Alexandrov - Stroke Flashcards
What is stroke?
- Injury to the brain caused by:
1. Interruption of its BF (ischemic) or
2. Bleeding (hemorrhagic) into or around brain - Clinically, the loss of blood supply to the brain produces abrupt onset of focal neuro deficits that frequently result in permanent disability or death
What is TIA?
- Transient ischemic attack
- Abrupt onset of focal neuro deficits that resolve in <1hr
- Important WARNING SIGN for future stroke
What are silent strokes?
- Acute focal neuro symptoms and signs that resolve completely, but take longer than 1 hr to do so
1. Invariably associated with detectable injury on MRI brain scans - May also be called resolving ischemic neuro deficits (RIND’s) -> although clinically detectable neuro deficit may appear to have resolved, MRI brain scan will show evidence of focal brain injury
What are the 2 “flavors” of stroke? How common are they, and what are some causes?
- HEMORRHAGIC: 20%, and may be caused by bleeding into brain parenchyma (intracerebral hem) or bleeding around surface of brain (subarachnoid hem), which occur in roughly equal portions
- ISCHEMIC: majority (80%), and can occur as result of atherosclerotic occlusion of intra-or extracerebral blood vessel, embolus to brain from heart of cerebral blood vessel, or disease of lumen of small arterioles (lacunar infarcts)
1. Sizable proportion of these are CRYPTOGENIC - IMAGES: IC hem on top L (bright white blood in basal ganglia), subarachnoid hem in lower L (star-shaped silhouette of basilar cistern)
1. Upper right digital subtraction arteriogram of atherosclerotic plaque in ICA (red arrow)
2. Coronal section through pons showing lacunar infarct in mid-pons (yellow arrow)
What is the epi of stroke?
- 3rd leading COD in the US, and leading cause of adult disability
- Death rate fell 13.9% from 1987-97, but # of strokes each year has INC
- Risk of having stroke and dying from one INC w/age, but significant # of strokes in ppl <65
1. Very high mortality rate in the SE: TN #3
What are the non-modifiable risk factors for stroke?
- AGE: doubles each decade >55
- GENDER: male 1.5x risk of F
- RACE: AA at 2x risk of European Americans
- FAMILY HX: other genetic factors
What are the modifiable risk factors for stroke?
- HTN
- Diabetes
- Hyperlipidemia
- Smoking
- Carotid artery stenosis
- Atrial fibrillation
- Obesity
- Physical inactivity
- NOTE: each of these is amenable to change via Rx tx, sx, or alteration of lifestyle
What is the #1 risk factor for stroke? List some other things with high relative risk.
- HTN is #1 risk factor for stroke: based on combo of relative risk (3-5x) and prevalence (>30%)
- RR for afib 5-17x, but low prevalence (<5%)
- Other risk factors around 2x RR and prevalence b/t 20-30% (except carotid artery stenosis = <10% prev)
What is the pathological consequence of focal brain ischemia?
- Cerebral infarct, where infarction is defined as focal necrosis of all cellular elements of brain, i.e., neurons, glia, and other supporting brain cells
- NOTE: brain utilization in conscious man attached
What is selective ischemic necrosis? When are you most likely to see it?
- ONLY brain neurons are injured (instead of the focal necrosis of all cellular elements of the brain seen with cerebral infarction)
1. Affects only specific pops of highly vulnerable neurons, like CA1 pyramidals of hippocampus and Purkinje cells of cerebellum - Encountered most commonly in pts suffering transient global brain ischemia from CARDIAC ARREST and successful cardiac resuscitation
What happens to an ischemic neuron vs. a normal neuron?
- NORMAL: metabolizes glu delivered by blood almost exclusively via aerobic metabolism; mito generate adequate ATP and PCr to sustain membrane ion pumping mechs that maintain fluctuating membrane ion gradients and membrane potential associated with depolarization and repolarization
- ISCHEMIC: w/in mins of loss of blood supply, brain energy stores depleted via metabolism of glu via glycolytic pathways w/accumulation of lactic acid -> if not rapidly reversed, catabolic mechs triggered and cell will die
How do hyperglycemia and hyperthermia affect stroke brain injury? Implications?
- They accelerate it, and exacerbate stroke brain injury
- Elevated brain glu/glycogen stores or elevated circulating glu will provide further fuel for glycolysis, resulting in higher concentrations of lactic acid
- A GOAL for acute stroke intervention is to normalize elevated body temp and rapidly treat hyperglycemia
What is the difference b/t core and penumbral ischemia? Implications?
- Reduction of BF NOT uniform
- CORE: severe ischemia, and tissue dies (or suffers irreversible injury) in <1hr (area most remote from blood vessels that may provide collateral BF)
- PENUMBRA: moderate ischemia, and tissue dies in 4-6hrs -> acute intervention that restores blood supply to this territory has potential for salvaging brain tissue otherwise destined to die
1. Basis for acute stroke intervention having a therapeutic window of 4-6 hours - NOTE: image shows L hemisphere w/pre-rolandic branch of MCA occluded by embolus
How does CBF autoregulation change in pts with chronic HTN? Implications?
