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Neurology
FA complete review
| Question | Answer |
|---|---|
| List of Epilepsy drugs: | 1. Benzodiazepines 2. Carbamazepine 3. Ethosuximide 4. Gabapentin 5. Lamotrigine 6. Levetiracetam 7. Phenobarbital 8. Phenytoin, fosphenytoin 9. Tiagabine 10. Topiramate 11. Valproic acid 12. Vigabatrin |
| What is the main use for Benzodiazepines as an epileptic agent? | Acute status epilepticus |
| What is the mechanism of action of Benzodiazepines? | Increase GABA-A action |
| What epilepsy drugs can be used a secondary treatment of Eclampsia seizures? | Benzodiazepines |
| What are side effects associated with Benzodiazepines? | Sedation, tolerance, dependence, and respiratory depression |
| Which could be the most fatal or severe adverse effect of benzodiazepine overdose? | Respiration depression |
| Which epilepsy drug(s) MOA is to increase the actions GABA-A? | Benzodiazepines and Phenobarbital |
| What is the common use of Carbamazepine? | Treatment of Partial (focal) seizures |
| Which type of generalized seizures can be treated, not commonly, with Carbamazepine? | Tonic-clonic seizures |
| What is MOA of Carbamazepine? | Blocks Na+ channels |
| Which partial seizure medication MOA is to block the sodium cation channels? | Cabazempine |
| List of known adverse effects caused by Carbamazepine? | 1. Diplopia 2. Ataxia 3. Blood dyscrasias 4. Liver toxicity 5. Teratogénesis 6. Induction of CYP450 7. SIADH 8. Stevens-Johnson syndrome |
| What is a severe cutaneous adverse effect of Carbamazepine? | Stevens-Johnson syndrome |
| What are the common blood dyscrasias caused by Carbamazepine? | Agranulocytosis and Aplastic anemia |
| What are the teratogenic side effects associated with the use of Carbamazepine? | Cleft lip/palate, and spina bifida |
| A newborn with cleft lip and palate, and a turf of hair in the lower back, was born to a mother with seizure hx. What is the most likely medication she was taking? | Carbamazepine |
| SIADH, SJS, and blood dyscrasias are known adverse effects of whichani-epilepsy drug? | Carbamazepine |
| What is the 1st line of treatment for Trigeminal neuralgia? | Carbamazepine |
| Besides focal seizures, what non-epileptic condition , is primarily treated with Carbamazepine? | Trigeminal neuralgia |
| What is treated with Ethosuximide? | Absence seizure |
| What drug is used to treat Absence seizures? | Ethosuximide |
| MOA of Ethosuximide | Blocks thalamic T-type Ca+ channels |
| Which anti-epilepsy drug works by blocking the Thalamic T-Type calcium cation channels? | Ethosuximide |
| A list of all adverse effects associated with Ethosuximide: | EFGHIJ: - Ethosuximide causes: Fatigue, GI distress, Headache, Itching (and urticaria) Stevens-Johnson syndrome |
| Thalamic T-type Ca2+ channel blocker epileptic | Ethosuximide |
| Which the only type of seizures treated with Gabapentin? | Partial (focal) seizures |
| What is the MOA of Gabapentin? | Primarily inhibits high-voltage-activated Ca2+ channels |
| Which antiepileptic was designed as a GABA analog? | Gabapentin |
| Inhibition of high-voltage-activated Ca2+ channels. | MOA of Gabapentin |
| Common side effects of Gabapentin | Ataxia and Sedation |
| What are non-epileptic uses of Gabapentin? | 1. Peripheral neuropathy 2. Postherpetic neuralgia |
| Which seizures are can be treated with Lamotrigine? | Partial seizures, Tonic-Clonic , and Absence seizures |
| MOA of Lamotrigine | - Blocks voltage-gated Na+ channels - Inhibits the release of glutamate |
| What NT release is inhibited by Lamotrigine? | Glutamate |
| Which channels are blocked by Lamotrigine? | Voltage-gated Na+ channels |
| What is the associated adverse effect of Lamotrigine? | Stevens-Johnson syndrome |
| How is SJS prevented when taking Lamotrigine? | Slow titration |
| Blocks voltage-gated Na+ channels and inhibits release of glutamate. | Mechanism of action of Lamotrigine |
| What is a possible effect of the mode of action of Levetiracetam? | Possible modulation of GABA and glutamate release |
| What are the adverse effects seen with Levetiracetam? | 1. Neuropsychiatric symptoms 2. Fatigue, drowsiness, and headache |
| Personality changes are seen in a person taking which antiepileptic? | Levetiracetam |
| What is the mode of action of Phenobarbital? | Increase GABA-A action |
| Phenobarbital share MOA with which other type of epilepsy medications? | Benzodiazepines |
| First line of seizures (focal, tonic-clonic) in neonates is: | Phenobarbital |
| What is probably the most severe side effect of Phenobarbital? | Cardiorespiratory depression |
| As side effects, both, benzodiazepines and Phenobarbital have certain organ depressons: Benzodiazepines cause __________________ depression. Phenobarbital causes___________________ depression. | Respiratory Cardiorespiratory |
| Which epilepsy drugs are known to cause induction of the CYP450 system? | Carbamazepine and Phenobarbital |
| 1st line of treatment for recurrent status epilepticus | Phenytoin |
| What is Fosphenytoin? | Water-soluble phenytoin prodrug used only in hospitals for the treatment of epileptic seizures. |
| Water-soluble phenytoin | Fosphenytoin |
| What is the mode of action of Phenytoin? | Blocks Na+ channels |
| What is the order kinetics of Phenytoin? | Zero |
| Zero order kinetics antiepileptic | Phenytoin |
| Which antiepileptics or seizure medication block Na+ channels as mechanism of action? | Carbamazepine, Phenytoin, and Topiramate |
| Blocks Na+ channels; zero order kinetics | Phenytoin |
| List of side effects associated with Phenytoin: | 1. P450 system induction 2. Hirturism 3. Enlarged gums 4. Nystagmus 5. Yellow-brown skin 6. Teratogenicity 7. Osteopenia 8. Inhibited folate absorption 9. Neuropathy |
| What rare adverse effects associated with Phenytoin? | Stevens-Johnson syndrome, DRESS syndrome, and SLE-like syndrome |
| Phenytoin is used as 1st line of treatment of acute ----> | Tonic-clonic seizures |
| Phenytoin is used as 1st line of treatment for which recurrent seizure type? | Status epilepticus |
| What is the main agent used for prophylaxis of Status epilepticus? | Phenytoin |
| Phenytoin is an inducer or inhibitor of the CYP450 system? | Inducer |
| Which anti-seizure medication is associated with possible development of SLE-like syndrome? | Phenytoin |
| What is the teratogenic effect caused by Phenytoin? | Fetal hydantoin syndrome |
| A newborn with Fetal Hydantoin syndrome most likely had a mother that took what medication during pregnancy? | Phenytoin |
| What is the common use of Tiagabine? | Partial (focal ) seizures |
| What is the MOA of Tiagabine? | Increasing GABA by inhibiting reuptake |
| MOA- inhibiting GABA reuptake, thus increasing GABA concentration. | Tiagabine |
| What is the mode of action of Topiramate? | 1. Blocks Na+ channels 2. Increases GABA action |
| This drug works by blocking Na+ channels and also by increasing GABA action. | Topiramate |
| Valproic acid is 1st line of treatment of acute -----> | Tonic-clonic seizures |
| What are the two parts of the MOA of Valproic acid? | 1. Increases Na+ channel inactivation 2. Increases GABA concentration by inhibiting GABA transaminase |
| Which enzyme is inhibited by Valproic acid? | GABA Transaminase |
| How does Valproic acid increases the concentration of GABA? | Inhibiting GABA transaminase |
| Which antiepileptic works by Increasing the Na+ channel inactivation? | Valproic acid |
| What are the associated adverse effects of Topiramate? | Sedation, mental dulling, word-finding difficulty, kidney stones, weight loss, and glaucoma. |
| A person with a seizure disorder started to complain about not remembering or finding the right words. She had been an avid writer and poet. What medication can cause this? | Topiramate |
| What is an non-seizure related use of Topiramate? | Migraine prevention |
| What are other uses for Valproic acid, other than as antiepileptic medication? | Myoclonic seizures, bipolar disorder, migraine prophylaxis |
| What teratogenic defects are expected for the use of Valproic acid? | Neural tube defects |
| Irreversible GABA transaminase inhibitor. | Vigabatrin |
| What is the associated black box warning of Vigabatrin? | Permanent visual loss |
| Permanent visual loss may be caused by which antiepileptic? | Vigabatrin |
| What are some common Barbiturates? | Phenobarbital, pentobarbital, thiopental, and secobarbital |
| What is the detailed MOA of Barbiturates? | Facilitate GABA-A action by increasing DURATION of Cl- channel opening, thus decreasing neuron firing. |
| Barbiturates increase or decrease, duration of Cl- opening? | Increase |
| Which type of drugs are known to increase DURATION of Cl-channel opening? | Barbiturate |
| What is the result of the increased duration of Cl- channel opening by Barbiturates? | Facilitation of GABA-A action |
| What are the clinical uses for barbiturates? | Sedative for anxiety, seizures, insomnia, induction of anesthesia |
| Which barbiturate is used as to induce anesthesia? | Thiopental |
| Thiopental is a _____________________. | Barbiturate |
| Increase duration of Cl- channel opening | Barbiturate |
| Barbiturates are to be avoided in people with _________________. | Porphyria |
| A patient with a known porphyria should avoid which type of drugs? | Barbiturate |
| CNS depression by barbiturates can be exacerbated by: | Alcohol use |
| What is the overdose by Barbiturates treatment? | Supportive (assist respiration and maintain BP) |
| List of common Benzodiazepines: | Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam |
| What is the mechanism of action of Benzodiazepines? | Facilitate GABA-A action by increasing frequency of Cl- channel opening |
| Which, benzodiazepines or barbiturates, enhance GABA-A action, by increasing the frequency of Cl- channel opening? | Benzodiazepines |
| Most Benzodiazepines have: | Long half-lives and active metabolites |
| Which mnemonic may be used to remember those Benzodiazepines with SHORT half-lives? | ATOM |
| What does the mnemonic ATOM stands for? | Short half-life benzodiazepines Alprazolam, Triazolam, Oxazepam, Midazolam |
| What is a risk or adverse effect of short half-live benzodiazepines? | Higher addictive potential |
| Which drugs are known to increase the frequency of Cl- channel opening? | Benzodiazepines |
| What drugs and substances bind to GABA-A receptors? | Benzodiazepines, Barbiturates, and Alcohol |
| GABA-A receptor is a : | Ligand-gated Cl- channel |
| Why are Oxazepam, Temazepam, and Lorazepam used to treat alcohol withdrawal safer than other benzodiazepines? | Due to minimal first-pass metabolism |
| What are some important Nonbenzodiazepine hypnotics? | Zolpidem, Zaleplon, and esZopiclone |
| What is the MOA of nonbenzodiazepines hypnotics? | Act via BZ1, subtype of GABA receptor |
| What is the GABA subtype used by nonbenzodiazepine hypnotics? | BZ1 |
| Nonbenzodiazepine hypnotic effects are reversible with: | Flumazenil |
| Why are nonbenzodiazepines hypnotics used for sleep? | They affect less the sleep cycle as compared to Benzodiazepines |
| Clinical use for Zolpidem? | Insomnia |
| What is the mechanism of action of Suvorexant? | Orexin (hypocretin) receptor antagonist |
| Orexin receptor antagonist | Suvorexant |
| What is the clinical use for Suvorexant? | Insomnia |
| Suvorexant is contraindicated in patients with _________________. | Narcolepsy |
| What are conditions are have Suvorexant administration contraindicated? | 1. Narcolepsy 2. Liver disease 3. Strong CYP3A4 inhibitors |
| What is the MOA of Ramelteon? | Melatonin receptor agonist, binds MT1 and MT2 in suprachiasmatic nucleus. |
| Ramelteon binds to: | MT1 and MT2 in the Suprachiasmatic nucleus |
| What is the clinical use of Ramelteon? | Insomnia |
| What is the most common Triptan? | Sumatriptan |
| Common 5-HT 1B/1D agonist. | Sumatriptan |
| What is the MOA of Triptans? | Inhibit trigeminal nerve activation Prevent vasoactive peptide release Induce vasoconstriction |
| What is the clinical use for Triptans? | - Acute migraine - Cluster headache attacks |
| What some adverse effects of Triptan therapy? | Coronary vasospasm, mild paresthesia, and serotonin syndrome |
| Which type of patients are at higher risk of coronary vasospasms due to Triptan intake? | CAD and/or Prinzmetal angina paites |
| When is it possible to develop serotonin syndrome with the use of Triptans? | When used in combination with other 5-HT agonists. |
| List of Na+ channel blocker epileptics: | 1. Carbamazepine 2. Fosphenytoin 3. Lamotrigine 4. Phenytoin 5. Topiramate 6. Valproic acid |
| SV2A receptor blocker (antiepileptic). | Levetiracetam |
| List of GABA-A agonists: | 1. Benzodiazepines 2. Topiramate 3. Phenobarbital 4. Propofol |
| Which epileptics are Ca2+ channel blockers? | Ethosuximide and Gabapentin |
| GABA reuptake inhibitor epileptic | Tiagabine |
| Which antiepileptics are GABA transaminase inhibitors? | Valproic acid and Vigabatrin |
| Parkinsonism is due to: | Loss of dopaminergic neurons and excess cholinergic activity |
| Parkinson drugs are categorized in strategies, which are: | 1. Dopamine agonists 2. Increase dopamine availability 3. Increase L-DOPA availability 4. Prevent dopamine breakdown 5. Curb excess cholinergic activity |
| The Dopamine agonists used for Parkinson disease are divided into: | 1. Ergot and, 2. Non-ergot |
| Which type of Dopamine agonist are preferred in treating of Parkinson disease? | Non-ergot |
| Which is the Ergot dopamine agonist used for Parkinson disease? | Bromocriptine |
| What are the Non-ergot dopamine agonists in Parkinson disease treatment? | Pramipexole and Ropinirole |
| Ropinirole and Pramipexole are: | Non-ergot Dopamine agonists |
| What are symptoms are included in Non-ergot dopamine agonist toxicity? | Impulse control disorder, postural hypotension, and hallucinations/confusion. |
| A person with a movement disorder is treated with a commonly used drug for such, but later develops a gambling problem. What are the more likely drugs given? | Pramipexole and Ropinirole |
| Parkinson drug that works by increasing dopamine availability. | Amantadine |
| How does Amantadine increase dopamine availability? | Increase dopamine release and decrease dopamine uptake |
| What are signs of Amantadine toxicity? | Ataxia and livedo reticularis |
| What is the mode of action of drugs that increase L-DOPA availability? | Prevent peripheral (pre-BBB) L-DOPA degradation, which increases the L-DOPA entering the CNS ---> increase central L-DOPA available for conversion to dopamine |
| What are the main drugs that increase L-DOPA availability? | Levodopa, Carbidopa, and Entacapone |
| Levodopa and Entacapone --> | Increase L-DOPA availability |
| MOA of Carbidopa: | Blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase |
| Which enzyme is inhibited by Carbidopa? | DOPA decarboxylase |
| How does Entacapone prevent peripheral L-DOPA degradation? | Inhibiting COMT |
| Which drug is used in conjunction with Entacapone? | Levodopa |
| Which enzyme is inhibited by Entacapone? | COMT |
| Peripheral COMT is inhibited by ____________________. | Entacapone |
| Entacapone prevents the degradation of L-DOPA into: | 3-O-methyldopa (3-OMD) |
| A reduction in 3-OMD levels might be seen with the use of which Parkinson disease drug? | Entacapone |
| Agents that inhibit or prevent dopamine breakdown, work pre- or post-BBB? | Post-BBB |
| Which are the two types of agents that prevent dopamine breakdown post-BBB? | MAO-B inhibitors and Central COMT inhibitor |
| A central COMT inhibitor means: | It prevents that breakdown of Dopamine post BBB into 3-methoxytyramine (3-MT) |
| Central or Peripheral COMT inhibitors prevent conversion of dopamine into 3-MT? | Central COMT inhibitors |
| Which is a common central COMT inhibitor used in Parkinson disease? | Entacapone |
| What is the overall purpose of Selegiline and Rasagiline? | Prevent dopamine breakdown post-BBB |
| How does Selegiline prevent Dopamine breakdown? | Block conversion of dopamine into DOPAC by selectively inhibiting MAO-B. |
| Which enzyme is selectively inhibited by selegiline and rasagiline, in the treatment of Parkinson disease? | MAO-B |
| How do MAO-B inhibitors help in treating Parkinson disease symptoms? | Prevent dopamine breakdown post-BBB |
| Which Parkinson drugs are known to curb excess cholinergic activity? | Benztropine, trihexyphenidyl |
| Benztropine and Trihexyphenidyl are ________________________. | Antimuscarinics |
| How do antimuscarinics help in Parkinson symptoms relief? | Improve tremors and rigidity but has little to no effect in bradykinesia |
| What is intended to "better" by the use of Benztropine in Parkinson disease? | Tremor and rigidity |
| What enzyme in the CNS converts L-DOPA into dopamine? | DOPA decarboxylase |
| What long term adverse effects of Levodopa/Carbidopa administration? | Dyskinesia following administration ("on-off" phenomenon), akinesia between doses |
| What is the function of MAO-B? | Metabolize dopamine |
| What is a possible adverse effect of Selegiline and Rasagiline? | May enhance adverse effects of L-DOPA |
| Tetrabenazine and Reserpine clinical uses are: | Huntington chorea and Tardive dyskinesia |
| MOA of Tetrabenazine and reserpine: | Inhibit vesicular monoamine transporter (VMAT) dopamine |
| What is the result of the inhibition of VMAT dopamine? | Decrease vesicle packaging and release |
| Which drugs may cause decrease vesicle packaging and release due to VMAT dopamine inhibition? | Tetrabenazine and reserpine |
| What is the use for Riluzole? | ALS |
| MOA of Riluzole? | Decreased neuron glutamate excitotoxicity |
| What medication is used to treat Lou Gehrig disease? | Riluzole |
| List of common Alzheimer drugs: | 1. Memantine 2. Donepezil, Rivastigmine, and Galantamine |
| What is the mechanism of action of Memantine? | NMDA receptor antagonist |
| NMDA receptor antagonist used to treat Alzheimer? | Memantine |
| What are the two types of Alzheimer disease drugs? | 1. NMDA receptor antagonists 2. AChE inhibitors |
| CNS drugs must be: | 1. Lipid soluble, in order to cross the BBB, or, 2. Actively transported across the BBB |
| Drugs with low solubility in blood = | Rapid induction and recovery times |
| Drugs with high solubility in lipids = | Increase in potency |
| 1 -------------- = MAC | Potency |
| What does MAC in anesthetics stand for? | Minimal Alveolar Concentration |
| What is MAC? | Minimal Alveolar Concentration required to prevent 50% of subjects from moving in response to noxious stimulus |
| Which anesthetic is an example of decreased blood and lipid solubility? | Nitrous oxide (N2O) |
| Halothane, propofol, and thiopental have: | Increase lipid and blood solubility, and thus high potency and slow induction. |
| Which anesthetics have high potency and slow induction? | Halothane, propofol, and thiopental |
| What are inhaled anesthetics examples? | Desflurane, halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, and N2O. |
| What are the physiological effects of inhaled anesthetics? | Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow. |
| Halothane adverse effect | Hepatotoxicity |
| What adverse effect is seen with Methoxyflurane? | Nephrotoxicity |
| Which inhaled anesthetics are proconvulsant if toxic levels are reached? | Enflurane and Epileptogenic |
| What is a possible adverse effect of the use of N2O as an inhaled anesthetic? | Expansion of trapped gas in a body cavity |
| What is Malignant hyperthermia? | Rare, life-threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions. |
| What are the genetic principles associated with Malignant hyperthermia? | The susceptibility of Malignant hyperthermia, is often inherited as AD with variable penetrance. |
| What type of mutations induced or cause increase levels of Ca2+ release from Sarcoplasmic Reticulum? | Voltage-sensitive Ryanodine receptor (RYR1 gene) mutations |
| A mutated RYR1 gene causes --> | Increase release of Ca2+ from SR |
| A mutated RYR1 gene may increase the subject's susceptibility to develop which anesthetic-induced emergency? | Malignant hyperthermia |
| What is the treatment for Malignant hyperthermia? | Dantrolene |
| Dantrolene is used to treat: | Malignant hyperthermia |
| A person under surgery spikes fever > 104 F and has muscle twitches, is going to be treated with: | Dantrolene |
| What is the MOA of Dantrolene? | Ryanodine receptor antagonist |
| Ryanodine receptor antagonist | Dantrolene |
| Is malignant hyperthermia associated with Intravenous (IV) or Inhaled anesthetics? | Inhaled anesthetics |
| What are the common Intravenous anesthetics? | Thiopental, Midazolam, Propofol, and Ketamine |
| Thiopental is a _______________________ anesthetic. | Intravenous anesthetic |
| Which IV anesthetic is a barbiturate? | Thiopental |
| Which IV anesthetic is a Benzodiazepine? | Midazolam |
| NMDA receptor antagonist IV anesthetic | Ketamine |
| What is the mode of action of Propofol? | Pontentiates GABA-A |
| Which GABA receptor type, is targeted by IV anesthetics, A or B? | GABA-A |
| Thiopental is used for long or short, surgical procedures? | Short |
| How is the effect of Thiopental quickly terminated? | Rapid redistribution into tissue and fat |
| Cerebral blood flow with Thiopental is increased or decreased? | Decreased |
| Which IV anesthetic decreases cerebral blood flow? | Thiopental |
| What are severe or significant adverse effects of IV anesthetic, Midazolam? | Severe postoperative respiratory depression, hypotension, and anterograde amnesia |
| What kind of amnesia may be provoked as adverse effect of Midazolam? | Anterograde amnesia |
| What are the common uses for Midazolam? | 1. Procedural sedation (endoscopy) 2. Anesthesia induction |
| Which IV anesthetic may be used in the ICU setting? | Propofol |
| Which IV anesthetic is used to rapid anesthesia induction? | Propofol |
| MOA of Ketamine | NMDA receptor antagonist |
| What are the anesthetic uses of Ketamine? | 1. Dissociative anesthesia 2. Sympathomimetic |
| Increased or Decreased. Cerebral blood flow with Ketamine? | Increased |
| What is a possible emergence reaction to Ketamine anesthesia? | Disorientation, hallucination, and vivid dreams |
| Which IV anesthetic is known to increase the cerebral blood flow? | Ketamine |
| What are the two types of local anesthetics? | Esters and Amides |
| List of Ester Local anesthetics: | Procaine, Tetracaine, Benzocaine, and Chloroprocaine |
| List of Amide Local anesthetics: | Lidocaine, Mepivacaine, Bupivacaine, and Ropivacaine |
| What is the MOA of Local anesthetics? | Block Na+ channels by dingin to specific receptors on inner portion of channels |
| On which neuros a local anesthetics the most effective? | Rapidly firing neurons |
| What can be given along with a local anesthetic to enhance the local action? | Epinephrine |
| How does the co administration of local anesthetic + epinephrine help to enhance effect? | Decrease bleeding, increase anesthesia by systemic concentration |
| What is the order of loss when a local anesthetic is administered? | Pain --> Temperature --> Touch --> Pressure |
| What is the first scenario that is loss or blocked by local anaesthetics? | Pain |
| What type of anesthetics are used for spinal anesthesia? | Local anesthetics |
| What is an bupivacaine specific adverse effect? | Cardiovascular toxicity |
| Which local anesthetic is known to cause Methemoglobinemia? | Benzocaine |
| Selective for Nm nicotinic receptors at NMJ but not autonomic Nn receptors. | Neuromuscular blocking drugs |
| Neuromuscular blocking drugs are divided into ________________ and _________________. | Depolarizing and Non-depolarizing |
| What are complications of Depolarizing neuromuscular blocking drugs? | Hypercalcemia, hyperkalemia, and malignant hyperthermia. |
| What is the most common Depolarizing neuromuscular blocking agent? | Succinylcholine |
| Succinylcholine is a strong___________________________________. | ACh receptor agonist |
| MOA of Succinylcholine: | ACh receptor agonist that produces sustained depolarizing and prevents muscle contraction |
| The reversal of blockade caused by Succinylcholine is reversed in how many phases? | 2 phases |
| Which phase pf Succinylcholine blockade is definced a prolonged depolarization? | Phase I |
| Phase II of Succinylcholine blocked is: | Repolarized but blocked; ACh receptors are available, but desentized |
| What some common Nondepolarizing Neuromuscular blocking drugs? | Atracurium, Cisatracurium, Pancuronium, and Vecuronium |
| What is MOA of Non-depoloarizing nuromulsclar blcking agents? | Competitive with ACh for receptors |
| What are some drugs used to reverse the Nondepolarizing neuromuscular drug blockade? | Neostigmine and Edrophonium |
| Why is neostigmine must be given with atropine or glycopyrrolate? | To prevent muscarinic effects such as bradycardia |
| Which drugs must be administered with Neostigmine in order to prevent muscarinic effects? | Atropine or Glycopyrrolate |
| _______________________, prevents the release of Ca2+ from the SR of skeletal muscle by binding to the ryanodine receptor. | Dantrolene |
| What are the two clinical sues for Dantrolene? | 1. Malignant hyperthermia, 2. Neuroleptic malignant syndrome |
| What is a severe toxicity of antipsychotic drugs treated with Dantrolene? | Neuroleptic malignant syndrome |
| MOA of Baclofen: | Skeletal muscle relaxant. GABA-B receptor agonist in spinal cord |
| What is the clinical use for Baclofen? | Muscle spasticity, dystonia, and multiple sclerosis |
| GABA-B receptor agonist in spinal cord | Baclofen |
| Which GABA receptor is used by Baclofen? | GABA-B |
| Skeletal muscle relaxant that acts within CNS | Cyclobenzaprine |
| What is the clinical use for Cyclobenzaprine? | Muscle spasms |
| List of antispasmodics or Spasmolytics: | - Baclofen - Cyclobenzaprine - Dantrolene - Tizanidine |
| What is the mechanism of action of Tizanidine? | a-2 agonist, acts centrally |
| What conditions which produce spams, are treated with Tizanidine? | Muscle spasticity, multiple sclerosis, ALS, and cerebral palsy |
| Which spasmolytics work centrally? | Cyclobenzaprine and Tizanidine |
| Back muscle pain/spasm is commonly treated with: | Baclofen |
| On which opioid receptors does opioid analgesics work? | u, g, and k |
| Which is the B-endorphin opioid receptor? | u |
| What is mechanism of action of opioid analgesics? | Agonists at opioid receptors to modulate synaptic transmission, which leads to closure of presynaptic Ca2+ channels and open K+ channels leading to a decrease in synaptic transmission. |
| What are common Opioid analgesics Full agonists? | Morphine, heroin, meperidine, methadone, codeine, and fentanyl |
| Which is a common Opioid analgesics Partial agonist? | Buprenorphine |
| Mixed agonist/antagonist opioid analgesics? | Nalbuphine, pentazocine, and butorphanol |
| Common Opioid analgesics antagonists | Naloxone, naltrexone, and methylnaltrexone |
| Clinical uses for Opioid analgesics: | - Moderate to severe or refractory pain - Diarrhea - Acute pulmonary edema - Maintenance programs for heroin addicts |
| Which opioid analgesics are used for maintenance programs for heroin addicts? | Methadone, buprenorphine + naloxone |
