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(3) Neurological Examination > S1_L2: Cerebrovascular Disease > Flashcards

S1_L2: Cerebrovascular Disease Flashcards

1
Q

4th leading cause of death and leading cause of long-term disability among adults

A

Stroke

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2
Q

1st leading cause of death

A

Heart disease

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3
Q

2nd leading cause of death

A

Cancer

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4
Q

Temporal classification: Symptoms last for a few minutes or hours, but does not last longer than 24 hours
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

A. Transient Ischemic Attack

Note: Once it is already >24 hours, it’s already a stroke.

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5
Q

Etiological classification: Most common ischemic type; formation of blood clot within the cerebral arteries or
their branches
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

A. Ischemic: Thrombotic

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6
Q

Saccular aneurysm is caused by progressive degeneration of ___.

A

tunica adventitia (outer layer of blood vessel)

Additional: The loss of outer layer leads to loss of outside support → BV can inc in size and burst

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7
Q

Caused by tangled arteries and veins, causing fusion of oxygenated and deoxygenated blood. This leads to fusion of pressure that will inc the pressure in the veins so it will burst

A

Arteriovenous malformation (AVM)

Note: Veins are supposed to have less pressure than arteries

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8
Q

Brainstem Stroke: Medial basal of the midbrain
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

A. Weber’s Syndrome

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9
Q

What does BE FAST stand for in spotting a stroke

A

Balance (loss of balance, headache or dizziness)
Eyes (blurred vision)
Face (one side of the face is drooping)
Arms (arm or leg weakness)
Speech (speech difficulty)
Time (to call for ambulance immediately)

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10
Q

Ischemic Stroke Theory: If there will be an increase in LDL compared to an
increase in HDL, the LDL will go to the arteries, specifically the tunica intima layer. Occurs until LDL
continues to increase and lead to blockage.
A. Endothelial Injury Theory
B. Lipid Infiltration Theory
C. Unified Hypothesis

A

B. Lipid Infiltration Theory

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11
Q

Will look away from the paretic side but
towards the affected lobe & away from
unaffected lobe
A. Frontal gaze pattern
B. Pontine gaze pattern

A

A. Frontal gaze pattern

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12
Q

Pt has Gait apraxia, Frontal gaze pattern, Disconnection apraxia, Transcortical motor aphasia, Urinary incontinence, Contralateral grasp reflex, Sucking reflexes, and behavioural problems (abulia and akinetic mutism)
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

A. ACA Stroke

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13
Q

Affectation of which structure leads to athetosis?
A. Putamen
B. Globus pallidus
C. Subthalamic nucleus
D. Caudate nucleus

A

B. Globus pallidus

PCGASH

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14
Q

Pt has Contralateral homonymous hemianopsia, may have frontal or pontine gaze pattern, and contralateral hemiplegia and hemianesthesia on the UE/face more than the LE
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

B. MCA Stroke

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15
Q

Enumerate the tetrad of Gerstmann Syndrome

A
  1. Right and left Indiscrimination
  2. Acalculia
  3. Agraphia
  4. Finger agnosia
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16
Q

Artery affected in amaurosis fugax or transient loss of vision upon the attack?

A

ophthalmic artery (branch of internal carotid artery)

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17
Q

The origin of the posterior circulation of the brain is the ___ via the vertebrobasilar artery.

A

subclavian artery

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18
Q

Enumerate the arteries that form the circle of Willis

A
  1. Anterior Cerebral Artery (2)
  2. Posterior Cerebral Artery (2)
  3. Posterior Communicating Artery (2)
  4. Anterior Communicating Artery (1)
  5. Middle Cerebral Artery (2)
  6. Internal Carotid Artery (2)
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19
Q

Affectation of which structure leads to chorea?
A. Putamen
B. Globus pallidus
C. Subthalamic nucleus
D. Caudate nucleus

