Stroke

Question 1

What are the 4 general causes of GLOBAL CEREBRAL ISCHEMIA?

Answer 1

1. LOW PERFUSION due to large vessel ATHEROSCLEROSIS (e.g. INTERNAL CAROTID ARTERY)
2. LOW PERFUSION due to acute decrease in blood flow (SHOCK)
3. LOW OXYGENATION due to CHRONIC HYPOXIA (anemia)
4. LOW ENERGY SUPPLY due to HYPOGLYCEMIA (INSULINOMA)

Question 2

How does an INSLULINOMA create a MILD GLOBAL ISCHEMIA?

Answer 2

INSULINOMA - Lots of insulin release -> Low Glc -> Low energy supply to brain -> GLOBAL ISCHEMIA -> TRANSIENT CONFUSION -> PROMPT RECOVERY with Glc transfusion = MILD

Question 3

Name the two possible causes of MODERATE GLOBAL CEREBRAL ISCHEMIA.

Answer 3

1. WATERSHED INFARCTS

2. HIGHLY VULNERABLE REGION INFARCTS

Question 4

Name the 3 highly vulnerable regions of MODERATE GLOBAL ISCHEMIA.

Answer 4

1. PYRAMIDAL NEURONS of CEREBRAL CORTEX (Gray matter = Layers 3,5,6) = CORTICAL LAMINAR NECROSIS
2. PYRAMIDAL NEURONS of HIPPOCAMPUS (Temporal lobe) = Long-term memroy
3. PURKINJE cells of the CEREBELLUM = Integration of SENSORY perception with motor control

Question 5

What is CORTICAL LAMINAR NECROSIS*** VERY HIGH YIELD

Answer 5

Damage to VULNERABLE AREA of MODERATE GLOBAL ISCHEMIA: Damage to PYRAMIDAL NEURONS of CORTEX LAYERS 3,5,6

Question 6

What is the difference between FOCAL ISCHEMIC STROKE and FOCAL TIA?

Answer 6

Difference in DURATION
FOCAL ISCHEMIC STROKE: Focal neurologic deficits >24hrs
FOCAL TIA: Focal neurologic deficits

Question 8

Which type of cerebral infarct will result in a PALE PERIPHERAL CORTEX? Where does this usually occur?

Answer 8

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)

Question 9

Which type of cerebral infarct will result in a HEMORRHAGIC PERIPHERAL CORTEX INFARCT?

Answer 9

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

Question 10

Describe the etiology and pathophysiology of LACUNAR STROKES

Answer 10

BENIGN HTN + DIABETES -> Protein hyaline leakage -> HYALINE ARTERIOLOSCLEROSIS of SMALL “arteriolar-like” LENTICULOSTRIATE ARTERIES supplying the deep structures -> LACUNAR INFARCT

Question 11

What are the 3 types of ISCHEMIC STROKES?

Answer 11

THROMBOTIC
EMBOLIC
LACUNAR

Question 12

**UW: Delineate the chronology of the pathophysiology of an ISCHEMIC STROKE.

Answer 12

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

Question 13

Name the most common LACUNAR ISCHEMIC STOKE and how it presents. Name the 2nd most common.

Answer 13

MCA DEEP LENTICULOSTRIATE ARTERIES supplying INTERNAL CAPSULE -> Pure contralateral MOTOR HEMIPARESIS

PCA DEEP THALAMOPERFORATOR BRANCHES supplying THALAMUS -> Pure contralateral SENSORY HEMIPARESIS

Question 14

What is the EARLIEST FINDING of an ISCHEMIC STROKE? How long after is this seen after an infarction?

Answer 14

12hrs later: RED NEURONS - Eosinophilic change of NEURON CYTOPLASM

Question 15

Which stage of an ISCHEMIC STROKE is CYSTIC LESION SURROUNDED BY GLIOSIS seen on biopsy?

Answer 15

>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)

Question 16

What are the two types of HEMORRHAGIC STROKES?

Answer 16

INTRACEREBRAL HEMORRHAGE: MCA Deep lenticulostriate arteries - Charcot Bouchard microaneurysms

SUBARACHNOID SPACE: ACommA branch point saccular berry aneurysms

Question 17

What is the most common source of an EMBOLIC STROKE and what cerebral artery does it most commonly involve?

Answer 17

LEFT ATRIUM during Afib = most common source

MIDDLE CEREBRAL ARTERY = most common artery involved

Question 18

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?

Answer 18

YES
BENIGN HTN/DIABETES -> Hyaline arteriolosclerosis of MCA DEEP LENTICULOSTRIATE ARTERIES -> Weaken BV wall -> CHARCOT BOUCHARD MICROANEURYSM -> HEMORRHAGIC STROKE

Question 19

What is a CHARCOT-BOUCHARD MICROANEURYSM? What stroke is it associated with? What structure is most commonly involved in?

Answer 19

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

Question 20

What is the most common cause of SAH (“the worst headache of my life”)?

Answer 20

SACCULAR BERRY ANEURYSMS: Thin-walled outpouchings of damaged vessels that LACK MEDIA

Question 21

Where is the most common saccular (berry) aneurysm causing a SAH? How is this diagnosed?

Answer 21

Branching point of ACommA - Anterior communicating artery (anterior circle of willis)
LP: CSF shows xanthochromia - YELLOW HUE due to bilirubin products

Question 22

What is the only possible cause of a BLEED SHOWN IN THE BOTTOM OF THE BRAIN?

Answer 22

SAH

Question 23

What are the two associations of SUBARACHNOID HEMORRHAGE? [Hint: Think cardiac, kidney]

Answer 23

MARFAN SYNDROME

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE

Question 24

What are 2 other possible causes of SAH?

Answer 24

AVM malformation

Anti-coagulated state