| What are some adverse effects of opioid analgesics? | N/V, pruritus, addiction, respiratory depression, constipation, sphincter of Oddi spasms, miosis, additive CNS depression with other drugs |
| What is used to treat Opioid analgesic toxicity? | Naloxone |
| What is used to treat relapse of a detoxified Opioid analgesic? | Naltrexone |
| What are the two common Mixed and antagonist opioid analgesics? | Pentazocine and Butorphanol |
| What is the mechanism of action of PENTAZOCINE? | 1. k-opioid receptor agonist and , - u-opioid receptor weak antagonist or partial agonist |
| What is the clinical use for Pentazocine? | Analgesia for moderate to severe pain |
| What is a severe adverse effect or result from the use of Pentazocine? | Opioid withdrawal symptoms if patient is also taking full opioid agonist. |
| What are the mechanisms of action of Butorphanol? | 1. k-opioid receptor agonist and, 2. u-opioid receptor partial agonist |
| What are common instances in which Butorphanol is used? | In severe pain such as migraines and labor. |
| What is the MOA of Tramadol? | Very weak opioid agonist |
| Which opioid analgesic is known to inhibit the reuptake of norepinephrine and epinephrine? | Tramadol |
| Very weak opioid agonist | Tramadol |
| What is the use for Tramadol? | Chronic pain |
| What are two specifics adverse effects of Tramadol? | - Decreases seizure threshold - Serotonin syndrome |
| What is the purpose of Glaucoma therapy? | Decreases IOP via decreased amount of aqueous humor |
| How is the aqueous humor decreased in Glaucoma therapy? | Inhibition of synthesis/ secretion or increase drainage of aqueous humor. |
| Which drug classes are in Glaucoma therapy are used to decrease aqueous humor synthesis? | B-blockers, a-agonists, and diuretics. |
| Which beta-blockers are used in Glaucoma? | Timolol, betaxolol, and carteolol |
| How do beta-blockers mechanism of action work for Glaucoma treatment? | Decreases aqueous humor synthesis |
| Which are common alpha-agonists used in Glaucoma therapy? | Epinephrine, apraclonidine, and Brimonidine |
| Decreases aqueous humor synthesis via vasoconstriction. | Epinephrine |
| Which a-agonist is contraindicated in treatment of closed-angle glaucoma? | Epinephrine |
| What is an adverse effect of Epinephrine in association of Glaucoma treatment? | Mydriasis |
| What are the adverse effects seen with Apraclonidine and Brimonidine, as they treat glaucoma? | Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, and ocular pruritus. |
| Which a common diuretic used for Glaucoma? | Acetazolamide |
| How does Acetazolamide help in treating glaucoma? | Decreases aqueous humor synthesis via inhibiting carbonic anhydrase |
| Which common prostaglandins are used in treating Glaucoma? | Bimatoprost, and Latanoprost |
| How do Prostaglandins MOA contribute to Glaucoma treatment? | 1. Increase outflow of aqueous humor via a decreaed resistace of flow through uveoscleral pathway |
| What are adverse effects of Glaucoma treating Prostaglandins? | 1. Darkens color of iris (browning) 2. Eyelash growth |
| Direct Cholinomimetics that are used to treat Glaucoma: | Pilocarpine and Carbachol |
| Pilocarpine and Carbachol are: | Direct cholinomimetics that are used to treat glaucoma |
| Which receptor are the cholinomimetics use to treat glaucoma? | M3 |
| Which are the Indirect cholinomimetics that treat glaucoma? | Physostigmine and Echothiophate |
| MOA of Cholinomimetics treating Glaucoma: | Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork |
| Why is Pilocarpine widely used in Closed-angle glaucoma? | Very effective at opening meshwork into canal of Schlemm |
| Which cholinomimetic is very effective in treatment of Closed-angle glaucoma? | Pilocarpine |
| What are the two main adverse effects of Glaucoma-treating cholinomimetics? | Miosis and cyclospasm |
| What causes the cyclospasms when using Cholinomimetics to treat glaucoma? | Contraction of ciliary muscle |
| Which muscle is stimulated to contract in order for cholinomimetics to treat Glaucoma? | Ciliary muscle |
| Which Glaucoma therapy drug classes work by increasing the outflow of aqueous humor? | Prostaglandins and Cholinomimetics (M3) |
| List of structures that are located in the Anterior segment of the eye: | 1. Ciliary body 2. Zonular fibers 3. Cornea 4. Iris 5. Pupil 6. Lens 7. Anterior chamber 8. Posterior chamber |
| What structure covers the whole eye? | Sclera |
| List of structures that are in the Posterior segment of the eye? | 1. Sclera 2. Choroid 3. Retina 4. Fovea 5. Optic disc 6. Central retinal artery and vein 7. Optic nerve 8. Vitreous chamber |
| Anterior chamber + Posterior chamber = | Anterior segment |
| In the posterior segment of the eye, what is the outermost structure? | Sclera |
| In the posterior segment of the eye, what is the middle and inner structures? | - Choroid (middle) - Retina (inner) |
| The iris, is the _______________ structure of the anterior segment of the eye. | Middle |
| What is Conjunctivitis? | Inflammation of the conjunctiva causing red eye |
| Clinical presentation of Allergic Conjunctivitis? | Itchy eyes, and bilateral |
| What are the clinical features of Bacterial conjunctivitis? | Pus; treatment with antibiotics |
| Pus in conjunctivitis most likely points to allergic, bacterial, or viral etiology? | Bacterial |
| What are the 3 main etiologies for Conjunctivitis? | Allergic, bacterial, and viral |
| What the most common type or etiology for Conjunctivitis? | Viral conjunctivitis |
| What is the most common viral pathogen that causes conjunctivitis? | Adenovirus |
| Clinical profile of viral conjunctivitis: | Sparse mucous discharge, swollen preauricular node; self-resolving |
| Which type of conjunctivitis is often seen with preauricular node involvement? | Viral conjunctivitis |
| List of REFRACTIVE errors: | 1. Hyperopia 2. Myopia 3. Astigmatism 4. Presbyopia |
| What do Refractive errors mean? | Means that the shape of your eye does not bend light correctly, resulting in a blurred image |
| What is a common cause of impaired vision, but corrected with eyeglasses? | Refractive errors |
| What is the common name for Hyperopia? | Farsightedness |
| What is the cause of Hyperopia? | Eye too short for refractive power of cornea and lens which causes the light to focus behind the retina. |
| Where do light focuses in Hyperopia, in front or behind the retina? | Behind retina |
| What type of lenses are used to correct hyperopia? | Convex (converging) lenses |
| Convex (converging) lenses are used to correct what type of refractive error? | Hyperopia |
| Eye to short or small for refractive power of cornea and lens. | Hyperopia |
| Light focused behind the retina. Dx? | Hyperopia |
| What is the common name for Myopia? | Nearsightedness |
| Nearsightedness = | Myopia |
| Farsightedness = | Hyperopia |
| What is the problem with Myopia? | Eye too long for refractive power of cornea and lens leading to light focused in front of retina |
| If the light is focused in front of retina. Dx? | Myopia |
| In myopia, the light is focused in front or behind the retina? | In front retina |
| Eye to long for refractive power of cornea and lens. | Myopia |
| What type of lenses are used to correct Myopia? | Concave (diverging) lens |
| A concave (diverging) lens is used to correct which refractive error? | Myopia |
| Abnormal curvature of the cornea. Dx? | Astigmatism |
| What is the result of abnormal curvature of the cornea? | Different refractive power at different axes |
| Which refractive error (condition) is characterized by having different refractive powers at different angles? | Astigmatism |
| What type of lens are used in Astigmatism? | Cylindrical lens |
| Cylindrical lens correct which refractive error? | Astigmatism |
| What is astigmatism? | Abnormal curvature of cornea leading to different refractory power at different angles. |
| A person with Astigmatism should buy eyeglasses with what type of lens? | Cylindrical lens |
| What is Presbyopia? | Aging-related impaired accommodation, primarily due to decreased lens elasticity, changes in lens curvature, decreased strength of ciliary muscle |
| Which is the age related refractive error? | Presbyopia |
| What type of glasses are used in Presbyopia patients? | "Reading glasses" (magnifiers) |
| What refractive error is due to impaired accommodation of the eyesight? | Presbyopia |
| 77 year old man with difficulty focusing on near objects. Dx? | Presbyopia |
| Which muscle usually looses its normal strength in Presbyopia? | Ciliary muscle |
| Eye inspection reveal a decrease in lens elasticity, changes in curvature of lens, and a weakening ciliary muscle. What is the most likely refractive error? | Presbyopia |
| Aging-related impaired accommodation. Dx? | Presbyopia |
| Common vision condition in which you can see distant objects clearly, but objects nearby may be blurry | Hyperopia |
| A "farsighted" describes his/her sight as: | Can see objects far away, but see blurry objects nearby |
| A "nearsighted" person would say that his/her vision is: | Can see objects nearby, but sees blurry or difficulty when objects are far away. |
| A person with Myopia cannot see objects that are __________. | Far away |
| A person with Hyperopia cannot see objects that are ____________. | Nearby |
| What is a Cataract? | Painless, often bilateral, opacification of lens, often resulting in glare and decreased vision, especially at night |
| Painless, bilateral, opacification of the lens leading to poor vision at night. Dx? | Cataracts |
| What known risk factor for Cataracts? | Increasing age Smoking Excessive alcohol use Excessive sunlight Prolonged corticosteroid use Diabetes mellitus |
| Which "blood sugar" condition is associated with development of cataracts? | Diabetes mellitus |
| List of congenital risk factors/ conditions that increase chances of developing Cataracts: | 1. Classic Galactosemia 2. Galactokinase deficiency 3. Trisomies (13, 18, 21) 4. TORCHES infections (rubella) 5. Marfan syndrome 6. Alport syndrome 7. Myotonic dystrophy 8. Neurofibromatosis 2 |
| Which type of NF is associated with Cataracts? | Neurofibromatosis 2 |
| Which TORCHES infection is especially associated with development of cataracts? | Rubella |
| Which saccharide metabolic conditions are associated with development fo Cataracts? | Galactose metabolism |
| Which canal is used by the Aqueous humor in Trabecular outflow pathway? | Canal of Schlemm |
| What type of medication is used to increase the Trabecular outflow? | M3 agonist |
| Drainage of aqueous humor into uvea and sclera is known as: | Uveoscleral outflow |
| What produces the Aqueous humor? | Nonpigmented epithelium on ciliary body |
| Which type of drugs or medications are used to decrease the production of Aqueous humor? | B-blockers, a2-agonists, and carbonic anhydrase inhibitors |
| What is the role of Muscular fibers in ciliary body? | Affect lens shape for accomodation |
| What eyesight function can be deficient in case of damage to the muscular fibers in ciliary body? | Accomodation |
| What is Glaucoma? | Optic disc atrophy with characteristic cupping, usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated |
| What is the ultimate purpose of Glaucoma treatment? | Lowering IOP with medications or surgically |
| What is "cupping" when used in association with Glaucoma? | Thinning of outer rim of optic nerve head versus normal |
| Thinning of outer rim of optic disc and increased IOP. Dx? | Glaucoma |
| What are the types of Glaucoma? | 1. Open-angle glaucoma 2. Closed- or Narrow-angle glaucoma |
| What is the main associated in develop of Open-angle glaucoma? | Increasing age, African-American, and family history |
| Which type of Glaucoma is most common in the USA? | Open-angle glaucoma |
| What is the cause of Secondary Open-angle glaucoma? | Due to blocked Trabecular meshwork from WBCs, RBCs, and/or retinal elements |
| What condition can lead to secondary open-angle glaucoma due to blockage of meshworkby WBCss? | Uveitis |
| What is a possible consequence or resulting pathology of a vitreous hemorrhage? | Secondary Open-angle glaucoma |
| Retinal detachment can led to what type of Glaucoma? | Secondary Open-angle glaucoma |
| Blockage of trabecular meshwork | General cause of Secondary Open-angle glaucoma |
| What is primary Closed (narrow)-angle glaucoma? | Enlargement or anterior movement of lens against central iris leading to obstruction of normal aqueous flow through pupil. |
| What is the result of the blockage of aqueous humor flow in primary Closed angle glaucoma? | Fluid builds up behind iris, pushing peripheral iris against cornea and impeding aqueous flow through trabecular meshwork |
| What part of the eye is either enlarged or moved anteriorly that lead to the development of Primary Closed (Narrow) angle glaucoma? | Lens against central iris |
| What is the cause for Secondary Closed (Narrow) angle glaucoma? | Hypoxia from disease induces vasoproliferative in iris that contacts angle |
| How does DM can cause Narrow-angle glaucoma? | It causes hypoxia, which as result induces the vasoproliferation in the iris that contracts the angle. |
| What is "Chronic closure" in Closed-angle glaucoma referred to? | Often asymptomatic with damage to optic nerve and peripheral vision |
| Which is a true ophthalmic emergency, acute or chronic closure, in Closed-angle glaucoma? | Acute closure |
| What are the symptoms seen in Acute closure in Closed angle glaucoma? | Very painful, red eye, sudden vision loss, ahos around lights, frontal headache, fixed and mid-dilated pupil. |
| What type of agents are contraindicated in Acute closure? | Mydriatic agents |
| What causes Acute closure in Closed angle Glaucoma? | Elevated IOP pushes iris foard leading to angle to close up abruptly. |
| What condition is suspected in diabetic mellitus patient, that has suddenly lost vision in right eye, complains of a headache, and indicates alot of pain in the right eye? | Acute closure in Closed angle glaucoma |
| What is Uveitis? | Inflammation of the uvea |
| What determines the specific name for uveitis type? | Location within affected eye |
| What are the types of uveitis? | Anterior uveitis, iritis, and posterior uveitis. |
| What is hypopyon? | Accumulation of pus in anterior chamber |
| What ocular condition is associated with Hypopyon? | Uveitis |
| What are associated symptoms along with Uveitis? | Hypopyon and conjunctival redness |
| What are common systemic inflammatory disorders associated with Uveitis? | Sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27-associated conditions. |
| What is and causes Age-related macular degeneration? | Degeneration of macula (central ara of retina), and causes distortion and eventual loss of central vision. |
| What causes loss of central vision in Age-related macular degeneration? | Scotomas |
| What are the two types of age-related macular degeneration? | Dry and Wet |
| Description of Dry macular degeneration due to age. | Deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium with gradual decreaes in vision |
| Non-exudative macular degeneration is another way to refer to: | Dry macular degeneration |
| What the simpler form to refer to Exudative age-related macular degeneration? | Wet macular degeneration |
| Rapid loss of vision due to bleeding secondary to choroidal neovascularization. | Wet macular degeneration |
| What is the treatment to prevent progression of age-related dry macular degeneration? | Multivitamins and antioxidant supplements |
| What is used to treat Age-related wet macular degeneration? | Anti-VEGF injections |
| What are some examples of anti-VEGF injections? | Bevacizumab and Ranibizumab |
| What is retinal damage due to chronic hyperglycemia? | Diabetic retinopathy |
| Diabetic retinopathy has two forms: | 1. Nonproliferative 2. Proliferative |
| How does Nonproliferative Diabetic retinopathy develops? | Due to damaged capillaries leak blood leading to lipids and fluid seep into retina causing hemorrhages and macular edema |
| What is the best treatment and/or management for Nonproliferative Diabetic retinopathy? | Blood sugar control |
| What is the result of the damaged capillaries in nonproliferative diabetic retinopathy? | Leak blood which lead to lipids and fluids to reach the retina causing hemorrhages and macular edema |
| What causes Proliferative Diabetic retinopathy? | Chronic hypoxia |
| Chronic hypoxia is the major cause for which type of Diabetic retinopathy? | Proliferative Diabetic retinopathy |
| What is the result of chronic hypoxia causing proliferative diabetic retinopathy? | New blood vessel formation with resultant traction on retina |
| What is the treatment for proliferative diabetic retinopathy? | Peripheral retinal photocoagulation, surgery, and anti-VEGF. |
| Which condition is known to be treated with Peripheral Retinal Photocoagulation? | Proliferative Diabetic retinopathy |
| Retinal damage due to chronic uncontrolled HTN | Hypertensive retinopathy |
| What ophthalmologic condition is associated with Flame-shaped retinal hemorrhages? | Hypertensive retinopathy |
| Clinical features of Hypertensive Retinopathy | 1. Flame-shaped retinal hemorrhages 2. Arteriovenous nicking 3. Microaneurysms 4. Macular star 5. Cotton-wool spots |
| Cotton-wool spots + Macular star + Flamed-shaped retinal hemorrhages. Dx? | Hypertensive retinopathy |
| What associated symptom if present in Hypertensive retinopathy, requires immediate lowering of the blood pressure? | Papilledema |
| What conditions are often associated with Hypertensive retinopathy? | 1. Increase risk of stroke 2. CAD 3. Kidney disease |
| A person with BP 190/112, that has not visited a physician in 20 years, and indicates some problems with sight. Dx? | Hypertensive retinopathy |
| Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis. | Retinal vein occlusion |
| "blood and thunder appearance" in fundoscopy is often used in describing what ophthalmologic pathology? | Retinal vein occlusion |
| What is a more common way to refer to the retinal hemorrhage and venous engorgement seen in retinal vein occlusion? | "blood and thunder appearance" |
| What are the clinical features of Retinal vein occlusion? | 1. Retinal hemorrhage and vein engorgement 2. Edema in affected area |
| What is Retinal vein occlusion? | The blockage of central or branch of the Retinal vein due to the compression from nearby arterial atherosclerosis. |
| What is the most common cause of blocking the central retinal vein or a branch of such vein? | Compression by nearby arterial atherosclerosis |
| What is Retinal detachment? | Separation of neurosensory layer of retina from outermost pigmented epithelium leading to degeneration of photoreceptors and eventually vision loss |
| Which parts of the eye anatomy are "detached" in Retinal detachment? | The neurosensory layer of the retina, form the outermost pigmented epithelium |
| What is degenerated by the detachment of the retina layer and the outermost pigmented epithelium, in Reitan detachment? | Photoreceptors |
| What is the results or degeneration of photoreceptors in Retinal detachment? | Vision loss |
| What are some secondary etiologies for Retinal detachment? | - Retinal breaks - Diabetic tration - Inflammatory effusions |
| What are the fundoscopic findings in Retinal detachment? | Crinkling of retinal tissue and changes in vessel direction |
| Retinal breaks, which cause retinal detachment are more common in: | Patients with high myopia and/or history of head trauma |
| What are common used words to describe the Posterior vitreous detachment which often precedes Retinal detachment? | "Flashes" and "floaters" |
| What are key features or symptoms seen in Retinal detachment? | 1. Posterior vitreous detachment 2. Monocular loss of vision |
| How is the loss in vision in Retinal detachment described? | - Monocular loss - Like "curtain drawn down" |
| A patient complains of unable to see from right eye, and describes it as a "curtain been drawn down" and indicate prior to losing vision, he could "feel and see" floaters in the right eye. Dx? | Right eye Retinal detachment |
| How is the progress and vision loss in Central Retinal artery occlusion? | Acute, painless monocular vision loss |
| Retinal cloudy with attenuated vessels and "cherry-red" spot at fovea. Dx? | Central Retinal artery occlusion |
| Which is most common, Central Retinal artery or Central Retinal vein, occlusion? | Central Retinal vein occlusion |
| Which is more severe, Central Retinal artery or Central Retinal vein, occlusion? | Central Retinal artery occlusion |
| Which most likely to occur, an occlusion of the Central Retinal vein or Branch Retinal vein? | Branch Retinal vein occlusion |
| In which Central Retinal vessel occlusion, is a "cherry-red" spot at the fovea seen? | Central Retinal artery occlusion |
| What is the first thing to evaluate in cases of suspected Central Retinal artery occlusion? | Embolic source |
| What are common conditions that predispose for Central Retinal artery occlusion? | Embolic-inducing conditions such as: Carotid Artery atherosclerosis, Cardiac vegetations, and PFO. |
| Clinical presentation of Central Retinal artery occlusion (CRAO)? | - Sudden, profound vision loss - Painless - Monocular |
| Clinical presentation of Central Retinal vein occlusion (CRVO)? | - Blurred vision to sudden vision loss - Painless - Monocular |
| Is vision loss in CRAO and CRVO, painful or painless? | Painless |
| Common etiologies for CRAO: | 1. Embolism 2. Vasculitis 3. Vasospasm 4. Sickle cell 5. Trauma 6. Glaucoma |
| Common etiologies for CRVO: | Hypercoagulable states, stokes, glaucoma, and compression of vein by thyroid or ocular tumors |
| Optic disc edema + Diffuse retinal hemorrhages. Dx? | Central Retinal vein occlusion |
| Retinal pallor, Macular "cherry-red" spot + Afferent pupillary defect. Dx? | Central Retinal artery occlusion |
| What is inherited retinal degeneration disorder? | Retinitis pigmentosa |
| What is Retinitis pigmentosa? | Inherited retinal degeneration. - Painless, progressive vision loss beginning with night blindness. |
| Progressive, painless vision loss that starts by losing vision at night. Dx? | Retinitis pigmentosa |
| What are the features findings in Macular of Retinitis pigmentosa? | Bone spicule-shaped deposits around macula |
| Finding; Bone spicule-shaped deposits around macula. Dx? | Retinitis pigmentosa |
| Which cells are affected first in Retinitis pigmentosa? | Rods |
| Early in Retinitis pigmentosa, are the rods or cones affected first? | Rods |
| What is the definition for Retinitis? | Retinal edema and necrosis leading to scar |
| What are the common viral pathogens that cause Retinitis? | CMV, HSV, VZV |
| What condition is often associated or seen with Retinitis? | Immunosuppression |
| What is Papilledema? | Optic disc swelling (usually bilateral) due increased ICP |
| Enlarged blind spot and elevated optic disc with blurred margins. Dx? | Papilledema |
| What is the most characteristic fundoscopic finding in Papilledema? | Elevated Optic disc with blurred margins |
| What ocular condition is often seen with enlarged blind spot, and optic disc swelling? | Papilledema |
| What are the three actions or functions of the eye that compose Pupillary control? | 1. Miosis 2. Pupillary light reflex 3. Mydriasis |
| Pupillary constriction is referred as __________________. | Miosis |
| Miosis is it controlled by the Parasympathetic or sympathetic system? | Parasympathetic |
| How many neurons make up the process of Miosis? | 2 neurons |
| What is connected by the 1st Neuron in Miosis? | Edinger-Westphal nucleus to ciliary ganglion via CN III |
| What is the role or connection of the 2nd Neuron in Miosis? | Short ciliary nerves to sphincter pupillae muscles |
| Medical term to "make pupil small" | Miosis |
| In testing the Pupillary light reflex, the light shone at either eye, sends signal to Pretectal nuclei via which cranial nerve? | CN II |
| Light going INTO the eye is transmitted to the LGN and Edinger-Westphal nucleus via the : | CN II |
| Once the light signal transmitted by CN II reaches the Pretectal nuclei in the midbrain it: | Activates bilateral Edinger-Westphal nuclei |
| The bilateral activation of the Edinger-Westphal nuclei causes: | Pupils constrict bilaterally |
| If the Light reflex on either eye, cause pupil contsticiton in boeth eyes, it is: | Positive (non affected) Direct and consensual reflex |
| A positive Direct and Consensual reflex in Pupillary light reflex means: | Both pupils constrict when light is shone to one eye |
| What is the expected (healthy) result for Pupillary light reflex? | Illumination of 1 eye result in blagearl pupillary constriction |
| Mydriasis is: | Sympathetic dilation of the pupil |
| How many neurons are involved in Mydriasis? | 3 neurons |
| What is "connected" by the 1st neuron of Mydriasis? | Hypothalamus to Ciliospinal center of Budge (C8-T2) |
| Where is the Pretectal nuclei? | Midbrain |
| In which pupillary function is the Ciliospinal center of Budge involved with? | Mydriasis 1st neuron |
| Where in the spinal cord is the ciliospinal center of Budge usually located? | C8-T2 |
| Where does the 2nd neuron of Mydriasis exits the spinal cord? | At T1 |
| Exit at T1 and travels to superior cervical ganglion | 2nd neuron of Mydriasis |
| What is the course followed by the 2nd neuron of Mydriasis? | Travels along cervical sympathetic chain near lung apex, and subclavian vessels |
| What is the course or path of the 3rd neuron involved in Mydriasis? | Plexus along internal carotid, through cavernous sinus; enter orbit as long ciliary nerve to pupillary dilator muscles |
| What do the sympathetic fibers of the 3rd neuron in mydriasis innervate? | Smooth muscle of eyelids and sweat glands of forehead and face |
| What is Marcus Gunn pupil? | When light shine into a normal eye, the pupillary reflex is intact, but when shown to the affected eye, both pupils dilate instead of constrict. |
| A "reverse" result in Pupillary light reflex? | Marcus Gunn pupil |
| What causes the abnormal Pupillary reflex that leads to Marcus Gunn pupil? | Impaired conduction of light signal along the injured optic nerve |
| What is the Direct reflex part of the Pupillary light reflex? | Constriction of the Ipsilateral eye |
| What is the Consensual reflex part of the Pupillary light reflex? | Constriction of the contralateral eye |
| What are the main symptoms of Horner syndrome? | 1. Ptosis 2. Anhidrosis 3. Miosis |
| What is Ptosis? | Slight drooping of eyelid |
| What muscle is associated with Ptosis? | Superior tarsal muscle |
| Horner syndrome is: | Sympathetic denervation of the face |
| Medical term for absence of sweating? | Anhidrosis |
| Horner syndrome is associated with a sympathetic chain composed of how many neurons? | 3 neurons |
| What are the lesions associated with 1st neuron associated with Horner syndrome? | - Pontine hemorrhage - Lateral medullary syndrome - Spinal cord lesion above T1 |
| What is the condition that is known to cause Horner syndrome at the level of the 2nd neuron? | Pancoast tumor |
