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Session 4 CM Neuro-3
CM- Neuro -3- CVA
| Question | Answer |
|---|---|
| This is characterized by an acute onset of neurologic deficit persists for at least 24 hours and reflect focal involvement of the central nervous system and is a result of disturbances to cerebral circulation/perfusion | Stroke/CVA |
| What are the 4 types of stroke | TIA, Reversible Ischemic Neurologic deficit, stroke in evolution, completed stroke |
| What is the difference typically between a TIA and a reversible ischemic neurologic deficit | TIA last less than 24hrs usually less than 4 and a RIND lasts less than a few days both don't have permanent deficits |
| What is a stroke in evolution | stroke where signs and symptoms (deficits) are still progressing IE getting worse |
| If you have an acute onset of stroke with deficits occurring almost immediately what is likely causing the stroke embolism, thrombotic, tumor, inflammation, or neurodegenerative disease | Embolic stroke- maximal deficit immediately |
| If you have an acute stroke that has deficits developing over minutes to hours what is the likely cause- embolism, thrombotic, tumor, inflammation, or neurodegenerative disease | Thrombotic stroke- maximal deficits over minutes to hours |
| If you maximal deficit takes days or weeks to evolve what is the likely cause of the stroke- embolism, thrombotic, tumor, inflammation or neurodegenerative | likely tumor, inflammation or neurodegenerative any one of these could take days or weeks to evolve into a maximal deficit |
| How do you narrow down where the stroke lesion is | first a neuro exam looking at symptoms of the deficit will key you into likely brain areas that you will want to look at with CT/MRI |
| What is the leading cause of morbidity in the USA | stroke |
| Where does stroke fall on causes of deaths in the USA | in third place |
| What is the most common etiology of a stroke | ischemic infarct 70-80% of which 80% result from occlusion of large or small vessels due to atherosclerotic vascular disease |
| What percent of strokes are caused by cardiac embolism | 15% |
| What percent of strokes are caused by hypercoagulable states | 5% |
| What is generally the underlying cause of atherosclerotic vascular disease that causes majority of strokes | HTN that precipitates deposition of lipohyalinosis in the vessels |
| What are the tow sub groups of hemorrhage that cause stroke | intracerebral hemorrhage (ICH) and Subarachnoid hemorrhage (SAH) |
| What are the 3 sub groups of ischemia that cause stroke | thrombosis, embolism, systemic hypotension |
| What are the likely causes of subarachnoid hemorrhage or precursors to it | cerebral aneurysm and AV malformation |
| what is the likely causes of intracerebral hemorrhage or precursors to its development | Arterial Disease or hematological disease/abnormality |
| What risk factors increase your likelihood of developing a stroke | diabetes, HTN, smoking/tobacco, family hx, hyperlipidemia, sedentary life style, heavy alcohol use, gender = male |
| What heart rhythm is at high risk for developing a stroke | atrial fibrillation |
| What heart conditions increase your risk for developing a stroke besides HTN | atrial fib, prosthetic heart valve, cardiac structural abnormalities patent foramen ovale, atrial septal defect, hx of MI, hx of CHF |
| is high serum homocysteine indicate risk or protection from a stroke | indicates higher risk for stroke |
| What are the two blood supplies to the brain and how are they connected | carotid arteries and vertebral basilar artery connected by circle of Willis and additional collaterals |
| What is the blood flow threshold for irreversible neuronal damage | 18ml/100mg/min |
| What is the most powerful cerebral vasodilator | CO2 |
| How is blood flow regulated in the cerebellum | through auto regulation keeping blood flow constant and is dramatically changed by altering arterial CO2 |
| What is the ischemic cascade | starts seconds to minutes after loss of glucose and oxygen delivery with cessation of normal electrophysiologic function of cells, then neuronal and glial injury produces edema within hours to days after stroke causing further injury |
| What is the ischemic penumbra | the zones of decreased marginal perfusion around the core region. Tissue in penumbra can remain viable for several hours because of marginal perfusion interventions target restoring penumbra perfusion as the core is already dead |
| What is the ischemic core | the area directly affected by stroke where cells are presumed to be dead within minutes after stroke onset |
