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ABPP > Stroke & anoxia > Flashcards

Stroke & anoxia Flashcards

1
Q

Binswanger disease

A

Subcortical ateriosclerotic encephalopathy; small vessel vascular dementia caused by damage to white matter

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2
Q

CADASIL

A

Cerebral autosomal dominant arteriopathy with subcortical infarcts & leukoencephalopathy

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3
Q

At what level of decreased arterial oxygen is cognitive affected? When does unconsciousness occur? Death?

A

75% arterial oxygen, 50%, 30-40%, respectively

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4
Q

Ischemia

A

Reduced blood flow due to interruption or reduction of blood delivery to the brain

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5
Q

Hypoxia

A

Tissue oxygen deprivation

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6
Q

Anoxia

A

Complete lack of O2 in the arterial blood or tissues

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7
Q

Hypoxemia

A

Reduced oxygenation of the blood

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8
Q

What is the most common cause of hypoxia/anoxia?

A

Cardiac arrest

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9
Q

What are some other causes of hypoxia/anoxia?

A

reduced arterial pressure due to lung disease, reduced hemoglobin due to anemia or blood loss, biochemical block of cerebral utilization of O2 due to cyanide poisoning

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10
Q

Why are some areas of the brain more vulnerable to anoxia/hypoxia?

A

Attributed to vascular or hemodynamic specificity, increased regional metabolism of glucose, and/or proximity to structures with high levels of excitatory amino acids

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11
Q

Brain regions most vulnerable to anoxia/hypoxia

A

Watershed regions, neocortex, hippocampus, BG, cerebellar Purkinje cells, primary visual cortex, frontal regions, thalamus

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12
Q

NP deficits associated with anoxia

A

Impaired memory, executive dysfx, apperceptive agnosia, visuospatial deficits, overall cognitive decline, extrapyramidal signs, cerebellar ataxia, intention or action myoclonus

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13
Q

Definition of stroke

A

Abrupt onset of a focal neurologic deficit that is consistent with a vascular distribution & lasts >24 hrs with or without an image positive for stroke OR <24 hours with a positive image

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14
Q

Ischemic stroke

A

Blood flow is insufficient to maintain neurologic function; infarction occurs when ischemia reaches threshold to produce cell death

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15
Q

Transient ischemic attack (TIA)

A

Acute transient neurological deficit that typically lasts <1 hr & is w/o persistent neuro abnormality or evidence of acute infarction on imaging

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16
Q

What is the risk of clinical stroke after TIA?

A

1/3 within 5 years

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17
Q

Lacunar infarct

A

Small cavity caused by a small deep cerebral infarct, most often associated with arterial HTN

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18
Q

What is the window for t-PA?

A

3 hours of onset

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19
Q

Risk factors for stroke

A

75+, AA/Hispanic, male, HTN, AFib, diabetes, high cholesterol, smoking, abdominal obesity, metabolic syndrome

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20
Q

How does smoking increase stroke risk?

A

Contributes to atherosclerosis, alters coagulation systems by increasing fibrinogen, platelet aggregation, & hematocrit level, reduces blood vessel distensibility

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21
Q

Thrombosis

A

Obstruction of blood flow due to blood clot formed locally with a blood vessel

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22
Q

Embolism

A

Material is formed elsewhere in the vascular system & travels to lodge in a vessel

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23
Q

What areas of the CNS are vulnerable to global cerebral ischemia?

A

Purkinje cells in cerebellum
Ca1 region of hippocampus
Watershed zones
Cerebral cortical layers

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24
Q

Brief global cerebral ischemia

A

Coma that persists <12 hrs, transient confusion or amnesia

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25
Q

Prolonged global cerebral ischemia

A

Comas that persist at least 12 hrs with lasting focal or multifocal motor, sensory, & cognitive deficits

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26
Q

Arteriovenous malformation

A

Tangle of dilated blood vessels; forms an abnormal connection between arteries & veins & can cause damage by compression of neighboring structures or shunting of blood away from the site leading to hypoperfusion of surrounding tissue

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27
Q

Cavernous malformation

A

Large vascular lumen with collagenous walls lined by a single layer of endothelial cells; affects veins with no arterial connections

Most common manifestation is recurrent seizures, but often clinically silent

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28
Q

Capillary telangiectasias

A

Small regions of abnormally dilated capillaries, rarely give rise to ICH

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29
Q

Venous angioma

A

Dilated veins visible on MRI scans as single flow void extending to brain surface; not known to cause any clinical symptoms themselves