A

A. Putamen

PCGASH

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20
Q

Affectation of which structure leads to hemiballismus?
A. Putamen
B. Globus pallidus
C. Subthalamic nucleus
D. Caudate nucleus

A

C. Subthalamic nucleus

PCGASH

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21
Q

Most commonly injured layer in ischemic stroke

A

Tunica intima

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22
Q

Temporal classification: No blood clot, interruption of blood vessels is temporary only; no neurologic/residual symptoms after 24 hours.
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

A. Transient Ischemic Attack

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23
Q

Temporal classification: Focal neurologic deficits fully recover within a week, may last for > 24 hrs but < 1 wk.
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

B. Reversible Ischemic Neurologic Deficit

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24
Q

Temporal classification: Progressive type of stroke, stepwise incremental increases in neurologic deficits
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

C. Stroke in Evolution

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25
Q

Temporal classification: No further deterioration in neurologic status is seen and the pt is already stable.
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

D. Complete Stroke

Note: The condition will no longer progress unless they experience another attack.

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26
Q

Temporal classification: Risk factor for stroke, for example: after 5 years of having this, the pt can have a major stroke attack.
A. Transient Ischemic Attack
B. Reversible Ischemic Neurologic Deficit
C. Stroke in Evolution
D. Complete Stroke

A

A. Transient Ischemic Attack

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27
Q

Trochlear nucleus, mesencephalic nuclei of CN V
A. Level of Facial colliculus
B. Level of Trigeminal nuclei
C. Level of Inferior colliculi
D. Level of Superior colliculi

A

C. Level of Inferior colliculi

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28
Q

Oculomotor nucleus, Edinger-Westphal nucleus, red nucleus, mesencephalic nucleus of CN V
A. Level of Facial colliculus
B. Level of Trigeminal nuclei
C. Level of Inferior colliculi
D. Level of Superior colliculi

A

D. Level of Superior colliculi

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28
Q

Main sensory and motor nucleus of CN V, pontine nuclei, trapezoid nuclei
A. Level of Facial colliculus
B. Level of Trigeminal nuclei
C. Level of Inferior colliculi
D. Level of Superior colliculi

A

B. Level of Trigeminal nuclei

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29
Q

Facial nucleus, abducens nucleus, medial vestibular nucleus, spinal nucleus of CN V, pontine nuclei, trapezoid nuclei
A. Level of Facial colliculus
B. Level of Trigeminal nuclei
C. Level of Inferior colliculi
D. Level of Superior colliculi

A

A. Level of Facial colliculus

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30
Q

Etiological classification: Usually affects the smaller arteries and is usually cardiac in origin
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

B. Ischemic: Embolic

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31
Q

Etiological classification: A pure motor or pure sensory stroke that is focal in nature
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

C. Ischemic: Lacunar

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32
Q

Etiological classification: Usually affects the lenticulostriate arteries
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

C. Ischemic: Lacunar

33
Q

Etiological classification: Gradual onset, usually occurs at night and affects the larger arteries
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

A. Ischemic: Thrombotic

34
Q

Etiological classification: Sudden onset, usually in the morning, and is d/t physical activity
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

B. Ischemic: Embolic

35
Q

Etiological classification: Hallmarks are seizures, aphasia, and unilateral neglect
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

B. Ischemic: Embolic

36
Q

Etiological classification: Due to long standing hypertension or diabetes mellitus
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

C. Ischemic: Lacunar

37
Q

Etiological classification: Has earlier, more rapid, greater degree of neurologic deficits
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

C. Ischemic: Lacunar

38
Q

Etiological classification: Composed of bits of matter (e.g. blood clot) formed elsewhere and released into bloodstream, traveling to the cerebral arteries
A. Ischemic: Thrombotic
B. Ischemic: Embolic
C. Ischemic: Lacunar

A

B. Ischemic: Embolic

39
Q

Etiological classification: anatomic pattern is in the subarachnoid space
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