| What is the difference between atherothrombotic disease and embolic disease with strokes | atherothrombotic is from lipid deposition that narrows vessel lumen from plaque causing turbulent flow activating clotting cascade clot forms and occludes vessel; Embolic disease dislodged clot from elsewhere goes to brain to occlude and cause stroke |
| What is the most common cause of embolic disease | 1/2 are caused by a-fib the rest are caused by ventricular dysfunction, severe CHF, paradoxical emboli (patent foramen ovale) and thrombi breaking off in aortic arch and carotid arteries |
| What is a watershed infarct/border zone infarct | where most distal arterial territories get hypoperfusion most produce bilateral symptoms frequent occur perioperatively or w/ prolonged hypotension |
| What is the most common cause of hemorrhagic stroke | HTN accelerates arteriosclerosis weakening larger arteries allowing formation of Charcot bouchard aneurysms that rupture and bleed |
| Where is the most common location of hemorrhagic stroke | basal ganglia (putamen, caudate nucleus) & thalamus 65% then pons 15% then cerebellum 10% |
| What are common causes of secondary intracerebral hemorrhage | aneurysm, AV malformation, neoplasms, trauma, anticoagulation, hemorrhagic conversion of ischemic stroke |
| Which imaging study is more sensitive for ischemic strokes- ct scan with out contrast, MRI, Diffusion weighted MRI or perfusion weighted MRI | Diffusion Weighted MRI 88-100% sensitivity and 95-100% specificity |
| What are the signs and symptoms of a stroke arising from occlusion of the internal carotid artery | similar to MCA stroke with transient monocular blindness, occasional unilateral blindness, severe contralateral hemiplegia, hemianesthesia, hemianopia, profound aphasia if dominant hemisphere is involved |
| A internal carotid stroke often presents with MCA symptoms the internal carotid also supplies the ACA why don't you see as profound of ACA s/sx | generally there is collateral flow between the two ACAs |
| What is the more common cause of ICA stroke | atherothrombotic is more common than embolic |
| What area of the brain does the ACA supply blood to | supplies blood to the parasagittal cerebral cortex motor and sensory cortex related to contralateral leg, bladder inhibitory and micturation center |
| What are the typical physical s/sx of ACA stroke | paralysis and sensory loss of contralateral leg > arm, grasp, sucking reflexes and urinary incontinence. Abulia, paratonic rigidity, gait apraxia |
| if the stroke is in the superficial ACA what s/sx may be seen more | weakness more prominent in leg than arm, involves distal muscles > proximal. Flaccid paralysis of bilateral arms and unilateral leg. Descending motor tracts of basal ganglia or brainstem as a result of small vessel disease |
| What is the most common cause of ACA stroke | embolism |
| What are some of the neuro signs of ACA stroke | emotional liability, confusion, amnesia, personality changes, urinary incontinence, impaired mobility >>>lower extremities |
| What area of the brain does the MCA supply blood to | structures of higher cerebral processes of communication, language, interpretation, perception and interpretation of space, sensation and voluntary movement. Also sensory and motor cortex of arms and proximal muscles |
| What motor s/sx would you likely see in an MCA stroke | motor and sensory deficit in face, arm more than foot or leg. Complete hemiplegia if internal capsule is involved (dominant hemisphere involved) |
| What neuro s/sx would you likely observe in an MCA stroke pt | homonymous hemianopia, neglect, anosognosia, |
| what is the most common cause of MCA stroke | embolic >>> atherothrombotic |
| If your occlusion takes out the superior division of the MCA what signs might you notice | contralateral hemiparesis with relative sparing of leg, contra-lateral hemi sensory loss and BROCA's aphasia (difficulty producing speech, understands just fine) |
| What signs will you note if stroke involves inferior division of the MCA | homonymous hemianopia, impaired cortical sensory function, anosognosia, apraxia and Wernicke's aphasia |
| What signs will you note if stroke involves lenticulostriate vessels | dense hemi-paresis affecting arm/leg/face equally |
| What areas of the brain does the posterior cerebral artery and its branches supply blood to | medial and inferior temporal lobes, medial occipital lobe, thalamus, posterior hypothalamus, visual receptive area |
| What are the signs of a posterior cerebral artery stroke (PCA) | homonymous hemianopia, hemianesthesia, cortical blindness, memory deficits. Alexia w/o agraphia (dominant hemisphere), choreoathetosis, spontaneous pain, III nerve palsy, |