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30
Q

4 major types of aneurysms

A

Saccular (most common)
Giant (>1 in across)
Fusiform (bulges from all sides & has no neck)
Mycotic (results from infection in artery wall)

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31
Q

Increased risk for aneurysm rupture is associated with

A

Size >10 mm in diameter, age, chronic HTN, cigarette smoking, alcohol use, atherosclerosis

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32
Q

Common symptoms of aneurysm rupture

A

Abrupt onset of severe HA, nausea & vomiting, stiff neck, loss or alteration of consciousness, confusion or slowed thinking, motor problems, visual disturbance

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33
Q

How are aneurysms treated?

A

Clipping, coiling

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34
Q

Where are aneurysms most likely to occur?

A

AComm, start of MCA, PComm

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35
Q

Stroke risk in sickle cell anemia

A

Sickled red blood cells adhere more readily to surface of blood vessels; increased CBF to compensate for decreased oxygenation of red blood cells reduces cerebrovascular reserve; stroke is usually large vessel, but chronic insufficiency leads to watershed infarcts

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36
Q

What are the signs of an incomplete (watershed) L ICA infarct?

A 
Aphasia (mostly mixed transcortical or transcortical motor)
R motor & sensory impairments
Gerstmann's syndrome
Agnosias
Memory deficits possible
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37
Q

What are the signs of an incomplete (watershed) R ICA infarct?

A

Aprosody
L motor & sensory impairment
Anosognosia, L neglect, ideational apraxia, constructional apraxia
Memory deficits possible

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38
Q

What are the signs of a complete L ICA infarct?

A 
R HP including lower face
R hemianesthesia
Aphasia (global or Broca's)
Gerstmann's syndrome
Apraxias
Acute IL monocular blindness, right HH
Frontal lobe behaviors
Memory, particularly verbal, may be impaired
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39
Q

What are the signs of a complete R ICA infarct?

A 
L HP including lower face
L hemianesthesia
Receptive & expressive aprosody
Acute IL monocular blindess, left HH
Frontal lobe behaviors
Memory, particularly nonverbal, may be impaired
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40
Q

What are the signs of a left ACA infarct?

A

R leg motor & sensory loss
Akinesia, mutism, abulia, frontal release signs
Transcortical motor aphasia
Memory deficits possible, particularly poor retrieval
Alien hand syndrome (R)

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41
Q

What are the signs of a right ACA infarct?

A 
L leg sensory & motor loss
L arm weakness
Apathy, stimulus-bound behaviors, jocularity, hypomania, frontal release signs
Left inattention
Alien hand syndrome (L)
42
Q

What are the signs of a left MCA stem infarct?

A 
R HP & hemianesthesia
R HH possible, left gaze preference
Global aphasia
Motor apraxias & visuoconstructional deficits
Acalculia & memory loss
Mood changes, particularly depression
43
Q

What are the signs of a right MCA stem infarct?

A 
L HP & hemianesthesia
Left HH possible, right gaze preference
Profound hemineglect
Visuoconstructional deficits
Motor apraxia
Memory impairments
Anosognosia, mood changes, aprosody
44
Q

What are the signs of a L MCA deep territory infarct?

A

R pure motor HP
Mild aphasia syndromes
Deficits in mvmt w/ BG involvement
Mood changes w/ depression

45
Q

What are the signs of a R MCA deep territory infarct?

A

L pure motor HP
L hemineglect
Visuoconstructional deficits

46
Q

What are the signs of a L MCA inferior division infarct?

A 
Fluent aphasia
R face & arm sensory loss
R visual field defect
R face & hand motor loss possible (mild)
Gerstmann's syndrome
Visuoconstructional/visuospatial deficits
Mood changes w/ depression
47
Q

What are the signs of a R MCA inferior division infarct?

A

L face & arm sensory loss
L visual field defect
L face & hand motor loss possible (mild)
L hemineglect
Visuoconstructional/visuospatial deficits
Mood changes, w/ hypomania or affective flattening
Receptive aprosody

48
Q

What are the signs of a L MCA superior division infarct?

A

R face & arm motor loss
Some face & arm sensory loss
Nonfluent aphasia
Mood changes w/ depression

49
Q

What are the signs of a R MCA superior division infarct?

