Stroke Flashcards
What are the 4 general causes of GLOBAL CEREBRAL ISCHEMIA?
- LOW PERFUSION due to large vessel ATHEROSCLEROSIS (e.g. INTERNAL CAROTID ARTERY)
- LOW PERFUSION due to acute decrease in blood flow (SHOCK)
- LOW OXYGENATION due to CHRONIC HYPOXIA (anemia)
- LOW ENERGY SUPPLY due to HYPOGLYCEMIA (INSULINOMA)
How does an INSLULINOMA create a MILD GLOBAL ISCHEMIA?
INSULINOMA - Lots of insulin release -> Low Glc -> Low energy supply to brain -> GLOBAL ISCHEMIA -> TRANSIENT CONFUSION -> PROMPT RECOVERY with Glc transfusion = MILD
Name the two possible causes of MODERATE GLOBAL CEREBRAL ISCHEMIA.
- WATERSHED INFARCTS
2. HIGHLY VULNERABLE REGION INFARCTS
Name the 3 highly vulnerable regions of MODERATE GLOBAL ISCHEMIA.
- PYRAMIDAL NEURONS of CEREBRAL CORTEX (Gray matter = Layers 3,5,6) = CORTICAL LAMINAR NECROSIS
- PYRAMIDAL NEURONS of HIPPOCAMPUS (Temporal lobe) = Long-term memroy
- PURKINJE cells of the CEREBELLUM = Integration of SENSORY perception with motor control
What is CORTICAL LAMINAR NECROSIS*** VERY HIGH YIELD
Damage to VULNERABLE AREA of MODERATE GLOBAL ISCHEMIA: Damage to PYRAMIDAL NEURONS of CORTEX LAYERS 3,5,6
What is the difference between FOCAL ISCHEMIC STROKE and FOCAL TIA?
Difference in DURATION
FOCAL ISCHEMIC STROKE: Focal neurologic deficits >24hrs
FOCAL TIA: Focal neurologic deficits
Which type of cerebral infarct will result in a PALE PERIPHERAL CORTEX? Where does this usually occur?
THROMBOTIC INFARCT: Rupture of atherosclerotic plaque -> Exposure of sub-endothelial collagen -> Thrombus dvlm -> Occlusion of blood supply to peripheral cortex -> PALE
Most commonly occurs at branch points (e.g. ICA branching to ACA and MCA)
Which type of cerebral infarct will result in a HEMORRHAGIC PERIPHERAL CORTEX INFARCT?
EMBOLIC STROKE
Left atrium thrombus embolizes -> Lodges in cerebral artery -> Occlusion of blood supply -> Neuronal damage -> CLOT EVENTUALLY LYSES -> Blood enters peripheral cortex -> HEMORRHAGIC
Unlike THROMBOTIC INFARCT: No matter what clot can NOT Be lysed because ATHEROSCLEROTIC PLAQUE keeps activating clotting
Describe the etiology and pathophysiology of LACUNAR STROKES
BENIGN HTN + DIABETES -> Protein hyaline leakage -> HYALINE ARTERIOLOSCLEROSIS of SMALL “arteriolar-like” LENTICULOSTRIATE ARTERIES supplying the deep structures -> LACUNAR INFARCT
What are the 3 types of ISCHEMIC STROKES?
THROMBOTIC
EMBOLIC
LACUNAR
**UW: Delineate the chronology of the pathophysiology of an ISCHEMIC STROKE.
12hrs: EOSINOPHILIC CHANGE RED NEURONS
24hrs: LIQUEFACTIVE NECROSIS (stimulus of acute inflammation)
1-3d: NEUTROPHILS
4-7d: MICROGLIAL CELLS (CNS Macrophages - See abundant LIPIDS** inside from extensive phagocytosis of MYELIN breakdown)
2-3wk: Reactive GLIOSIS (Granulation-like tissue)
>1mo: CYSTIC SPACE surrounded by GLIOSIS (dense glial fibers =reactive CT astrocytes lining cystic space)
1wk-1mo: LIQUEFACTIVE NECROSIS
Name the most common LACUNAR ISCHEMIC STOKE and how it presents. Name the 2nd most common.
MCA DEEP LENTICULOSTRIATE ARTERIES supplying INTERNAL CAPSULE -> Pure contralateral MOTOR HEMIPARESIS
PCA DEEP THALAMOPERFORATOR BRANCHES supplying THALAMUS -> Pure contralateral SENSORY HEMIPARESIS
What is the EARLIEST FINDING of an ISCHEMIC STROKE? How long after is this seen after an infarction?
12hrs later: RED NEURONS - Eosinophilic change of NEURON CYTOPLASM
Which stage of an ISCHEMIC STROKE is CYSTIC LESION SURROUNDED BY GLIOSIS seen on biopsy?
>1mo: After healing from acute inflammation of ischemic-stroke induced liquefactive necrosis CYSTIC SPACE (Liquefactive necrosis), GLIOSIS (granulation-like tissue that becomes scar by CT astrocytes)
What are the two types of HEMORRHAGIC STROKES?
INTRACEREBRAL HEMORRHAGE: MCA Deep lenticulostriate arteries - Charcot Bouchard microaneurysms
SUBARACHNOID SPACE: ACommA branch point saccular berry aneurysms
What is the most common source of an EMBOLIC STROKE and what cerebral artery does it most commonly involve?
LEFT ATRIUM during Afib = most common source
MIDDLE CEREBRAL ARTERY = most common artery involved
BENIGN HTN-mediated HYPERPLASTIC ARTERIOLOSCERLOSIS of MCA LENTICULOSTRIATE ARTERIES can result in a LACUNAR ISCHEMIC INFARCT resulting in a pure motor contralateral hemiparesis. Can it also result in a HEMORRHAGIC STROKE? If so, how?
YES
BENIGN HTN/DIABETES -> Hyaline arteriolosclerosis of MCA DEEP LENTICULOSTRIATE ARTERIES -> Weaken BV wall -> CHARCOT BOUCHARD MICROANEURYSM -> HEMORRHAGIC STROKE
What is a CHARCOT-BOUCHARD MICROANEURYSM? What stroke is it associated with? What structure is most commonly involved in?
ANEURYSM of the DEEP LENTICULOSTRIATE ARTERIES of the MCA that have undergone HTN-mediated HYALINE ARTERIOLOSCLEROSIS
Most commonly associated with HEMORRHAGIC STROKE (ICH - bleeding into parenchyma)
Specifically BASAL GANGLIA
What is the most common cause of SAH (“the worst headache of my life”)?
SACCULAR BERRY ANEURYSMS: Thin-walled outpouchings of damaged vessels that LACK MEDIA
Where is the most common saccular (berry) aneurysm causing a SAH? How is this diagnosed?
Branching point of ACommA - Anterior communicating artery (anterior circle of willis)
LP: CSF shows xanthochromia - YELLOW HUE due to bilirubin products
What is the only possible cause of a BLEED SHOWN IN THE BOTTOM OF THE BRAIN?
SAH
What are the two associations of SUBARACHNOID HEMORRHAGE? [Hint: Think cardiac, kidney]
MARFAN SYNDROME
AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE
What are 2 other possible causes of SAH?
AVM malformation
Anti-coagulated state
