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Clinical Medicine: Neurology

Hemispheric lesion whole half of body
Brainstem lesion Half of face, opposite half of body
Spinal Cord lesion lower half of body (depending on where the lesion is)
Polyneuropathy stocking/glove involvment
Myopathy shoulders and thighs
Degenerative examples of neurologic disorders Alzheimer disease, Huntington disease, Parkinson disease, amyotrophic lateral sclerosis
Developmental or genetic examples of neurologic disorders Muscular dystrophies, Arnold-Chiari malformation, syringomyelia
Immune examples of neurologic disorders Multiple sclerosis, Guillain-Barré syndrome, myasthenia gravis
Infectious examples of neurologic disorders Bacterial meningitis, brain abscess, viral encephalitis, HIV-associated dementia, neurosyphilis
Metabolic examples of neurologic disorders Hypo/hyperglycemic coma, diabetic neuropathies, hepatic encephalopathy
Neoplastic examples of neurologic disorders Glioma, metastatic carcinoma, lymphoma, paraneoplastic syndromes
Nutritional examples of neurologic disorders Wernicke encephalopathy (vitamin B1/thiamine ), combined systems disease (vitamin B12 )
Toxic examples of neurologic disorders Alcohol-related syndromes, intoxication with recreational drugs, side effects of prescription drugs
Traumatic examples of neurologic disorders Sub/epidural hematoma, entrapment neuropathies
Vascular examples of neurologic disorders Ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage
What kind of meningitis is most lethal? Acute bacterial meningitis
What can cause a type of atypical chronic meningitis? TB
Define meningitis. inflammation of meninges. Can be acute or chronic.
Define encephalitis. inflammation of brain; usually infx (viral most common)
Bacterial meningitis: Severity, Initial Tx Neurological emergency that should be Tx w/ ABX as soon as possible Dx considered.
Bacterial Meningitis Pathophysiology (common infxs & etiology); Risk Factors (RF) H. Influenzae, Meningococcus, Pneumococcus cause 75%; reaches meninges either by direct extension from ears, skin, skull infx or hematogenously (bacteremia); RF: extremes of age, immunocompromised, trauma/surgery, lung/ear/sinus infx, alcoholism, asplenia
Clinical presentation of bacterial meningitis Classic triad: fever, HA, stiff neck; other Sx: N/V, seizures, photophobia, confusion, abscess. Nuchal rigidity, Kernigs, Brudzinskis. Petechial/purpuric rash suggestive of meningococcus.
Kernig’s sign resistance to knee extension after passive flexion of the hip and knees
Brudzinski’s involuntary flexion of the knees in response to passive, rapid neck flexion
Bacterial meningitis complications Hearing impairment, hydrocephalus, brain damage- in general, cognitive deficits: sensory/motor deficits, learning disabilities, MR, cortical blindness, seizures
Bacterial meningitis Management/Tx Blood Cx-> LP (CT before LP if higher risk of herniation: ICP/mass). IV ABX after Cx; Vancomycin and 3rd gen cephalo (ceftriaxone/Rocephin) and if >50 add Ampicillin; Corticos minimize inflammation but must be started IMMEDIATELY PRIOR TO ABX
8 Indications for a CT prior to a LP 1 Altered LOC, 2 altered mental status, 3 focal neurological deficit, 4 immunocompromised, 5 Hx of CNS disease, 6 new-onset seizure, 7 papilledema, 8 Hx or evidence of head trauma
Aseptic meningitis: Patho, presentation, Tx mostly viral: 90% enteroviruses, aseptic aka Lymes, RMSF, etc; less severe than bacterial, preceding viral illness, LP shows bacterial vs viral; Tx: supportive (hydration and pain), If herpes meningitis or HIV: antivirals (associated w/ ^ mortality)
Viral (V) vs Bacterial (B) bigger CSF findings WBCs: B- 100 to 10,000 (for sure if >2000), V- <300; B-neutrophils V-lymphocytes; Proteins: B- >100 V- normal; Opening Pressure B- elevated (200-300) V- normal
Encephalitis Patho, presentation, Management and Tx Patho: usually viral: arboviruses, enteroviruses, herpes; Pres: lethargy, behavioral change, neurological deficit are characteristic; M: CT before LP, but MRI>CT early. CSF Cx; Tx: primarily supportive but acyclovir for herpes improves survival to 90%
Apraxia inability to perform a learned task, despite desire, physical ability and understanding of the command
Agnosia inability to recognize (objects, people, sounds, odors)
Aphasia difficulty with speech, can be receptive or expressive
7 Risk Factors for Dementia; What are several of these associated with? 1) Advancing age, 2) genetics, 3) smoking/alcohol, 4) Atherosclerosis, 5) Elevated LDL, 6) Diabetes, 7) Down Syndrome; Cardiovascular health
Difference between progressive vs static dementia? Progressive: happens over time and is most common. Static: 1 time trauma/stroke.
