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Neurology-Week 4 & 5 > 3. Vascular Disease & Stroke > Flashcards

3. Vascular Disease & Stroke Flashcards

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1
Q

SUDDEN onset of a focal neurological impairment due to ischemia or hemorrhage; NOT reversible; more common in older men; risk factors are DM, HTN, Smoking, Hyperlipidemia, Obesity and Sleep Apnea

A

Stroke

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2
Q

Two types of Strokes

A

Ischemic
Hemorrhagic *

  • less common but more fatal
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3
Q

(Ischemic/Hemorrhagic) strokes are more common

A

Ischemic (~80%)

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4
Q

(Ischemic/Hemorrhagic) strokes are commonly caused by atherosclerosis with thrombosis in LARGE vessels and/or embolic occlusion of DISTAL vessels; can also occur due to venous thrombosis like in superior sagittal sinus (due to infection or hyper-coagulation states in pregnancy)

A

Ischemic

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5
Q

Emboli causing an ischemic stroke often originate from

A

EXTRA-cranial thrombi (atherosclerosis of Carotid artery bifurcation or from the heart)

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6
Q

What is the spectrum of consequences of brain ischemia (best to worst)

A
  1. No effect (thanks to anastomoses!)
  2. TIA (brief, focal neurologic deficits but reversible)
  3. “Incomplete” infarct (neuronal necrosis)
  4. “Complete” infarct (BOTH neuronal AND glial necrosis)

*neurons are more vulnerable that glial cells to ischemia

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7
Q

There typically no gross changes in the brain with CT until ________ HOURS after the infarct

A

6-8

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8
Q

CT findings of brain infarct (remember that it takes 6-8 hours for anything to be grossly visible)

A

Early (1-2 days): congestion, discoloration of grey matter

Late: cavitation (phagocytosis of dead tissue)

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9
Q

Histologic findings of a brain infarct

A
  1. Hours: Red (“dead”) neurons
  2. 24 hours: neutrophilic infiltrate
  3. 48 hours: Macrophage infiltrate –> discoloration of grey matter
  4. Weeks: Macrophage clear debris –> cavitation
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10
Q

(Focal/Global) ischemia is due to the occlusion of a blood vessel; infarct in local area; commonly due to…

  1. atherothrombosis (1 large vessel or many small vessels)
  2. intra-arterial (artery to artery) emboli, and
  3. cardiogenic emboli.
A

Focal (or “territorial” or “local”)

  • more common than global
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11
Q

(Focal/Global) ischemia is due to cardiac arrest, systemic hypotension or increased ICP cutting off cerebral perfusion; causes widespread necrosis that can be accentuated or limited to watershed areas

A

Global (or “generalized”)

*note watershed areas (시냇물 shape)

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12
Q

The maximal amount of swelling after an infarct is usually within

A

one week

*can cause a mass lesion

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13
Q

Peripheral rim of “lesser” ischemia surrounding a central core of maximal ischemia

A

Penumbra

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14
Q

Consequences of Brain Infarcts

A 
Focal neurologic deficites
Cognitive impairment (Vascular dementia)
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15
Q

Common causes of Brain Hemorrhage

A 
Hypertensive small-vessel disease
Ruptured Berry Aneurysm
Ruptured arteriovenous malformation
Cerebral amyloid angiopathy
Drugs/Neoplasm/Trauma
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16
Q

MOST common cause of Intracerebral Hemorrhage

A

Hypertension

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17
Q

Acute hypertensive hemorrhage typically occurs in what two vessels?

A
  1. Lenticulostriate vessels (branches of MCA supplying deep cerebral nuclei like putamen)
  2. Pontine arteries (branches of Basilar artery)
    * note that they are “SMALL” vessels
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18
Q

Most common cause of a Subarachnoid Hemorrhage (hemorrhage that moves into CSF space b/w arachnoid and pia maters); patients often say worst HA of my life; CSF xanthochromic (bilirubin in CSF)

A

Ruptured Berry Aneurysms

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19
Q

Abnormal dilation of an artery (due to weakening of vessel wall) that arise at the base of the brain where the major blood vessels meet (“Circle of Willis”); most occurs in Anterior circulation; MOST don’t rupture but still a concern; NEVER occurs in children

A

Berry Aneurysm

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20
Q

Berry aneurysms are more likely in the (anterior/posterior) circulation of the Circle of Willis

A

Anterior

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21
Q

Mean age of Berry Aneurysm rupture (remember vast majority don’t ever rupture)

A

50

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22
Q

HTN, smoking, cocaine, heavy alcohol consumption, and heritable CT disorders (Ehlers-Danlos, ADPKD, etc.) are the major risk factors of

A

Berry aneurysm RUPTURE

  • rarely ruptures though
23
Q

Consequences of Aneurysm rupture

A

Inc. ICP (can cause mass effect)
Hydrocephalus
Re-bleeding of aneurysm
Secondary vasospasm of cerebral arteries

24
Q

Tangle of abnormal arteries and veins bypassing capillary bed; often WEDGE-shaped area involving brain and leptomeninges (arachnoid+pia); may rupture and hemorrhage

A

Arteriovenous malformations (AVM)

25
Q

Brain tumor composed of small, tightly packed thin-walled blood vessels; can rupture and may cause seizures

A

Cavernous Angioma (aka. Cavernoma)

26
Q

Examples of brain vasculitis

A 
Giant Cell (aka. Temporal) arteritis*
Primary angiitis of the CNS
Polyarteritis Nodosa

