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Neurology - Physiology > CVD 2 > Flashcards

CVD 2 Flashcards

1
Q

This is a segmental, nonatheromatous, noninflammatory
arterial disease of unknown etiology, almost exclusively
in women

A

Fibro m u scu l a r Dysplasia

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2
Q

Arteries involved in FMD

A

internal carotid artery is involved most frequently,

followed by the vertebral and cerebral arteries

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3
Q

Histology of FMD

A

The narrowed arterial segments show degeneration
of elastic tissue and irregular arrays of fibrous and
smooth muscle tissue in a mucous ground substance

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4
Q

Mechanisms of ischemia in FMD

A

from thrombi in the pouches or in relation to intraluminal septa

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5
Q

In pts with FMD, between 7 and 20 percent of affected individuals are found to have intracranial
_________ (rarely a giant aneurysm),

A

saccular aneurysms

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6
Q

the process formerly

known as Erdheim’ s medionecrosis aortica cystica

A

I nte r n a l Ca rot i d Artery D i ssect i o n

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7
Q

The frequency of cerebral stroke with aortic dissection
has varied from ______ percent and that of spinal
stroke has been approximately ______ percent

A

10 to 50

10

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8
Q

___________are also associated with an increased risk of vascular dissection

A

The Ehlers-Danlos and Marfan syndromes,
osteogenesis imperfecta,
Loeys-Dietz syndrome (transforming growth factor [TGF]-,B receptor mutation), and alpha1 -antitrypsin deficiency

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9
Q

In most cases, dissection of the internal carotid artery
can be detected by ultrasonography and confirmed by
MRl and CTA, which show a _____

A

double lumen

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10
Q

In pts with Carotid artery dissection,

angiography usually reveals an elongated, but variable
length, irregular narrow column of dye, usually
begiruting 1 .5 to 3 em above the carotid bifurcation and
extending to the base of the skull, a picture that Fisher
has called the ________

A

string sign

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11
Q

Rapid
and extreme rotational movement of the neck is the most
common identifiable cause of ____________

A

vertebral artery dissection

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12
Q

Another interesting but rare

association with dissection has been the ________

A

reversible cerebral vasoconstriction syndrome

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13
Q

___________percent of patients
with the angiographic signs of cervical artery dissection;
mainly, these were patients who had fluctuating
ischemic symptoms but without stroke have a complete or excellent recovery

A

85%

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14
Q

Tx of cervical artery dissection

A

anticoagulation for several weeks

or months and followed up with some form of arteriography.

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15
Q

relative CI to anticoagulation in pts with cervical artery dissection

A

there is existing
subarachnoid blood on a CT scan or if there is a pseudoaneurysm
within the intracranial portion of the dissection

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16
Q

refer to an extensive basal
cerebral rete mirabile-a network of small anastomotic
vessels at the base of the brain around and distal to the
circle of Willis,

A

Moya-Moya

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17
Q

Associations of Moya-Moya dse

A

segmental stenosis or occlusion of the terminal intracranial parts of both internal carotid arteries

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18
Q

Certain hemoglobinopathies, particularly sickle cell anemia, may cause a vasoocculsive condition equivalent to moyamoya disease, possibly because of sickling of red blood cells in the vasa vasorum of the_______

A

supraclinoid carotid artery.

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19
Q

MC initial presentation of Moya Moya in adults

A

subarachnoid hemorrhage was the most common initial

manifestation.

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20
Q

in pts with Moya Moya, EEG phenomenon in which high-voltage slow waves reappear 5 min after the end of hyperventilation is called?

A

rebuild up

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21
Q

Histology of pts with Moya Moya

A

The adventitia, media, and internal
elastic laminae of the stenotic or occluded arteries were
normal, but the intima was greatly thickened by fibrous
tissue

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22
Q

Theories on the origin of the rete mirabile

A

congenital vascular malformation (i.e., a
persistence of the embryonal network) or a rich collateral
vascularization secondary to a congenital hypoplasia,
acquired stenosis, or occlusion of the internal carotid
arteries early in life.

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23
Q

Tx of Moya Moya

A

transplantation of a vascular muscle flap,
omentum, or pedicle containing the superficial temporal
artery to the pial surface of the frontal lobe temporal pial
synangiosis with the idea of creating neovascularization
of the cortical convexity

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24
Q

The term has come to denote a widespread degeneration of cerebral white matter having a vascular causation and observed in the context of hypertension, atherosclerosis of the small blood vessels, and multiple strokes.

A

Binswanger Disease

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25
Q

Imaging feature of Binswanger

A

leukoaraiosis describes the imaging appearance
of hypointense periventricular tissues, presumably
damaged by chronic ischemia

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26
Q

Clinical features of Binswanger

A

Dementia, a pseudobulbar state, and a gait disorder,
alone or in combination, are the main features of
Binswanger cases

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27
Q

A process with an imaging appearance of large confluent
cerebral white matter changes, somewhat similar to
Binswanger leukoencephalopathy, has been identified
as an autosomal dominant familial trait linked in several
families to a missense mutation on chromosome 19.