Difference between Primary and Secondary causes of dementia with examples? Primary: signs of neurologic disease other than cognitive decline. Ex: Alzheimers, Multiinfarct dementia, dementia w/ Lewy bodies. Secondary: Accompanied by signs and Sx of medical disease. Ex: toxins/alcohol/meds, metabolic/endocrine, nutritional, infx
Most common etiology of dementia? Alzheimer's Disease: 65%
Causes of possible dementias? 1) Vascular dementia (MID) 2) normal-pressure hydrocephalus 3) mass lesion 4) Parkinson's 5) Lewy-body disease 6) HIV/Neurosyphilis/Depression 1) Smoking, HTN, hyperlipidemia 2) prior meningitis/SAH, abnormal gait, incontinence 3) head trauma, focal neuro deficit, progressive HA 4) tremor/rigidity 5) extrapyramidal Sx: dysarthria, poor coordination 6) High-risk sex behavior
Alzheimer's:General, epidemiology Progressive/degenerative, most common, sporadic but can be familial, no specific physical signs until post-mortem. Epi: ^ w/age, M=W, AA x2>whites
Alzheimer's: Dx criteria Mini-Mental State Exam, Deficits in 2+ areas of cognition (orientation, registration, visuospatial and executive functioning, language, attention, memory), progression, NO disturbances in consciousness, absence of systemic disorders.
Alzheimer's: Pathology 1) Neurofibrillary tangles of Tau protein (normal protein involved w/microtubule fn that is twisted to -> nonfunctioning in AD. 2) Senile plaques of Beta-amyloid peptides that build up in the brain due to protein deposits.
Apolipoprotein E (APOE) gene Risk factor for development of AD and influences age of onset. Not everyone who has AD has APOE, but people w/APOE are 4x as likely to get AD. Helps Dx but doesn't exclude.
Alzheimer's: Tx Acetylcholinesterase inhibitors: donepezil (Aricept). NMDA/Glutamine Antagonist: Memantine (Namenda) for AD and vascular dementia- slows rate of decline
Alzheimer's: Prevention regular exercise, better nutrition, mentally stimulating activity, Tx of atherosclerotic risks, moderate alcohol intake, folate/B12/B6, antioxidants A, C, E
Vascular/Multi-infarct Dementia: General, Risk 2nd most common form of dementia. Infarcts occur in different parts of brain over time. Higher mortality than AD. Clinical course: progressive, stepwise decline. Risk: AA, Japanese, ^ age, HTN, smoking, DM, AFib, carotid disease, CAD
Vascular/Multi-infarct Dementia: Pathology, Evaluation, Tx Patho: depression, personality change, signs of UMN injury, gait problems prevalent; Eval: MRI, neuroimaging, Echo/Holter (AFib), Carotid evals; Tx: Aspirin/warfarin, Memantine, depression meds PRN
Dementia w/ Lewy Bodies: General, Patho Gen: fluctuating cognition, visual hallucinations, delusional Parkinsonism. Patho: cortical and substantia nigra damage, Lewy bodies (aggregating protein) in nerve cells, mild brain atrophy.
Dementia w/ Lewy Bodies: Sx Visual hallucinations, delirium, fluctuating cognitive difficulties, and parkinsonism and extrapyramidal motor symptoms [can be more prominent than memory issues] (dysarthria, poor coordination of voluntary movements), sensitivity to neuroleptic meds
Dementia w/ Lewy Bodies: Tx Treat Psych/Parkinsonism Sx, only use newer atypical anti-psychotis, donepezil, memenatine; Selegiline may slow progression (MAO inhibitor boosting dopamine)
Normal-Pressure Hydrocephalus: General, Sx, Tx potentially reversible cause of dementia: ventricular enlargement w/o cortical atrophy resulting from poor reabsorption of CSF. Sx: dementia, gait disturbance, urinary/fecal incontinence. Tx: Peritoneal shunting or serial lumbar punctures that remove CSF
Alzheimer's disease main features Frontal lobe release signs (later stages; primitive reflexes return), extrapyramidal signs. Enlarged ventricles and cortical atrophy by CT or MRI
Multi-infarct dementia main features Focal deficits stepwise course. Multiple areas of infarction, often subcortical on CT/MRI
Normal-pressure hydrocephalus main features Gait disorder, incontinence. Enlarged ventricles with little or no cortical atrophy
Dementia with Lewy bodies main features Visual hallucinations, periodic confusion, parkinsonism. Marked exacerbation of extrapyramidal symptoms with use of standard neuroleptics
Parkinson's disease and Huntington's disease main features Subcortical dementias with significant motor dysfunction and no prominent aphasia or agnosia. Parkinson’s dementia
Frontotemporal dementia main features Affects younger patients. Behavioral and executive function (planning AND judgment) abnormalities
Peripheral Neuropathy: types, management, Mononeuropathy: One nerve: carpal tunnel, bell's palsy- entrapment or injury. Polyneuropathy: multiple nerves not following nerve pattern- diabetes and alcoholism most common. Managment: Rest, protection of area, anti-inflammatories, PT, surgery.
Cervical radiculopathy: General, Patho, Dx Dysfn of nerve root often due to aging. Foraminal narrowing due to osteophyte/spur formation, disc herniation. Dx: Provocative compression tests recreate Sx. Eval:
Myotome of shoulder abduction C5
Myotome of elbow flexion C5, C6
Myotome of elbow and wrist extension C7
Myotome of wrist flexion C8
Myotome of finger extension C7
Myotome of finger flexion C8
Myotome of finger abduction T1
Myotomes of ankle reflexes S1, S2
Myotomes of knee reflexes L3, L4
Myotomes of biceps C5, C6
Myotomes of triceps C7, C8
Cervical radiculopathy: Evaluation, Tx XRay < MRI esp if radicular pain is severe, motor/sensory/reflex deficit, myelopathy suspected (after UMN signs). Tx: rest, ice, NSAIDs, cervical collar
Myelopathy: General, Causes may lead to motor, sensory, sphincter disturbances. Spasticity common w/UMN lesions. Causes: trauma, MS, infx, infarct, B12 deficiency, cervical spondylosis, tumor; recall this ISN'T a peripheral nerve disorder.