| What condition may lead to Horner syndrome due to 3rd neuron lesion? | Carotid dissection |
| What are common spinal cord lesion above T1 that cause Horner syndrome? | Brown-Sequard syndrome and Late-stage syringomyelia |
| Which condition is seen with Ptosis, Anhidrosis, and Miosis? | Horner syndrome |
| Where is the synapse of the first and second neuron in Horner syndrome sympathetic chain? | Lateral horn |
| Where or which structure locates the synapse between the second and third neuron in Horner syndrome? | Superior cervical ganglion |
| At what point of spinal cord is the Superior Cervical ganglion? | C2 |
| What what level of the spinal cord is the second synapse in Horner syndrome sympathetic chain? | T1 |
| Which arterial bodies are in proximity to the 3rd neuron of Horner syndrome? | Internal and External Carotid artery |
| List of Ocular motility muscles: | 1. Superior Rectus muscle 2. Lateral Rectus muscle 3. Inferior Oblique muscle 4. Superior Oblique muscle 5. Medial Rectus muscle 6. Inferior Rectus muscle |
| Which ocular motility muscle is innervated by cranial nerve VI? | Lateral rectus muscle |
| Which ocular motility muscle ins innervated by CN IV? | Superior oblique muscle |
| What is the mnemonic to depict the all the ocular motility cranial nerve innervation? | LR6 SO4 R3 |
| What is the strongest action of the Superior Oblique muscle? | Depression when the eye is adducted |
| In ocular muscles, the "obliques" go: | Opposite side |
| If patient is looking to the right, which ocular muscles are been tested? | Left SO and Left IO |
| How is the patient asked to look in order to test the Inferior Oblique muscle? | Up |
| What are common causes of CN III damage? | 1. Ischemia --> pupil sparring 2. Uncal herniation --> coma 3. PCA aneurysm --> sudden-onset headache 4. Cavernous sinus thrombosis --> proptosis, involvement of CNs IV, V1/V2, VI 5. Midbrain stroke --> contralateral hemiplegia |
| What type of pathology affects in CN III damage, affects most the motor output to extraocular muscles? | Vascular disease due to decreased diffusion of oxygen and nutrients to the inferior fibers form compromised vasculature that reside on outside of nerve. |
| What are the CN III palsy deficits due to vascular disease? | Ptosis, "down and out" gaze |
| What are the two main components of CN III? | Motor (central) and Parasympathetic (peripheral) |
| What affects the parasympathetic component in CN III damage? | Compression by PCom aneurysm or Uncal herniation |
| What are the signs seen by Parasympathetic (peripheral ) CN III damage? | 1. Diminished or absent Pupillary light reflexes 2. "blown pupil" often with "down-and-out" gaze |
| What type of gaze is seen in CN III palsy? | Down and Out |
| Eyes move upward, particularly with contralateral gaze. Dx? | CN IV palsy |
| How does one can easily distinguish CN IV palsy in a person by non-ocular signs? | Going down stairs, head may tilf in the opposite direction to compensate |
| Cranial Nerve VI damage (palsy) is defined as: | Affected eye unable to abduct and is displaced medially in primary position of gaze |
| Which ocular palsy is characterized by inability to abduct affected eye? | CN VI palsy |
| What condition is suspected if a person can abduct eye, and instead it is "maintained" at primary position (medial) of gaze? | CN VI palsy |
| Ask patient "look to the left" and the patient immediately has upward eye deviation. Dx? | Right sided CN IV palsy |
| List of Visual field defects: | 1. Right/Left anopia 2. Bitemporal hemianopia 3. R/L homonymous hemianopia 4. R/L Upper quadrantanopia 5. R/L lower quadrantanopia 6. R/L hemianopia with macular sparing 7. Central Scotoma |
| Which conditions can cause Bitemporal hemianopia? | Pituitary lesion and compression of Pituitary chiasm |
| A left upper quadrantanopia is most likely due to: | Left temporal lesion or MCA lesion |
| A right parietal lesion may me responsible for which visual field defect? | Left lower quadrantanopia |
| Visual field defect caused by a Left PCA infarct? | Left hemianopia with macular sparing |
| The Meyer loop course: | Lower retina; Loops around inferior horn of Lateral ventricle |
| Dorsal optic radiation: | Superior retina; takes shortest path via internal capsule |
| Which brain area is traversed or caused by the Dorsal Optic radiation? | Internal capsule |
| An infarct to the internal capsule will most likely cause defects to the superior or lower retina? | Superior retina |
| Meyer Looop damage or lesion will cause problems with the lower or superior retina? | Lower retina |
| What areas of the brain are involved or anatomically approximate to with the Meyer Loop? | Inferior horn of lateral ventricle |
| When an image hits the Primary visual cortex, it is ===> | Upside down and left-right reversed |
| Where is the light of an image if it is upside down, and Left-right reverse? | Primary visual cortex |
| What is the Cavernous sinus? | Collection of venous sinuses on either side of pituitary. |
| Where does the blood from eye and superficial cortex drains into? | Cavernous sinuses |
| Collection of venous sinuses on either side of the pituitary. | Cavernous sinuses |
| The contents oft he Cavernous sinuses drain into ----> | Internal jugular vein |
| The internal jugular vein receives content (blood) from which structure? | Cavernous sinuses |
| Which Cranial nerves and other nervous system structures pass through the Cavernous sinus? | - CNs: III, IV, V1, and V2 - Postganglionic sympathetic pupillary fibers en route to orbit |
| What are signs and features of Cavernous sinus syndrome? | 1. Ophthalmoplegia, 2. Decreased corneal sensation 3. Horner syndrome 4. Occasional decreased maxillary sensation |
| What are secondary causes for Cavernous sinus syndrome? | Pituitary tumor mass effect, Carotid-cavernous fistula, or Cavernous sinus thrombosis related to infection |
| Which cranial nerve that goes through the cavernous sinus is most susceptible to injury in Cavernous sinus syndrome? | CN VI |
| What is Internuclear Ophthalmoplegia? | A disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. |
| What is the Medial Longitudinal fasciculus? | Pair of tracts that allows for crosstalk between CN VI and CN III nuclei. |
| What it the role of the MLF? | Coordinates both eyes to move in same horizontal direction |
| Which structure is in charge to move eyes to same horizontal side, together? | Medial longitudinal fasciculus (MLF) |
| Bilateral lesions to the MLF are common in: | Multiple sclerosis |
| Why is the MLF highly myelinated? | Must communicate quickly so eyes move at the same time |
| What is the most common conditions due to MLF damage? | Internuclear Ophthalmoplegia (INO) |
| Conjugate horizontal gaze palsy. | Internuclear Ophthalmoplegia (INO) |
| Lack of communication such that when CN 6 nucleus activités ipsilateral lateral rectus, contralateral CN 3 does not stimulate medial rectures to contract | Internuclear Ophthalmoplegia (INO) |
| What action causes eye to get nystagmus in INO? | Abducting the eye |
| What causes the nystagmus in INO by abducting the affected eye? | CN VI overfires to stimulate CN III |
| In Right INO, which eye is paralyzed, right or left? | Right |
| How is convergence in INO? | Normal |
| What is Leukocoria? | Loss (whitening) of the red reflex |
| What are some causes for Leukocoria in children? | Retinoblastoma, congenital cataract, and toxocariasis |
| What are the 4 herniation syndromes? | 1. Cingulate (subfalcine) herniation under falx cerebri 2. Central/downward transtentorial herniation 3. Uncal transtentorial herniation 4. Cerebellar tonsillar herniation into the foramen magnum |
| A Cingulate herniation syndrome can ---> | Compress anterior cerebral artery |
| Which artery is at risk of compression by a Cingulate herniation under the falx cerebri? | Anterior cerebral artery (ACA) |
| ACA may be compressed by which herniation syndrome? | Cingulate herniation under the falx cerebri |
| What is a Central/downward transtentorial herniation? | Caudal displacement of brain stem which causes rupture of Paramedian basilar artery branches causing Duret hemorrhages |
| Duret hemorrhages are due to rupture of which arteries? | Paramedian basilar artery branches |
| What causes the rupture of Paramedian basilar artery branches in a Central transtentorial herniation? | The caudal displacement of the brain stem |
| The presence of Duret hemorrhages are associated with which herniation syndrome? | Central/downward transtentorial herniation |
| Uncus = | Medial Temporal lobe |
| What word can be used to refer to the "Medial Temporal lobe"? | Uncus |
| What does an early Uncal transtentorial herniation causes? | Ipsilateral blown pupil and contralateral hemiparesis |
| What does a late Uncal Transtentorial herniation causes? | Coma and Kernohan phenomenon |
| What is the "Kernohan phenomenon"? | Misleading contralateral blown pupil and ipsilateral hemirarers due to contralateral compression against Kernohan notch |
| Which herniation syndrome is associated with Kernohan phenomenon? | Late Uncal Transtentorial herniation |
| Misleading contralateral blown pupil and ipsilateral hemiparesis due to contralateral compression against Kernohan notch. | Kernohan phenomenon |
| What are the consequences of a Cerebellar tonsillar herniation into the foramen magnum? | Coma and death result when these herniations compress the brain stem |
| What is the most feared structure to be compressed by a Cerebellar tonsillar herniation into the foramen magnum? | Brain stem |
| Why is does a Cerebellar tonsillar herniation into the foramen magnum so feared? | If it compresses the brain stem it can cause comma and death |
| What are the MOTOR neurons signs? | 1. Weakness 2. Atrophy 3. Fasciculations 4. Reflexes 5. Tone 6. Babinski 7. Spastic paresis 8. Flaccid paralysis 9. Clasp knife spasticity |
| Motor neuron lesions are divided into: | Upper and Lower |
| Lower motor neuron injury means: | Less muscle mass, decreased muscle tone, decreased reflexes, and downgoing toes |
| Upper motor neuron injury means: | Everything up (tone, DTRs, toes) |
| What are fasciculations? | Muscle twitching |
| When is a (+) Babinski sign normal? | In an infant |
| UMN and LMN injuries, both show with a positive _______________. | Weakness |
| Which Motor neuron signs are (+) in LMN injury? | Weakness, Atrophy, Fasciculations, and Flaccid paralysis |
| A person with Fasciculations, most likely suffered a UMN or LMN lesion? | LMN lesion |
| Flaccid paralysis is seen in UMN or LMN lesion? | LMN lesion |
| Which motor neuron sings are DECREASED in a LMN lesion? | Reflexes and Tone |
| Which are (+) motor neuron signs in a UMN lesion? | Weakness, Babinski, Spastic paresis, and Clasp knife spasticity |
| Reflexes and tone, are increased in a __________ motor neuron lesion. | UMN lesion |
| List of Spinal lesion diseases: | 1. Spinal muscular atrophy 2. Amyotrophic lateral sclerosis 3. Complete occlusion of anterior spinal artery 4. Tabes dorsalis 5. Syringomyelia 6. Vitamin B12 deficiency 7. Cauda Equina syndrome |
| Congenital degeneration of anterior horns of spinal cord. Dx? | Spinal muscular atrophy |
| What type of motor neuron deficits are seen in Spinal muscular atrophy? | LMN symptoms |
| What mutation is associated with Spinal muscular atrophy? | AR mutation in SMN1 leading to defective snRNP assembly |
| What is the clinical presentation of Spinal muscular atrophy? | - LMN symptoms only, - Symmetric weakness - "Floppy baby" with marked hypotonia - Tongue fasciculations |
| What is another way to refer to Spinal Muscular Atrophy (SMA) type 1? | Werdnig-Hoffmann disease |
| Werdnig-Hoffmann disease is the same as: | Spinal muscular atrophy type 1 |
| What part(s) of the Spinal cord is affected in Werdnig-Hoffmann disease? | Anterior horns of spinal cord |
| What is the common name for Amyotrophic lateral sclerosis (ALS)? | Lou Gehrig disease |
| What symttoms are seen in ALS? | Combined UMN and LMN degeneration. |
| In ALS (Lou Gehrig disease) what produces the UMN deficits? | Degeneration of the corticobulbar and corticospinal tracts |
| What tract degeneration produces the LMN deficits seen in ALS? | Degeneration of medullary and spinal cord |
| UMN + LMN lesion deficits with no sensory or bowel/bladder deficits. Dx? | Amyotrophic lateral sclerosis |
| What is a common cause of Lou Gehrig disease? | Defect in Superoxide dismutase 1 |
| Defective Superoxide dismutase 1. Dx? | Amyotrophic lateral sclerosis |
| What are the common LMN deficits seen in ALS? | Flaccid limb weakness, fasciculations, atrophy, bulbar palsy |
| What is seen in Bulbar palsy? | Dysarthria, dysphagia, and tongue atrophy |
| Which Spinal cord disorder is associated with Bulbar palsy? | Amyotrophic lateral sclerosis |
| What are the UMN deficits seen with ALS? | Spastic limb weakness, hyperreflexia, clonus, pseudobulbar palsy |
| What symptoms are associated with Pseudobulbar palsy? | Dysarthria, dysphagia, and emotional lability |
| What is the common treatment for ALS? | Rilouzole |
| What condition is treated with Rilouzole? | Amyotrophic lateral sclerosis |
| Which tracts (parts of spinal cord) are spared in "Complete occlusion of ASA"? | Dorsal columns and Lissauer tract |
| Which artery supplies the ASA below T8? | Artery of Adamkiewicz |
| What is a common cause for Complete Occlusion of Anterior Spinal artery? | Aortic aneurysm repair |
| What are the common clinical signs or symptoms of Complete Occlusion of ASA? | 1. UMN deficit below the lesion (corticospinal tract), 2. LMN deficit at the level of the lesion (anterior horn), 3. Loss of pain and temperature sensation below the lesion (spinothalamic tract). |
| What parts of the Spinal cord are affected by the complete occlusion of the ASA? | Corticospinal tract, anterior horn, and Spinothalamic tract. |
| What UMN deficits are seen in Complete Occlusion of the ASA? | Deficit below the level of lesion |
| LMN or UMN deficits are seen at the level of lesion by Complete occlusion of ASA? | LMN deficits |
| What is the result of damage to the Spinothalamic tract in Complete occlusion of the ASA? | Loss of pain and temperature sensation below the lesion |
| What causes Tabes dorsalis? | Tertiary syphilis |
| What are the pathological changes or results caused by Tabes dorsalis? | Degeneration/ demyelination of dorsal columns and roots leading to progressive sensory ataxia |
| What are the clinical features caused by Progressive sensory ataxia caused by Tabes dorsalis? | Impaired proprioception with causes poor coordination |
| (+) Romberg sign and absent DTRs. Dx? | Tabes dorsalis |
| What are featured signs of Tabes dorsalis? | - Charcot joints, - Shooting pain - Argyll Robertson pupils |
| (+) Argyll Robertson pupils. Dx? | Tabes dorsalis |
| What spinal cord condition is associated with tertiary syphilis? | Tabes dorsalis |
| Syrinx expand and damages anterior white commissure of spinothalamic tract. | Syringomyelia pathogenesis |
| What is the result of Syringomyelia pathogenesis? | Bilateral symmetric los of pain and tempreatio nsesaton in cape-like distribution |
| Chiari I malformation are associated with which Spinal cord condition? | Syringomyelia |
| What is the featured sensation loss of Syringomyelia? | Cape-like distribution loss of pain and temperature |
| What condition is known to affect the anterior white commissure of the Spinothalamic tract? | Syringomyelia |
| What another name given to Vitamin B12 deficiency? | Subacute combined degeneration |
| What tracts are demyelinated in Subacute combined degeneration? | - Spinocerebellar tracts - Lateral Corticospinal tracts - Dorsal columns |
| What are the neurological symptoms seen in Vitamin B12 deficiency? | Ataxic gait, paresthesia, impaired position/vibration sense, and UMN symptoms. |
| Cauda equina syndrome is due to: | Compression of spinal roots L2 and below, often due to intervertebral disc herniation or tumor. |
| The herniation if the intervertebral disc, causing compression of spinal roots L2 and below. Dx? | Cauda equina syndrome |
| What the clinical signs of Cauda equina syndrome? | Radicular pain, absent knee and ankle reflexes, loss of bladder and anal sphincter control, and saddle anesthesia |
| Absence of the knee and ankle reflexes could represent what spinal cord condition? | Cauda equina syndrome |
| What is saddle anesthesia? | A loss of sensation restricted to the area of the buttocks, perineum and inner surfaces of the thighs. |
| What type of pain is associated with Cauda equina syndrome? | Radicular pain |
| What pathogen causes Poliomyelitis? | Poliovirus |
| Poliomyelitis is due to: | Infections causes destruction of cells in anterior horn of spinal cord (LMN death) |
| Where does the Poliovirus replicate to cause Poliomyelitis? | Oropharynx and small intestine before spreading via bloodstream to CNS. |
| What are the common LMN deficits seen in Poliomyelitis? | Asymmetric weakness, hypotonia, flaccid paralysis, fasciculation, hyporeflexia, and muscle atrophy. |
| How does the LMN deficits different in Poliomyelitis and Spinal muscular atrophy? | Poliomyelitis develops ASYMMETRIC weakness, while, Spinal muscular atrophy develos symmetric weakness. |
| If the patient demonstrates asymmetric weakness, is it Spinal muscular atrophy or poliomyelitis? | Poliomyelitis |
| What condition is due to hemisection of spinal cord? | Brown-Sequard syndrome |
| What is the cause of Brown-Sequard syndrome? | Hemisection of spinal cord |
| What are the main 5 findings of Brown-Sequard syndrome? | 1. Ipsilateral loss of all sensation at level of lesion 2. Ipsilateral LMN signs at level of lesion 3. Ipsilateral UMN signs below level of lesion 4. Ipsilateral loss of proprioception, vibration, light touch, and tactile sense below level of lesion 5. Contralateral loss of pain, temperature, and crue touch below level of lesion |
| What is a risk or a consequence, of Brown-Sequard syndrome above (lesion) T1? | Ipsilateral Horner syndrome due to damage to oculosympathetic pathway |
| LMN deficits in Brown-Sequard syndrome? | Ipsilateral LMN signs at level of lesion |
| What are the contralateral deficits seen in Brown-Sequard syndrome? | Loss of pain, temperature, and crude touch below level of lesion |
| What are the ipsilateral symptoms below the level of lesion of Brown-Sequard syndrome? | 1. UMN signs 2. Impaired proprioception, vibration, light touch, and tactile sense |
| What are the deficits seen ipsilaterally at the level of the lesion of Brown-Sequard syndrome? | 1. Loss of sensation 2. LMN signs |
| Contralateral or Ipsilateral signs: Impaired pain, temperature, crude touch sensation in Brown-Sequard syndrome. | Contralateral |
| Autosomal recessive trinucleotide repeat disorder (GAA)n on chromosome 9 in gene that encodes frataxin. Dx? | Friedreich ataxia |
| What chromosome is involved in the mutation of Friedreich ataxia? | Chromosome 9 |
| What is "frataxin"? | Iron binding protein |
| Which tracts are degenerated in Friedreich ataxia? | 1. Lateral Corticospinal tract 2. Spinocerebellar tract 3. Dorsal columns 4. Dorsal root ganglia |
| What is the clinical result of degeneration of the lateral corticospinal tract in Friedreich ataxia? | Spastic paralysis |
| What produces the loss of DRTs in Friedreich ataxia? | Degeneration of dorsal root ganglia |
| What are symptoms of Friedreich ataxia? | Staggering gaint, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy |
| Which condition is often associated with childhood with Kyphoscoliosis? | Friedreich ataxia |
| What featured bone abnormalities in Friedreich ataxia? | Pes cavus and Hammer toes |
| Cardiac abnormality associated with Friedreich ataxia? | Hypertrophic cardiomyopathy. |
| Hypertrophic, Restrictive, or Dilated cardiomyopathy, which is associated with Friedreich ataxia? | Hypertrophic cardiomyopathy |
| A person with trinucleotide condition associated with Staggering gain and frequent falls? | Friedreich ataxia |
| What is the most common cause of death in Friedreich ataxia? | Hypertrophic cardiomyopathy |
| What is the trinucleotide associated with Friedreich ataxia? | GAAn |
| What are the consequences of CN V motor lesion? | Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle |
| In a CN V motor lesion , does the jaw deviate away or toward the side of lesion? | Toward |
| Why does a CN V motor lesion has a ipsilateral jaw deviation? | Due to unopposed force from the opposite pterygoid muscle |
| Which muscle has not enough forced by itself to counteract the deviation toward injured side of CN V motor nerve? | Pterygoid muscle |
| What is the consequence or clinical presentation of CN X lesion? | Uvula deviates away from side of lesion |
| Is the uvula deviation toward or away from side of lesion in a CN X injury? | Away |
| What causes the contralateral deviation of the uvula in a CN X lesion? | Weak side collapse and uvula points away |
| Upon physical examination the uvula is deviated away from presented injured side. What is the suspected CN damaged? | CN X |
| What is the clinical presentation of CN XI lesion? | Weakness turning head to contralateral side of lesion |
| Weakness turning head to contralateral side of lesion is due to what kind of cranial nerve damage? | CN XI lesion |
| What are the clinical results of CN XI lesion? | 1. Weakness turning head to contralateral side of lesion 2. Shoulder drop on side of lesion |
| What ipsilateral muscle is damaged in CN XI lesion that cause the shoulder drop? | Trapezius |
| Which muscle is affected by CN XI lesion? | Contralateral Sternocleidomastoid |
| What is the ipsilateral sign of a CN XI lesion? | Shoulder drop |
| The left SCM contract to help ====> | Turn the head to the right |
| What is the consequences of a CN XII lesion? | Tongue deviates toward side of lesion |
| Why is the tongue deviates toward of CN XII lesion? | Due to weakened tongue muscles on affected side |
| A CN XII lesion is considered a _______________ lesion. | LMN lesion |
| Does tongue deviate toward or away from affected side in a CN XII lesion? | Toward |
| The expression "lick your wounds" is used to describe aht type of CN lesion? | CN XII lesion |
| If the tongue is deviated, which cranial nerve is most likely affected? | CN XII |
| If the Jaw is deviated, which cranial nerve is most likely affected? | CN V motor |
| What body part is affected and by consequence deviated in a CN X? | Uvula |
| What two parts of the body are affected in a CN XI lesion? | Sternocleidomastoid muscle (neck) and Trapezius muscles (shoulder) |
| What is the most common cause of peripheral facial palsy? | Bell palsy |
| What is the most common pathogen associated with the development of Bell palsy? | Reactivation of HSV |
| What is the treatment for Bell palsy due to HSV reactivation? | Corticosteroids + acyclovir |
| List of causes of peripheral facial palsy? | 1. Reactivation of HSV infection 2. Lyme disease 3. Herpes zoster (Ramsay Hunt syndrome) 4. Sarcoidosis 5. Tumors 6. Diabetes mellitus |
| What is Ramsay Hunt syndrome? | A complication of shingles. It is the name given to describe the symptoms of a shingles infection affecting the facial nerve |
| What is the location of the lesion of Facial nerve palsy that produces UMN deficits? | Motor cortex, connection from motor cortex to facial nucleus in pons |
| If the Facial nerve palsy prices UMN deficits, will these be contralateral or ipsilateral? | Contralateral |
| What are the muscles involved or affected in Facial nerve palsy with UMN deficits? | Lower muscles of facial expression |
| If the forehead is spared (not involved), the facial nerve palsy is of UMN or LMN affectio? | UMN |
| Why is the forehead spared in facial nerve palsy with UMN lesion? | Due to bilateral UMN innervation |
| Is UMN or LMN innervation bilateral, that a facial nerve palsy does not affect the foreadhad? | UMN |
| Lesion location of facial nerve palsy with a LMN injury? | Facial nucleus, anywhere along CN VII |
| Which nerve is affected in LMN Facial nerve palsy? | CN VII |
| Ipsilateral or contralateral, the effects of LMN facial nerve palsy? | Ipsilateral |
| Which type of lesion deficits in facial nerve palsy, affect the Upper and lower muscles of facial expression? | LMN Facial nerve palsy |
| If both, upper and lower muscles of facial expression are affected by Facial nerve palsy, it is safe to assume the forehead will be or will not be affected? | Affected forehead |
| LMN lesion or UMN lesion if facial nerve palsy involves only lower muscles of facial expression? | UMN lesion |
| What are associated symptoms of LMN Facial nerve palsy? | - Incomplete eye closure, - Hyperacusis - Loss of taste and sensation to anterior tongue |
| CN VII LMN lesion ---> | Peripheral; cannot wrinkle forehead |
| If patient present with a facial nerve palsy, and is UNABLE to wrinkle the forehead, it indicates a ______________ lesion. | LMN |
| What are the main division of the ear? | Outer ear, Middle ear, and Inner ear |
| What accounts for the Outer ear? | Visible portion of ear (pinna), includes auditory canal and tympanic membrane. |
| How does the Outer ear transmit sound? | Via vibration of tympanic membrane |
| What is the "pinna"? | Visible portion of ear |
| What is included, besides the pinna, in the Outer ear? | Auditory canal and tympanic membrane |
| What is the Middle ear? | Air-filled space with three bones called the ossicles |
| What is the name given to group of three bones found in the Middle ear? | Ossicles |
| In which division of ear are the "ossicles" located? | Middle ear |
| The auditory canal is in the ______________ ear. | Outer ear |
| Which division or part of the ear has the tympanic membrane? | Outer ear |
| What are the names of the 3 ossicles? | Malleus, incus, and Stapes |
| What is the Malleus? | One of three ossicles (bones) in the middle ear. |
| The Malleus, ______________ and ______________, are the ossicles. | Incus and Stapes |
| What is the role or function of the ossicles? | Conduct and amplify sound from tympanic membrane to inner ear |
| What ear structure(s) is responsible to conduct and amplify sound from the tympanic membrane to the inner ear? | Ossicles |
| Snail-shaped, fluid-filled cochlea. | Inner ear |
| What part of the ear contains the basilar membrane? | Inner ear |
| Vibrates secondary to sound waves | Basilar membrane |
| How is vibration transduced in the inner ear? | Via specialized hair cells --> auditory nerve signaling --> brain stem. |
| Where in the inner ear does low frequency sounds are heard? | Apex near helicotrema |
| What type of frequency is perceived at the cochlea? | High frequency |
| Sound heard best at base of cochlea. | High frequency |
| What are the two types of hearing loss (diagnostically)? | 1. Conductive hearing loss 2. Sensorineural hearing loss |
| What are the two common tests performed to diagnose hearing loss? | Weber test and Rinne test |
| What type of hearing loss produces an abnormal Rinne test? | Conductive hearing loss |
| Which hearing test when performed it test the localization of sound? | Weber test |
| Which type of hearing loss is seen with Weber test that localized sound to affected ear? | Conductive hearing los |
