CAPLAN CH9: Penetrating and Branch Artery Flashcards

1
Q

Can chronic white matter abnormalities present as Parkinson’s disease?

A

Yes. Multiple dilated perivascular spaces can be accompaned by WM changes and can be accompanied by cognitive and behavioral abnormalities and basal ganglioninc clinical dysfunction resembling PD.

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2
Q

What was the finding in the SPS 3 trial in terms of medications and bleeding?

A

Aspirin 325mg/day vs Aspirin 325mg/day + Clopidogrel 75mg/day

There is no significant reduction in recurrent stroke but inreased risk of bleeding and death

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3
Q

Small, discrete, often irregular lesions, ranging from 1 to 15mm in size

A

Lacunar infarcts

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4
Q

Most common locations of lacunes

A

putamen and pallidum
pons, thalamus, caudate, IC and corona radiata

RARE: peduncles, pyramid, SC white matter

NOT found: cerebral and cerebellar cortices

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5
Q

Characteristic vascular pathology

A

Focal enlargements and small hemorrhagic extravasation through the walls of the arteries

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6
Q

Arteries in spots being replaced by whorls, tangles and wisps of connective tissue obliterating the usual vascular layers

A

segmental arterial disorganization, fibrinoid degeneration and lipohyalinosis

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7
Q

Similar pathophysiology of penetrating artery disease and ICH?

A

Lipohyalinosis

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8
Q

The clinical-neurological findings of CADASIL are similar to CARASIL except___

A
  1. Premature baldness and back pain and severe spondylitis are additional major features.
  2. Arteries in CARASIL do not contain osmiophiliic materials
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9
Q

COL4A1 vs CADASIL

A

Unlike CADASIL, the in COL4A1, the temporal lobes are spared of the chronic white matter abnormalities

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10
Q

Major cause of fibrinoid degeneration and lipohyalinosis?

A

Hypertension

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11
Q

TRUE/FALSE. Headache caused by vascular distension OCCURS in patient with lacunes?

A

FALSE. Lacunes are small and deep. Because there is no accompanying overdistension of superficial arteries and deep arteries have no pain fibers.

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12
Q

Prior TIA occur in approximately __% of patients with lacunes?

A

20%

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13
Q

Most common cause of worsening of clinical neurological signs during the first week after stroke onset?

A

Lacunar infarction

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14
Q

TRUE OR FALSE. Lacunar syndromes are highly suggestive of deep cerebral infarction. 100% of the time, lacunar infarcts are found.

A

FALSE. In 16% of the time, it is not due to lacunar infarcts.

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15
Q

Combination of weakness, pyramidal signs and cerebellar-type ataxia

A

Homolateral ataxia and crural paresis (predominantly the lower limbs)

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16
Q

Abnormalities of motor function on one side of the body BUT no true paralysis and reflexes are not exaggerated, plantar response is flexor

A

non-pyramidal hemimotor syndrome (affected usually is the striatum and globus pallidus)

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17
Q

Can lacunar infarcts present with aphasia?

A

YES. In some patients with left caudate infarcts, the aphasia is slight and transient.

18
Q

Three major syndromes in the pons related to infarcts in the basis pontis?

A
  1. pure-motor hemiparesis (paramedian basis pontis)
  2. ataxic hemiparesis
  3. dysarthria clumsy-hand syndrome
19
Q

Compare the location of the lesions of ataxic hemiparesis vs pure motor syndrome in the pons?

A

smaller, more rostral, dorsal and lateral than lesions of pure motor syndrome

20
Q

Describe the development of a rubral tremor.

A

Usually develops as the hemiparesis improves and is present at rest and on intention.

21
Q

Describe the ataxia in patients with midbrain infarcts.

A

If focal lesions involve the decussation of the brachium conjunctivum in the midbrain, patient present with bilateral limb ataxia and tremor. (Wernekick commissure syndrome).

22
Q

What are the two most important and consistent paramedian thalamoperforating arteries?

A
  1. polar (tuberothalamic) artery- from the middle third PCOM

2. thalamic- subthalamic artery- from the medial PCA

23
Q

Usual presentation of polar artery infarction?

A

Polar artery supplies teh anteriomedial and anterolateral thalamic nuclei hence present with cognitive and behavioral changes.

24
Q

Counterpart of the lenticulostriate branches of the MCA?

A

thalamogeniculate group of arteries

25
Q

TRUE OR FALSE. The numbness of the inner mouth, eye, ear, scalp, chest, back, abdomen and genitalia is MUCH MORE COMMON in thalamic lacunes than in superfiicial lesions of the parietal cortex?

A

TRUE

26
Q

Hemianopia, hemisensory symptoms, and behavioral abnormalities may occur in patients with ____ infarcts.

A

Posterior choroidal artery territorial infarcts

27
Q

Characteristic visual field defect in a patient with PChA territory infarct vs AChA territory

A

Sectoranopia

In AchA territory: loss of the upper and lower quadrants, with sparing of vision in a line along the median horizontal meridian.

28
Q

What is the finding of the SPS 3 (Secondary Prevention of Small Subcortical Strokes) in terms of cognitive impairment?

A

Nearly half of stroke patients recruited presented with mild cognitive impairment between 2 weeks and 6 months after the qualifying lacunar stroke.

29
Q

What was the finding in the ESPS 2 (European Stroke PRevention Studies 2)?

A

That a combination of ASA + Dipyridamole is better than ASA or Dipyridamole alone.

30
Q

How many percent of lacunes were there in the WARRS trial?

A

40%

31
Q

What was the finding in the PROFESS trial?

A

No difference between Clopidogrel and Aspirin + extended-release dipyridamole with regard to effectiveness in prevention of recurrent strokes.

32
Q

What is the iMAGES trial?

A

Intravenous Magnesium Efficacy in Stroke- this checked the utility of Magnesium as vasodilator

33
Q

Where are the white matter lesions of CADASIL found?

A

Usually in the external capsule and anterior temporal lobes. (Characteristic lesion)

34
Q

What are the findings of the LADIS study (Leukoaraiosis and disability study)?

A

Increasing severity of whit matter abnormalities and number of lacunes were related to poorer cognitive performance.

When WM and lacunes were considered together, strong association of WM than number of lacunes.

35
Q

What is the usual age of onset of CADASIL?

A

less than 40 years old

36
Q

What is the difference between leukocariosis and white matter disease?

A

Leukoaraiosis is a general term and many patients with white matter abnormalities do not have a vascular disease.

37
Q

Cerebral microbleeds are present in approximately __ of patients with ICH and ischemic CVD?

A

70%

40%

38
Q

Mechanisms when white matter abnormalities are larger than the territory of a single penetrator?

A
  1. tandem penetrating arterial lesions.

2. increased vascular permeability

39
Q

What metalloproteinase is elevated in patients with Binswanger-type pathology?

A

Matrix metalloproteinase-9

40
Q

How does matrix metalloproteinases affect the BBB?

A

They degrade the tight junction proteins found within the blood vessels.

41
Q

Mechanism of brain edema in patients with Binswanger disease?

A

Degenerative changes in the veins within the white matter.