Brachial Plexus Neuropathy: Causes, Tx, Dx Causes: Injury: football "burner/stinger", birth injury w/ difficult delievery; Idiopathic; Tx: pain management, PT; Dx: Erb's Palsy: "waiter's tip", C5/C6. Can lead to scapular winging.
Thoracic Outlet Syndrome: General, Etiology Impingement on brachial plexus or subclavian vessels passing through throacic outlet. Eti: cervical rib/bony abnormality, repetitive overhead activity, trauma
Thoracic Outlet Syndrome: Sx, Tx Sx: pain in arm in certain positions, pallor/cyanosis, edema, coolness of extremity, weak pulse, sensory loss and weakness. Tx: PT, Rest, Shoulder exercises, NSAIDs, Conservative therapy effective in 90%, surgical excision
Carpal Tunnel Syndrome: General, Sx Median nerve entrapment, most common peripheral nerve entrapment. 90% respond to conservative therapy. Sx: pain/paresthesias/numbness in median nerve, worse at night, referred pain to shoulder, muscle weakness, thenar atrophy
Carpal Tunnel Syndrome: Associations, Dx, Tx DM, RA, preg, hypothyroidism, fracture, occupational repetitive actions; Dx: Tinel's: tapping on wrist along median nerve -> tingling, Phalen's: performed w/ wrist at max flexion. Tx: splinting in neutral position, rest, NSAIDs, steroid injection, surgery
Ulnar Nerve Entrapment: General, Sx, Tx Most commonly entrapped at medial elbow (vulnerable to trauma/fracture), cubital tunnel syndrome. Sx: pain/paresthesias, sensory lost in 4th/5th finger, wasting of grip muscles. Tx: rest, elbow padding, extension splint, NSAIDs, steroid injection, surgery
Radial Nerve Compression: General, Causes, Sx most often in axilla or upper arm. Causes: injury/fracture of humerus, improper crutch use, prolonged pressure during sleep (Saturday night palsy). Sx: pain, paresthesias, wrist drop
Meralgia Paresthetica: General/Patho, Sx LFC nerve enters thigh in close relation to inguinal ligament, ASIS and sartorius muscle insertion and is compressed. Purely sensory (motor deficit excludes this) of anterior thigh. Sx: burning pain, improves w/ sitting/lying down.
Meralgia Paresthetica: Risk Factors, Tx Risks: obesity, preg, tight clothing, DM. Dx: clinical nerve conduction studies. Tx: resolve spontaneously, but weight loss encouraged, loose clothing.
Femoral Neuropathy: General, Sx, Tx supplies motor/sensory to quads and sensation to anteromedial lower extremities; caused by diabetes. Sx: thigh pain, weakness, wasting. Absent/decreased knee jerk. Tx: PT, knee bracing, pain meds (specifically designed for neuropathic pain)
Sciatic Compression: General, Sx provides sensation to posterior thigh, lateral calf, gluteus, hamstrings, lower leg and foot. Compression due to prolonged pressure, trauma, misplaced injections. Sx: pain/weakness, sensory changes
Common Peroneal (fibular) Compression: General, Sx, Tx Common @ level of fibular head, seen in cachectic patients w/prolonged bed rest, alcoholics, DM, fractures, tight casts, prolonged crossing of legs. Sx: anterolateral lower leg sensory changes and foot drop/slapping gait. Tx: foot brace, avoid compresison
Lumbar Disc Syndromes: general, types, Sx sudden, severe low back pain after minimal/no activity. Sx: Disk btwn L4/L5 (weakness of dorsiflexion/sensation of great toe) and L5/S1 (weakness of plantar flexion, loss of ankle jerk reflex) most affected.
Lumbar Disc Syndromes: Imaging, Tx, Warning signs calling for immediate imaging Imaging: plain films, MRI; Tx: relative rest (not complete), PT, NSAIDs, muscle relaxants, heat/ice, prednisone, surgical eval if no improvment. WARNING SIGNS: Hx of Ca, immunosuppression, incontinence
Cauda Equina Syndrome: General, Sx, Imaging, Tx compression of multiple nerve roots suggested by combo of: progressive limb weakness/numbness, uncontrollable pain, saddle anesthesia, bladder/bowel dysfn. Imaging: Urgent MRI needed. Tx: surgery to prevent permanent paralysis of lower extremities.
Peripheral Polyneuropathy: Sx, PE, Causes Sx: distal, symmetric sensory and/or motor symptoms; may also include autonomic nerves. PE: decreased sensation or motor abnormalities in a “stocking-glove” distribution. Causes: DM, chronic alcoholism, idiopathic, meds, many others.
Peripheral Polyneuropathy durations -Chronic (years): suggests a hereditary cause -Subacute (weeks to months): may be toxic/metabolic cause -Acute (days): toxin or Guillain–Barré syndrome
Peripheral Polyneuropathy: Studies, Management, CBC, ESR, Glucose, Lipids, TSH, B12, BUN, LFT; difficult to Tx, management of underlying causes like zoster. Antidepressants, antiseizure meds, topicals, narcotics, pain specialist referral.