*most common

27
Q

Most common primary vasculitis involving the CNS; peak age of about 80; twice as often in females; temporal artery usually involved; highly associated with polymyalgia rheumatica; histologic findings of granulomatous inflammation, multi-nucleated giant cells, and fragmented internal elastic lamina

A

Giant Cell Arteritis

  • aka. Temporal Arteritis
28
Q

TRANSIENT episode of neurologic dysfunction resulting from focal brain, spinal cord or retinal ischemia; usually only lasts <1 hour; NOT associated with permanent cerebral infarction (if yes, then it’s a stroke)

A

Transient Ischemic Attack

29
Q

(Intracerebral/Subarachnoid) hemorrhages are more common

A

Intracerebral (70%)

30
Q

A-fib, prosthetic valves, acute MI, dilated cardiomyopathy, endocarditis, and ventricular aneurysm are some cardiac sources of ______ causing ischemic stroke.

____________ is less likely to cause an emboli in elderly but is a common cause of “young stroke”.

A

Emboli

Patent Foramen Ovale

31
Q

Basal ganglia (striatum + GP) and internal capsule are supplied by

A

lenticulostriate arteries (from MCA)

32
Q

Midbrain and thalamus are supplied by

A

perforators from PCA

33
Q

Caudate is supplied by

A

perforators from ACA (“recurrent artery of Heubner”)

34
Q

Internal capsule is supplied by

A
  1. lenticulostriate arteries (from MCA)

2. Anterior choroidal artery (from Internal Carotid Artery)

35
Q

Effects of stroke caused by “carotid” ischemia (anterior circulation)

  • think about the anterior portion of brain supplied by internal carotid arteries and its branches
A
  1. TIA
  2. Motor (CONTRALATERAL weakness)
  3. Language disturbance (if dominant hemisphere)
36
Q

Effects of MCA Stroke

  • think about the brain area supplied by MCA (lateral parietal lobe, lateral frontal lobe, and temporal lobe)
A
  1. Contralateral paralysis and sensory loss of face and upper limb (lateral homunculus)
  2. Broca’s Aphasia (if lesion in dominant hemisphere)
  3. Wernicke’s Aphasia
37
Q

Effects of ACA Stroke

  • think about the brain area supplied by ACA (medial parietal lobe, medial frontal lobe, and caudate)
A
  1. Contralateral paralysis and sensory loss of lower limb (medial homunculus)
  2. Urinary incontinence (loss of bladder control)
38
Q

Effects of PCA Stroke

  • think about the brain area supplied by PCA (occipital lobe, thalamus)
A
  1. Contralateral hemianopia with macular sparing
  2. Hemisensory loss
  3. Anton syndrome (denial of blindness)
39
Q

Effects of stroke caused by “vertebrobasilar” ischemia (posterior circulation)

  • think about the posterior portion of brain supplied by vertebrobasilar arteries
A
  1. Diplopia/Binocular blurring or loss of vision
  2. Unilateral or bilateral weakness in limbs
  3. Vertigo/lack of coordination (look drunk)
40
Q

Small infarcts deep in the hemispheres, brainstem or cerebellum; often associated with HTN/DM

A

Lacunar Infarcts

  • lacunar = small vessels
41
Q

Lacunar infarct in what area of brain causes PURE MOTOR syndrome?

  • contralateral F, A, L motor loss
A

Posterior limb of internal capsule (supplied by “anterior choroidal artery”, a branch of ICA)

42
Q

Lacunar infarct in what area of brain causes PURE SENSORY syndrome?

  • contralateral Face, Arm, Leg sensory loss
A

Thalamus (supplied by perforating arteries of PCA)

43
Q

Often described as “worst HA in my life”; LP shows CSF xanthochromic (bilirubin is found in CSF)

A

Aneurysm rupture —> subarachnoid hemorrhage

44
Q

Non-contrast CT scan is sensitive for

A

Hemorrhage

  • blood will appear WHITE
45
Q

Why do we use NON contrast for CT scans of the brain

A

With contrast, lit up areas could be either bone, blood or contrast

*non-contrast means it can only be blood or bone

46
Q

MRI scan is sensitive for

A

Early detection of ISCHEMIC stroke

*CT can take days to show effects, while MRI can show within hours

47
Q

When should you use Thrombolysis (rt-PA) for strokes?

A

ISCHEMIC ONLY

48
Q 
>5 hours since onset
Head trauma
Hx of intracranial hemorrhage
Low platelets
Recent surgery

are contraindications for

  • they all increase risk of bleeding
A

thrombolytics for strokes

49
Q

(Carotid Endarterectomy/stenting) is preferred in asymptomatic with at >60% stenosis or symptomatic with 70-99%

A

Carotid Endarterectomy

50
Q

(Carotid Endarterectomy/stenting) is preferred in symptomatic or asymptomatic with high grade ICA stenosis

A

Stenting

51
Q

Drug for the treatment of acute stroke/TIA

A

rt-PA (Tissue Plasminogen Activator)

52
Q

Drugs for secondary prevention of Stroke/TIA

A

Antiplatelets (Aspirin + Clopidogrel for 21-90 days)

Anticoagulants (Warfarin, Dabigatran, Apixaban, etc.)

53
Q

Treatment plan for Hemorrhagic Stroke

A
  1. Identify/fix cause of bleed
    • BP management

*because usually due to HTN

Neurology-Week 4 & 5 (14 decks)

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