- NORMAL: CBF relatively constant (independent of MAP) b/t MAP of 55 - 155 mm Hg -> this is important bc MAP can fluctuate rapidly and widely w/changing position, but CBF does NOT fluctuate w/body position changes in normal folk
1. MAP < 55 = severe hypoTN, reduced CBF, and syncope
2. MAP > 155 = hypertensive encephalopathy - CHRONIC HTN: curve shifted to the R, so less severe hypotension or even BP levels considered normal can now result in DEC CBF
1. Majority of stroke pts are HTNsive, so must be careful not to acutely lower BP bc risk of further reducing CBF to already ischemic vascular bed
a. Loss of auto-regulation in penumbra and core, so depend on MAP -> lowering BP may cross infarction threshold in penumbral zone, INC extent of cerebral infarct
2. Recommendation NOT to lower BP in pts who aren’t candidates for thrombolytic therapy unless systolic >220 or diastolic >120
a. Lower BP only by 10-15% in first 24hrs if above these #’s
What is the equation for CBF? Approximate measure in normal folk/threshold for infarction?
- CBF = MAP/CVR where MAP = mean arterial pressure and CVR = cerebral vascular resistance
- About 55mL/100gm brain/min in normal ppl
1. Threshold for infarction = 20
What are the neuro signs and symptoms of stroke?
- Common neuro deficits include:
1. Weakness or paralysis (acute onset on 1 side of body)
2. Loss of sensation in 1 limb or on 1 side of body
3. Loss of vision in one eye (amaurosis fugax: painless, transient monocular vision loss) or field
4. Difficulty talking/understanding what is being said
5. Difficulty w/organization or perception (cognitive abilities)
6. Clumsiness of lack of balance
What are the ischemic stroke categories/subtypes?
- CIRCULATION:
1. Anterior: ICA, MCA, ACA, any of their branches
2. Posterior: PCA, VA, SCA, AICA, PICA, branches - VESSEL SIZE:
1. Large: ICA, MCA, ACA, PCA, VA, SCA, AICA, PICA
2. Small: long and short penetrating branches of these aa
Briefly describe the cerebral circulation (image).
What functional areas of the brain are supplied by the MCA (image)?
- Motor/sensory cortical regions
- FEF
- Broca’s
- Wernicke’s
- Optic radiations
What parts of the cortical homunculus are supplied by the ACA vs. the PCA? What do the lenticulostriate aa supply?
- ACA: lower limb + trunk, shoulders
-
MCA: upper limbs and face
1. Lenticulostriate: pyramidal tract axons to cortex + putamen, globus pallidus, and caudate
What structures are supplied by the ACA vs. the PCA (midsagittal view)?
- ACA: medial frontal lobe, corpus callosum, motor + sensory to lower limbs/trunk
- PCA: temporal lobe and hippocampal formation, optic radiations, deep perforating branches to thalamus and hypothalamus
Describe the Circle of Willis. What is it for?
- Functions to provide collateral BF in instances of proximal occlusions (closer to heart) of cerebral blood vessels
Describe the blood supply to the brainstem (image).
What is medullary stroke syndrome (Wallenberg’s; image)?
What is pontine stroke syndrome (image)?
What is midbrain stroke syndrome (Benedikt; image)?
What are the signs/symptoms of an anterior circulation stroke? Potentially affected vessels?
- ICA, MCA, ACA, or any of their branches
- Ipsilateral blindness or contralateral inferior quadrantanopsia
- Contralateral gaze paresis
- Contralateral mono/hemiparesis and/or mono/hemi-sensory deficit
- Aphasia in dominant hemisphere or neglect in nondominant hemisphere
- Any combo of the above
- EX: occlusion of parietal-temporal branches of left MCA would produce R-sided inferior quadrantanopsia
- NOTE: image shows signs/symptoms 2o to occluded aa in graphic (ICA, ophthalmic, central retinal) -> clot + emboli
Why is it important to be able to distinguish b/t anterior and posterior circulation strokes?
Bc these 2 vascular territories carry slightly different prognoses and tx options
What are the signs/symptoms of a posterior circulation stroke? Potentially affected vessels?
- PCA, VA, SCA, AICA, PICA, or any of their branches
- Unilateral, bilateral, or crossed (face/body) weakness or sensory deficits
- Contralateral homonymous hemianopsia or superior quadrantanopsia
- Vertigo, N/V, gait ataxia, diplopia, dysphagia, Horner’s syndrome
- Altered consciousness and amnesia
- Any combo of the above
- EX: L PCA occlusion will cause homonymous hemi-anopsia of R visual field (visual field loss on same side of both eyes bc left 1/2 of brain has visual pathways for R hemifield of both eyes, and vice versa)
- NOTE: crossed extremity signs, while possible, are very rarely caused by lesion above foramen magnum (not unusual to have crossed motor or sensory signs involving ipsilateral face and contralateral limbs)
What are lacunar strokes? What are the 4 classic syndromes?
- Small areas of ischemic necrosis caused by occlusion of small, penetrating arteries
- SYNDROMES:
1. Pure hemiparesis: can occur at any of several locations along corticospinal/spinothalamic tracts, but most common sites are INTERNAL CAPSULE and PONS
2. Pure hemisensory deficit: same as above + lacunes involving VPL nucleus of THALAMUS
3. Ataxia hemiparesis (pontine stroke syndrome)
4. Dysarthria: clumsy hand syndrome (medullary stroke syndrome = Wallenberg) - IMAGE: left arrows pointing to 2 of several lacunar infarcts; right arrows pointing to bilateral thalamic lacunes