Diabetic Neuropathy: General common source of sensorimotor polyneuropathy. Sx improve w/ improved glucose control.
Peripheral neuropathy symmetric pain or sensory loss in the digits, feet, legs, hands, arms (feels like walking on hot coals). Most common form of diabetic neuropathy.
Autonomic neuropathy gastroparesis, Orthostatic hypotension, hypoglycemic unawareness, silent MI, impotence, bowel/bladder dysfunction
Proximal neuropathy Diabetic amyotrophy; pain in the thighs, hips, or buttocks, with weakness and muscle atrophy, usually b/l and may be associated with weight loss
Focal neuropathy sudden weakness of one nerve (typical) or group of nerves, causing muscle weakness or pain
Guillian-Barre Syndrome: General, Risk Factors (RF) Acute, inflammatory demyelinating polyneuropathy, mostly motor. Acquired autoimmune disease. Presentation: 1-3 weeks after viral illness w/rapid progression ascending from lower extremities. RF: preg, influenza immunization, post op, HIV, campylobacter
Guillian-Barre Syndrome: clinical presentation Rapid progression of ascending symmetric weakness, pain, paresthesias, sensory loss, hypo/hyperreflexia, respiratory muscle paralysis requiring vent support. 50% have autonomic neuropathy
Guillian-Barre Syndrome: Evaluation, Tx Nerve conduction studies reveal evidence of demyelination. CSF has increased protein BUT NORMAL cell count (cytoalbumin dissociation). Tx: plasmapheresis (getting rid of antibodies) and IV immunoglobulin (IVIG). No steroids.
Complex Regional Pain Syndromes: General, Types begin secondary to inciting event and consisting of pain disproportionate to injury. Type of post-traumatic neuralgia. Type 1: reflex sympathetic dystrophy pain- pain caused by variety of insults like soft tissues injury. 2: causalgia: due to nerve damage
Complex Regional Pain Syndromes: Sx, Tx Sx: Sensory: burning pain. Vasomotor: temperature/color change. Autonomic dysfn: edema/increased sweating. Motor: weakness, clumsiness, decreased ROM, tremor, atrophy. Tx: Steroids, calcitonin, analgesics, SSRIs, nerve blocks, lido, pain specialist
Bell's Palsy: General, Presentation, Evaluation acute paralysis of facial muscles (CN VII). Pres: ear pain, fever, tinnitius, hearing loss, difficulty closing eyelid, alteration in taste, evaluate for skin lesions that cause Bell's, glucose, MRI if atypical features, EMG for severe and persistent
Hyperacusis oversensitivity to certain frequencies heard
Red Flags suggesting alternative Dx than Bell's Palsy CN involvement other than VII. Bilateral facial weakness. Weakness, numbness of arms or legs. Unaffected upper facial muscles (forehead). HA, visual deficits, N/V. Hx of travel in woods/tick bite (Lyme). Recurrent unilateral facial paralysis
Bell's Palsy Tx supportive, preventing corneal injury w/lubricating drops. STEROIDS are a must have and antiviral therapy for possible herpes may be considered. Start w/in first few days of onset.
Myasthenia Gravis: General chronic autoimmune process w/antibodies against Ach receptor of neuromuscular jn -> decrease in normal receptors availability leads to fatigue and weakness w/ progressive nerve stimulation. Only motor.
Myasthenia Gravis: Epidemiology, Pathology, Sx more common in women and associate w/ Thymoma (CT for chest ->remove and Sx decrease), thyroid disease (20%). Sx: weakness, fatigue, ptosis, diplopia, facial muscle weakness, dysphagia, nasal quality to speech, resp distress
Myasthenia Gravis: Dx, Tx fluctuating muscle weakness and fatiguability. Dx: lab- blood Ach receptor antibodies. Tx: Ach-ase inhibitors (overdose causes cholinergic crisis tx w/ atropine. Prednisone, thymectomy, plasmapheresis, IVIG, supportive.
Causes of Resting tremor usually due to Parkinson's
Causes of Postural tremor Physiologic (albuterol, caffeine); essential/familial/senile
Cause of intention tremor cerebellar (finger to nose)
Physiologic tremors: Causes and Tx usually not noticable, increased by anxiety, muscle fatigue, caffeine, meds, hyperthyroidism. Decreased w/ alcohol, benzos, BB, primidone. Tx: BB for special occasions
Familial/Benign/Senile Essential Tremors: Causes, Tx half are autosomal dom. Onset: early AND late adult. May affect hands, head, voice, legs, trunk, symmetrically. Increases w/writing, carrying, age, stress, fatigue. Decreased w/ BB, rest, alcohol. Tx: BB, primidone, benzos, surgery/deep brain stim
Intention Tremor: General, Causes, Tx dramatic action tremor progressively increasing in amplitude as pt brings limb toward target. No tremor at rest. WORSE w/ alcohol. No effective Tx
Dysdiadochokinesis is the inability to perform rapid alternating movements.
Dysmetria is the inability to judge distances which leads to the difficulty with finger to nose testing and heel to shin– overshooting the target.
Resting Tremor "pill-rolling" movement (70%). Old psych drugs (haldol) worsen tremor. Anticholinergics may improve tremor.
