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Neurology
FA complete review Part 3.1 Pathology
| Question | Answer |
|---|---|
| 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 |
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rakomi
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