| Sensorineural hearing loss Weber test: | Localizes to affected ear |
| A Weber test in the Conductive hearing loss: | Localizes to affected ear |
| Weber test n Sensorineural hearing loss: | Localizes to affected ear |
| Which auditory test is directed to indicate the localization of sound? | Weber test |
| Which auditory test is intended to indicate bone and air conductivity? | Rinne test |
| A person with Conductive hearing loss will have _______________ Rinne test. | Abnormal |
| What indicates a Normal Rinne test? | Air conductive > Bone conductivity |
| If the sound/vibratory conductivity of bone is larger, then Rinne test is _____________________. | Abnormal |
| Which type of hearing loss experiences a normal Rinne test? | Sensorineural hearing loss |
| Which type of hearing loss experiences an abnormal Rinne test? | Conductive hearing loss |
| Weber test -> Localized to affected ear Rinne test --> Abnormal What is the hearing loss type? | Conductive hearing loss |
| Weber test --> Localizes to unaffected ear Rinne test --> Normal What is the hearing loss type? | Sensorineural hearing loss |
| Which type of hearing loss has the sound localized to the "good" ear in a Weber test? | Sensorineural hearing loss |
| Which type of hearing loss will have the sound/vibration to localized at the "bad" or affected ear? | Conductive hearing loss |
| Bone > air | Abnormal Rinne test seen in Conductive hearing loss |
| What are the two most common types of hearing loss? | 1. Noise-induced hearing loss 2. Presbycusis |
| What is "Noise-induced hearing loss"? | Damage to stereociliated cell in organ of Corti |
| In Noise-induced hearing loss, which hearing frequency is lost first? | High-frequency hearing |
| What is a severe consequence of a sudden, extremely loud noise? | Hearing loss due to tympanic membrane rupture |
| The rupture of the tympanic membrane due to a sudden and extremely loud noise, is an example of which type of hearing loss? | Noise-induced hearing loss |
| What is Presbycusis? | Aging-related progressive bilateral/symmetrical sensorineural hearing loss du tot destruction of hari cell at the cochlear base. |
| Destruction of hair cell at the cochlear base, leads to what type of hearing loss? | Presbycusis |
| What population is most common to develop Presbycusis? | Elderly |
| Hearing loss associated with increasing age. | Presbycusis |
| What hearing is preserved in Presbycusis? | Low-frequency hearing at apex |
| What is destroyed in Presbycusis that leads to hearing loss? | Hair cells at the cochlear base |
| Overgrowth of desquamated keratin debris within the middle ear space. | Cholesteatoma |
| What is a Cholesteatoma? | Overgrowth of desquamated keratin debris within the middle ear space |
| Which part of the ear develops Cholesteatomas? | Middle ear |
| What type of hearing loss, conductive or sensorineural, is seen with Cholesteatoma? | Conductive hearing loss |
| What causes the conductive hearing loss in a Cholesteatoma? | The erosion ossicles, mastoid air cells |
| Painless otorrhea is a common symptom of _____________________. | Cholesteatoma |
| Middle ear mass + Painless otorrhea. Dx? | Cholesteatoma |
| Vertigo: | Sensation of spinning while actually stationary |
| What is a subtype of "dizziness," but distinct form "lightheadedness"? | Vertigo |
| What are the two types of vertigo? | - Central vertigo - Peripheral vertigo |
| What is more common , peripheral or central vertigo? | Peripheral vertigo |
| __________________ vertigo is an inner ear etiology. | Peripheral vertigo |
| What parto fo the ear etiology is peripheral vertigo considered? | Inner ear |
| What is the difference in etiology between Peripheral and Central vertigo? | Peripheral vertigo is an inner ear condition, while Central Vertigo is due to Brain stem or cerebellar lesion |
| What are common etiologies or condition that lead to development of Peripheral vertigo? | 1. Semicircular canal debris 2. Vericular nerve infection 3. Meniere disease 4. Benign Paroxysmal Positional Vertigo (BPPV) |
| What is the treatment for Peripheral vertigo? | Antihistamines, anticholinergics, antiemetics |
| Besides the general medications for Peripheral vertigo, what else is used to treat Peripheral vertigo caused by Meniere disease? | Low-salt diet + diuretics (if needed) |
| For which condition is the Epley maneuver performed? | Treatment of BPPV |
| BPPV causes _______________ vertigo. | Peripheral vertigo |
| What is the common triad associated with Meniere's disease? | 1. Sensorineural hearing loss 2. Vertigo 3. Tinnitus |
| A person with normal Rinne test, Weber test localized sound to non-affected ear, describes currently the room spinning around and a constant ring in the affected ear. Dx? | Meniere disease |
| What would be the Weber test for a Meniere's disease patient? | Localizes to unaffected ear |
| What does the Rinne test on a person with Meniere's disease demonstrate? | Normal; Air conduction is greater than bone conduction of sound and vibration. |
| What are two examples of etiologies that may cause brainstem or cerebellar lesions, leading to develop Central vertigo? | Stroke affecting vestibular nuclei or posterior fossa tumor |
| What ar the findings in Central vertigo? | - Directional or purely vertical nystagmus - Skew deviation - Diplopia - Dysmetria - Focal neurologic findings |
| Which type of vertigo is associated with vertical nystagmus and skew deviation? | Central vertigo |
| A ________________- fossa tumor may cause Central vertigo. | Posterior |
| What is Benign Paroxysmal Positional vertigo (BPPV)? | Sudden sensation that you're spinning or that the inside of your head is spinning |
| What is the Epley manuveur? | Type of exercise help that helps to treat the symptoms of benign paroxysmal positional vertigo (BPPV) |
| List of Vagal nuclei: | 1. Nucleus Solitarius 2. Nucleus Ambiguus 3. Dorsal motor nucleus |
| What is the function of the Nucleus solitarius? | Visceral sensory information (taste, baroreceptors, gut distension) |
| Which cranial nerves associated with the Vagal Nucleus solitarius? | VII, IX, and X |
| Motor innervation of pharynx, larynx, and upper esophagus. Which vagal nuclei is described? | Nucleus ambiguus |
| What actions are performed or regulated by Nucleus ambiguus? | Swallowing and palate elevation |
| CNs involved in the nucleus ambiguus | IX, X, and XI |
| Which is the only cranial nerve involved with the Dorsal motor nucleus? | X |
| What is the function of the Dorsal motor nucleus? | Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI. |
| What are some common cranial nerve reflexes? | Corneal, Lacrimation, Jaw jerk, Pupillary, and gag reflexes. |
| Afferent corneal reflex is done by which nerve? | V1 Ophthalmic (nasociliar y branch) |
| Which CN gives rise to the efferent Corneal reflex? | Bilateral VII (temporal branch: orbicularis oculi) |
| Which reflex is checked by testing Bilateral VII (temporal branch)? | Efferent Corneal reflex |
| Which cranial nerve reflexes are regulated by the CN V1? | Afferent Corneal and Afferent Lacrimation reflexes |
| Does the loss of the afferent lacrimation reflex does not ---> | Preclude emotional tears |
| Which CN must be tested in order to check for Efferent lacrimation reflex? | VII |
| CN V3 cranial afferent reflex? | Jaw jerk |
| Cranial nerve reflex: Sensory-muscle spindle form masserter | Afferent Jaw jerk reflex due to V3 stimulation |
| Efferent Jaw jerk cranial reflex: | V3 (motor -masseter) |
| Which muscle is involved in both efferent and afferent Jaw jerk cranial nerve reflex? | Masseter |
| Which CN is involved in the efferent part of the Pupillary cranial reflex? | CN III |
| What is the cranial nerve involved in the afferent part of the Pupillary reflex? | CN II |
| Which reflex is checked by testing CN II? | Afferent Pupillary reflex |
| A damaged CN III, will cause loss of what part of the pupillary reflex? | Efferent Pupillary reflex |
| CN _____ is involved in afferent gag reflex. | IX |
| Which CN is involved in the efferent part of the gag reflex? | X |
| Damaged CN X will cause a deficit in which cranial nerve reflex? | Efferent Gag reflex |
| How many (number) muscles close the jaw? | 3 |
| How many (number) muscles are needed to open the jaw? | 1 |
| Which muscles are used to close the jaw? | Masseter, Temporalis, and Medial pterygoid |
| Which muscle is used to open the jaw? | Lateral pterygoid |
| All mastication muscles ar innervated by which cranial nerve? | CN V3 |
| Which subdivision of the Trigeminal nerve is in charge to innervate all opening and closing jaw muscles? | V3 |
| Which Pterygoid muscle is used to open the jaw, lateral or medial? | Lateral |
| The Medial pterygoid muscle _______________ the jaw. | Closes |
| Masseter, Temporalis, and Medial pterygoid. | Mastication muscles that close the jaw |
| Total number of pairs of spinal nerves | 31 |
| How are all 31 pairs of spinal nerves categorized? | - 8 cervical pairs - 12 thoracic pairs - 5 lumbar pairs -5 sacral pais - 1 coccygeal pair |
| How many Cervical Spinal nerve pairs exist? | 8 |
| Which subdivision has the most spinal nerve pairs? | Thoracic with 12 pairs |
| Which spinal nerves have each 5 pairs? | Lumbar and Sacral |
| How many coccygeal spinal nerve pairs exist? | 1 |
| Which spinal nerves exit above the corresponding vertebra? | Nerves C1-C7 |
| What is anatomically important about Spinal nerves C1-C7? | Exit ABOVE the corresponding vertebra |
| Do spinal nerves form C1-C7 exit above or below, the corresponding vertebrae? | Above |
| Which is the only spinal nerve that exits above and below the corresponding vertebra? | C8 spinal nerve |
| C8 spinal nerve exits ---> | Below C7 and above T1 |
| C8 spinal nerve exits above the _________. | T1 |
| C8 spinal nerve exits below the ________. | C7 |
| Nerves below the C8 exit ____________ corresponding vertebra. | Below |
| Where would C3 spinal nerve exit the vertebrae? | Above the 3rd cervical vertebra |
| Where would L2 spinal nerve exits the vertebra? | Below the 2nd lumbar vertebra |
| What is a Vertebral Disc herniation? | Nucleus pulposus herniates through annulus fibrosus |
| MC location anatomically for Vertebral disc herniation | Posterolaterally at L4-L5 or L5-S1 |
| In a vertebral disc herniation, which nerve is usually affected? | Nerve below the level of herniation |
| Absent ankle reflex is due to compression of which spinal nerve root? | S1 |
| Compression of S1 nerve root ----> | Absent ankle reflex |
| In a vertebral disc herniation of L3-L4, which nerve is affected and which would be spared? | L3 would be spared, while L4 is affected |
| What is the soft central disc of vertebrae also known as? | Nucleus pulposus |
| Another way to refer to the outer ring by which a vertebral disc herniation goes through? | Annulus fibrosus |
| How far does an adult lower spinal cord normally extend to? | L1-L2 vertebrae |
| The subarachnoid space extends how far in healthy adults? | Lower border of S2 vertebra |
| Most common and best locations for a Lumbar puncture? | L3-L4 or L4-L5 |
| Why is an LP (lumbar puncture) usually performed in L3-L5 area? | Level of Cauda Equina |
| What is the most likely location of the cauda equina in a healthy adult? | L3-L5 vertebrae |
| What is the ultimate goal of a Lumbar puncture (LP)? | Obtain sample of CSF without damaging spinal cord |
| What are the two DESCENDING spinal cord tracts? | 1. Lateral Corticospinal tract 2. Anterior Corticospinal tract |
| What are the divisions of the Lateral corticospinal tracts? | Sacral and Cervical tracts |
| What is controlled or regulated by the Descending tracts of the Spinal cord? | Voluntary motor |
| List of all ASCENDING spinal tracts: | 1. Dorsal column (Fasciculus gracilis, and Fasciculus Cuneatus) 2. Lateral spinothalamic tract 3. Anterior spinothalamic tract |
| What type of sensory information is controlled or sensed by the Dorsal column? | Pressure, vibration, fine touch, and proprioception. |
| What are the divisions of the Dorsal column?? | 1. Fasciculus gracilis 2. Fasciculus cuneatus |
| Fasciculus gracilis controls which part of the body? | Lower body, legs |
| Fasciculus cuneatus provides sensory information to which part of the body? | Upper body, arms |
| An injury to the F. cuneatus will cause deficits in sensation in the ______________. | Upper body and arms |
| What spinal tract sense pressure, vibration, fine touch, and proprioception? | Dorsal column |
| What is sense the Lateral Spinothalamic tract? | Pain and temperature |
| What is sense by the Anterior Spinothalamic tract? | Crude touch, and pressure |
| Which parts of the dorsal column are the most medial in respect of the spinal cord? | Sacral an lumbar |
| Damage to the Lateral spinothalamic tract will cause | Deficit in sensing pain and temperature |
| Ascending or Descending. Lateral Spinothalamic tract: | Ascending |
| Ascending or Descending: Anterior Spinothalamic tract: | Ascending |
| The Dorsal Column is ascending or Descending tract? | Ascending |
| Ascending and Descending. Fasciculus gracilis? | Ascending |
| Fasciculus Cuneatus is it descending or ascending? | Ascending |
| Ascending or Descending. Lateral corticospinal tract? | Descending |
| Ascending or Descending. Anterior Corticospinal tract? | Descending |
| Name of the anterior descending spinal cord tract: | Anterior Corticospinal tract |
| Key. If the name of the of the spinal tract has the cord "Cortico-" is ascending or descending? | Descending |
| The spinothalamic tracts are both ____________________________. | Ascending |
| Pain and temperature are sensed by which spinal cord tract? | Lateral Spinothalamic tract |
| Crude touch and pressure are sensed or relayed by which cord tract? | Anterior Spinothalamic tract |
| Complete sentence. "Ascending tracts ________________........" | Synapse and then cross |
| Which tracts synapse and then cross? | Ascending tracts |
| 1st-Orden Neuron of Dorsal column: | Sensory nerve ending --> bypass pseudounipolar cell body in dorsal root ganglion --> enter spinal cord --> ascend ipsilaterally in dorsal column |
| Where is the Synapse 1 of Dorsal column? | Nucleus gracilis, nucleus cuneatus (ipsilateral medulla) |
| Decussates in medulla and then ascends contralaterally as the medial lemniscus. | 2nd-order neuron in Dorsal column tract |
| Where is the Synapse 2 of the Dorsal column? | VPL of the Thalamus (sensory cortex) |
| What are the two division of the Spinothalamic tract? | Lateral and Anterior |
| Describe the mechanism of the 1st order neuron in the Spinothalamic tract: | Sensory nerve ending --> bypass pseudounipolar cell body in dorsal root ganglion and finally entering the spinal cord |
| Where is the Synapse 1 of the Spinothalamic tract? | Ipsilateral gray matter (in spinal cord) |
| 2nd-order Neuron of the Spinothalamic tract: | Decussates in spinal cord as the anterior white commissure and then ascends contralaterally |
| The dorsal column 2nd-order neuron decussates in the ___________________ to tehn ascend contralaterally. | Medulla |
| Which important structure provides the ascend of the second order neuron of the Dorsal column? | Medial lemniscus |
| What can be found to travel up alongside the second order neuron of the dorsal columns? | Medial lemniscus |
| Where is the Synapse 2 of the spinothalamic tract? | VPL of the Thalamus (sensory cortex) |
| If the Synapse 2 is the VPL of the thalamus, which are the two possible tracts? | Dorsal columns and Spinothalamic tracts |
| Crossing the spinal cord at the white commissure is seen in which ascending tract? | Spinothalamic tract |
| Which tract has function for Voluntary movement of contralateral limbs? | Lateral corticospinal tract |
| What is the 1st-order neuron function of the Lateral corticospinal tract? | UMN: cell body in primary motor cortex --> descends ipsilateral, and most fibers decussate at the caudal medulla |
| At what point the first-order neuron of the lateral corticospinal tract decussatus? | Caudal medulla |
| The decussation of the first-order neuron of the lateral corticospinal tract is known as: | Pyramidal decussation |
| Which gtract is known to "descend contralaterally"? | Lateral corticospinal tract |
| Which is the 1st-order neuron of the lateral corticospinal tract, UMN or LMN? | UMN |
| Where does the Synapse 1 of the Lateral corticospinal tract occurs? | Cell body of anterior horn of the spinal cord |
| What is the most likely referred tract, if the synapse 1 happens that the cell body of anterior horn of spinal cord? | Lateral corticospinal tract |
| LMN of the Lateral corticospinal tract is the ----> | Second-order neuron pathway |
| Where is the synapse 2 of the lateral corticospinal tract? | Neuromuscular junction (NMJ) ---> muscle fibers |
| What are the 4 main clinical reflexes? | 1. Achilles reflex 2. Patellar reflex 3. Biceps and brachioradialis reflexes 4. Triceps reflex |
| Nerve roots of the Achilles reflex | S1 and S2 |
| Which is the main nerve root of the Achilles reflex? | S1 |
| A damage to the S1, S2 nerve roots will cause --> | Weak or absent Achilles reflex |
| Damage to nerve roots L3 , L4 causes: | Weak or absent Patellar reflex |
| What are the nerve roots of the Patellar reflex? | L3 and L4 |
| Which is the main nerve root for the Patellar reflex? | L4 |
| Which reflex is tested by checking L3/L4 nerve roots? | Patellar reflex |
| The Biceps and Brachioradialis reflexes are tested by checking which nerve roots? | C5 and C6 |
| Which is the main nerve root for the Biceps and Brachioradialis reflexes? | C5 |
| Which important clinical reflex is tested by the C5 and C6 nerve roots? | Biceps and Brachioradialis reflexes |
| S1, S2 nerve roots ------> reflex? | Achilles |
| L3, L4 nerve roots -----> reflex? | Patellar |
| C5, C6 nerve roots ------> reflex? | Biceps and Brachioradialis |
| Which are the nerve roots involved in the Triceps reflex? | C7 and C8 |
| Which is the main nerve root in the Triceps reflex? | C7 |
| C7, C8 nerve roots -----> reflex? | Triceps |
| To check the Triceps reflex, the clinician must stimulate which nerve roots? | C7 and C8 |
| A injury to the C7 or C8 nerve roots will cause: | Weak or absent Triceps reflex |
| Damage to the C5 or C6 nerve roots will cause: | Weak or absent Biceps and Brachioradialis reflexes |
| "testicles move" reflex. | Cremasteric reflex |
| Which clinical reflex is directed to the testicles? | Cremasteric reflex |
| Which are the nerve roots involved in the Cremasteric reflex? | L1 and L2 |
| Damage to L1 or L2 nerve roots will probable cause abnormal __________ reflex. | Cremasteric reflex |
| The phrase "winks galore" is used to describe or indicate which clinical reflex? | Anal wink reflex |
| Which are the nerve roots involved in the Anal wink reflex? | S3 and S4 |
| Damage to the S3 or S4 nerve roots result in ----> | Weak or absent anal wink reflex |
| CNS reflexes that are present in a healthy infant, but are absent in a neurologically intact adult | Primitive reflexes |
| What are Primitive reflexes? | CNS reflexes that are present in a healthy infant, but are absent in a neurologically intact adult |
| By when are Primitive reflexes normally gone? | 1st year of life |
| What part of the brain is inhibit the primitive reflexes? | Frontal lobe |
| What is a possible consequence of a frontal lobe lesion? | Loss of inhibition (reemergence) of primitive reflexes |
| Description of the Moro reflex: | "Hang on for life" reflex - abduct/extend arms when startled, and the draw together |
| The abduction/extension of arms when a baby is startled, and then draw back them together. | Moro reflex |
| What is the rooting (primitive) reflex? | Movement of head toward one side if cheek or moth is stroked |
| What is a common way to refer to the rooting reflex? | Nipple seeking |
| The movement of an infant's head toward the side side of cheek or mouth that is stroked. | Rooting reflex |
| What is the description of the Sucking reflex? | Sucking response wehn roof of mouth is touch |
| Placing a finger in an infant roof of mouth should elicit what refeed in a healthy baby? | Sucking reflex |
| What is the Palmar (primitive) reflex? | Curling of fingers if palm is stroked |
| Curling of fingers as the palm of an infant is stroked. | Palmar reflex |
| Definition of the Plantar reflex | Dorsiflexion of large toe and fanning of other toes with plantar stimulation |
| What is the Babinski sign? | Presence of Plantar reflex in an adult |
| A (+) Babinski sign indicates: | UMN lesion |
| What reflex is seen with UMN lesion? | (+) Babinski sign |
| What is the Galant reflex? | Stroking alongside of the spine while newborn is in ventral suspension causes lateral flexion of lower body toward stimulated side |
| A physician places baby laying on its stomach and then gently strokes along side the right side of the spine. What is the reflex been tested? | Galant reflex |
| What is the possible age of a healthy human with (+) plantar, Moro, and Rooting reflexes? | Less than one year |
| What is the expected result or reaction of the Gallant reflex? | Lateral flexion of lower body toward the stimulated side |
| If the galant reflex test is done on the left side, toward which side is the lower body flexion expected to occur? | Left side |
| Dermatome C2 distribution | Posterior half of skull |
| What dermatome is distributed or covers the posterior half of the skull? | C2 |
| Which dermatome distribution is described as "high turtle neck"? | C3 |
| What dermatomes are the ones that refer diaphragm and gallbladder pain to the right shoulder? | C3, C4, and C5 |
| Referred pain to the right shoulder is done via which nerve? | Phrenic nerve |
| Low-collar shift dermatome distribution | C4 |
| What is the distribution of the C4 dermatome? | Low-collar shirt |
| Which digits are included in C6 dermatome distribution? | Thumbs |
| What is a Dermatome? | An area of the skin supplied by nerves from a single spinal root. |
| An area of the skin supplied by nerves from a single spinal root | Dermatome |
| By which dermatome are thumbs covered or prove skin nerve sensation? | C6 |
| Which dermatome location is described by "At the nipple"? | T4 |
| Which dermatome covers the nipple? | T4 |
| T4 dermatome distribution is at the ______________. | Nipple |
| Which dermatome covers the Xiphoid process? | T7 |
| What part of body is covered by T7 dermatome? | Xiphoid process |
| Which dermatome is located or distributed at the umbilicus? | T10 |
| Damage to spinal root T10 will cause lack of skin sensation tow which part of body (dermatome)? | Umbilicus |
| T10 is a point referred with pain in which condition? | Appendicitis |
| A patient will have pain at which dermatome ? | T10 |
| L1 dermatome distribution: | At the Inguinal Ligament |
| What dermatome covers the Inguinal ligament? | L1 |
| L4 includes what part of the lower extremities? | Kneecaps |
| Kneecap dermatome coverage is done by which spinal nerve root? | L4 |
| Dermatomes S2, S3, and S4 provide skin sensation to: | Penile and anal zones |
| What areas of body would experience decreased or absent skin sensation case of S2-S4 dermatome damage? | Penile and anal zones |
| Sensation of penile and anal zones is done by which dermatomes? | S2, S3, and S4 |
| What actions and/or functions are controlled by the Temporal lobe? | 1. Language comprehension 2. Behavior 3. Memory 4. Hearing 5. Emotions |
| Which lobe has the area of the brain in charge of language comprehension? | Temporal lobe |
| A person with changes in behavior, hearing, and memorey, as well with deficits in language comprehension, most likely suffered from an injury to which brain lobe? | Temporal lobe |
| What functions and roles are controlled by the Pituitary gland? | - Hormones - Growth - Fertility |
| Damage to the pituitary gland may represent damage into which overall characteristics: | Hormonal activity, growth, and fertility |
| What physiological features are controlled by the Brain stem? | 1. Breathing 2. Blood pressure 3. Heartbeat 4. Swallowing |
| Breathing, swallowing, BP, and HR are controlled all by which area of the CNS? | Brain stem |
| What is coordinated by the actions of the Cerebellum? | Balance, coordination, and Fine muscle control |
| A deficit in balance and coordination may represent damage to the ______________________. | Cerebellum |
| Occipital lobe has which physiological feature under its control? | Vision |
| Which brain lobe houses the vision control and ability? | Occipital lobe |
| What are the roles/functions coordinated or controlled by the Parietal lobe? | 1. Telling right from left 2. Calculations 3. Sensations 4. Reading 5. Writing |
| A person unable to distinguish "right" from "left" may present with damage to: | Parietal lobe |
| A person that prior to a severe car accident was a math teacher, but after that was unable to read, write, or do mathematical calculations, may have injured which part of the brain? | Parietal lobe |
| Reading is controlled by which lobe? | Parietal lobe |
| Writing is controlled by which brain lobe? | Parietal lobe |
| Acalculia is due to damage or injury to the _____________ lobe. | Parietal lobe |
| List of actions controlled or managed by the Frontal lobe of the brain: | 1. Movement 2. Reasoning 3. Behavior 4. Memory 5. Personality 6. Planning 7. Decision making 8. Judgement 9. Initiative 10. Inhibition 11. Mood |
| Which actions are controlled or coordinated by the Frontal and Temporal lobes of the brain? | Behavior and memory |
| A person with movement deficits may have suffered an brain injury involving which lobe? | Frontal lobe |
| Personality changes, may be due to injuries to the _____________ lobe. | Frontal lobe |
| Unable to make decisions, as well as bad judgement calls, may represent an injury to which brain lobe? | Frontal lobe |
| Which brain area or lobe has more actions or roles under its control? | Frontal lobe |
| What is the sensory information conveyed by the Parietal lobe? | Taste, smell, touch, sight, hearing, temperature, and pain |
| Which lobe of the brain is in charge of coordinating Spatial relationships? | Parietal lobe |
| What are the Spatial relationships? | - Hand-eye coordination - Recognizing body position - Judging distances - Moving between objects |
| Understanding what you see | Sight |
| Sight is controlled by which brain lobe? | Occipital lobe |
| Executive functions are controlled by which lobe? | Frontal lobe |
| What are (list) of Executive functions? | Planning, organizing, problem solving, decision-making, reasoning |
| Broca's area in frontal lobe is in charge of: | Speaking fluently and with meaning |
| Wernicke's area in the Temporal lobe is in charge of: | Understanding language and speech |
| List of Adult primary brain tumors: | 1. Glioblastoma multiforme 2. Oligodendroglioma 3. Meningioma 4. Hemangioblastoma 5. Pituitary adenoma 6. Schwannoma |
| What is a Grade IV astrocytoma? | Glioblastoma multiforme |
| Glioblastoma multiforme is: | Grade IV astrocytoma |
| Adult or Childhood brain tumor: Glioblastoma multiforme? | Adult |
| Common, highly malignant primary brain tumor with ~ 1 year median survival. Dx? | Glioblastoma multiforme |