Parkinson's Disease: General (3 Cardinal features) Progressive neurodegenerative disease characterized by 3 cardinal features: 1) Resting tremor 2) Rigidity- “cogwheeling” during passive motion (goes and then stops) 3) Bradykinesia-slowness in all activities.
Parkinson's Disease: Cause and Associated Features/Sx Cause: unknown, combo of genetic and environmental factors, increased in rural environment, Micrographia, masked facies, shuffling gait, postural instability (later finding), anosmia, cognitive impairment, dementia, depression, sleep disturbance
Parkinson's Disease: Evaluation Eval: CT/MRI (best) to rule out vascular or other disease, screening labs, Dx is clinical, rule out secondary Parkinsonism (drug/toxin-induced, structural lesions, hydrocephalus, infx).
Drug-Induced Parkinsonism crucial to rule out as it is reversible, need med history. Often: anti-psychotics (haldol), antiemetics (metoclopramide-Reglan), Dopamine depleters (methyldopa), Combo drugs.
Parkinson's Disease: Tx (Neuroprotective and Sx) Tx: Neuroprotective: MAO inhibitors (selegiline) delays early need for levodopa; Sx relief: Levodopa, Dopamine agonists, anticholinergics (for tremors), Catechol-O-Methyltransferase Inhibitor (increase 1/2 life of L-Dopa), amantadine, neurosurgery.
Levodopa limited duration of efficacy. Most effective Tx for bradykinesia, rigidity, tremor. Often given in combo with cabidopa to prevent peripheral conversion to dopamine. Side effects: N/V, anorexia, dyskinesias, hallucinations
Huntington's Disease: General, Dx, Sx, Tx Incurable, adult onset, degenerative, neurological condition usual onset : 35-44 yo. Autosomal dominant inheritance. Dx w/ genetic testing. 1) Huntington's chorea 2) dementia 3) behavioral changes. Tx: Sx Tx for Chorea. exercise beneficial. Fatal ~ 15 yrs
Amyotrophic Lateral Sclerosis (ALS): General, Etiology Lou Gehrig's disease; progressive neurodegenerative disorder affecting anterior horn of spinal cord (LMN) and corticospinal UMNs, most common btwn 40-60 yo men w/ 90% mortality in 6 years averaging 3 years. Eti: genetic, autoimmune, viral, smoking
Amyotrophic Lateral Sclerosis (ALS): Sx Purely upper and lower motor neuron deficits. Sx: atrophy, weakness, spasticity, fasciculations, hyperreflexia, dysphagia, dyspnea, hypotonia. Cognition, eye movements, sensation and bathroom fns remain intact. Death due to resp. failure or infx
Amyotrophic Lateral Sclerosis (ALS): Tx Sx relief, Riluzole may prevent progression and prolong life for several months by delaying need for invasive vent support.
Tourette's Syndrome: General, Etiology, Epidemiology, Associated disorders movement disorder presenting in childhood, 50 % resolve in early adulthood. Sudden, brief, intermittenent repetitive movements or sounds w/unknown etiology. Males>Females. Associated w/ OCD, ADD, learning difficulties, impulse control difficulties.
Tourette's Syndrome: Sx, Tx, coprolalia, echolalia 80% motor 20% vocal (coprolalia (vulgar/obscene speech) or echolalia (parroting speech of others)). Tx: ID of triggers, self-esteem boosting, alpha2-adrenergic agonist (clonidine), Benzos, anti-psychotics, topiramate
Multiple Sclerosis (MS): General chronic, progressive degenerative disease affecting myelin sheath. Most common demyelinating disease of CNS. Characterized by remitting and relapsing neuro dysfunction affecting multiple areas, locations, times. Clinical course highly variable pt to pt
Multiple Sclerosis: Etiology, Pathophysiology More common in women 20-50; Et: unknown but may have genetics, exposure, defective reg of immune response. Patho: discrete episodes of autoimmune demyelination injury to CNS -> plaques. Some remyelination occurs w/ partial resolution of Sx.
Multiple Sclerosis: Presentation/Sx; Lhermitte's Exacerbations occur w/ stress, illness, heat. Sx: sensory: paresthesias, decreased. Motor: OPTIC NEURITIS, diplopia, weakness, spasticity, ataxia, intention tremor, bowel/bladder dysfn, memory loss. Lhermitte's: electrical sensation down spine w/ neck fle
Relapsing-Remitting Disease 85%; Younger patients may have a relapsing–remitting course, characterized by attacks followed by complete or nearly complete remission. Typical course; sometimes this will go to Secondary Progressive Disease
Multiple Sclerosis: Dx MRI w/ gadolinium (most sensitive for plaques). Key to diagnosis is evidence of lesions separated in “space and time”. Dx: evidence of damage at 2+ areas in CNS AND evidence damage occurred 1+ month apart.
Multiple Scelrosis: Testing, Tx 90% of MS patients have increased IgG and oligoclonal IgG bands on electrophoresis. Plaques found on 90% on MRI. Labs exclude other things. Tx: acute: SUPER DUPER HIGH DOSE Prednisone. Relapse prevention: interferon, Natalizumab.
Multiple Sclerosis: Prognosis After 15 years of clinical disease, about 50% can still walk, 30% can still work. 5-10% mild, benign course- can’t predict which patients do not need disease-modifying therapy.
