Stroke Flashcards
What are some common and uncommon signs of stroke?
Common:
- Unilateral weakness/numbness
- Visual disturbance*
- Vertigo
- Double vision
- Imbalance, lack of coordination
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Uncommon - Aphasia
- Neglect
- Confusion
- Behavioral abnormality
Describe the zones of cerebral autoregulation
- Passive collapse
- Vasodilatory cascade zone
- Zone of normal autoregulation
- Autoregulation breakthrough zone
Vasodilatory cascade zone & Zone of normal autoregulation are in the realm of okay.
The concept is Cerebral perfusion pressure can cause changes in cerebral blood flow and from 50-150 mm Hg, cerebral blood flow is held constant.
As cerebral perfusion pressure goes up, vasculature vasoconstricts and cerebral flow is constant.
Above 150 mm Hg (autoregulation break through zone): pressure becomes too high, the blood vessels break down, no longer control increased pressure and edema starts. Cerebral blood flow soars.
Below: 50 mm Hg, vasodilated as much as possible but blood flow is just not enough to neurons or endothelial cells, start getting damaged, the vessels collapse
ICP - falls in passive collapse, rises in break through zone. Is kinda high at the start of vasoconstriction and then drops steadily
*also the lower your blood flow the less time you can tolerate it, duh
What is the concept of penumbra
The penumbra is area surrounding an ischemic event such as thrombotic or embolic stroke. Immediately following the event, blood flow and therefore oxygen transport is reduced locally, leading to hypoxia of the cells near the location of the original insult. This can lead to hypoxic cell death (infarction) and amplify the original damage from the ischemia; however, the penumbra area may remain viable for several hours after an ischemic event due to the collateral arteries that supply the penumbral zone.
As time elapses after the onset of stroke, the extent of the penumbra tends to decrease; therefore, in the emergency department a major concern is to protect the penumbra by increasing oxygen transport and delivery to cells in the danger zone, thereby limiting cell death. The existence of a penumbra implies that salvage of the cells is possible. There is a high correlation between the extent of spontaneous neurological recovery and the volume of penumbra that escapes infarction; therefore, saving the penumbra should improve the clinical outcome.
What are TPA contraindications?
Efficacy decreases after 4.5 hours
(Head CT) • ACTIVE INTERNAL BLEEDING • ACUTE INTRACRANIAL HEMORRHAGE • RECENT INTRACANIAL OR SPINAL SURGERY OR SERIOUS HEAD TRAUMA • BLEEDING DIATHESIS (INR >1.7, ELEVATED PTT, PLATELET COUNT <100,000) • CURRENT SEVERE UNCONTROLLED HYPERTENSION • HISTORY OF RECENT STROKE
Describe thrombotic ischemic stroke
large vessel vs lacunar
Large vessel: -Age > 40 -Vascular risk factors (cholesterol, high BP) -Preceding TIA's -Mechanism: Artherosclerosis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Lacunar:
-milder symptoms
-absence of cortical deficits (field cut, aphasia, neglect)
-Mechanism: lipohyalinosis - Lipohyalinosis - is artherosclerosis of small vessels - destroy endothelium, byproduct is hyalin and deposit that. Lipohyalinosis is a small-vessel disease in the brain, it is characterised by vessel wall thickening and a resultant reduction in luminal diameter.
-Microartheromas: clots at origin of arteries
-Microembolism: small clots still
Radiographic: <1.5CM diameter lesion on MRI
-subcortical lesions
Embolic ischemic stroke
CLots are LARGE, blocks a major blood vessel.
You will have have a ton of shitty symptoms - hemiparisis, gaze deviation, aphasia.
-shower of emboli, you can block a lot of vasculature.
Sources:
• atrial fibrillation - top of heart and bottom don’t beat in synchrony, blood pools in left atrium, when it goes back to normal rhythm it dislodges.
• Structural heart disease: left ventricle is barely pumping, blood pools in left ventricle, clot forms and a piece of that can leave
• paradoxical embolus through PFO- clot in leg vein, if it goes up, it will go to right side of heart and go to lungs. From DVT, you get pulmonary emoblism, however if you have a patent foramen ovale , a clot can cross the hole and go up to the brain because we don’t expect venous clots to end up in brains, instead lungs
-valvular disease
-aortic arch plaques
-cardiac tumor (pieces of tumor)
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RADIOGRAPHIC FEATURES:
-LARGE ZONE OF INFARCT
-INFARCTS IN MULTIPLE VASCULAR TERRITORIES
-DENSE VESSEL SIGN ON CT
What are some rare causes of ischemic brain infarcts?
- Arterial dissection: occurs when a small tear forms in the innermost lining of the arterial wall (known as the tunica intima). Blood is then able to enter the space between the inner and outer layers of the vessel, causing narrowing (stenosis) or complete occlusion.
- Sickle Cell: damage the same branch points which leads to reactive thickening of the blood vessels, internal carotid is especially vulnerable to that.
- Hypercoagulable states
- Vasculitis: inflammed vessels can occlude
- Vasospasm: (a blood vessel spasms causing less blood flow) can be induced by COCAINE and SSRI
- Venous sinus thrombosis - usually caused by subarachnoid hemorrhage impairing drainage
- COMplicated migraine: headache causes change in blood flow in the brain. Low blood flow can be low enough and long enough to cause damage.