| What is a "common" way to refer to Glioblastoma multiforme? | Butterfly glioma |
| Severe astrocytoma that can cross corpus callosum. Dx? | Glioblastoma multiforme |
| - Astrocyte origin, GFAP (+) - "Pseudopalisading" What is the possible brain tumor? | Glioblastoma multiforme |
| What is the characteristic of the astrocytes in Glioblastoma multiforme? | GFAP (+); "Pseudopalisading" pleomorphic tumor cells border central aras of necrosis, hemorrhage, and/or microvascular proliferation |
| "Pseudopalisading" pleomorphic tumor cells border central areas of necrosis. Dx? | Glioblastoma multiforme |
| What is the main cell proliferation in Glioblastoma multiforme? | Astrocytes |
| What causes Glioblastoma multiforme to adopt the term "butterfly glioma"? | The fact it can cross the corpus callosum, gives it a butterfly appearance |
| Where is a Glioblastoma multiforme most likely found? | Cerebral hemispheres |
| Which primary adult brain tumor is found in the Cerebral hemispheres? | Glioblastoma multiforme |
| Where do most often Oligodendroglioma appear? | Frontal lobe |
| "Chicken-wire" capillary pattern. Brain tumor? | Oligodendroglioma |
| What is origin cell of Oligodendroglioma? | Oligodendrocytes |
| What is the histology of Oligodendrogliomas? | "Fried egg" cells- round nuclei with creal cytoplasm. Often calcified |
| Which adult brain tumor appears in the frontal lobes? | Oligodendroglioma |
| Adult or Childhood brain tumor: Oligodendroglioma? | Adult |
| Adult or Childhood brain tumor: Meningioma? | Adult |
| Adult or Childhood brain tumor: Hemangioblastoma? | Adult |
| Adult or Childhood brain tumor: Pituitary adenoma? | Adult |
| Which adult brain tumor is common, typically benign, more common in females than males? | Meningioma |
| Most common location for Meningioma? | Near surfaces of brain and in parasagittal region |
| Which is brain tumor is often seen with dural attachment? | Meningioma |
| Which tumor is seen with a "tail" attached to the dura? | Meningioma |
| Arachnoid cell origin brain tumor. | Meningioma |
| Histology of a Meningioma: | Spindle cells concentrically arranged in a whorled pattern; psammoma bodies |
| (+) Psammoma bodies brain tumor | Meningioma |
| Spindle cells concentrically arranged in whorled pattern; (+) Psammoma bodies. | Meningioma |
| Blood vessel oring adult brain tumor. | Hemangioblastoma |
| Near surfaces fo brain and parasagittal regions. | Meningioma |
| Hemangiomas are most often __________________. | Cerebellar |
| What conditions are associated with Hemangioblastomas? | von Hippel-Lindau syndrome, when found with retinal angiomas |
| What is a possible consequence produced by Hemangioblastomas | Secondary polycythemia |
| How does a Hemangioblastoma cause secondary polycythemia? | It produces Erythropoietin |
| What is the histology found in Hemangioblastomas? | Closely arranged, thin-walled capillaries with minimal intervening parenchyma. |
| Adult or Childhood brain tumor: Schwannoma? | Adult |
| What are the tow types of Pituitary adenoma? | 1. Non-functioning (silent) 2. Hyperfunctioning (hormone producing) |
| What is meant by a Hyperfunctional Pituitary adenoma? | Brain tumor that produces hormones |
| What is the most common hyperfunctional pituitary adenoma? | Prolactinoma |
| What is the hormone consequence of the most common hyperfunctional pituitary adenoma? | Hyperprolactinemia |
| What are rare, hyperfunctional pituitary adenomas? | 1. Adenoma of somatotrophs (GH) --> acromegaly/gigantism 2. Adenoma of corticotrophs (ACTH) --> Cushing disease |
| What mass effect is seen with nonfunctional pituitary adenomas? | Bitemporal hemianopsia, hypopituitarism, and headache |
| What structure is compressed by pituitary adenoma that causes bitemporal hemianopsia? | Optic chiasm |
| The Optic chiasm is often compressed by which adult brain tumor? | Nonfunctional pituitary adenoma |
| What is the normal presentation of Prolactinoma in women? | Galactorrhea, amenorrhea, and decreased bone density due to suppression of estrogen. |
| What is the reason for the female clinical symptoms due to a Prolactinoma? | Suppression of estrogen by increased prolactin |
| How is a prolactinoma clinically presented in men? | Low libido and infertility |
| What is the non-surgical treatment of a Pituitary adenoma? | Dopamine agonists |
| Dopamine agonist are used to treat what type of adult brain tumor? | Pituitary adenoma |
| A transsphenoidal resection is a surgical treatment for: | Pituitary adenoma |
| What are common dopamine agonists used in Pituitary adenoma treatment? | Bromocriptine and Cabergoline |
| What is the location for a Schwannoma? | Cerebellopontine angle |
| What brain tumor is commonly found in the Cerebellopontine angle? | Schwannoma |
| What cranial nerves are involved in Schwannoma? | CN VII and VIII |
| Vestibular Schwannoma is localized in: | CN VIII in internal acoustic meatus |
| What brain tumor is located at Internal acoustic meatus? | Vestibular Schwannoma |
| Bilateral Schwannomas are associated with what condition? | NF-2 |
| What is the origin cell for Schwannomas? | Schwann cell |
| What are features that mark or indicate Schwann cell? | S-100 (+), and Biphasic |
| Histology of Schwannoma: | Dense, hypercellular areas containing spindle cells alternating with hypocellular, myxoid areas |
| Histology findings: Dense, hypercellular areas alternating with hypocellular, myxoid areas. | Schwannoma histology |
| S-100 (+). Brain cancer? | Schwannoma |
| List of childhood primary brain tumors: | 1. Pilocytic astrocytoma 2. Medulloblastoma 3. Ependymoma 4. Craniopharyngioma 5. Pinealoma |
| Adult or Childhood brain tumor: Pilocytic astrocytoma? | Childhood |
| Adult or Childhood brain tumor: Medulloblastoma? | Childhood |
| Adult or Childhood brain tumor: Ependymoma? | Childhood |
| Adult or Childhood brain tumor: Craniopharyngioma? | Childhood |
| Adult or Childhood brain tumor: Pinealoma? | Childhood |
| Low-grade astrocytoma in children. | Pilocytic astrocytoma |
| What is the most common primary brain tumor in children? | Pilocytic astrocytoma |
| Where is most often found a Pilocytic astrocytoma? | Posterior fossa (cerebellum) |
| The Posterior fossa (cerebellum) is the most common location for which childhood primary brain tumor? | Pilocytic astrocytoma |
| What is the cell of origin for Pilocytic astrocytoma? | Glial cell |
| GFAP (+). Glial cell oring. Child. Dx? | Pilocytic astrocytoma |
| Histologic findings in Pilocytic astrocytoma: | - Rosenthal fibers - eosinophilic, corkscrew fibers |
| Rosenthal fibers are seen in which childhood brain malignancy? | Pilocytic astrocytoma |
| What is the most malignant primary childhood brain tumor? | Medulloblastoma |
| What is the most common location for a Medulloblastoma? | Cerebellum |
| What structure may be compressed by a Medulloblastoma? | 4th ventricle |
| What is the result of compression to the 4th ventricle by a Medulloblastoma? | Noncommunicating hydrocephalus |
| What type of hydrocephalus is seen in Medulloblastoma? | Noncommunicating hydrocephalus |
| From of primitive neuroectodermal tumor (PNET). | Medulloblastoma |
| What are the important histological findings of a Medulloblastoma? | Homer-Wright rosettes, small blue cells |
| Small blue cells found in Medulloblastoma histological view. | Homer-Wright rosettes |
| (+) Homer-Wright rosettes. Dx? | Medulloblastoma |
| "Drop metastases" to spinal cord. | Medulloblastoma |
| What are the symptoms caused by the noncommunicating hydrocephalus often found in Medulloblastoma patients? | Headaches and Papilledema |
| What is the most likely childhood brain tumor that involves or may cause 4th ventricle compression? | Medulloblastoma |
| Where is an ependymoma most likely found? | 4th ventricle |
| An autopsy of a deceased child shows a large mass in the 4th ventricle. Dx? | Ependymoma |
| Ependymoma may cause ---> | Hydrocephalus |
| How is the prognosis of a Ependymoma? | Poor |
| Ependyma cell origin childhood brain tumor. | Ependymoma |
| What is the main histological characteristic of an Ependymoma? | Perivascular pseudorosettes |
| What, histological finding, is seen near the nucleus of Ependymoma cells? | Rod-shaped blepharoplasts |
| What are the Blepharoplasts? | Basal ciliary bodies near the nucleus of ependymal ells |
| Tumor cells arranged radially around a central vessel | Perivascular pseudorosettes |
| What is the most common childhood supratentorial tumor? | Craniopharyngioma |
| A Craniopharyngioma is often mistaken or misdiagnosed with a ___________________. | Pituitary adenoma |
| What complication or symptoms do both, Craniopharyngioma and Pituitary adenoma, cause that may indicate why there are often mistaken by each other? | Bitemporal hemianopsia |
| Which childhood tumor is derived from remnants of Rathke's pouch (ectoderm)? | Craniopharyngioma |
| What is a key or featured histological finding of a Craniopharyngioma? | Cholesterol crystal found in "motor-oil"-like fluid within tumor |
| Cholesterol crystal in what seems to be motor oil fluid. Dx? | Craniopharyngioma |
| What is a Pinealoma? | Childhood brain tumor of pineal gland |
| What is a common consequence of a Pinealoma? | Parinaud syndrome |
| How does a Pinealoma causes Parinaud syndrome? | Compression of tectum which presents with vertical palsy gaze |
| What is Parinaud syndrome? | Compression of tectum leading to vertical gaze palsy |
| List of common compression compilation by a Pinealoma? | 1. Parinaud syndrome 2. Obstructive hydrocephalus 3. Precocious puerbty in males |
| How does a Pinealoma cause Obstructive hydrocephalus? | Compression of cerebral aqueduct |
| The compression of the cerebral aqueduct by a Pinealoma leads to development of: | Obstructive hydrocephalus |
| How does Pinealoma cause precocious puberty in males? | Increase B-hCG production |
| Which childhood primary brain tumor is similar to germ cell tumors? | Pinealoma |
| A testicular seminoma can be said to be the ____________ of the brain tumors. | Pinealoma |
| What are the deficits or symptoms seen with frontal lobe tumors? | 1. One sided paralysis 2. Seizures 3. Defective memory 4. Impaired judgement 5. Personality changes |
| What are the common symptoms seen with Temporal lobe tumors? | - Occasional seizures - Language disorders |
| Brain stem CNS tumors present what common symptoms? | 1. Uncoordinated walk 2. Muscle weakness 3. Difficulty in speech 4. Drowsiness 5. Hearing loss |
| A person with a CNS tumor located in the cerebellum will likely experience the following symptoms: | 1. Vomiting 2. Headache 3. Uncoordinated muscle movement 4. Problems in walking |
| Parietal lobe tumors/cancer will likely present the patient with: | - Seizures - Speech disturbance - Loss ability to write |
| An occipital lobe tumor very likely will present with: | Blindness and seizures |
| One sided paralysis due to CNS tumor, is most likely found in which lobe? | Frontal lobe |
| What is the most common symptom of a Supratentorial tumor? | Symptoms of raised ICP |
| Papilloedema, seizures, raised ICP, and focal neurological deficits, are seen in what type of brain tumors? | Supratentorial tumors |
| Posterior fossa tumours main symptoms are: | Nausea and vomiting |
| Which brain tumors are often seen with Pyramidal signs? | Brain stem tumors |
| What are the top 3 symptoms of Brain stem tumors? | 1. Abnormal gait and coordination difficulties 2. Cranial nerve palsies 3. Pyramidal signs |
| Spinal cord tumors main clinical symptom is: | Back pain |
| What brain tumors are located in the Corpus callosum? | Astrocytoma and Oligodendroglioma |
| Which brain tumors are located in the Cerebral hemisphere? | Astrocytoma, Meningioma, Oligodendroglioma, and Ependymoma. |
| Brain tumors in the ventricles: | Ependymoma, Choroid plexus papilloma, and Subependymoma |
| Where is the common location for a hemangioblastoma? | Cerebellum |
| What is Aphasia? | Higher-order language deficit |
| Inability to understand/produce/use language appropriately. | Aphasia |
| What is the cause for Aphasias? | Pathology in dominant cerebral hemisphere |
| A condition that affects the dominant cerebral hemisphere, that causes the patient to inappropriately verbally express. | Aphasia |
| Which is the most commonly affected Dominant cerebral hemisphere in aphasia? | Left (usually the dominant side) |
| What is Dysarthria? | Motor inability to speak |
| Is Aphasia or Dysarthria the inability to produce movement in order to speak? | Dysarthria |
| What are the two criteria tested or analyzed in Aphasias? | Speech fluency and Comprehension |
| What are the main two categories in which aphasias are usually divided into? | 1. Repetition impaired 2. Repetition intact |
| What specific language and speech characteristic is used to categorize the most significant types of aphasias? | Repetition ability |
| List of the Repetition IMPAIRED aphasias: | 1. Broca (expressive) 2. Wernicke (receptive) 3. Conduction 4. Global |
| Which repetition impaired aphasia have NON-fluent speech fluency? | Broca and Global |
| Which is the only repetition impaired aphasia that has both affected, speech fluency and comprehension? | Global aphasia |
| Broca area location | Inferior frontal gyrus of frontal lobe |
| What area/structure is at the inferior frontal gyrus of frontal lobe? | Broca area |
| How is a Broca aphasia patient commonly found (emotionally) during doctor's visits or therapy? | Frustrated |
| A patient with a broken language, goes to doctor's office, but during the visit the patient, loses patience and acts extremely frustrated and agitated. Dx? | Broca aphaia |
| Broca aphae is _______________________. | Expressive |
| Wernicke aphasia is denominated a __________________ aphasia. | Receptive |
| What type of aphasia is most likely indicated if it's described as an "expressive aphasia" with repetition impaired? | Broca aphasia |
| Speech fluency = Nonfluent Comprehension = Intact Repetition = Impaired What is the most likely Dx? | Broca aphasia |
| Speech fluency = Fluent Comprehension = Impaired Repetition = Impaired | Wernicke's aphasia |
| How are the speech fluency and comprehension in a Wernicke's aphasia? | Fluent speech but impaired or poor comprehension |
| Patients do not have insight. Aphasia? | Wernicke's aphasia |
| Superior temporal gyrus of temporal lobe. | Wernicke area |
| How is the "insight" of a Broca aphasia patient? | Intact |
| What kind of aphasia is seen by damage to the Arcuate fasciculus? | Conduction aphasia |
| What is the only deficit seen in Conduction aphasia? | Repetition |
| Speech fluency = Fluent Comprehension = Intact Repetition = Impaired | Conduction aphasia |
| If both areas, Broca and Wernicke areas, are affected, what is the most likely type of repetition impaired aphasia to be developed? | Global aphasia |
| What are the two repetition impaired aphasias that develop due to damage to the Arcuate fasciculus? | Conduction and Global aphasias |
| What is the key word in the name of aphasias that have INTACT repetition? | Transcortical |
| If the aphasia in question has the word "Transcortical" it always depicts what characteristic? | Repetition is INTACT |
| What are the 3 types of Repetition intact aphasias? | 1. Transcortical motor 2. Transcortical sensory 3. Transcortical, mixed |
| Speech fluency = Nonfluent Comprehension = Intact Repetition = Intact | Transcortical motor aphasia |
| Affects frontal love around Broca area, but Broca area is spared. Dx? | Transcortical motor aphasia |
| What area is spared from damage in Transcortical motor aphasia? | Broca area |
| What areas are affected in Transcortical motor aphasia? | Frontal lobe around Broca area |
| Speech fluency = Fluent Comprehension = Impaired Repetition = Intact | Transcortical sensory aphasia |
| Which aphasia affects the temporal lobe around the Wernicke area, but Wernicke area is actually spared (non affected)? | Transcortical sensory aphasia |
| Speech = Nonfluent Comprehension = Impaired Repetition = Intact | Transcortical, mixed aphasia |
| What areas are spared from damage in Transcortical, mixed aphasia? | Broca and Wernicke areas and Arcuate fasciculus remain intact. |
| What is affected in order to develop Transcortical, mixed aphasia? | Watershed areas |
| Watershed areas of brain are affected. What pathology is associated or develope due to this effect? | Transcortical, mixed aphasia |
| When is comprehension affected in aphasias? | The Wernicke area or its surroundings are affected |
| When is Speech fluency affected in aphasias? | Broca area or its surroundings are affected/damaged |
| What is the definition of aneurysms? | Abnormal dilation of an artery due to weakening of vessel wall |
| Abnormal dilation of an artery due to weakening of vessel wall | Aneurysm |
| What are the two main types of aneurysms? | 1. Saccular aneurysm 2. Charcot-Bouchard microaneurysm |
| What is another way to name a Saccular aneurysm? | Berry aneurysm |
| Where do Berry (Saccular) aneurysms occur? | Bifurcations of the circle of Willis |
| Where is the MC site for a Berry aneurysm? | Junction of Anterior Communicating artery (ACom) and ACA. |
| What are two conditions associated with development of Berry aneurysms? | ADPKD and Ehlers-Danlos syndrome |
| What are secondary (minor) associated risk factors of Berry aneurysm development? | Advance age, hypertension, smoking, African-American race |
| Which race is most commonly affected by Berry aneurysms? | African-Americans |
| Pathway in which a Saccular aneurysm develops focal neurological deficits: | Rupture of Saccular aneurysm --> Subarachnoid hemorrhage leading to focal neurological deficits |
| What common ways patients describe the symptoms of Subarachnoid hemorrhage? | 1. "worst headache of my life", 2. "thunderclap headache" |
| The direct compression of the Anterior Communicating artery by a Saccular aneurysm produces the following symptoms: | - Bitemporal hemianopia; - Visual acuity deficits - Rupture --> ischemia in ACA distribution leading to contralateral lower extremity hemiparesis, and sensory deficits |
| What is the result of ACom rupture because of a Berry aneurysm in the ACA? | Contralateral lower extremity hemiparesis and sensory deficits |
| What is the result of MCA distribution obstruction due to a Berry aneurysm ruptures? | Contralateral upper extremity and lower facial hemiparesis, and sensory deficits |
| PCom compression due to direct compression of a Berry aneurysm ---> | Ipsilateral CN III palsy leading to mydriasis; and possible ptosis, "down and out" eye. |
| What are arteries commonly directly compressed by a Saccular aneurysms? | 1. ACom 2. MCA 3. PCom |
| What is a common aneurysm, associated with chronic hypertension? | Charcot-Bouchard microaneurysm |
| What small vessels are commonly affected by Charcot-Bouchard microaneurysm? | Lenticulostriate arteries in basal ganglia and Thalamus |
| What is a common severe complication of Charcot-Bouchard aneurysms? | Lacunar strokes |
| What is a common cause of Lacunar strokes? | Charcot-Bouchard microaneurysms |
| Seizures are characterized by: | Synchronized, high-frequency neuronal firing |
| What are the two main categories of Seizures? | 1. Partial (focal) seizures 2. Generalized seizures |
| What are partial (focal) seizures? | Affect single area of the brain. Most commonly originate in medial temporal lobe. |
| What are the types of Partial (focal) seizures? | 1. Simple partial seizures 2. Complex partial seizures |
| Description of Simple partial seizures? | - Consciousness intact - Motor, sensory, autonomic, and psychic |
| Which type of focal seizure is characterized with impaired consciousness, and automatisms? | Complex partial seizures |
| What conditions (pathologies) are associated with Partial (focal) seizures? | 1. Epilepsy 2. Status epilepticus |
| What is Epilepsy? | A disorder of recurrent seizures |
| What is Status epilepticus? | Continuous (> 5 mins) or recurring seizures that may result in brain injury |
| Condition of recurrent seizures less than 5 minutes, that result in brain injury. | Status epilepticus |
| Diffuse seizures = | Generalized seizures |
| What are the types of Generalized seizures? | 1. Absence 2. Myoclonic 3. Tonic-clonic 4. Tonic 5. Atonic |
| What is another way to name an absence seizure? | Petit mal |
| 3 Hz spike-and-wave discharges, no postictal confusion, and blank stare. | Absence seizure |
| What type of generalized seizures is featured by a "blank stare"? | Absence seizure |
| Description of Myoclonic seizures: | Quick, repetitive jerks |
| What is another way to refer to a Tonic-clinic seizure? | Grand mal |
| If a vignette describes a "grand mal" seizure, it refers to: | Tonic-clonic seizure |
| What is the description of and Tonic-clonic seizure? | Alternating stiffening and movement |
| Person fall on floor and has a pattern of body stiffening and movement alternation. Dx? | Tonic-clonic seizure |
| What is the term "tonic" refer in seizures? | Stiffening |
| Description Atonic seizure? | "drop" seizures (falls to floor); commonly mistaken for fainting |
| "drop" seizures | Atonic seizures |
| What is the MCC of elderly seizures? | Stokes |
| What is another way to refer infection seizure? | Febrile seizure |
| What is a headache? | Pain due to irritation of structures such as the dura, cranial nerves, or extracranial structures. |
| What types of headaches are more common in males? | Cluster headaches |
| What are the types of headaches important for USMLE? | 1. Cluster 2. Tension 3. Migraine |
| Which type (s) of headache are unilateral? | Cluster and Migraine |
| Which type of headache is bilateral? | Tension |
| What is the duration of a Cluster headache? | 15 min - 3 hour; repetitive |
| What is the description of a Cluster headache? | - Excruciating periorbital pain with lacrimation and rhinorrhea - (+/-) Horner syndrome - More common in males |
| What is the acute treatment of a Cluster headache? | Sumatriptan, 100% oxygen |
| What is the prophylaxis medication for cluster headache? | Verapamil |
| What is the average duration of a Tension headache? | > 30 minutes |
| Description of Tension headache | - Steady, "band-like" pain. - No photophobia or phonophobia - No aura |
| What are the common drugs used for acute tension headache? | Analgesics, NSAIDs, and acetaminophen |
| What medication is commonly used to treat chronic tension headaches? | Amitriptyline |
| Unilateral, intense 4-72 hour headache. | Migraine |
| What is the duration of a migraine? | 4 - 72 hours |
| What is the description of a Migraine? | - Pulsating pain with nausea, photophobia, or phonophobia - (+/-) have "aura" |
| What is the cause for a migraine? | Irritation of CN V, meninges, or blood vessels |
| What serum substances are secreted in the pathogenesis of a migraine? | Substance P, calcitonin gene-related peptide, and vasoactive peptides |
| What is the acute treatment of a migraine? | NSAIDs, triptans, and dihydroergotamine |
| Prophylaxis of a migraine: | Lifestyle changes, B-blockers, amitriptyline, topiramate, and valproate. |
| What is a common mnemonic of migraine characteristics? | POUND Pulsatile One-day duration Unilateral Nausea Disabling |
| What are less common causes of headache? | Subarachnoid hemorrhage, meningitis, hydrocephalus, neoplasia, and giant cell (temporal) arteritis. |
| A cluster headache is often compared with what other pathology? | Trigeminal neuralgia |
| Producers repetitive, unilateral, shooting pain in the distribution of CN V. | Trigeminal neuralgia |
| What is the first line of therapy for Trigeminal neuralgia? | Carbamazepine |
| What can trigger Trigeminal neuralgia? | Chewing, talking, touching certain parts of the face |
| What is "Akathisia"? | Restlessness and intense urge to move |
| Restlessness and intense urge to move. | Akathisia |
| Possible side effect of Parkinson treatment | Akathisia |
| What is Asterixis? | Extension of wrists causes "flapping" motion |
| What pathologies and/or conditions are associated with Asterix? | Hepatic encephalopathy, Wilson disease, and other metabolic derangements. |
| What are two common movement disorders associated with lesion of the Basal ganglia? | Athetosis and Chorea |
| What is Athetosis? | Slow, snake-like, writhing movements; especially in the fingers |
| Slow, snake-like, writhing movements in the fingers | Athetosis |
| Definition of Chorea: | Sudden, jerky, purposeless movements |
| Sudden, jerky, and purposeless movements | Chorea |
| What conditions are seen with Chorea? | Huntington disease and Rheumatic fever |
| Dystonia is: | Sustained, involuntary muscle contractions |
| An involuntary muscle contraction that is sustained for short period of times. | Dystonia |
| Associated conditions that may produce Dystonia: | Writer's cramp, blepharospasm, and torticollis |
| "Writer's cramp" is an example of what type of movement disorder? | Dystonia |
| What is Essential tremor? | High-frequency tremor with sustained posture, worsened with movement or when anxious |
| High-frequency tremor with sustained posture, that is worst in movements of anxiety or movement. | Essential tremor |
| What is the common treatment that individual may choose to treat Essential tremor? | Alcohol, since it decreases tremor amplitude |
| Why is common to find alcoholism in a patient with Essential tremor? | Alcohol- it decreases amplitude of the tremor |
| What is the medically relevant (not alcohol) treatment for Essential tremor? | Non-selective B-blockers, and primidone. |
| Sudden, wild flailing of 1 arm, +/_ ipsilateral leg. | Hemiballismus |
| What is Hemiballismus? | Sudden, wild flailing of one arm, and possible the ipsilateral leg |
| Where is the lesion of Hemiballismus? | Contralateral subthalamic nucleus |
| Contralateral or Ipsilateral lesion is seen in Hemiballismus? | Contralateral |
| What type of movement disorder is seen with Cerebellar dysfunction? | Intention tremor |
| What is Intention tremor? | Slow, zigzag motion when pointing/extend toward a target |
| Slow, zigzag motion when pointing/extending toward a target | Intention tremor |
| A person that extends on purpose the arm pointing to a target is seen with slow, zigzag movements of such extremity. Dx? | Intention tremor |
| What is the definition of Myoclonus? | Sudden, brief, uncontrolled muscle contraction |
| If the muscle contraction is sudden and brief, it is _______________. | Myoclonus |
| What is the difference between the muscle contraction, in odr to be either dystonia or myoclonus? | Brief contraction is myoclonus Sustained contraction is dystonia |
| What are two common examples of Myoclonus? | Jerks and hiccups |
| Which organ failures are common to develop myoclonus? | Liver and kidneys |
| How is Resting tremor defined? | Uncontrolled movement of distal appendages; tremor alleviated by intentional movement. |
| What area is affected in Parkinson disease that leads to development of Resting tremor? | Substantia nigra |
| Which type of tremor occurs at rest? | Resting tremor |
| "Pill-rolling tremor" of Parkinson disease | Resting tremor |
| How is Resting tremor alleviated? | Producing intentional tremor |