Seizure transient alteration in a cerebral cortical function due to synchronous activation of neurons either focally or throughout the brain
Seizure: partial (simple and complex) and Generalized Both involve one area of the brain. Simple: focal neurologic events w/ normal consciousness. Jacksonian March. Complex: consciousness impaired. Generalized: involve both hemispheres, LOC, bilateral symmetric (not focal)
Epilepsy recurrent, unprovoked seizures; 1/100 in the U.S.
Jacksonian March jerking movements go from hand to arm to face etc. as stimulation travels through the brain.
Simple Partial Seizures consciousness is preserved; can be motor, sensory, autonomic or psychic. Jacksonian March. Psychic: dejavu, fear; Autonomic: pallor, sweating, vomiting, hypersalivation
Complex Partial Seizures Consciousness/memory impaired. May begin w/ aura. Sx: coordinating/involuntary motor activity (ex: lip smacking/grimacing); olfactory hallucinations. Resemble psychosis. Begins in TEMPORAL LOBE
Generalized Seizures: Types 1) Absence (petit mal) brief impaired consciousness often found in young children. Usually resolve by adulthood. 2) Tonic-clonic seizures (grand mal seizures) "typical full on seizures" often w/ incontinence/tongue biting.
Tonic-Clonic Extended-flexed
Causes of Seizure and by age Idiopathic, tumor (focal suggests), cerebral hypoxia, stroke, toxins/drugs, fever, head injury, infx, metabolic disturbances, alcohol withdrawal. By age: Infants: birth trauma, febrile, Teens: trauma, infx, toxic, idio. Older: toxins, trauma, CVD
Risk Factors of first seizure in adults AIDS, head trauma, >40, fever, malignancy, anticoag, new focal deficit, Hx of stroke, persistent HA, altered mental status. ->get CT (emergency setting) or MRI
Seizure: Evaluation Eval: EEG confirms type, MRI recommended for non-febrile seizure. LP if indicated, toxicology.
Seizure Recurrence and risk factors for it 36-77% after first unprovoked seizure. 50% recur in 1st 6 months. 70% recur after 2, 80% recur after 3. RF: neurologic lesions, Hx of epilepsy in sibling
Seizure Tx risks life threatening idiosyncratic rxns, teratogenicity, cog. impairment, systemic toxicity, adverse behavioral effects, P450 interactions
Anti-epileptic drugs (AEDs) 70% controlled on 1 drug. 20% more controlled w/ multiple ones. Rest should consider surgery/experimental drug therapy. Biggest cause for failure is NONCOMPLIANCE
What type of anti-epileptics cause acute stoppage of seizures? Benzodiazepines
AEDs for Seizure types: Tonic/Clonic, Absence, Partial Simple and Complex Valproic acid can be used for them all. Ethosuximide can only be used for Absence. Carbamazepine, phenytoin, phenobarbital, primidone can bed used on both tonic-clonic and simple/complex partial seizures.
Advantages for newer AEDs Effective, fewer toxic effects, better tolerated, no need for blood level monitoring
Prognosis of Seizures Primary generalized have best overall prognosis. 50%+ child-onset cease by age 20. 80% recur w/in 5 years of discontinuation of med.
Discontinuing AEDs May be considered if seizure-free for 2-5 years on AEDs AND if 1) single type of partial seizure 2) normal neuro exam/IQ 3) EEG normal w/ Tx
Precautions/First Aid for Seizures Pre: uncontrolled seizure pts should not do certain things until control maintained: driving, water, height, fire, power tools. F/A: When having seizure: move hot/hard/sharp objects, pillow under head, turn on side, activate EMS, don't restrain
Status Epilepticus: General, Management, Prevention 5-30+ min of seizure activity. ABC, Vitals, IV access, labs esp glucose. Give and D50 and Thiamine (which can be depleted in process of metabolizing sugar)
Wernicke's encephalopathy: General, Presentation Caused by administration of D50 w/o Thiamine in those already Thiamine (B1) deficient (required in oxidation of glucose). Necessary for alcoholics, frail, elderly, malnourished, (good practice in everyone else). Pres: confusion, ataxia, oculomotor dysfn
Meds for Status Epilepticus 1) Lorazepam (ativan) 2) Phenytoin (dilantin) 3) Phenobarbital (barbituate)
Stroke: General (Causes, ID, Types Management) rapid onset of neurological deficit due to loss of perfusion, 15% mortality. Ischemic (80-90%- Thrombosis 2/3 and Embolic 1/3), Hemorrhagic: 10-20%
Ischemic Stroke: Pathogenesis: Thrombosis: large (carotid, cerebral, vertebral) or small vessels. Emboli: platelets, fibrin from carotid artery or heart due to A-Fib.
Hemorrhagic stroke: Pathogenesis aneurysm, HTN, coagulopathies, cocaine, trauma, neoplasm
Stroke: Risk Factors (Modifiable and non-modifiable) M: HTN, smoking, AFib, hypercholesterolemia. N-M: age, ethnicity, Hx of migraines, sickle cell, heredity
Stroke: Presentation Ischemic: acute onset of focal, unilateral, weakness and speech disturbances. Hemorrhagic: worst headache of my life, decreased level of consciousness
Where is a vascular distribution of anterior circulation? Carotid
Vascular distribution of posterior circulation? Vertebral
Lacunar small vessel disease strokes, most common with chronic hypertensives and diabetics, pure motor or pure sensory symptoms
Transient Ischemic Attack (TIA): General, Sx, Tx Transient neurological fn due to ischemic, w/o infarct. MAJOR risk for stroke or MI. Unilateral paresis/speech disturbance, amaurosis fugax/retinal artery occlusion. 1) search for treatable cause (AFib, carotid stenosis), 2) R/O other causes 3) anticoag
TIA/Stroke: Evaluation, Risk of Stroke after TIA ABCs -> extent of neuro deficits -> ID potential causes -> ID comorbid conditions -> determine timing of onset; 10-20% in 90 days, 50% of those that occur occur w/in 48 hours; CT w/o contrast, blood glucose, EKG etc.