Wat is the mechanism of venous infarctions, 4 stages
- Thrombosis of cerebral vein (subarachnoid hemorrhage)
-Increased venous
pressure
-Decreased capillary perfusion pressure
-Increased CerebralBVolume Decreased CBFlow - Recruitment of collaterals
-Dilatation of cerebral veins
-Recruitment of
collateral pathways
-Initially
compensates - Compensatory failure
-Vasogenic edema (blood brain barrier
disruption)
-Increase in intravascular
pressure
-Still potentially
reversible - Parenchymal lesion
-Failure of energy
metabolism
(Na+/K+ pump
failure)
-Venous infarct (cytotoxic edema)
-Venous hemorrhage
(venous rupture)
What is TIA
Transient ischemic attack:
-sudden focal neurologic deficit: usually weakness on one side lasting 10-60 min
Risk factors
Age >60 yrs
- unilateral weakness or speech disturbance
- duration of 10-60 minutes
- history of diabetes
Intracerebral hemorrhages
Over 2/3’s are small vessel hypertensive
-most are in the basal ganglia/thalamus
- Hypertensive
-small penetrating arterioles rupture
-basal ganglia, thalamus, pons, cerebellum
-it is subcortical like hypertensive hemorrhage
**R: small ball of white surrounded by hypodense (edema)
___________________________ - Lobar
-Arteriovenous malformation: veins are not built to handle the blood from an artery so it is likely to rupture and bleed.
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Cavernous Angioma: just a venous malformation: abnormally dilated vein. -Somebody falls down, emergency room does a cat scan and finds a bright spot. What is different is that its contained in the venous channel, if blood goes to parenchyma, it will cause dark rim of swelling (like in the other example), this one has not swelling it doesn’t touch the brain.
- TUMORS (METASTATIC DISEASE, OR PRIMARY) glioblastoma
- COAGULOPATHY
-VASCULOPATHY (CEREBRAL AMYLOID ANGIOPATHY, VASCULITIS) DRUGS (E.G. COCAINE)
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-cerebral amyloid angiopathy
Age > 60
-multiple lobar hemorrhages (many microbleeds)
-amyloid deposits in leptomeningeal and cortical arterioles (stain congo red)
-associated with dementia
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-TRAUMA (FRONTAL, OCCIPITAL, TEMPORAL)
What are causes of coagulopathy?
(3)
What are hallmark signs on radiology?
CAUSES • Anticoagulants • Platelet dysfunction • Low levels of clotting factors (e.g. liver dysfunction)
Meniscus in non-contrast head CT ; blood is remaining liquid and conforming to the patient laying supine
Intraventricular hemorrhage would pool at the bottoms.
Subarachnoid hemorrhage
CLINICAL FEATURES:
-SEVERE HEADACHE (97%)
-MENINGEAL SIGNS: the blood is irritating the meninges so you get nuccal rigidity
-LETHARGY, NAUSEA, VOMITING
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COMPLICATIONS:
REBLEEDING (24-48 HRS) VASOSPASM (7-10 DAYS) - the longer it sits in subarachnoid space it can cause vasospasm
HYDROCEPHALUS (>24 HRS): plugs CSF outlets
CAUSES:
-TRAUMA
-SACCULAR (BERRY) ANEURYSMS AT BRANCH POINTS IN CIRCLE OF WILLIS -VASCULAR MALFORMATIONS
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R: HYPERDENSITY IN SUPRACELLAR CISTERN, QUADRIGEMINAL CISTERN, SYLVIAN FISSURES, AND SULCI
“explosion and avalanche of hematoma growth
EXPLOSION:
” CONTINUOUS BLEEDING FROM SINGLE RUPTURED VESSEL”
“AVALANCHE:” SECONDARY SHEARING OF ADJACENT VESSELS
What would each of these present as?
Right Motor cortex Left Somatosensory cortex Left FEF Right Primary visual cortex Right primary auditory cortex Broca's area (dominant) Wwernicke area (dominant)
Right Motor cortex: left hemiparesis (lateral - face/arm, medial - leg)
Left Somatosensory cortex: right sensory loss, graphesthesia, stereognosis
Left FEF: loss of rightward gaze
Right Primary visual cortex: Left contralateral homonymous visual hemianopsia
Right primary auditory cortex: just diminished localization of auditory cortex, no deafness because of connections
Broca’s area (dominant): motor aphasia
Wwernicke area (dominant): sensory aphasia
Major frontal lobe lesion signs
- Perseveration (inability to change focus/behaviors
- working memory deficits (dorsolateral)
- Abulia, lack of empathy (dorsolateral)
- Disinhibited behavior (orbitofrontal)
- Limited insight (confabulation) - fabricate imaginary experiences as compensation for loss of memory.
- Impersistence: unable to sustain certain movements
- Frontal release signs - innate reflexes that reemerge, grasp, root (touch side of mouth they will turn to it, suck, snout (touching lips will purse)
- Gegenhalten - increased voluntary tone
- Mood changes, left = depressed, right = manic
- shuffling magnetic gait.