A

L face & arm motor weakness
Some face & arm sensory loss
Variable L inattention
Expressive aprosody
Dorsolateral syndrome (poor problem-solving, impaired sequencing, perseveration, poor reasoning)
Mood changes w/ hypomania & hollow jocularity

50
Q

What are the signs of a L PCA infarct?

A 
R HH or some kind of visual field defect
Visual agnosia
Alexia w/o agraphia
Transcortical sensory aphasia
Motor & sensory loss of hand & face
Mood changes w/ depression
51
Q

What are the signs of a right PCA infarct?

A 
L HH or some kind of visual defect
Visual agnosias
Receptive aprosody
Motor & sensory loss of hand & face
Mood changes w/ anxiety or depression
52
Q

What are the signs of a left ACA-MCA watershed infarct?

A

Transcortical motor aphasia

R motor & sensory impairment of trunk, hips, & proximal extremities

53
Q

What are the signs of a right ACA-MCA watershed infarct?

A

L motor & sensory impairment of trunk, hips, & proximal extremities
Visuoconstructional deficits

54
Q

What are the signs of a left MCA-PCA watershed infarct?

A

Transcortical sensory aphasia
Gerstmann’s syndrome
Agnosias
Memory deficits possible, particularly verbal

55
Q

What are the signs of a right MCA-PCA watershed infarct?

A

Visuoconstructional & visuoperceptual deficits
Visual agnosias
Memory deficits possible, particularly nonverbal

56
Q

Pure sensory stroke

A

Taste may be impaired, no vision loss, motor deficits, or NP impairment

57
Q

Vasculature involved in pure sensory stroke

A

Inferiolateral (thalamo-geniculate) artery

58
Q

Localization of pure sensory stroke

A

VPL nuclei of thalamus, taste impaired if VPM is affected

59
Q

Pure sensorimotor stroke

A

Hemisensory loss of hand, face, leg; taste may be impaired; HP of face, hand, leg; no NP impairments

60
Q

Vasculature involved in pure sensorimotor stroke

A

Thalamogeniculate & lenticulostriate arteries

61
Q

Localization of pure sensorimotor stroke

A

Ventrolateral & VPL, thalamic somato-sensory projections, corticospinal & corticobulbar pathways, VPM involvement = loss of taste

62
Q

Vasculature involved in pure motor HP

A

lenticulostriate arteries, perforating branches of PCA, anterior choroidal artery

63
Q

Localization of pure motor HP

A

posterior limb of IC, pons (anterior portion), cerebral peduncle, corona radiata

64
Q

Vaculature involved in pure motor HP with dysarthria

A

Penetrating branches of the basilar artery, lenticulostriate arteries

65
Q

Localization of pure motor HP with dysarthria

A

Medial pons, cerebral peduncle, genu of IC

66
Q

Vasculature involved in pure motor HP with ataxia (ataxic hemiparesis)

A

Penetrating branches of the basilar artery, lenticulostraite arteries

67
Q

Localization of ataxic hemiparesis

A

medial pons, less often due to IC including corona radiata

68
Q

Hemi-dystonic lacunar stroke

A

may be asymptomatic, may see mvmt disorders, rarely NP deficits, OC symptoms reported

69
Q

Vasculature involved in hemi-dystonic lacunar stroke

A

lenticulostriate arteries, anterior choroidal artery, recurrent artery of Heubner

70
Q

Localization of hemi-dystonic lacunar stroke

A

putamen and/or globus pallidus

71
Q

Hemiballism/chorea lacunar stroke

A

Hemiballismus of extremity due to infarct in the subthalamic nucleus (thalamogeniculate artery)

72
Q

Clinical features of a thalamogeniculate artery stroke

A 
Hemisensory loss
Hemiataxia
Possible thalamic pain syndrome
HP (mild) & loss of taste
No NP deficits
73
Q

Clinical features of stroke of the paramedian arteries

A

Impairment of declarative memory (retrieval deficits & inefficient consolidation)
Behavioral apathy w/ somnolescence
Vertical gaze palsy
Confabulation may be present

74
Q

Clinical features of a stroke of the tuberothalamic artery

A

Dominant hemisphere: aphasia symptoms, verbal memory w/ impaired encoding & consolidation

Nondominant hemisphere: nonverbal memory impairment, hemineglect, visuoconstructional & visuospatial deficits