Ischemic Stroke: Tx Thrombolysis is currently the most effective Tx for acute ischemic stroke, but must be 100% sure it is not hemorrhagic stroke with CT.
Door to medical evaluation for stroke 10 min from presentation to ER
Access to stroke specialist 15 min from presentation to ER
Door to CT completion for stroke 25 min from presentation to ER
Door to CT interpretation for stroke 45 min from presentation to ER
Door to treatment (tPA) for stroke 60 min from presentation to ER, 3 hours from onset of Sx to Tx of tPA
4 Criteria for Tissue plasminogen activator (tPA) 1) Dx of ischemic stroke causing measurable neurological deficit 2) Over 18 yo 3) CT w/o evidence of hemorrhage 4) less than 4.5 hours since onset of Sx (intra-ARTERIAL thrombolysis can be administered up to 6 hours in some pts w/ stroke)
tPA CONTRAs BP> 185/110 (must get it down before admin). Glucose <50 or >400 (just give insulin or glucose before admin). SUSPICION OF SUBARACHNOID HEMORRHAGE, obviously. Hx of brain hemorrhage or tumor, stroke/head trauma in past 3 months, 2 weeks since surgery/LP
Management of BP while treating w/ tPA or about to Tx w/ tPA If not receiving t-PA: monitor BP as long as it is less than 220/120 and asymptomatic. IF receiving t-PA: must treat if greater than 185/110. Uncontrolled hypertension increases the risk of hemorrhagic complication.
Primary stroke/TIA prevention lifestyle modifications, control BP/cholesterol/DM, ASA in high risk, warfarin for AFib
Secondary stroke/TIA prevention For someone who has had a stroke before...preventing another. Anti-platelet therapy: ASA, plavix (clopidogrel), anticoag (warfarin), aggressive control of atherosclerotic RF
Carotid Artery Stenosis: General, Tests, Tx bruit suggest atherosclerotic lesion..often a source of emboli. USPSTF doesn't recommend screening for asymptomatic population. Tests: U/S, MRA, CTA. Tx: anti-platelet, cholesterol/BP control, endarectomy (>70% stenosis in symptomatic pts)
Indications of carotid endarterctomy *Sx pts with greater than 70% stenosis. Sx pts with greater than 50-69% stenosis-marginal benefit (more in men). ASx pts with greater than 60% stenosis- some benefit, but much less than if Sx. No endarterectomy if < 50% stenosis, even if Sx -no benefit
Hemorrhagic Stroke: Presentation, Tx HA: severe and sudden, N/V, Seizures, HTN, altered LOC, ICP. Tx: STAT neurology/neurosurgery consult. Correction of coagulopathy. BP management, seizure control, ICP control.
Hemorrhagic Stroke: Causes Trauma, ruptured aneurysm, HTN, polycystic kidney disease, cocaine/ampheetamine use
Cerebral Aneurysms: General, Causes, Studies, Tx most caused by SAH, focal dilations of cerebral blood vessels prone to rupture. Can be congenital, traumatic, infx, atherosclerotic. Dx: CT IDs 90%, LP, angiography, ECG changes (peaked P waves, prolonged QT, tall T waves). Tx: ABCs, ICU, angio, Surgery
Xanthrochromia yellowish color caused by presence of blood in the CSF
Acute post stroke complication cerebral edema, increased ICP and possible herniation (hemorrhagic), hemorrhagic transformation(ischemic ->hemorrhagic), aspiration pneumonia, and seizures. Secondary cerebral vasospasm may lead to further ischemia/infarct after anueurysmal SAH
Post-thrombolytic post stroke complication bleeding. Of greatest concern is intracerebral hemorrhage, typically occurring within the first 12 hours after treatment. Other potential sites of bleeding include GI tract, GU tract (associated with Foley catheters), and skin, typically at IV sites
Subacute post stroke complication include pneumonia, DVT, PE, urinary tract infections, decubitus ulcers, contractures, spasticity, joint problems and malnutrition
Chronic post stroke complication depression
Primary HAs clinical syndromes not indicative of underlying disease: migraine, tension, cluster HA
Secondary HAs 2ndary to wide range of pathology some serious some not: sinusitis, temporal arteritis, SAH, tumor, subdural hematoma
Acute onset HAs Subarachnoid hemorrhage, Meningitis or encephalitis, Ophthalmic disorders (glaucoma, acute iritis). Less common
Subacute onset HAs Temporal arteritis, Intracranial mass (tumor, subdural hematoma, abscess), Pseudotumor cerebri (ICP; papilledema but no tumor), Trigeminal neuralgia (severe pain in C2 or C3) , Postherpetic neuralgia
Chronic HAs Migraine, Medication overuse headache, Cluster headache, Tension headache, Cervical spine disease, Sinusitis, Dental disease
HA: Studies CT to rule out hemorrhage. MRI preferable for brain tumor and posterior fossa. LP: subarachnoid hemorrhage/meningitis. Low/elevated CSF pressure can cause HA.