| When is Restless legs syndrome the worst? | During rest or nighttime |
| What are associated conditions that are seen with Restless legs syndrome? | Iron deficiency and CKD |
| What is the treatment for Restless legs syndrome? | Dopamine agonists |
| Which movement disease or condition is treated with Dopamine agonists, such as ropinirole and Pramipexole? | Restless legs syndrome |
| What are two common Dopamine agonists used in Restless legs syndrome? | Pramipexole and Ropinirole |
| Pathophysiology of FEVER: | Cytokine activation during inflammation, such in an infection |
| What is the pathophysiology of a Heat stroke? | Inability of body to dissipate heat |
| Incapacity to get rid of body heat. | Heat stroke |
| What is the temperature for fever? | < 40 C |
| > 40 C. Fever or Heat stroke? | Heat stroke |
| What are the possible complications of fever? | Febrile seizure |
| List of complication from Heat Stroke: | - CNS dysfunction - End-organ damage - Acute respiratory distress syndrome - Rhabdomyolysis |
| What are the common drugs used to treat Fever? | 1. Acetaminophen or ibuprofen for comfort 2. Antibiotic therapy if indicated |
| How is Heat Stroke managed? | Rapid external cooling, rehydration and electrolyte correction |
| Decrease in cognitive ability, memory, or function with intact consciousness. | Neurodegenerative disorder |
| What is the term given to dementia caused by depression? | Pseudodementia |
| What mood disorder must be rule-out as the cause of dementia? | Depression |
| What are some reversible causes of dementia? | Hypothyroidism, vitamin B12 deficiency, neurosyphilis, normal pressure hydrocephalus, and depression. |
| What is the histologic and gross findings in Parkinson disease? | 1. Loss of dopaminergic neurons of substantia nigra pars compacta 2. Lewy bodies: composed of a-synuclein |
| What are Lewy bodies composed of? | a-synuclein |
| What are Lewy bodies? | Intracellular eosinophilic inclusions found in Parkinson disease |
| What is MPTP? | Contaminant in illegal drugs, is metabolized to MPP+, which is toxic to substantia nigra |
| What is a common toxic metabolic to the substantia nigra? | MPP+, a metabolite of MPTP |
| TRAPSS | Tremor Rigidity Akinesia Postural instability Shuffling gait Small handwriting |
| Medical term for small handwriting | Micrographia |
| Autosomal dominant trinucleotide (CAG)n. Dx? | Huntington disease |
| What is the gene involved in Huntington disease? | Trinucleotide expansion of CAGn in the huntingtin (HTT) gene on chromosome 4 |
| Which chromosome is affected in Huntington's disease? | Chromosome 4 |
| What is the common age range of onset of Huntington's symptoms? | 20-50 years old |
| What are the symptoms seen with Huntington disease? | Chorea, athetosis, aggression, depression, dementia. |
| Caudate loses ACh and GABA | Huntington disease |
| What genetic phenomenon is associated with Huntington disease? | Anticipation |
| Pathogenesis of Huntington's disease: | Atrophy of caudate and putamen with ex vacuo ventriculomegaly |
| Neurotransmitter levels in Huntington disease: | Increase dopamine, and decrease ACh and GABA |
| How do neurons "die" in Huntington disease? | Via NMDA-R binding and glutamate excitotoxicity |
| GAGn repeat. Dx? | Huntington disease |
| Which NTs are decreased in Huntington disease? | ACh and GABA |
| Which neurotransmitter is elevated in Huntington disease? | Dopamine |
| What is the MCC of dementia in the elderly? | Alzheimer disease |
| Which trisomy condition is associated with a higher risk of developing Alzheimer disease? | Down syndrome |
| Why are Down syndrome patients at higher risk of eventually developing Alzheimer disease? | APP is located in chromosome 21 |
| What neurotransmitter is decreased in Alzheimer's disease? | ACh |
| What are some associated altered proteins of Alzheimer disease? | 1. ApoE-2 2. ApoE-4 3. APP, presenilin-1, presenilin-2 |
| What protein is associated with a decrease risk of sporadic form of Alzheimer disease? | ApoE-2 |
| A person with an altered ApoE-4 protein ----> | Increase risk of sporadic form of Alzheimer disease |
| What proteins are associated with familial forms with earlier onset of Alzheimer disease? | APP, presenilin-1, and presenilin-2 |
| Widespread cortical atrophy, especially hippocampus. Narrowing gyri and widening of sulci. | Gross findings of Alzheimer disease |
| What are some histological findings in Alzheimer disease? | Senile plaques in gray matter: extracellular B-amyloid core |
| What are the Neurofibrillary tangles found in histology of Alzheimer disease patient? | Intracellular, hyperphosphorylated tau protein = insoluble cytoskeletal elements |
| What part of the brain is most affected by Alzheimer disease? | Hippocampus |
| What neurodegenerative condition is associated with Hirano bodies? | Alzheimer disease |
| What are the intracellular rods found in Alzheimer disease? | Hirano bodies |
| What are Hirano bodies? | Intracellular eosinophilic proteinaceous rods in hippocampus |
| Where in the brain are Hirano bodies found? | Hippocampus |
| What is the old name for Frontotemporal dementia? | Pick disease |
| What is the new name of Pick disease? | Frontotemporal dementia |
| What are the histological findings of Frontotemporal dementia? | Inclusions of hyperphosphorylated tau or ubiquitinated TDP-43 |
| Histological findings: Hyperphosphorylated Tau proteins and Ubiquitinated TDP-43. Dx? | Frontotemporal dementia |
| What are clinical feurs to Lewy body dementia? | Visual hallucinations, dementia with fluctuating cognition/alertness, REM sleep behavior disorder, and parkinsonism. |
| Where are Lewy bodies are primarily found? | In cortex |
| What neurologic disorder is associated with REM sleep behavior disorder? | Lewy body dementia |
| When is it called Lewy body dementia? | If cognitive and motor symptom onset is < 1 year apart |
| If the cognitive deficit in is over a year apart form motor deficit, it is not longer considered Lewy body dementia, instead it is considered: | Secondary to Parkinson disease |
| What is the cause of Vascular dementia? | Result of multiple arterial infarcts and/or chronic ischemia |
| What is the second MCC of dementia in elderly? | Vascular dementia |
| Step-wise decline in cognitive ability with late-onset memory impairment. | Vascular dementia |
| MRI or CT show multiple cortical and/or subcortical infarcts. Dx? | Vascular dementia |
| What do the images of a MRI or CT of vascular dementia patient most likely show? | Multiple cortical and/or subcortical infarcts |
| What is Creutzfeldt-Jakob disease? | Rapidly progressive dementia with myoclonus and ataxia |
| What is commonly seen in EEG of CJD? | Periodical sharp waves |
| Important CSF finding in CJD? | Incread 14-3-3 protein |
| Elevated 14-3-3 protein in CSF. Dx? | Creutzfeldt-Jakob disease |
| - Rapid progressive dementia, + - "Startle myoclonus", + - Ataxia. Dx? | Creutzfeldt-Jakob disease |
| Spongiform cortex. Dx? | Creutzfeldt-Jakob disease |
| Prion neurodegenerative condition. | Creutzfeldt-Jakob disease |
| What is another name for Idiopathic intracranial hypertension? | Pseudotumor cerebri |
| Elevated ICP with no apparent cause on imaging. Dx? | Idiopathic intracranial hypertension |
| What are conditions the cause increased ICP with no imaging evidence? | Hydrocephalus, and obstruction of CSF outflow |
| What are common risk factor for Idiopathic intracranial hypertension? | Female gender, Tetracycline, Obesity, vitamin A excess, and Danazol |
| What the common physical findings seen with Idiopathic intracranial hypertension? | Headache , tinnitus, diplopia, no change in mental status |
| What is the treatment of Pseudotumor cerebri? | Weight loss, acetazolamide, invasive procedures for refractory cases. |
| What cause the papilledema seen in Pseudotumor cerebri? | Impaired optic nerve axoplasmic flow |
| What is accomplished by performing a LP on a patient with Idiopathic intracranial hypertension? | Reveals elevated opening pressure and provides temporary headache relief. |
| What is the pathogenesis of Hydrocephalus? | Increased CSF volume leads to ventricular dilation and possible increase in ICP |
| How are types of hydrocephalus mainly divided into? | Communicating, Non-communicating,and Hydrocephalus mimics |
| WHat are the two types Communicating hydrocephalus? | 1. Communicating hydrocephalus 2. Normal pressure hydrocephalus |
| What is the cause of Communicating hydrocephalus? | Decreased CSF absorption by arachnoid granulations leading to development of elevated ICP, papilledema, and herniation |
| Arachnoid scarring post-meningitis is a common cause for: | Communicating hydrocephalus |
| What population is most affected by normal pressure hydrocephalus (NPH)? | Elderly |
| CSF pressure elevated only episodically; does not result in increased subarachnoid space volume; expansion of the ventricles. Dx? | Normal Pressure Hydrocephalus |
| What is the result of the expansion of the ventiluces in NPH? | Distorts the fibers of the corona radiata leading to development of trial do urinary incontinence, gait apraxia, and cognitive dysfunction. |
| What is the common triad associated with NPH? | 1. Urinary incontinence 2. Gait apraxia 3. Cognitive dysfunction |
| What is another way to describe the gait apraxia seen in NPH patient? | Magnetic gait |
| What part is distorted in NPH ventricle expansion leading to developing of its famous clinical triad? | Fibers of the corona radiata |
| What is the treatment that often lead to reversivion of cysmtpos in NPH? | CSF shunt placement |
| What type of hydrocephalus is classified as Obstructive? | Non-communicating hydrocephalus |
| Caused by structural blockage of CSF circulation within ventricular system | Pathogenesis of Non-communicating hydrocephalus |
| What are examples that cause the obstruction in Non-communicating hydrocephalus? | - Stenosis of aqueduct of Sylvius - Colloid cyst blocking foramen of MOnro - Tumor |
| Ex vacuo ventriculomegaly | Appearance of increased CSF on imaging, but is actually due to decreased brain tissue and neuronal atrophy |
| Apparent increase in CSF + Normal ICP + (-) NPH triad. Dx? | Ex vacuo ventriculomegaly |
| What condition mimics a Hydrocephalus? | Ex vacuo ventriculomegaly |
| Which conditions are often associated with Ex vacuo ventriculomegaly? | Alzheimer's disease, advanced HIV, Pick disease, and Huntington's disease |
| Why are Huntington and Alzheimer's, and other neurodegenerative conditions associated with Ex vacuo ventriculomegaly? | Decreased brain tissue and nurutonal atrophy |
| What is Multiple sclerosis? | Autoimmune inflammation and demyelination of CNS with subsequent axonal damage. |
| Autoimmune inflammation and demyelination of CNS with subsequent axonal damage. | Multiple sclerosis |
| What are the general features presented in Multiple sclerosis? | 1. Acute optic neuritis 2. Brain stem/cerebellar syndromes 3. Pyramidal tract weakness 4. Spinal cord syndromes |
| Description Acute Optic neuritis in MS: | Painful unilateral visual loss associated with Marcus Gunn pupil |
| What are the clinical symptoms of the brainstem/cerebellar syndromes seen with Multiple sclerosis? | Diplopia, ataxia, scanning speech, intention tremor, nystagmus/INO. |
| INO deficit is often associated with _________ ___________. | Multiple sclerosis |
| What is Lhermitte phenomenon? | Electric shock-like sensation along spine on neck flexion |
| What neurological autoimmune condition is associated with Lhermitte phenomenon? | Multiple sclerosis |
| What physical condition may exacerbate symptoms of Multiple sclerosis? | Increased body temperature |
| What is the common pattern or characteristic of MS clinical course? | Relapsing and remitting |
| Which population are most affected with Multiple sclerosis? | Women in their 20s and 30s; more common in Caucasians living away from the equator |
| Oligoclonal bands are diagnostic for what condition? | Multiple sclerosis |
| What is found in CSF sample of a Multiple sclerosis patient? | Elevated IgG level aodn myelin basic protein |
| What is the gold standard test/imagining procedure for Multiple sclerosis? | MRI |
| What are the findings in MRI of a MS patient? | Periventricular plaques |
| MRI (+) periventricular plaques | Multiple sclerosis |
| What are the periventricular plaques found in MRI of MS? | Areas of Oligodendrocyte loss and reactive gliosis |
| Multiple white matter lesions disseminated in space and time. Dx? | Multiple sclerosis |
| Multiple sclerosis affects white or gray matter? | White matter |
| What is used to treat acute flares of MS? | IV steroids |
| What is the treatment (chronic) for Multiple sclerosis? | Stop relapses and halt/slow progression with disease-modifying therapies |
| What are common drugs denominated as Disease-modifying therapies? | B-interferon, glatiramer, and Natalizumab |
| What is another name for Osmotic demyelination syndrome? | Central pontine myelinolysis |
| What is Osmotic demyelination syndrome? | Massive axonal demyelination in pontine white matter |
| What is the cause for Osmotic demyelination syndrome? | Secondary to rapid osmotic changes, most commonly iatrogenic correction of hyponatremia but also rapid shifts of other osmolytes |
| Clinical features of Osmotic demyelination syndrome? | Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness |
| What is a possible severe complication of Osmotic demyelination syndrome? | "Locked-in syndrome" |
| Problems arise from correcting serum Na+ too fast or too slow? | Too fast |
| Excessively rapid correction of low serum Na+ to high serum Na+ leads to development of: | Osmotic demyelination syndrome |
| Serum Na+ form high to low rapid correction lead to: | Cerebral edema/herniation |
| Massive axonal demyelination in pontine white matter secondary to rapid osmotics changes, especially rapid correction of low serum Na+ to high serum Na+? | Osmotic demyelination syndrome |
| What is the most common subtype of Guillain-Barre syndrome? | Acute inflammatory demyelinating polyradiculopathy |
| What is acute inflammatory demyelinating polyradiculopathy? | Autoimmune conditions associated with infections and motor fibers likely due to molecular mimicry, inoculation, and stress, but no definitive link to pathogens |
| What infection is associated to Acute inflammatory demyelinating polyradiculopathy? | Campylobacter jejuni, virus (Zika) that destroy Schwann cells by inflammation and demyelination of peripheral nerves III-XII |
| What is the clinical presentation of Acute inflammatory polyradiculopathy, common subtype of GBS? | 1. Symmetric ascending muscle weakness/paralysis and depressed /absent DTRs beginning in lower extremities 2. Facial paralysis (MC bilaterally) 3. Respiratory failure 4. +/- Autonomic dysregulation and/or sensory abnormalities |
| What is albuminocytologic dissociation? | Increased CSF protein with normal cell count |
| What conditions is seen with albuminocytologic dissociation? | Acute inflammatory demyelinating polyradiculopathy |
| What is the treatment for Acute inflammatory demyelinating polyradiculopathy? | Disease-modifying treatment with plasmapheresis, and IV immunoglobulins |
| What is Acute disseminated (postinfectious) encephalomyelitis? | Multifocal inflammation and demyelination after infection or vaccination |
| What is the common clinical presentation of Acute disseminated encephalomyelitis? | Rapidly progressive multifocal neurological symptoms and altered mental status. |
| What is the common name for Hereditary motor an sensory neuropathy? | Charcot-Marie-Tooth disease |
| What is Charcot-Marie-Tooth disease? | Group of progressive hereditary nerve disorders related to the detective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath. |
| Defective production of proteins involved in the structures and function of peripheral nerves or myelin sheath. Dx? | Charcot-Marie-Tooth disease |
| The defective protein in Charcot-Marie-Tooth disease lead to abnormal structure and function of which neurologic structure? | Peripheral nerves and myelin sheath |
| What is a clinical relevant feature of Charcot-Marie-Tooth disease? | Foot deformities |
| What are the common foot deformities in CMT disease? | Pes cavus, and hammer toe |
| Mode of inheritance of Charcot-Marie-Tooth disease? | Autosomal dominant |
| What are the symptoms seen in Charcot-Marie-Tooth disease? | 1. Foot deformities 2. Lower extremity weakness, and 3. Sensory deficits |
| What is and what causes the most common type of Charcot-Marie-Tooth disease? | CMT1A, is caused by PMP22 gene duplication |
| Duplication of gene PMP22 leading to synthesis of CMT1A. Dx? | Charcot-Marie-Tooth disease |
| Demyelination of CNS due to destruction of oligodendrocytes secondary to JC virus infection. Dx? | Progressive multifocal leukoencephalopathy |
| What type of patients is PML encephalopathy often seen? | AIDS |
| What is the clinical course often seen by JC virus induced PML? | Rapidly progressive and most often fatal |
| What areas of the brain are most commonly affected by PML? | Parietal and occipital areas |
| What therapies or medication increase firsl of developing PML by JC viral infection? | Natalizumab and Rituximab |
| What is a possible severe complication in AIDS patient by the reactivation of latent JC virus infection? | Progressive multifocal leukoencephalopathy |
| Krabbe disease, Metachromatic leukodystrophy, and adrenoleukodystrophy, are examples of: | Demyelinating disorders |
| List of Neurocutaneous disorders: | 1. Sturge-Weber syndrome 2. Tuberous sclerosis 3. Neurofibromatosis type 1 4. Neurofibromatosis type 2 5. von Hippel-Lindau disease |
| What is another name for Sturge-Weber syndrome? | Encephalotrigeminal angiomatosis |
| What is the cause of Sturge-Weber syndrome? | Congenital, non-inherited, developmental anomaly of neural crest derivatives due to somatic mosaicism for an activating mutation in one copy of the GNAQ gene |
| What causes the "stain in face" in a patient with Sturge-Weber syndrome? | Small (capillary-seized) blood vessels |
| What is the port-wine stain of the face in a Sturge-Weber syndrome? | Nevus flammeus, a non-neoplastic "birthmark" in CN V1/V2 distribution |
| What are the clinical features of Sturge-Weber syndrome? | 1. Port-wine stain of the face 2. Ipsilateral leptomeningeal angioma --> seizures/epilepsy 3. Episcleral hemangioma leading to increased IOP --> early-onset glaucoma |
| What is the affected gene in Sturge-Weber syndrome? | GNAQ gene |
| What is the result of the elevated IOP of Sturge-Weber syndrome? | Glaucoma |
| TSC1 mutation on chromosome 9 or TSC2 mutation on chromosome 16. Dx? | Tuberous sclerosis |
| What are features of Tuberous sclerosis? | - Hamartomas in CNS and skin - Angiofibromas - Mitral regurgitation - Ash-leaf spots - Cardiac Rhabdomyoma - Autosomal dominant inheritance - Mental retardation - Renal Angiomyolipoma - Seizures - Shagreen patches |
| What malignancies or tumors have increased incidence in Tuberous sclerosis, but not are part of the disorder? | Subependymal giant cell astrocytomas and Ungual fibromas |
| Hamartomas in CNS and skin. Dx? | Tuberous sclerosis |
| What kind of murmur is seen in Tuberous sclerosis? | Mitral regurgitation |
| What AD neurocutaneous disorder is associated with cardiac rhabdomyoma and Ash-leaf spots? | Tuberous sclerosis |
| What renal tumors are seen in Tuberous sclerosis? | Renal angiomyolipoma |
| Shagreen patches are seen in : | Tuberous sclerosis |
| What type of skin lesions or "stains" are seen in Tuberous sclerosis? | Ash-leaf spots and Shagreen patches |
| How else is Neurofibromatosis type I? | Recklinghausen disease |
| What chromosome of is affected in NF I? | Chromosome 17 |
| What are the most significant features of NF I? | 1. Cafe-au-lait spots 2. Cutaneous neurofibromas 3. Optic gliomas 4. Pheochromocytomas 5. Lisch nodules |
| What condition is associated with Lisch nodules? | Neurofibromatosis type I |
| What is Lisch nodules? | Pigmented iris hamartomas |
| What are main clinical features of Neurofibromatosis type II? | 1. Bilateral acoustic schwannomas 2. Juvenile cataracts 3. Meningiomas 4. Ependymomas |
| Which neurocutaneous conditions is associated with Bilateral acoustic schwannomas? | Neurofibromatosis type II |
| What are the associated brain tumors of NF II? | 1. Acoustic Schwannomas 2. Meningiomas 3. Ependymomas |
| Deletion of VHL gene of chromosome 3p. Dx? | von Hippel-Lindau disease |
| What is the role of pVHL? | Ubiquinates hypoxia-inducible factors 1 |
| What are the characteristics of vHL disease? | Numerous tumors, both benign and malignant |
| What mnemonic is sued by von Hippel-Lindau disease? | HARP: - Hemangioblastomas with hyperchromatic nuclei in retina, brain stem, cerebellum, and spine - Angiomatosis - Bilateral Renal Carcinomas - Pheochromocytomas |
| Which organs and tissues develop hemangioblastomas in vHL disease? | Retina, brain stem, cerebellum, and spine |
| What is the associated angiomatosis developing in vHL disease? | Cavernous hemangiomas in skin, mucosa, and other organs |
| Bilateral renal carcinomas + Pheochromocytomas + Hemangioblastomas. Dx? | von Hippel-Lindau disease |
| What is the consequence of frontal lobe lesion? | Disinhibition and deficits in concentration, orientation, judgement |
| What is a possible secondary result of frontal lobe lesion? | Reemergence of primitive reflexes |
| What kind of brain lesion may lead to reemerge of primitive reflexes? | Frontal lobe |
| Disinhibition and deficits in concentration, orientation, and judgement is caused aftera ___________ ____________ lesion. | Frontal lobe lesion |
| What are the consequences Frontal eye fields lesions? | Eyes look toward (destructive) side of lesion. In seizures (irritative), eyes look away from side of the lesion |
| Is it classified as destructive or irritative, a frontal eye field lesion, if the eyes look to the side of lesion? | Destructive |
| Irritative frontal eye field lesion: | Seizures, eyes look away from side of the lesion |
| What are the two types of Frontal eye field lesions? | Destructive and Irritative |
| How are the eyes deviated in a irritative frontal eye field lesion? | Away from the side of lesion |
| If the eyes of a patient with a frontal eye field lesions are deviated toward the side of the lesion, is it a destructive or irritative injury? | Destructive |
| Consequence of Paramedian pontine reticular formation (PPRF) lesion? | Eyes look away from side of lesion |
| What is an example of an Paramedian Pontine Reticular formation lesion? | Ipsilateral gaze palsy |
| What is Ipsilateral gaze palsy? | The inability to look toward side of lesion due to PPRF lesion |
| Which area of the brain is injured in Internuclear Ophthalmoplegia? | Medial longitudinal fasciculus |
| Injured Medial Longitudinal fasciculus lead to development of: | Internuclear ophthalmoplegia |
| What is Internuclear ophthalmoplegia? | Impaired adduction of ipsilateral eye + nystagmus of contralateral eye with abduction |
| What are the two main clinical pathological components of Internuclear Ophthalmoplegia? | 1. Impaired adduction if ipsilateral eye 2. Nystagmus of contralateral eye with abduction |
| What conditoin is often associated with injury to the MLF? | Multiple Sclerosis |
| What is the ophthalmic condition associated with MS? | Internuclear ophthalmoplegia |
| Which area of the brain is damaged or injured in Gerstmann syndrome? | Dominant parietal cortex |
| What condition is seen to develop by injury to the dominant parietal cortex? | Gerstmann syndrome |
| What are the clinical consequences of Dominant parietal cortex injury? | Agraphia, acalculia, finger agnosia, left-right disorientation |
| A person with trouble writing, simple calculations, and not seem to recognise fingers. Dx? | Gerstmann syndrome |
| Male accountant that after a severe car accident develops inability to carry simple mathematical calculations. What is the most likely area of the brain that was injured? | Dominant parietal cortex |
| What condition is often seen in a person that can't distinguish the LEFT Index finger, by side or name? | Gerstmann syndrome |
| What are the clinical consequences of lesion to the Non-dominant parietal cortex? | Agnosia of the contralateral side of the world |
| Ignoring the right side of the world, is a result of: | Left sided non-dominant parietal cortex lesion |
| What is the syndrome developed by injury to the non-dominant parietal cortex of the brain? | Hemispatial neglect syndrome |
| Hemispace neglect syndrome is due to: | Damage to Non-dominant parietal cortex |
| Are the clinical consequences of Non-dominant parietal cortex injury, ipsilateral or contralateral? | Contralateral |
| What are the clinical signs or consequences of the Hippocampus? | Anterograde amnesia |
| What is anterograde amnesia? | Inability to make new memories |
| Inability to create or make new memories | Anterograde amnesia |
| What area of the brain is injured if the patient develops anterograde amnesia? | Hippocampus |
| What are the clinical features seen in injured basal ganglia? | Tremor at rest, chorea, and athetosis |
| Which conditions are associated with Basal ganglia damage or lesion? | Parkinson disease and Huntington disease |
| Which part of area is damaged or with lesion in Parkinson's or Huntington's disease? | Basal ganglia |
| What is the main consequence of Subthalamic nucleus damage? | Contralateral hemiballismus |
| What ishte result of right-sided Subthalamic nucleus damage? | Left side hemiballismus |
| Contralateral or Ipsilateral, the hemiballismus caused by damage to the Subthalamic nucleus? | Contralateral |
| Contralateral hemiballismus is probably due to: | Injured Subthalamic nucleus |
| What is the main associated syndrome due to lesion to the Mammary bodies? | Wernicke-Korsakoff syndrome |
| What are the clinical characteristics of Wernicke-Korsakoff syndrome? | Confusion, Ataxia, Nystagmus Ophthalmoplegia Memory loss (anterograde and retrograde), Confabulation, and, Personality changes |
| What type of memory loss is seen in Wernicke-Korsakoff syndrome? | Anterograde and Retrograde amnesia |
| Alcoholic patient in ER severely confused, difficulty walking, with no memory of the reason he was in the park, and creating a ever changing story. Dx? | Wernicke-Korsakoff syndrome |
| What part of the brain is injured n Wernicke-Korsakoff syndrome? | Mammillary bodies |
| What is the associated syndrome with lesioned Amygdala? | Kluver-Bucy syndrome |
| What are the key features of Kluver-Bucy syndrome? | Hyperphagia, hypersexuality, and hyperorality |
| Obese woman with Hx of multiple STIs and a online-channel for adults in which practices oral sex to multiple men. What type of brain physical damage can explain her risky behavior? | Lesion to amygdala developing Kluver-Bucy syndrome |
| What viral infection-condition is associated with Kluver-Bucy syndrome? | HSV-1 encephalitis |
| What important condition is due to Dorsal midbrain injury? | Parinaud syndrome |
| What is the Parinaud syndrome? | Vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus |
| What palsy is seen in Parinaud syndrome? | Vertical gaze palsy |
| Vertical gaze palsy + lid retraction + dorsal midbrain lesion. Dx? | Parinaud syndrome |
| What events or conditions can provoke an lesion to the Dorsal midbrain? | Stroke, hydrocephalus, and pinealoma. |
| What area of the brain may result damaged in a person with a Pinealoma? | Dorsal midbrain |
| What brain area is injured in Parinaud syndrome? | Dorsal midbrain |
| What is seen in Reticular activating system (midbrain)? | Reduced levels of arousal and wakefulness |
| A person in coma, is seen what kind of brain lesion (area)? | Reticular activating system (midbrain) |
| What are the most common consequences of lesion of the Cerebellar hemisphere? | Intention tremor, limb ataxia, and loss of balance |
| Damage to the cerebellum causes what type of deficits? | Ipsilateral |
| A person with damage to right side of cerebellum most likely will fall ---> | Toward side of lesion (right side) |
| Cerebellar hemispheres are _________________ located. | Laterally |
| A person with tendency to fall to right rise, most likely present what kind of cerebellar hemisphere injury? | Damage to the right cerebellar hemisphere |
| Which has worst prognosis, decorticate or decerebrate posturing? | Decerebrate |
| What are the two types of injury to the Red nucleus? | 1. Decorticate posturing 2. Decerebrate posturing |
| Another way to refer to Decorticate posturing? | Flexor posturing |
| How else is Decerebrate posturing referred as? | Extensor posturing |
| Extensor posturing = | Decerebrate postring |
| Flexor posturing = | Decorticate posturing |
| What area of the brain is injured in decorticate/decerebrate posturing? | Red nucleus |
| Description of Decorticate posturing? | Lesion above red nucleus, presents with flexion of upper extremities and extension of lower extremities |
| Lesion at or below the red nucleus | Decerebrate posturing |
| Decorticate posturing is due to lesion ---> | Above red nucleus |
| Decerebrate posturing is due to lesion ---> | At or below red nucleus |
| How is decerebrate posturing presented clinically? | Extension of upper and lower extremities |
| How is Decorticate posturing presented clinically? | Flexion of upper extremities and extension of lower extremities |
| If lower and upper extremities are extended, is it decerebrate or decorticate? | Decerebrate |
| Upper extremities flexioned + Lower extremities extended; Decerebrate or Decorticate? | Decorticate |
| Consequence of Cerebellar vermis | Truncal ataxia and dysarthria |
| Description of Truncal ataxia due to Cerebellar vermis lesion: | Wide-based, "drunken sailor" gait |
| Cerebellar vermis is _________________ located. | Centrally |
| Central vermis lesioned ---> | Affects central body |
| What action is associated with degeneration of cerebellar vermis? | Chronic alcohol use |
| How long after initial event of an ischemic brain stroke, does the damage is irreversible? | After 5 minutes of hypoxia |
| What brain areas are the most susceptible to ischemic brain stroke/disease? | Hippocampus, neocortex, cerebellum, and watershed areas |
| What cells of the Cerebellum are known to be severely affected in an ischemic brain disease/stroke? | Purkinje cells |
| What area of the brain is the MOST vulnerable to ischemic hypoxia? | Hippocampus |
| What kind of imaging is done in an stroke prior to administration of tPA? | Noncontrast CT to exclude hemorrhage |
| Why is a non-contrast CT performed before giving tPA to a stroke victim? | To exclude hemorrhage |
| What is detected in a CT of a stroke patient? | Ischemic changes in 6-24 hours |
| What is the purpose of Diffusion-weighted MRI in a person with a stroke? | Detect ischemia within 3-30 minutes |
| What are the histologic features of a stroke within 12-24 from initial ischemic event? | 1. Eosinophilic cytoplasm 2. Pyknotic nuclei (red neurons) |
| Time frame after initial ischemic event of stroke in which red neurons appear histologically? | 12-24 hours |
| What are the "red neurons"? | Neurons affected by ischemic brain event in the first 12-24 hours, that have pyknotic nuclei |
| Histologic features of an ischemic attack after 24-72 hours form initial event? | Necrosis + neutrophils |
| How soon can neutrophils be seen in an ischemic brain event? | 24-72 hours |
| The histological examination of a person with an recent ischemic brain event shows necrosis and neutrophils. What is the approximate timeframe? | 24-72 hours from initial event |
| Time in which macrophages (microglia) apperats after initial ischemic brain event? | 3-5 days |
| What histological features is seen around 3-5 days after initial ischemic brain event? | Macrophages (microglia) |
| What cells are involved in Reactive gliosis? | Astrocytes |
| What are the histological findings in a stroke victim after 1-2 weeks form initial ischemic event? | 1. Reactive gliosis (astrocytes) 2. Vascular proliferation |
| Approximate time in which pathologist can see reactive gliosis in an ischemic brain attack victim? | 1-2 weeks from initial event |
| Vascular proliferation is seen after __________________ from initial ischemic event. | 1-2 weeks |
| A Glial scar is seen after _______________- from initial ischemic brain event. | > 2 weeks |
| How long after initial ischemic attack, is a glial scar hisotoligally found? | > 2 weeks |
| (+) Red neurons ---> | Initial histological finding after a ischemic brain event, alongside with an eosinophilic cytoplasm. |
| What is the definition of an Ischemic stroke? | Acute blockage of vessels leading to disruption of blood flow and subsequent ischemia, ultimately producing liquefactive necrosis |
| What type of necrosis is achieved by an ischemic stroke? | Liquefactive necrosis |
| What kind of necrosis is found in a patient suffering of an ischemic stroke? | Liquefactive necrosis |
| Acute blockage of brain blood vessels leading to a disruption of blood flow in the brain and causing ischemia. | Ischemic stroke |
| What are the 3 types of ischemic strokes? | 1. Thrombotic 2. Embolic 3. Hypoxic |
| Thrombotic ischemic stroke: | Due to a clot forming directly at site of infaction, usually over an athrosclerotic plaque |
| What arterial body is commonly affected by development of an Thrombotic ischemic stroke? | MCA |
| What is the most likely cause of an Embolic stroke? | Embolus from another part of the body obstruct the brain vessel. |
| Which type of ischemic stroke is known to affect multiple vascular territories? | Embolic |
| What are conditions that are associated with the development of an Embolic ischemic stroke? | Atrial fibrillation, carotid artery stenosis, DVT with patent foramen ovale. |
| What is the most common cause for a Hypoxic ischemic stroke? | Hypoperfusion or hypoxemia |
| Which is common type of ischemic stroke that develops during cardiovascular surgeries? | Hypoxic |
| What areas are most affected or more commonly affected by a Hypoxic ischemic stroke? | Watershed areas |
| When is tPA used in treating an ischemic stroke? | - Within 3.-4.5 hours of onset - No hemorrhage/risk of hemorrhage |
| A patient with with an ischemic stroke that stated 5 hours ago, that has no signs of hemorrhage, should be treated with tPA? | No, tPA administration should be only within 3-4.5 hours from onset. |
| What medications are known to reduce risk of developing an ischemic stroke? | Aspirin and Clopidogrel |
| Brief, reversible episode of focal neurologic dysfunction without acute infarction, with majority resolving in < 15 minutes. | Transient ischemic attack |
| The deficits seen in TIA are due to: | Focal ischemia |
| Most TIAs are resolved (time): | < 15 minutes |
| What is Neonatal Intraventricular hemorrhage? | Bleeding into ventricles in neonates |
| Which conditions of neonates increase risk Neonatal intraventricular hemorrhage? | Prematurity and Low-birth-weight infants |
| Where do neonatal intraventricular hemorrhage originate? | Germinal matrix, a highly vascularized layer within the subventricular zone. |
| A highly vascularized layer within the subventricular zone. | Germinal matrix |
| What is the cause of Neonatal Intraventricular hemorrhage? | Due to reduced glial fiber support and impaired autoregulation of BP in premature infants. |
| What clinical signs of NIH? | Altered level of consciousness, bulging fontanelle, hypotension, seizures, and coma. |
| Reduced glial fiber support and impaired autoregulation of BP in premature infants. Dx? | Neonatal Intraventricular Hemorrhage (NIH) |
| List of causes or types of Intracranial hemorrhage: | 1. Epidural hematoma 2. Subdural hematoma 3 .Subarachnoid hemorrhage 4. Intraparenchymal hemorrhage |
| What is the MCC of Epidural hematoma? | Rupture of middle meningeal artery, often secondary to skull fracture involving the pterion. |
| Common branch of the Maxillary artery involved in Epidural hematoma? | Middle Meningeal artery |
| What is the Pterion? | Thinnest areal of the lateral skull |
| A blow to the lateral side of the skull, rupturing the MMA. Dx? | Epidural hematoma |
| Which type f intracranial hematoma is seen with an "lucid interval"? | Epidural hematoma |
| Scalp hematoma and rapid intracranial expansion under systemic arterial pressure causing transtentorial herniation, and CN III palsy? | Epidural hematoma |
| Which type of intracranial hemorrhage is associated with development of Transtentorial herniation and CN III palsy? | Epidural hematoma |
| What is shown in CT on an Epidural hematoma? | Biconvex (lentiform), hyperdense blood collection not crossing suture lines |
| CT --> Hyperdense blood collection not crossing suture lines. Dx? | Epidural hematoma |
| CT--> Biconvex (lentiform) blood collection | Epidural hematoma |
| What is the MCC of Subdural hematoma? | Rupture of bridging veins |
| What condition is due to the rupture of bridging veins? | Subdural hematoma |
| What are acute causes of a Subdural hematoma? | Traumatic, high-energy impact --> hyperdense of CT |
| What are the chronic causes of a Subdural hematoma? | Mild trauma, cerebral atrophy, elderly, alcoholism --> hypodense on CT |
| If the CT of an Subdural hematoma shows a hypodense image is it chronic or acute cause? | Chronic |
| What infant condition is associated with developing Subdural hematoma? | Shaken babies |
| A baby abused by shaken, may develop what type of intracranial hematoma? | Subdural hematoma |
| What are predisposing factors of Subdural hematoma? | Brain atrophy and trauma |
| Crescent-shaped hemorrhage that crosses suture lines on CT. Dx? | Subdural hematoma |
| Lentiform or Crescent-shaped on CT of Subdural hematoma. | Crescent |
| Lentiform or Crescent-shaped on CT of Epidural hematoma. | Lentiform |
| What is a Subarachnoid hemorrhage? | Bleeding due to trauma, or rupture of an aneurysm or AVM. |
| What is the intracranial hemorrhage due to rupture of an aneurysm? | Subarachnoid hemorrhage |
| Patients complain of "worst headache of my life". Dx? | Subarachnoid hemorrhage |
| Bloody or yellow spinal tap. Dx? | Subarachnoid hemorrhage |
| What condition is seen with a xanthochromic spinal tap? | Subarachnoid hemorrhage |
| What is a serious complication of Subarachnoid hemorrhage? | - Vasospasm due to blood breakdown, or - Rebleed 3-10 days after hemorrhage |
| What medication or drug is used to prevent vasospasm due to Subarachnoid hemorrhage? | Nimodipine |
| Why is Nimodipine used in Subarachnoid hemorrhage? | It used to prevent/reduce vasospasm due to SAH. |
| What are conditions that have increased risk of developing in a patient with SAH? | Communicating and/or obstructive hydrocephalus |
| What is the MCC of intraparenchymal hemorrhage? | Systemic hypertension |
| What are conditions associated with developing an intraparenchymal hemorrhage? | Amyloid angiopathy, vasculitis, neoplasm. |
| What are the most common causes of hypertensive hemorrhages in the brain? | Charcot-Bouchard microaneurysm |
| Where do most Charcot-Bouchard microaneurysm occur? | Putamen of basal ganglia |
| What are the vessels most likely affected in Charcot-Bouchard microaneurysms? | Lenticulostriate vessels |
| Other than the Putamen of basal ganglia, where else is common to Charcot-Bouchard aneurysms? | Thalamus, pons, and cerebellum, |
| Intraparenchymal hemorrhage due to amyloid angiopathy presents with: | Recurrent lobar hemorrhagic stroke in elderly |
| If a stroke affects the Middle Cerebral artery, which area(s) of the brain are most affected? | 1. Motor and sensory cortices-- upper limb and face 2. Temporal lobe (Wernicke area); 3. Frontal lobe (Broca area) |
| Which arterial body is most likely affected if the patient presents with contralateral paralysis and sensory loss of face and upper limb? | MCA |
| What ophthalmological deficit is associated with Wernicke aphasia? | Right superior quadrant visual field defect due to temporal lobe involvement |
| Which anterior brain circulation artery if suffers a stroke affects the Wernicke and Broca areas? | MCA |
| What area of lesion in a stroke affecting the Anterior cerebral artery? | Motor and sensory cortices --- lower limb |
| Arterial body affected in a stroke that presents with contralateral paralysis and sensory loss of the lower limb and with urinary incontine? | ACA |
| ACA occlusion/stroke affects the ----> | Contralateral legs |
| MCA occlusion/stroke affects the ---> | Contralateral face and arms |
| What are the clinical signs presented if a patient suffers a right ACA stroke? | Left motor paralysis and sensory loss of lower extremity. |
| A patient presents with left sided face and left side arm numbness and difficulty moving it. What arterial body most lifkely has been affecred by a stroke? | MCA |
| Areas of lesion of a Lenticulostriate artery stroke? | Striatum and internal capsule |
| Areas affected: Striatum and Internal capsule. What is the most likely stroke? | Lenticulostriate artery stroke |
| What are the symptoms of Lenticulostriate artery stroke? | 1. Contralateral paralysis 2. Absence of cortical signs |
| What is a common location for Lacunar infarcts due to hyaline arteriosclerosis secondary to uncontrolled hypertension? | Lenticulostriate artery |
| What is the reason of Lacunar infarcts? | Hyaline arteriosclerosis secondary to uncontrolled hypertension |
| How would the absence of cortical signs present as? | Neglect, aphasia, and visual field loss |
| What arterial bodies compose the anterior circulation of the brain? | 1. MCA 2. ACA 3. Lenticulostriate artery |
| Main stroke related posterior brain circulation arteries: | 1. Anterior spinal artery 2. Posterior inferior cerebellar artery (PICA) 3. Anterior Inferior cerebellar artery (AICA) |
| What structures are affected by Anterior spinal artery stroke/occlusion? | 1. Lateral corticospinal tract 2. Medial lemniscus 3. Caudal medulla - hypoglossal nerve |
| Clinical features of Anterior spinal artery stroke affecting the Lateral corticospinal tract: | Contralateral paralysis -- Upper and Lower limbs |
| How is a ASA stroke affecting the lateral corticospinal tract different to a MCA or ACA stroke? | ASA stroke to the lateral corticospinal tract, affects both legs and arms of the contralateral side, while ACA affects contralateral leg, and MCA contralateral face and arm. |
| What area affected in a ASA stroke causes a decrease in contralateral proprioception? | Medial lemniscus |
| What is the symptom that indicated medial lemniscus injury in an ASA stroke? | Decrease contralateral proprioception |
| What is the consequence of ASA stroke affecting the Cauda medulla (Hypoglossal nerve)? | Ipsilateral hypoglossal dysfunction with causes tongue deviation ipsilateral |
| Ipsilateral or Contralateral. Tongue deviation in ASA stroke. | Ipsilateral |
| Which cranial nerve is involved with an ASA stroke? | Hypoglossal nerve |
| What is the common syndrome associated with Anterior spinal artery stroke? | Medial Medullary syndrome |
| What is the cause of Medial medullary syndrome? | Infarct of Paramedian branches of ASA and/or vertebral arteries |
| Infarct to the branches of the ASA and/or vertebral arteries. Dx? | Medial Medullary syndrome |
| Associated affected artery in Medial medullary syndrome? | Anterior Spinal artery |
| Associated syndrome of due to occlusion/stroke of the PICA? | Lateral medullary syndrome |
| What is another way to refer to Lateral medullary syndrome? | Wallenberg syndrome |
| What are the 5 main areas of lesion in occlusion/stroke of the Posterior inferior cerebellar artery (PICA)? | 1. Lateral medulla: Nucleus ambiguus (IX, X, XI) 2. Vestibular nuclei 3. Lateral spinothalamic tract, spinal trigeminal nucleus 4. Sympathetic fibers 5. Inferior cerebellar peduncle |
| What is the clinical result of PICA occlusion affecting the Lateral medulla? | Dysphagia, hoarseness, decreased gag reflex, and hiccups |
| What area is affected in PICA occlusion that lead to symptoms of dysphagia, decreased gag reflex, hoarseness, and hiccups? | Latear medulla (nucleus ambiguus CN IX, X, XI) |
| Affecting the vestibular nucleus in PICA occlusion is presented with: | Vomiting, vertigo, and nystagmus |
| What are is there result of damage to the Lateral spinothalamic tract and spinal trigeminal nucleus in PICA stroke? | Decreased pain and temperature sensation from contralateral body, and ipsilateral face |
| What part of the face losses sensation in PICA occlusion? | Ipsilateral |
| What are the clinical effects of affects of the inferior cerebellar peduncle, due to PICA occlusion? | Ipsilateral ataxia and dysmetria |
| What is the Lateral medullary (Wallenberg) syndrome? | Condition due to PICA stroke/occlusion. |
| What are the main clinical effects Wallenberg syndrome? | Nucleus ambiguus effects such as dysphagia, hoarseness, decreased gag reflex, and hiccups. |
| What is affected in PICA occlusion that leads to development of Ipsilateral Horner syndrome? | Sympathetic fibers |
| What areas are affected by AICA stroke/ occlusion? | 1. Lateral pons: Facial nucleus 2. Vestibular nuclei 3. Spinothalamic tract, spinal trigeminal nucleus 4. Sympathetic fibers 5. Middle and inferior cerebellar peduncles 6. Labyrinthine artery |
| What artery is affected in AICA occlusion that leads to deafness and vertigo? | Labyrinthine artery |
| What is the syndrome associated with AICA occlusion or stroke? | Lateral pontine syndrome |
| Lateral pontine syndrome. Associated with what cerebral artery? | AICA |
| Lateral medullary (Wallenberg) syndrome. Associated with ____________ occlusion. | PICA |
| Medial medullary syndrome. Associated with deficits in which posterior circulation cerebral artery? | Anterior spinal artery (ASA) |
| What deficits give Lateral Pontine syndrome its main symptoms? | Facial nucleus effects such as: Paralysis of face, decreased lacrimation, salivation , and taste from anterior 2/3 tongue. |
| What are the clinical effects of defects in the Facial nucleus? | - Paralysis of face - Decreased lacrimation, salivation, - Decreased taste from anterior 2/3 of tongue |
| Which syndrome is associated with the development of a "facial droop" and decreased lacrimation, salivation, and taste of anterior 2/3 of tongue? | Lateral pontine syndrome |
| What are the symptoms due to deficits to the Labyrinthine artery in AICA occlusion? | Ipsilateral sensorineural deafness and vertigo |
| What are the effects of damage to the Spinothalamic tract, and spinal trigeminal nucleus? | Decreased pain and temperature sensation from contralateral body, and ipsilateral face |
| What areas are affected by occlusion of the Basilar artery? | 1. Pons, medulla, lower midbrain 2. Corticospinal and corticobulbar tracts 3. Ocular cranial nerve nuclei, paramedian pontine reticular formation |
| What is the associated condition with a Basilar artery stroke? | Locked-in syndrome |
| Locked-in syndrome is due to occlusion/stroke to which artery? | Basilar artery |
| What are the significant symptoms in Locked-In syndrome? | 1. Preserved consciousness 2. Quadriplegia 3. Loss of voluntary facial, mouth, and tongue movements 4. Loss of horizontal, but not vertical, eye movements |
| What area is lesioned in Locked in syndrome, that causes the movement defectis? | Corticospinal and corticobulbar tracts |
| Which tracts are affected in Locked in syndrome? | Corticospinal and corticobulbar tracts |
| Patient in bed, unable to speak, move, or make facial grimaces. Communicates only by vertical eye movements, and is conscious of surrounding. Dx? | Locked-in syndrome |
| Locked-In syndrome associated artery? | Basilar artery |
| If the PCA is occluded or suffers a stroke, what area of the brain is lesioned? | Occipital lobe |
| If the occipital lobe is damaged due to ischemia, which is the most likely obstructed/occluded arterial body? | PCA |
| What are the common symptoms of PCA occlusion? | 1. Contralateral hemianopia with macular sparing 2. Alexia without agraphia |
| What is "Alexia without agraphia"? | Dramatic disorder of higher visual function in which patients can still write but are unable to read. |
| What artery is at suspicion of occlusion if a patient can write, but is unable to read? | PCA |
| Higher visual function in which patients can still write but can't read. | Alexia without agraphia |
| What Cerebral Posterior circulation artery, if obstructed or suffer an stroke, causes contralateral hemianopia with macular sparing? | PCA |
| What is Central Post-stroke pain syndrome? | Neuropathic pain due to thalamic lesions |
| What it the initial course of Central post-stroke pain syndrome? | Paresthesias followed in weeks to moth by allodynia and dysesthesia on the contralateral side. |
| What is allodynia? | It is when a patient that experiences ordinarly painless stimuli causes him/her pain. |
| Extreme, exaggerated, not fictional but intense sensation of pain, in stimuli that commonly is painless. | Allodynia |
| Contralateral or Ipsilateral. The dysesthesia seen in Central post-stroke pain syndrome. | Contralateral |
| What causes Diffuse axonal injury? | Traumatic shearing forces furin rapid acceleration and/or deceleration of the brain. |
| What is a common example of something that causes diffuse axonal injury? | Motor Vehicle accident (MVA) |
| What are the severe results of diffuse axonal injury? | Coma or persistent vegetative state |
| Which condition is known to show multiple lesions (punctate hemorrhages) involving the white matter tracts? | Diffuse axonal injury |
| What is the name of CN I? | Olfactory |
| What is the function of CN I? | Smell |
| Smell is sensed by which cranial nerve? | Olfactory |
| Which is the only cranial nerve without Thalamic relax to cortex? | Olfactory |
| What is a unique CN characteristic? | Only cranial nerve without thalamic relay to cortex |
| Sensory or Motor. Olfactory cranial nerve? | Sensory |
| CN I is an sensory or motor cranial nerve type? | Sensory |
| Name of CN II | Optic |
| What is the function of CN II? | Sight |
| Which cranial nerve's function is sight? | Optic |
| Sensory or Motor. Optic cranial nerve? | Sensory |
| Is CN II an sensory or motor type cranial nerve? | Sensory |
| What number is the Oculomotor nerve? | III |
| Name of CN III | Oculomotor |
| List of functions of the CN III: | 1. Eye movement 2. Pupillary constriction 3. Accomodation 4. Eyelid opening |
| Which eye movement (ocular) muscles are innervated by CN III? | SR, IR, MR, and IO |
| What are features of the sphincter pupillae? | 1. Edinger-Westphal nucleus 2. Muscarinic receptors |
| What type of receptors are associated with the sphincter pupillae? | Muscarinic receptors |
| Which muscle makes eyelid opening possible? | Levator palpebrae |
| Sensory, Motor, or Both. Oculomotor nerve? | Motor |
| What type of nerve is the CN III? | Motor |
| What is the name of CN IV? | Trochlear |
| What number is the Trochlear nerve? | IV |
| What is the function of CN IV? | Eye movement |
| Eye movement by the Trochlear nerve is done by the innervation of which ocular muscle? | SO |
| Which is the only eye muscle innervated by the CN IV? | SO |
| Sensory, Motor, or Both. CN IV? | Motor |
| What is the name of CN V? | Trigeminal |
| What are the functions of the Trigeminal nerve? | 1. Mastication 2. Facial sensation 3. Somatosensation from anterior 2/3 of tongue 4. Dampening of loud noises |
| What are the divisions of the CN V that provide Facial sensation? | Ophthalmic, Maxillary, and Mandibular |
| To what part of the tongue does the Trigeminal nerve provide somatosensation? | Anterior 2/3 of tongue |
| What muscle is innervated by the CN V that dampens loud noises? | Tensor tympani |
| The Tensor tympani is innervated by which cranial nerve? | Trigeminal |
| Sensory, Motor, or Both. Trigeminal nerve? | Both |
| Which cranial nerves are both, motor and sensory? | Trigeminal (V), Facial (VII), Glossopharyngeal (IX), and Vagus (X) |
| Name of CN VI? | Abducens |
| The Abducens cranial nerve is what number? | VI |
| What is the involved action of CN VI? | Eye movement |
| Which ocular muscle is innervated by CN VI? | LR |
| The lateral rectus is innervated by the ________________ nerve. | Abducens |
| Sensory or Motor. Abducens nerve? | Motor |
| What is the name for CN VII? | Facial |
| List of functions of CN VII: | - Facial movement - Taste from anterior 2/3 of tongue - Lacrimation - Salivation - Eye closing - Auditory volume modulation |
| Which glands innervated by CN II cause salivation? | Submandibular and Sublingual glands |
| What muscle causes eye closing? | Orbicularis oculi |
| The Orbicularis oculi is innervated by which CN? | Facial |
| The Chorda tympani is innervated by the ______________ nerve. | Facial |
| Auditory muscle innervated by the __________ nerve. | Facial |
| What is the function of the Stapedius muscle? | Auditory volume modulation |
| Sensory, Motor, or Both. CN VII? | Both |
| What type of nerve is the Facial cranial nerve, sensory or motor? | Both |
| What is the name for CN VIII? | Vestibulocochlear |
| What Roman number is given to the Vestibulocochlear nerve? | VIII |
| What are the associated functions of the Vestibulocochlear nerve? | Hearing and balance |
| Damage to the CN VIII may cause deficits in: | Hearing and balance |
| A person with a clear loss of balance and hard of hearing, might suffered from either compression or damage to which cranial nerve? | Vestibulocochlear |
| What type of nerve is CN VIII, sensory or motor? | Sensory |
| Sensory or motor. Vestibulocochlear nerve? | Sensory |
| What is the name for CN IX? | Glossopharyngeal |
| What is the roman numeral designated for the Glossopharyngeal nerve? | IX |
| What are some of the associated functions of CN IX? | 1. Taste and sensation from posterior 1/3 of tongue, 2. Swallowing 3. Salivation 4. Monitoring carotid body and sinus chemo- and baroreceptors, 5. Elevation of pharynx/larynx |
| Which part of the tongue is innervated by the Glossopharyngeal nerve? | Posterior 1/3 |
| CN IX innervation of the posterior 1/3 of tongue provides: | Taste and sensation |
| CN associated with Carotid body and sinus chemo- and baroreceptor monitoring? | Glossopharyngeal |
| Which chemo- and baroreceptors are monitored by the CN IX? | Carotid body and sinus |