| What is the most common cause of PCA stroke | embolic >>> atherothrombotic |
| What are the signs of a vertebral/basilar artery stroke | vertigo, tinnitus, syncope, dysphasia, dysarthria, drowsiness, confusion |
| What are the signs if you have a stroke of either the anterior, inferior or superior cerebellar arteries | difficulty in articulation, swallowing, movement of limbs, nystagmus |
| What specific signs will you have if you have a stroke of the anterior inferior cerebellar artery | ipsilateral cerebellar ataxia, loss of pain and temperature sensation and decreased light touch sensation of face; impaired taste sensation; central Horner's syndrome; deafness; facial palsy, loss of pain/temp contralateral limb |
| What brain areas are likely involved in an occlusion of the anterior inferior cerebellar artery | lateral inferior pontine (AICA syndrome), principle and spinal nucleus of CN V, CN VII nucleus or fibers, middle cerebellar peduncle, inferior cerebellar peduncle, corticospinal tract, inferior surface of cerebellar hemisphere |
| What brain areas does the posterior inferior cerebellar artery supply | lateral and posterior portion of medulla, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguous ( CN X(Vagus), and CN IX (glossopharyngeal), vestibular system, desc. sympathetic fibers, tegmental tract, inferior cerebellar peduncle |
| Occlusion of the Posterior Inferior Cerebellar artery can cause Wallenberg syndrome (lateral medullary syndrome) what is the characterized by | ipsilateral anesthesia of face and cornea for pain and temperature, ipsilateral Horner syndrome, contralateral loss of pain and temperature sensation in trunk and extremities, ipsilateral cerebellar signs |
| What is Horner's syndrome | ptosis, pupillary meiosis, facial anhidrosis |
| What are the sigs of posterior inferior cerebellar artery occlusion | loss of pain/temp ipsilateral face and contralateral body, decrease ipsi corneal reflex, weakness ipsi soft palate, loss of gag reflex, paralysis of ipsi vocal cord, ipsi central Horner's syndrome, nystagmus |
| What is the primary cause of posterior inferior cerebellar artery stroke | ischemia |
| What part of the brain does the vertebral artery/basilar arteries supply | brainstem, anterior portion of pons, cerebellum |
| What are the signs of a stroke from occlusion of the basilar arteries or vertebral arteries | drop attacks, unilateral or bilateral weakness of extremities, diplopia, homonymous hemianopia, nausea, Locked in syndrome (can only move eyes/eyelids), sensation and consciousness preserved |
| If pt is having bilateral cranial nerve palsies, crossed sensory deficits, diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, hiccup, limb and gait ataxia, motor deficits where is the stroke likely coming from | basilar artery disease |
| What is the most common cause of vertebral /basilar artery stroke | embolic=atherothrombotic |
| What are the signs of a complete occlusion/hemorrhage (internal capsule, thalamus, pons) | coma, miotic pupils, decerebrate rigidity, respiratory/circulatory abnormalities, DEATH |
| What are the signs of a stroke of the anterior spinal artery | flaccid paralysis, loss of pain, touch and temperature but proprioception is preserved!!!! |
| What are the signs of a stroke of the posterior spinal artery | Sensory loss, loss of proprioception, vibration loss, touch and pressure lost but MOVEMENT IS PRESERVED |
| What is a lacunar infarct | occlusion of a penetrating vessel that supplies with and deep gray matter typically the basilar ganglia. |
| How does the affected area appear in a lacunar infarct | small hypodense area |
| What are the signs of a lacunar infarct | pure motor hemiparesis, pure sensory deficit, hemiparesis, homolateral ataxia, dysarthria/clumsy hand |
| Lacunar infarcts have four classic syndromes what is a pure motor syndrome | hemiparesis involving face, arms, legs most common location of infarct that causes this is posterior limb of internal capsule |
| Lacunar infarcts have four classic syndromes what is a pure Sensory syndrome | Hemibody sensory symptoms involving face, arm, leg and trunk are lost indicating infarct in thalamus |
| Lacunar infarcts have four classic syndromes what is an ataxia hemiparesis | combination of cerebellar and motor symptoms on the same side of the body Leg is worse than arm indicates and infarct in pons, internal capsule or midbrain |
| Lacunar infarcts have four classic syndromes what is the clumsy hand dysarthria | unilateral hand weakness and dysarthria, dysarthria is usually severe hand involvement more subtle, usually from an infarct in the pons |