Migraine HA: General, Dx for w/o aura 12% of adults, women 3x, 2/3 have family Hx. Dx: 5 attacks w/ at least 2 of following: unilateral, pulsating, moderate/severe intensity inhibiting daily activity, aggravated by routine physical activity and ONE: N/V, photophobia/phonophobia
Migraine HA: Dx w/aura at least 2 attaacks w/ 3 of following: 1 aura Sx, no aura >60 min, HA follows aura w/in 60 min
POUNDing Mneumonic Pulsatile, hOurs: 4-72, Unilateral, N/v, Disabling intensity
Migraine HA: Presentation including prodrome and postdrome Prodrome of irritability, difficulty concentrating, nausea, aura, HA, HA termination, Postdromal: fatigue, sleepiness, irritability
Scotoma White spot in vision
Hemianopsia half of vision blacked out
Scintillating scotoma fuzziness of vision
Migraine HA: Pathophysiology and Triggers neuronal and inflammatory processes -> vasodilation due to triggers (caffeine, alcohol, cheeses, meats, stress, smoking, abn sleep, meds, strong odors)
Migraine w/ aura complications ^ risk of ischemic stroke esp w/ use of oral contraceptives, smoking, HTN
Migraine HA: Tx quiet, dark room, sleep, analgesics (NSAIDs/Acetaminophen, TRIPTANS BEST, ergot alkaloids, moderate caffeine, sedatives, antiemetics
Triptans Vasoconstriction (cerebral and coronary) and inhibit neurogenic inflammation. Theoretical concern of coronary ischemia.
Migraine Prophylaxis Indications and Tx Frequency > 2/month, duration >24 hrs, major disruptions in pt lifestyle, abortive therapy fails/overused, abortive meds used 2x+/week. Tx: BB, CCB, ACE, anticonvulsants, antidepressants, NSAIDs, B12, Magnesium
Tension HA: General, Sx, Precipitants Most common/recurrent, 90% bilateral, dull steady pressure or band-like sensation around head, progressively more painful. Pressing/tightening (nonpulsatile), no N/V; Precipitants: anxiety/depression/stress, muscle strain,
Tension HA: Tx stress reduction and exercise, PT/Massage, ergonomic eval, NSAIDs, amitriptyline (tricyclic ant-depressant), muscle relaxant
Cluster HA: General, Presentation Rare; Distinguished by location, timing, periodicity. Presents: Intense, non-throbbing, unilateral, ptosis, miosis, stabbing/burning behind eye w/lacrimation, attacks occur nightly for 2-3 months; severe distress for pt; suicidal ideology
Cluster HA: Triggers, Epidemiology stress, allergens, seasonal changes, nitroglycerin, alcohol. 80% are heavy smokers, 50% have Hx of heavy drinking. Epi: Male: Female 2:1, middle aged men
Cluster HA: Tx O2 inhalation 7-12 liters, sumatriptan, corticosteroids, capsaicin. Prophylactic: Verapamil: CCB
SNOOPS mnemonic for RED FLAGS Systemic Sx. Neurologic Sx. Onset (sudden, abrupt). Older (w/new onset) Previous HA Hx (changing or worst). Secondary RF (HIV, Ca, trauma)
Giant Cell Artertitis/Temporal Arteritis: General, Management >50 yo, systemic, ->BLINDNESS, jaw muscle claudication. Management: Sed rate, BX OF ARTERY is DX (done by Ophthalmologist), Prednisone start immediately
Pseudotumor cerebri (Idiopathic intracranial HTN): General, Sx Management, Tx unknown etiology, primarily affecting young obese women, variable type of HA, visual Sx present...risk of perm visual loss. Papilledema. "Worse in morning but gets better". Drug induced, referral, MRI then LP. Tx: carbonic anhydrase inhibitor diuretic
Trigeminal Neuralgia: General, Sx, Tx paroxysms of piercing sudden, severe pain lasting seconds to minutes in the mouth, cheek, jaw. 85% idiopathic, MRI to rule out secondary cause. Usually middle-aged/elderly women. Tx: carbamazepine (seizure meds)
Postherpetic Neuralgia: General, Sx, Tx constant, severe pain after zoster reactivation, V1 most frequently affected: dysethesia. Tx: Zoster w/acyclovir, corticos, zoster vaccine. PHN: tricyclic antidepressants (amitriptyline), antiseizure meds, topical (lidocaine/capsaicin)
Concussion: General, Sx, Causes mild TBI; disturbance of brain fn, caused by direct or indirect force to head. HA most common Sx; rapid onset, w/ short-lived impairment. Causes: MVC, Falls, sports (football esp). Sx: disorientation, dizziness/poor balance, HA.
Post-concussive syndrome weeks to months w/ 3 of the following: HA, dizziness, fatigue, irritability, impaired memory/concentration, insomnia, lowered tolerance for noise/light
8 Concussive indications for neuroimaging focal neuro deficit, GCS < 15, >60 yo (<16 yo), intoxication, coagulopathy, severe injury, LOC > 60 secs, skull fracture, severe HA, Vomiting
Concussion Management Cognitive rest, physical rest, slow transition back to school (limit hours, no standardized tests, longer breaks)
Created by: crward88