B. Hemorrhagic: Subarachnoid

40
Q

Etiological classification: Associated with Charcot-Bouchard aneurysms that are d/t long-standing hypertension
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

A. Hemorrhagic: Intracerebral

41
Q

Etiological classification: Associated with saccular aneurysm or
arteriovenous malformation
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

B. Hemorrhagic: Subarachnoid

42
Q

Etiological classification: “Worst headache of my life”
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

B. Hemorrhagic: Subarachnoid

43
Q

Etiological classification: Deep perforating cerebral arteries are the sites of rupture, which do not obey the anatomic distribution of a vessel
but dissects through tissue planes (massive affectation)
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

A. Hemorrhagic: Intracerebral

44
Q

Etiological classification: Usually occurs in younger patients and has dramatic clinical onset.
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

A. Hemorrhagic: Intracerebral

Note: Most commonly caused by hypertension (Merritt’s, 14th ed)

45
Q

Etiological classification: More common in females than males
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

B. Hemorrhagic: Subarachnoid

46
Q

Etiological classification: Occurs within the dural space around the brain and fills the basal cisterns
A. Hemorrhagic: Intracerebral
B. Hemorrhagic: Subarachnoid

A

B. Hemorrhagic: Subarachnoid

47
Q

Management classification: Presence of stable and severe type of impairments
A. Transient Ischemic Attack
B. Major Stroke
C. Deteriorating Stroke
D. Young Stroke

A

B. Major Stroke

48
Q

Management classification: Affecting individuals younger than age 45
A. Transient Ischemic Attack
B. Major Stroke
C. Deteriorating Stroke
D. Young Stroke

A

D. Young Stroke

49
Q

Management classification: neurological status deteriorates after hospitalization, similar to stroke in evolution
A. Transient Ischemic Attack
B. Major Stroke
C. Deteriorating Stroke
D. Young Stroke

A

C. Deteriorating Stroke

50
Q

Brainstem Stroke: Tegmentum of the midbrain
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

B. Benedikt’s Syndrome

51
Q

Brainstem Stroke: Bilateral pons
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

C. Locked-In Syndrome

51
Q

Brainstem Stroke: Lateral pons
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

D. Millard-Gubler Syndrome

52
Q

Brainstem Stroke: Lateral medulla
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

E. Wallenberg Syndrome

53
Q

Brainstem Stroke: manifests with Contralateral hemiplegia & Ipsilateral CN III palsy
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

A. Weber’s Syndrome

53
Q

Brainstem Stroke: Corticospinal tract and Oculomotor nerve (CNIII) are affected
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

A. Weber’s Syndrome

54
Q

Brainstem Stroke: Pt has CN III affectation & presents with contralateral chorea, athetosis, problem on the joint position, and contralateral loss of pain and temperature.
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

B. Benedikt’s Syndrome

55
Q

Brainstem Stroke: Spinothalamic tract, medial lemniscus, superior cerebellar peduncle, oculomotor nerve, and red nucleus are affected.
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

B. Benedikt’s Syndrome

56
Q

Brainstem Stroke: Paralysis on all fours or (B) UE & LE
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

C. Locked-In Syndrome

57
Q

Brainstem Stroke: Corticobulbar tract and Corticospinal tract are affected
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

C. Locked-In Syndrome

58
Q

Brainstem Stroke: Has Bilateral hemiplegia and bilateral CN palsy, but upward gaze is spared
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

C. Locked-In Syndrome

Note: Pt can’t move the head. Pt uses the eyes to communicate.