| What are the s/sx that a pt is having a subarachnoid hemorrhage | presents with worst headache of their life may rapidly have LOC and signs of meningeal irritation |
| What are the common etiologies of subarachnoid hemorrhage | aneurysm, av malformation, |
| Where do the majority of subarachnoid hemorrhages occur | anterior circle of Willis |
| How likely is a pt to rebleed after their subarachnoid hemorrhage | 20% rebleed in first 2weeks |
| What is the tx for AV malformations that may cause subarachnoid bleeds | surgical excision or embolization |
| If patient presents with neglect, hemianopsia, aphasia, gaze preference to side of weakness what brain level are you thinking the stroke is at | in higher cortical areas/superficial territory of the brain |
| If pt presents with vertigo, diplopia, bilateral abnormalities, gaze deviation, ataxia and lower cranial nerve dysfunction what brain level are you thinking the stroke is at | brainstem level |
| What is the most important point to obtain in your history of a stroke pt in the ED | time of onset of symptoms |
| What differentials should you consider in a possible stroke pt | hypoglycemia, tumor, abscess, syncope, seizure, trauma "classic migraine", MS, bell's palsy, conversion reaction |
| What dx study are you most likely to order for a stroke pt | ct noncontrast |
| What dx imaging study is useful to help prevent the major cause of embolic strokes | Echocardiogram- can help identify clots in the atrium from A-Fib can also show aortic arch atheroma, patent foramen ovale |
| What is the tx for a pt with a hypercoagulable state that has caused a stroke or TIA | thrombolysis (tPA), Aspirin, Antiplatelet agents, Fluids, Blood Thinner (heparin) |
| What antiplatelet agents can be administered to a stroke pt | aspirin, ticlopidine, clopidogrel, dipyridamole |
| What anticoag tx are good for stroke pts w/o contraindications | heparin, coumadin, LMWH |
| What Thrombolytic will likely be andministred to a pt w/o contraindications | tPA (tissue plasminogen activator), Streptokinase but this can cause allergy |
| What surgical procedures are available for stroke pts | carotid endarterectomy, extracranial-intracranial bypass |
| What is the time frame for administering tPA to stroke pt without contraindications | must be given within 4.5 hours the sooner the better this increases likelihood of an excellent recovery 30% |
| What are the only types of stroke that tPA can be administered for | only for strokes that have occurred no more than 4.5 hours ago and are 1-atherothrombotic, 2-Atheroembolic, 3-Cardioembolic, 4- Small Vessel Occlusive stroke (lacunar) DO NOT GIVE tPA for hemorrhagic stroke |
| What color does blood appear on CT no contrast scan | White |
| What color does an ischemic area appear on CT scan no contrast | Dark Gray |
| What are the contraindications to using tPA therapy for a stroke | HEMORRHAGIC s/sx, hx of prior brain hemorrhage, seizure during stroke, AVM or aneurysm, Recent (3mo) surgery, trauma, stroke. Onset more than 3 hours ago. Uncontrolled B/P, Abnormal Coag factors, Active internal bleeding, recent major surgery |
| What percent of pt treated with tPA will develop symptomatic intracranial hemorrhage | 6.4% watch for s/sx, if suspected stop tx, get a CT, stat bleed time, PT/PTT, plts, fibrinogen, cryoprecipitate 6-8 units, platelets 6-8 units get consult stat |
| What tx can you give if pt is not a candidate for t-PA | Anticoags but make sure it is not a hemorrhage first |
| You suspect your pt has carotid artery stenosis what non invasive dx technique can you order that may help demonstrate your suspicion | Doppler Ultrasonography (60% accuracy) |
| When is heparin therapy indicated in stroke pts | A-Fib, artificial valves, left atrial or ventricular thrombi, cardiac akinesia (dilated cardiomyopathy), symptomatic high grade stenosis, basilar thrombosis, coagulopathy (protein S, Protein C) |
| What is one way to reduce intracranial pressure from cerebral edema | Mannitol |
| What is the classic tx from TIAs | 75% are due to stenosis of carotid and subclavian artery so carotid endarterectomy, anticoag therapy, clopidogrel, aspirin, dipyridamole |
| What is the tx for a parenchymal hemorrhage | same as ischemic infarct control BP diastolic 90-100 and NO LP if cerebellar stroke. Get a neurosurgery consult |
| What is the tx for a subarachnoid hemorrhage | Neurosurgical Unit, sedation, keep diastolic below 100, Fluid Restriction, Catheterize pt, CCB to prevent vasospasm |
Created by:
smaxsmith
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