Bilateral: apathy, lethargy, anterograde amnesia

75
Q

Dejerine-Roussy syndrome (thalamic pain syndrome)

A

Severe burning pain CL to lesion w/ allodynia (conversion of benign pain to unbearable pain) & hyperapthia (testing for Babinski produces severe pain)

76
Q

Top-of-the-basilar syndrome

A

CL ataxia, HP or tetraparesis
IL CN III palsy
Somnolence
Visual hallucinations (poorly formed), memory impairment (anterograde), apathy & abulia, akinetic mutism in some cases

77
Q

Watershed zones

A

Border zone of anastomoses that lies between territories of 2 major cerebral arteries

Anastomose: to unite by contact, e.g., 2 vessels at their extremities

78
Q

What is the main clinical significance of watershed zones?

A

A significant drop in blood pressure will lead to drop in oxygenated blood supply where 2 arterial distributions overlap - become infarcted

79
Q

Where do thrombi usually occur?

A

At the site of a pre-existing stenosis of an artery

80
Q

What is the most common embolic source?

A

Heart

81
Q

Embolization

A

Method used to close vessels feeding AVMs

82
Q

Common conditions that require embolization

A
  • Reduce size of AVM before resection
  • Treat aneurysms & cavernous fistulas that cannot be resected
  • Stop uncontrollable bleeding of an artery following head or neck injury
83
Q

Anterior communicating artery syndrome

A

Dense anterograde amnesia, disorientation, & confabulation combined with disturbances of attention & behavior

84
Q

Arteriosclerosis

A

Thickening & hardening of smaller arteries; assoc. w/ chronic HTN

85
Q

Atherosclerosis

A

Build-up of fatty deposits in arterial walls, assoc. w/ MI

Most often affect MCA, ACA, ophthalmic artery

86
Q

Cerebral amyloid angiopathy

A

Dementia through multifocal recurrent hemorrhages & WM ischemic disease; often familial

87
Q

Chronic obstructive pulmonary disease (COPD)

A

Disease with poor expiratory airflow, may cause chronic hypoxia resulting in cognitive decline

88
Q

Hemosiderin

A

Protein residual of the breakdown of blood

Can cause nervous system dysfunction

89
Q

Temporal arteritis (giant cell arteritis)

A

Vasculitis affecting temporal arteries, including those supplying the eye

HA in temporal lobes, may have jaw pain when chewing, malaise, fever, weight loss; may lose vision

90
Q

Vasculitis

A

Inflammation or vasospasm causing narrowing of vessels

91
Q

Weber’s syndrome

A

Midbrain arterial thrombosis damaging CN III and corticospinal tract

92
Q

Neuroimaging correlates of anoxia/hypoxia

A

Focal & diffuse neuropathologic lesions & atrophy, lesions in hippocampus, BG, cerebellum, WM changes; significant hippocampal atrophy

93
Q

Neurologic syndromes/symptoms associated with anoxia/hypoxia

A

Persistent coma or stupor, dementia w/ or w/o extrapyramidal signs, extrapyramidal syndrome w/ cognitive impairment, choreoathetosis, cerebellar ataxia, intention or action myoclonus

94
Q

Prolonged periods of hypotension affect when structures?

A

Watershed zones, cerebellum, BG, spinal cord

95
Q

Global cerebral ischemia is associated with what conditions?

A

Cardiac arrest, respiratory failure, hyperglycemia, status epilepticus

96
Q

Wallenberg’s syndrome

A

Lateral medullary syndrome (PICA)

Ipsilateral cerebellar ataxia, Horner’s syndrome, facial sensory deficit, CL impaired pain & temp sensation, nystagmus, vertigo, nausea, dysphagia & dysarthria, hiccup, sparing of motor system

97
Q

Most common sites of primary hypertensive hemorrhage

A

Putamen, thalamus, cerebellum, pons, caudate, lobar subcortical

98
Q

Symptoms of primary hypertensive hemorrhage

A

Severe HA, vomiting, oculomotor disturbance, nuchal rigidity, altered consciousness

99
Q

Lobar hemorrhage in the elderly is most often related to

A

Amyloid angiopathy

100
Q

Children with sickle cell anemia tend to have _____ strokes, adults usually have _____ strokes

A

Ischemic, hemorrhagic

This is the reversal of the usual trend

ABPP (34 decks)

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