59
Q

Brainstem Stroke: Affectation of the abducens and facial nerves, and corticospinal tract
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

D. Millard-Gubler Syndrome

60
Q

Brainstem Stroke: Pt has contralateral hemiplegia and ipsilateral CN VI & CN VII palsy
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

D. Millard-Gubler Syndrome

61
Q

Pt has loss of consciousness and is in a coma, has bilateral motor deficits, cranial nerve and cerebellar dysfunction. Pt has intact cognition.
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

E. Vertebrobasilar Artery Stroke

62
Q

Cerebral blood flow (100 gm-min)

  1. Severe ischemia
  2. Metabolic changes
  3. Mild ischemia
  4. Moderate ischemia “PENUMBRA”
  5. Normal range

A. 10 ml
B. 20 ml
C. 30 ml
D. 40 ml
E. 50 ml

A
  1. A
  2. D
  3. C
  4. B
  5. E
63
Q

Cerebral blood flow (%)

  1. Severe ischemia
  2. Metabolic changes
  3. Mild ischemia
  4. Moderate ischemia “PENUMBRA”
  5. Normal range

A. 100%
B. 80%
C. 60%
D. 40%
E. 20%

A
  1. E
  2. B
  3. C
  4. D
  5. A
64
Q

Occurs when almost 60% of cerebral blood flow is lost. It surrounds the part of the cell which is irreversibly
damaged/dead. After 8 mins with no management, it will become irreversible cell damage and the
area surrounding it will become the new one.

A

Ischemic penumbra

65
Q

Ischemic Stroke Theory: Linear blood flow (normal) becomes turbulent
causing inner blood vessel layer damage that is d/t Htn
A. Endothelial Injury Theory
B. Lipid Infiltration Theory
C. Unified Hypothesis

A

A. Endothelial Injury Theory

66
Q

Ischemic Stroke Theory: Turbulent blood flow causes scar damage until
blockage while low-density lipoprotein (LDL) also travels to the artery and
further clots it.
A. Endothelial Injury Theory
B. Lipid Infiltration Theory
C. Unified Hypothesis

A

C. Unified Hypothesis

67
Q

Will look towards the paretic side but away from the affected lobe & towards the unaffected lobe
A. Frontal gaze pattern
B. Pontine gaze pattern

A

B. Pontine gaze pattern

68
Q

Stroke caused by the most commonly occluded artery that supplies the UE and the Face
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

B. MCA Stroke

Additional: MCA is largest branch of internal carotid artery

69
Q

Stroke caused by the artery supplying LE
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

A. ACA Stroke

70
Q

Normal cerebral blood flow

A

50mL/min/100g of brain tissue

OR

O’Sullivan: 60mL/min/100g

71
Q

TRUE OR FALSE: Occlusion on the proximal MCA produces minor
neurologic deficits.

A

False

produces major / extensive

72
Q

TRUE OR FALSE: Occlusion on the distal PCA produces minor neurologic deficits.

A

False

produces major / extensive

73
Q

Pt has thalamic pain syndrome (Dejerine Roussy Syndrome), contralateral hemiplegia and hemianesthesia, amnesic syndrome, prosopagnosia, visual agnosia, and homonymous hemianopsia.
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

C. PCA Stroke

74
Q

Pt has equal affectation of the face, UE, and LE. Pt also complains of temporary loss of vision upon the attack.
A. ACA Stroke
B. MCA Stroke
C. PCA Stroke
D. ICA Stroke
E. Vertebrobasilar Artery Stroke

A

D. ICA Stroke

75
Q

Stroke that always has ipsilateral affectation d/t double decussation, presents with hypotonia and coordination problems.

A

Cerebellar stroke

76
Q

Brainstem Stroke: Spinocerebellar tract, CN V, spinothalamic tract, vestibular nuclei, sympathetic tract, and nucleus ambiguus are affected.
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

E. Wallenberg Syndrome

77
Q

Brainstem Stroke: Pt has anhydrosis, ptosis, myosis, and exophthalmos. Pt also has ipsilateral hemiataxia and CN V palsy; loss of pain and temperature on contralateral side.
A. Weber’s Syndrome
B. Benedikt’s Syndrome
C. Locked-In Syndrome
D. Millard-Gubler Syndrome
E. Wallenberg Syndrome

A

E. Wallenberg Syndrome

(3) Neurological Examination (8 decks)

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