| Sensory, Motor, or Both. Cranial nerve 9? | Both |
| What muscle is innervated by the Glossopharyngeal nerve that elevate pharynx/ larynx? | Stylopharyngeus |
| The Stylopharyngeus is innervated by the ______________ nerve. | Glossopharyngeal |
| Vagus nerve roman numeral | X |
| What is the name for CN X? | Vagus |
| List of functions for CN X? | - Taste from supraglottic region - Swallowing - Soft palate elevation - Midline uvula - Talking - Cough reflex - Parasympathetics to thoracoabdominal viscera - Monitoring aortic arch chemo- and baroreceptors |
| Which chemo- and baroreceptors are monitored by the Vagus nerve? | Aortic arch |
| Deficient response of aortic arch chemoreceptors and baroreceptors may be due to damage to which cranial nerve? | Vagus |
| Which reflex is associated with proper Vagus nerve functioning? | Cough reflex |
| (-) Cough reflex. Dx? | Damage/injury to CN X |
| Which CN is involved in Soft palate elevation? | Vagus |
| CN that provides taste to the Supraglottic region? | Vagus |
| Sensory, Motor, or Both. Vagus nerve? | Both |
| Motor and sensory CN that is involved in swallowing, talking and midline uvula location? | Vagus |
| Name of the CN XI? | Accessory |
| What is the Roman numeral given to the Accessory nerve? | XI |
| What are the functions involved with the Accessory nerve? | Head turning, shoulder shrugging (SMC, trapezius) |
| Which shoulder/neck muscles are innervated by CN XI? | Sternocleidomastoid and Trapezius |
| What type of nerve is CN XI, sensory or motor? | Motor |
| A person with difficulty shrugging the shoulder, most likely indicates injury to which cranial nerve? | Accessory |
| Name of CN XII: | Hypoglossal |
| What is the function associated with CN XII? | Tongue movement |
| Sensory or Motor. Hypoglossal nerve? | Motor |
| What action would be deficient or abnormal in case of injury to Hypoglossal cranial nerve? | Tongue movement |
| Which medulla nucleus coordinates the vomiting center? | Nucleus tractus solitarius (NTS) in the medulla |
| Which areas or zones send to NTS in medulla? | 1. Chemoreceptor trigger zone (CTZ) 2. GI tract via vagus nerve 3. Vestibular system 4. CNS |
| Where is the CTZ located? | Within area postrema in 4th ventricle |
| CTZ and adjacent vomiting center nuclei receive input form 5 major receptos: | 1. Muscarinic (M1), 2. Dopamine (D2), 3. Histamine (H3), 4. Serotonin (5-HT), 5. Neurokinin (NK-1) |
| What muscarinic receptor is associated with the CTZ and vomiting centers nuclei? | M1 |
| Which receptor antagonists are used to treat chemotherapy-induced vomit? | 5-HT3, D2, and NK-1 receptors |
| Which two of the five antagonists are sued to motion sickness and hyperemesis gravidarum? | M1 and H1 receptors |
| M1 and H1 antagonists are used to treat? | Motion sickness and hyperemesis gravidarum |
| Serotonin, D2, and NK-1 antagonists are used to treat: | Chemotherapy-induced vomiting |
| What important physiologic center is located in the NTS in the medulla? | Vomiting center |
| The sleep cycle is regulated by the _______________ rhythm. | Circadian rhythm |
| The Suprachiasmatic nucleus of hypothalamus ---> | Drives the sleep cycle with regulates the circadian rhythm. |
| What is controlled by the Circadian rhythm? | Nocturnal release of ACTH, prolactin, melatonin, norepinephrine |
| What regulates Suprachiasmatic nucleus (SCN)? | Environment (light) |
| Which gland releases melatonin? | Pineal gland |
| SCN --(+)---> NE release ==> | Pineal gland which releases melatonin |
| What are the two stages of Sleep physiology? | Rapid-eye movement (REM) and non-REM |
| What substances and drug types are associated with a decrease in REM sleep and delta wave sleep? | Alcohol, benzodiazepines, and barbiturates |
| What happens to REM sleep with increase norepinephrine? | Decrease REM sleep |
| A patient with decreased REM sleep and a decreased delta wave is often associated to consumption of : | Alcohol, benzodiazepines, and barbiturates |
| Which type of medications are proven to help for night terrors? | Benzodiazepines |
| Which sleep disorder conditions are treated with Benzodiazepines? | Night terrors and sleepwalking |
| What is the MOA of benzodiazepines ahta aid in treating Night terrors and sleepwalking? | Decreased N3 and REM sleep |
| What are the main sleep stages? | 1. Awake (eyes open/closed) 2. Non-REM sleep (N1, N2, and N3) 3. REM sleep |
| Which is the description for the awake with eyes open sleep stage? | Aleer, active mental concentrations |
| What is the associated EEG waveform of the Awake with eyes open of the sleep stages? | Beta waves |
| Which sleep stages have Beta waves in the EEG? | 1. Awake (eyes open) 2. REM sleep |
| Alpha waves of EEG are associated with which sleep stage? | Awake (eyes closed) |
| What are the subdivisions of Non-REM sleep? | Stage N1, Stage N2, and Stage N3 |
| Which non-REM sleep is the largest or with the largest percentage? | Stage N2 |
| What is the description of Stage N1 of sleep? | Light sleep |
| Which stage of sleep is described as "light sleep"? | Stage N1 |
| What are the associated EEG waveforms of Non-REM Stage N1? | Theta waves |
| (+) Theta waves on EEG. | Stage N1 |
| Which sleep stage accounts for approximately 75% of all sleep cycle? | Non-REM sleep |
| Description of N2 stage of Non-REM sleep | Deeper sleep that Stage N1; bruxism occurs |
| Which sleep stage is associated with Bruxism? | Stage N2 |
| What is Bruxism? | Teeth grinding |
| EEG waveform of Non-REM stage N2 sleep | Sleep spindles and K complexes |
| (+) Sleep spindles and K complexes on EEG | Non-REM sleep stage N2 |
| Which stage has the deepest non-REM sleep? | Stage N3 |
| Which EEG waveform has the lowest frequency and highest amplitude? | Delta wave |
| Associated waveform of Stage N3 of sleep? | Delta wave |
| Slow-wave sleep? | Stage N3 |
| What is the description of non-REM sleep Stage N3? | Deepest non-REM sleep; associated with sleepwalking, night terrors, and bedwetting |
| Which conditions are associated with non-REM Stage N3 sleep? | 1. Sleepwalking 2. Night terrors 3. Bedwetting |
| Loss of motor tone, increased brain oxygen use, and increase variable pulse and BP, and elevated ACh | Description of REM sleep |
| What physiological conditions are associated REM sleep? | - Dreaming - Nightmares - Penile/clitoral tumensce |
| Which sleep stage may present with penile erection? | REM sleep |
| Which mood disorder is associated with increased REM sleep but decreased REM latency? | Depression |
| What accounts for the extraocular movements in REM sleep? | Activity of PPRF |
| What is the PPRF? | Paramedian Pontine Reticular formation/ conjugate gaze center. |
| How often does REM sleep occur? | Every 90 minutes, and duration increases through the night |
| REM sleep associated EEG waves | Beta waves |
| Dreams happen during __________________ sleep. | REM |
| Major relay for all ascending sensory information except olfaction | Thalamus |
| Which are the nuclei of the Thalamus? | 1. Ventral Postero-Lateral nucleus 2. Ventral Postero-Medial nucleus 3. Lateral geniculate nucleus 4. Medial geniculate nucleus 5. Ventral lateral nucleus |
| The VPL and VPM nucleus are part of the _________________. | Thalamus |
| Which ascending sensory information does not relay in the Thalamus? | Olfactory |
| What is the input of the Ventral Posterolateral nucleus of the Thalamus? | Spinothalamic and dorsal columns/ medial lemniscus |
| The Spinothalamic and dorsal columns and medial lemniscus is the input of the: | Ventral Posterolateral nucleus of the Thalamus |
| What is sensed by the VPL nucleus of the Thalamus? | Vibration, Pain, Pressure, Proprioception, Light touch, and temperature. |
| What is the destination of of the sensory information coming from the VPL nucleus of thalamus? | Primary somatosensory cortex |
| Which thalamic nucleus have as destination the Primary somatosensory cortex? | VPL and VPM nuclei |
| What is the input of the Ventral posterolateral nucleus of the thalamus? | Trigeminal and gustatory pathway |
| What are the sensation of the VPM nuclei of the thalamus? | Face sensation and taste |
| Which hypothalamic nucleus is damaged if there is decreased sensation of the face and taste? | Ventral Postero-Medial nucleus |
| Input Trigeminal and gustatory pathway. Thalamic nucleus? | Ventral Postero-Medial nucleus |
| What is the input of the Thalamic lateral geniculate nucleus? | CN II, Optic chiasm, and Optic tract |
| Associated thalamic nucleus of the CN II, optic chiasm, and optic tract? | Lateral geniculate nucleus |
| What is sensed by LGN of the thalamus? | Vision |
| Vision associated ________ _________ nucleus of the thalamus | Lateral geniculate nucleus |
| What is the destination of the Lateral geniculate nucleus sensory input? | Calcarine sulcus |
| The Calcarine sulcus receives sensory information of which Thalamic nucleus? | Lateral geniculate nucleus |
| Medial geniculate nucleus receives input from the: | Superior olive and inferior colliculus of tectum |
| What senses the Medial geniculate nucleus sensory fibers? | Hearing |
| Hearing is sense by the ____________ nucleus of the thalamus | Medial geniculate nucleus |
| What is the destination of the sensor pathways that relay by the Medial geniculate nucleus? | Auditory cortex of temporal lobe |
| Associated destination of the MGN of the thalamus? | Auditory cortex of temporal lobe |
| The ventral lateral nucleus has input of : | Basal ganglia and cerebellum |
| The Ventral lateral nucleus senses ________________ functions. | Motor |
| What is the final destination of the sensory information relayed in the thalamus ventral lateral nucleus? | Motor cortex |
| What is the Limbic system? | Collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, and ANS function |
| What does the Limbic system consists of? | Hippocampus, Amygdala, Mammillary bodes, anterior thalamic nuclei, cingulate gyrus, and entorhinal cortex. |
| What neurological structure or system is made up of the hippocampus, amygdala, mammillary bodies, anterior thalamic nuclei, cingulate gyrus, and entorhinal cortex? | Limbic system |
| The limbic system is responsible for: | 1. Feeding, 2. Fleeing, 3. Fighting, 4, Feeling, 5. Sex (fucking) |
| What are the famous 5 F's of the limbic system? | Feeding, fleeing, fighting, feeling, and Fukcing (sex) |
| List of Dopaminergic pathways: | 1. Mesocortical 2. Mesolimbic 3. Nigrostriatal 4. Tuberoinfundibular |
| What are the "negative"symptoms associated with Dopamine? | Anergia, apathy, and lack of spontaneity |
| A decreased in which dopaminergic pathway lead to development of negative symptoms? | Mesocortical |
| Decreased activity in the mesocortical dopaminergic pathway --> | "negative" symptoms |
| Antipsychotic drugs have a limited effect on which dopaminergic pathway? | Mesocortical |
| Increased activity in the Mesolimbic dopaminergic pathway lead to: | Development of "positive" symptoms |
| What are the positive symptoms associated with Dopamine? | Delusions and hallucinations |
| Which dopaminergic pathway represents the primary target of the antipsychotic drugs? | Mesolimbic |
| Inhibition of the mesolimbic dopaminergic pathway lead to: | Decrease positive symptoms in Schizophrenia |
| Dopaminergic pathways are altered by which drugs? | Antipsychotics |
| Which two features alter the Dopaminergic pathways? | Drugs (antipsychotics) and movement disorders (Parkinson disease). |
| What is the major dopaminergic pathway in the brain? | Nigrostriatal |
| Decreased activity of this dopaminergic pathway leads to the development of Extrapyramidal symptoms? | Nigrostriatal |
| What are the Extrapyramidal symptoms? | Dystonia, Akathisia, parkinsonism, and tardive dyskinesia |
| Which Dopaminergic pathway is most affected by drugs and movement disorders? | Nigrostriatal |
| Disorder that leads to an undeveloped or nonfunctional Nigrostriatal dopaminergic pathway will present clinically be the development of: | Extrapyramidal symptoms |
| Which Dopaminergic pathway is associated with libido, sexual function, galactorrhea and gynecomastia in men? | Tuberoinfundibular |
| A decrease activity in the Dopaminergic Tuberoinfundibular pathway leads to a ____________________ in prolactin. | Increase |
| Hyperprolactinemia may be due to damage to which dopaminergic pathway? | Tuberoinfundibular |
| What are the results of decrease activity in the Tuberoinfundibular pathway? | Hyperprolactinemia which leads to decreased libido, sexual dysfunction, galactorrhea, and gynecomastia in men. |
| Functions of the Cerebellum: | 1. Modulates movement 2. Aids in coordination and balance |
| What are the 2 inputs of the Cerebellum? | 1. Contralateral cortex via middle cerebellar peduncle 2. Ipsilateral cerebellar peduncle from spinal cord |
| What i the contralateral input of the cerebellum? | Cortix via middle cerebellar peduncle |
| What is the is ipsilateral input of the cerebellum? | Proprioceptive information via inferior cerebellar peduncle form the spinal cord |
| Output of the Cerebellar cortex: | Purkinje cells --> deep nuclei of cerebellum ----> contralateral cortex via superior cerebellar peduncle |
| Which cerebellar peduncle is used output information from the cerebellar cortex? | Superior cerebellar peduncle |
| What cells are involved in the output of information form the cerebellar cortex? | Purkinje cells |
| Cerebellar Purkinje cells are always _________________. | Inhibitory |
| True or False. Cerebellar Purkinje fibres are stimulatory and inhibitory. | False; Always and only inhibitory |
| What is the deep nuclei out of the cerebellum? | Dentate, Embolofrm, Globose, and Fatigal |
| Direction of output for the cerebellum deep nuclei output? | Lateral to medial |
| What is affected by LATERAL lesions to the cerebellum? | Voluntary movement of the extremities |
| What is a common symptom of a cerebellum lateral injury? | Propensity to fall toward ipsilateral side |
| A person falls has a tendency to fall to the right side, and has difficulty moving arms on command. Dx? | Right side cerebellum injury |
| What are the medial structures of the Cerebellum? | Vermis, fastigial nuclei, and floculonodular lobe |
| What clinical features of a medial cerebellar lesion? | 1. Truncal ataxia 2. Nystagmus 3. Head tilting |
| Lateral of Medial lesions to the cerebellum cause bilateral motor deficits affecting axial and proximal limb musculature? | Medial |
| What structures, medial or lateral cerebellum, in order to show wide-based cerebellar gait? | Medial |
| Modulates movement and aids in coordination and balance. | Cerebellum |
| The contralateral cortex input of the cerebellum is via the: | Middle cerebellar peduncle |
| Function of middle peduncle of cerebellum | Provide input to the contralateral cortex of the cerebellum |
| Function of the Inferior cerebellar peduncle? | Provide input concerning ipsilateral proprioception |
| Which structure is important in voluntary movements and making postural adjustments? | Basal ganglia |
| What type of input is received by the Basal ganglia? | Cortical input |
| Provides negative feedback to cortex to modulate movement. | Basal ganglia |
| What type of feedback is provided by the Basal ganglia? | Negative feedback to cortex to modulate movement |
| Putamen + Caudate = | Striatum |
| What composes the Striatum? | Putamen and Caudate |
| What provides the motor part of the Striatum? | Putamen |
| Which component of the Striatum provides the cognitive features? | Caudate |
| Lentiform = | Putamen + globus pallidus |
| Putamen and the Globus pallidus, compose the ________________, of the basal ganglia. | Lentiform |
| If the putamen is added to the caudate, it then makes up the _______________. | Striatum |
| Lentiform = Putamen + _____________________. | Globus pallidus |
| Which, D1 or D2, is the direct pathway in the basal ganglia? | D1 |
| Which is the inhibitory pathway of the basal ganglia, D1 or D2? | D2 |
| What is another way to refer to the Direct pathway of the Basal ganglia? | Excitatory |
| What is another form to refer to the Indirect pathway of the Basal ganglia? | Inhibitory |
| SNc input stimulate the striatum, stimulating the release of GABA, which inhibits GABA release from the GPi, disinhibiting the thalamus via the GPi. | Direct (excitatory) pathway of the basal ganglia |
| The direct pathway of the Basal ganglia, stimulates the striatum which causes ---> | Striatal release of GABA |
| What is the overall result of the direct pathway of the basal ganglia? | Increase motion |
| Which pathway of the basal ganglia is designed to decrease motion? | Indirect (inhibitory) pathway |
| Which structure stimulates the striatum in both, the indirect and direct pathways of the basal ganglia? | SNc (Substantia nigra) |
| How does dopamine causes increased motion by acting on the Basal ganglia pathways? | Binding to D1 to stimulate the excitatory pathway, and D2, by inhibiting the inhibitory pathway |
| Inhibition of the inhibitory pathway leads to increased movement | Dopamine binding to D2 receptor in the Basal ganglia |
| Which areas of the brain are located in the Frontal lobe? | - Primary motor - Premotor cortex - Frontal eye field - Prefrontal association area - Broca area |
| The Sylvian fissure borders with brain lobes? | Frontal lobe and Temporal lobe |
| On which brain lobe is the Wernicke area located? | Temporal lobe |
| Which important area or brain region is located at the Occipital lobe of the brain? | Primary visual cortex |
| Which lobe would be affected if there is traumatic damage to the Primary visual cortex? | Occipital lobe |
| On which brain lobe is the Primary auditory cortex located? | Temporal lobe |
| Which are the gyri and areas associated with the Parietal lobe? | - Primary somatosensory gyrus - Somatosensory association cortex |
| What association area is located in the anterior part of the Temporal lobe of the brain? | Limbic association area |
| Which areas and cortex are located in the Temporal lobe of the brain? | Limbic association area, Wernicke area, and Primary auditory cortex. |
| What is the "Homunculus"? | Topographic representation of motor ans sensory areas in the cerebral cortex |
| Which is the Homunculus presented with a "distorted appearance"? | Due to certain body regios being more richly innervated and thus having increased cortical representation |
| Brain perfusion relies strongly on ____________________. | Autoregulation |
| Cerebral perfusion is primarily driven by: | P CO2 |
| At what point is PO2 also a modulator of cerebral perfusion? | Severe hypoxia |
| What is the pressure gradient by which cerebral perfusion is based on? | Between mean arterial pressure (MAP) and ICP |
| A decrease on BP has what effect on cerebral perfusion pressure? | Decreased cerebral perfusion pressure |
| A decrease or increase on ICP will result in a decrease on CPP (cerebral perfusion pressure)? | Increase in ICP |
| Therapeutic hyperventilation: | 1. Decreases Partial CO2 (PCO2), which leads to ---> 2. Vasoconstriction, ---> 3. Decrease in cerebral blood flow which causes: 4. Decreased ICP |
| In order to achieve physiological decrease of ICP, the patient can be instructed to modified his/her breathing in what way? | Hyperventilate |
| What does the hyperventilation causes to the levels of PCO2 in the brain vasculature? | Decreases PCO2 with causes vasoconstriction |
| What is a possible reason to apply therapeutic hyperventilation? | Treat acute cerebral edema unresponsive to other interventions |
| CPP = (mathematical equation) | MAP - ICP |
| What is the difference of MAP -ICP? | Cerebral perfusion pressure |
| What does a CPP = 0, indicate? | No cerebral perfusion leading to brain death |
| When can hypoxemia cause an increase in CPP? | Only if P O2 is < 50 mm Hg |
| CPP is directly proportional to PCO2 until? | PCO2 is > 90 mm Hg. |
| Which cerebral artery supplies the anteromedial surface of the cortical brain? | Anterior cerebral artery |
| What is irrigated by the Middle cerebral artery? | Lateral surface of the cortical brain |
| Which cortical surfaces of the brain are supplied by the Posterior cerebral artery? | Posterior and Inferior surfaces |
| Watershed areas of the brain: | 1. Between the ACA and MCA 2. Between the PCA and MCA 3. Between the Superficial and deep vascular territories of the MCA |
| What condition affects the brain watershed areas? | Severe hypotension |
| What are the symptoms of damage of watershed areas by severe hypotension? | - Proximal upper and lower extremity weakness - Higher order visual dysfunction |
| What are the expected clinical signs of watershed zone damage if the internal border zone was damaged? | Proximal upper and lower extremity weakness |
| What is clinically seen in damgate to the watershed area formed between the PCA and MCA border zone? | Higher order visual dysfunction |
| What is the Circle of Willis? | System of anastomoses between anterior and posterior blood supplies to brain. |
| Which arteries form the anterior circulation of the brain? | ACA, ICA, and MCA |
| PCA, Basilar artery, and the Vertebral artery make up the _______________ circulation of the brain. | Posterior |
| The Lenticulostriate arteries branch off the ___________. | MCA |
| What are the Dural venous sinuses? | Large venous channel that run through the periosteal and meningeal layer of the dura mater |
| What is the function of the dural venous sinuses? | 1. Drain blood from cerebral veins and, 2. Receive CSF from arachnoid granulations |
| Into which important venous body do dural venous sinuses drain? | Internal jugular vein |
| The internal jugular vein receives drainage from: | The dural venous sinuses |
| What is the main clinical presentation of a patient with a Venous sinus thrombosis? | Increased ICP |
| What are the common clinical signs of increased ICP? | Headache, seizures, papilledema, and focal neurological defects |
| Serious complication of venous sinus thrombosis? | Venous hemorrhage |
| What are the associated hypercoagulable states that increase risk for venous sinus thrombosis development? | Pregnancy, OCP use, and factor V Leiden |
| Which is the main location of CSF return via the arachnoid granulations? | Superior sagittal sinus |
| Anatomically, wheres is the Cavernous sinus located with respect to the Sphenoparietal sinus? | Posteriorly |
| Which dural venous sinus is the the most superior? | Superior sagittal sinus |
| On which lobe of the brain is the Confluence of the sinuses located? | Occipital lobe |
| What are the ventricles that make up the CNS ventricular system? | Lateral ventricles, Third ventricle, and the Fourth ventricle |
| In the ventricular system, arrange from the most superior to the inferior the ventricles involved: | Lateral ventricles, Third Ventricle Fourth Ventricle |
| What structure is between the 3rd and 4th Ventricles? | Cerebral aqueduct of Sylvius |
| Which structure connects the 3rd ventricle with the Lateral ventricle? | Interventricular foramina of Monro |
| Which foramina connect or serve as conducts between the 4th Ventricle and the Subarachnoid space? | 1. Foramina of Luschka 2. Foramen of Magendie |
| Which is the medial foramina that allows 4th ventricle CSF to reach the subarachnoid space? | Foramen of Magendie |
| Foramina of Luschka, is it Lateral or Medial? | Lateral |
| What makes the CSF? | Choroid plexuses located in the lateral and fourth ventricles |
| Where are the choroid plexuses located? | Lateral and Fourth ventricles |
| What structures reabsorb the CSF from the Foramina of Luschka and Magendie? | Arachnoid granulations, which then drain into the dural venous sinuses |
| CSF in the arachnoid granulations is drain into the: | Dural venous sinuses |
| Which are the 4 Cranial nerves above the Pons? | I, II, III, and IV |
| Which 4 CNs exit the pons? | V, VI, VII, and VIII |
| Which 4 cranial nerves are in the medulla? | IX, X, XI, and XII |
| Which cranial nerve nuclei are MEDIAL ? | III, IV, VI, and XII |
| What is common in CNs 3, 4, 6, and 12? | Nuclei are medial |
| Actions or roles of the Pineal gland: | 1. Melatonin secretion 2. Circadian rhythms |
| The circadian rhythm and melatonin secretion are actions performed by the __________ ___________. | Pineal gland |
| What is the function of the Superior colliculi? | Direct eye movements to stimuli or objects of interests |
| The inferior colliculi is involved in __________________. | Auditatory |
| Where are the nuclei of the cranial nerves? | In tegmentum portion of brain stem |
| Which CN nuclei are located in the midbrain? | III and IV |
| Which cranial nerve nuclei are located in the Pons? | CN V, VI, VII, and VIII |
| What structure is known to divide the lateral nuclei from the medial nuclei of the cranial nerves? | Sulcus limitans |
| Cranial nerve LATERAL nuclei = | Sensory (alar plate) |
| Cranial nerve MEDIAL nuclei = | Motor (basal plate) |
| CN nerves in the medulla: | CN IX, X, XII |
| Which cranial nerve's nucleus in in the Spinal cord? | CN XI |
| Associated foramina of the Anterior cranial fossa? | Cribriform plate |
| Which cranial nerve goes through the Cribriform plate? | CN I |
| What structures (nerve/artery) pass through the Optic canal? | CN II and Ophthalmic artery |
| Which foramen is used by the CN II? | Optic canal |
| Which canal is used by the Ophthalmic artery? | Optic canal |
| What are the associated foramina of the Middle Cranial fossa? | 1. Optic canal 2. Superior orbital fissure 3. Foramen Rotundum 4. Foramen Ovale 5. Foramen Spinosum |
| What cranial nerves are known to pass through the Superior orbital fissure? | CN II, IV, VI, and V1. |
| Which foramen is used by CN V2? | Foramen Rotundum |
| Which foramen is used by CN V3? | Foramen Ovale |
| Foramen Rotundum provides passage to which cranial nerve? | CN V2 |
| Foramen Ovale is used by which cranial nerve? | CN V3 |
| What structure goes through the Foramen Spinosum? | Middle meningeal artery |
| The MMA uses which middle cranial fossa foramen? | Foramen spinosum |
| Anterior cranial fossa is through the | Ethmoid bone |
| Which cranial fossa is associated with "through sphenoid bone"? | Middle cranial fossa |
| Through temporal or occipital bone. Cranial fossa? | Posterior cranial fossa |
| What are the foramina associated with the Posterior cranial fossa? | - Internal auditory meatus - Jugular foramen - Hypoglossal canal - Foramen magnum |
| What cranial nerves go through the Internal auditory meatus? | CN VII and CN VIII |
| Which foramen is used by cranial nerves VII and VIII in the Posteror cranial fossa? | Internal auditory meatus |
| Damage to the Jugular foramen will probably damage which cranial nerves and vein? | CN 9, 10, 11, and Jugular vein |
| What foramen is used by Cranial nerve XII? | Hypoglossal canal |
| What structures traverse by the Foramen magnum? | 1. Brain stem 2. Spinal root of CN XI 3. Vertebral arteries |
| Which foramen is used in the Posterior cranial fossa by the Brain stem and Vertebral arteries? | Foramen magnum |
| What is the associated cranial nerve that goes through the Foramen Magnum? | Spinal root of CN XI |
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