A

Fa m i l i a l Su bcortica l I nfarction

CADASI L a n d CARAS I L

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28
Q

A syndrome of early alopecia and lumbar spondylosis
with the white matter changes typical of CADASIL has
been identified as a recessively inherited disease _______________

A

(cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy [CARASIL])

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29
Q

Mutation associated with Binswanger

A

missense change on
chromosome 19 of the NOTCH 3 gene, in the same locus
as the gene for familial hemiplegic migraine

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30
Q

Biopsy of Binswanger disease

A

eosinophilic inclusions in the arterioles of a skill

biopsy

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31
Q

Mutation associated with CARASIL

A

HTAR1 gene

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32
Q

Result of HTAR1 gene mutation

A

fragmentation and duplication of the internal elastic

lamina of cerebral vessels with narrowing of their lumens

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33
Q

MC cause of inherited deficiencies of naturally

occurring anticoagulant factors as a cause of stroke

A

heterozygous mutations
in the genes encoding proteins in the clotting cascade
(antithrombin III, proteins S and C) and from those that
disturb clotting balance (resistance to activated protein C,
or factor V Leiden mutation, and prothrombin mutations
as well as excess factor VIII)

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34
Q

___________ in young women with an established history of migraine as a risk for strokes, most of which occurred in the posterior circulation

A

prolonged

aura

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35
Q

women who take oral
contraceptives in the childbearing years-particularly if
they are _________, _________, ________, _____________–are at increased risk of
cerebral infarction

A

older than 35 years of age and also smoke, are

hypertensive, or have migraine

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36
Q

The vascular lesion underlying cerebral

thrombosis in women taking oral contraceptives consists of__________

A

nodular intimal hyperplasia of eccentric distribution with increased acid mucopolysaccharides and replication of the internal elastic lamina.

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37
Q

The use of ________ has not been associated with stroke as far as can be currently determined

A

progestin-only

pills or of subcutaneously implanted capsules of progestin

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38
Q

The risk of both
cerebral infarction and intracerebral hemorrhage appears
to be mainly in the________ period after delivery rather
than during the pregnancy itself

A

6-week

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39
Q

The occurrence of ________ embolus is always a
consideration in pregnancy because of a tendency to form clots in the pelvic and leg veins, coupled with increased right heart pressures

A

paradoxical

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40
Q

Atherosclerotic
plaques may be dislodged during ________ and are an important source of cerebral
emboli.

A

cross-clamping of the

proximal aorta

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41
Q

Frequency of stroke depending on location

A

(1) the putamen and adjacent internal capsule (SO percent);
(2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension);
(3) the thalamus;
(4) one or the other cerebellar hemisphere;
and (5) the pons

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42
Q

Phagocytosis of red cells begins within 24 h, and hemosiderin is first observed around the margins of the clot in ________

A

5 to 6 days

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43
Q

The _________ the appearance of contrast within the
hemorrhage during CT angiography, is associated with a
high rate of hematoma expansion

A

“spot sign,”

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44
Q

As _______ and _______ form, the hematoma signal becomes bright on Tl-weighted images and dark on T2

A

deoxyhemoglobin and

methemoglobin

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45
Q

The hypertensive vascular lesion that leads t o arteriolar
rupture in most cases appears to arise from an arterial
wall altered by the effects of hypertension, i.e., the change referred to in a preceding section as ______ and _________

A

segmental lipohyalinosis and the false aneurysm (microaneurysm)

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46
Q

The immediate prognosis for large and medium-sized
cerebral clots is grave; some _______ percent of patients
die in 1 to 30 days.

A

30 to 35

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47
Q

Scoring system for ICH

incorporates the patient’s age, size and location of hematoma, the presence of preexisting cognitive impairment, and Glasgow Coma score

A

FUNC

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48
Q

Scoring system for ICH

uses GCS, volume, presence of intraventricular hemorrhage, the location-supra- or infratentorial, and age above or below 80 years

A

ICH

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49
Q

Target Osm and serum Na in ICH Tx

A

osmolality kept at 295 to 305 mOsm/L and Na at 145 to

150 mEq

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50
Q

Findings of the STITCH Trial

A

failed to show a benefit from early surgery on survival or

neurologic functioning at 6 months.

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51
Q

Hematomas that are _______or more in largest diameter,
especially if located in the vermis, pose the greatest risk,
and some surgeons have recommended evacuation of
lesions of this size no matter what the clinical status of the
patien

A

4 em

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52
Q

They take the form of small, thin-walled blisters
protruding from arteries of the circle of Willis or its
major branches

A

“berry” aneurysms.

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53
Q

aneurysmal process is initiated by focal destruction
of the__________ which is produced
by hemodynamic forces at the apices of bifurcations

A

internal elastic membrane,

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54
Q

4 MC sites of aneurysms

A

(1) the proximal portions of the anterior communicating artery,
(2) at the origin of the posterior communicating artery
from the stem of the internal carotid,
(3) at the first major bifurcation of the middle cerebral artery, and
(4) at the bifurcation of the internal carotid into middle and anterior cerebral arteries.

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55
Q

Aneurysms of the carotid artery that rupture in the

cavernous sinus give rise to an ______

A

arteriovenous fistula

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56
Q

The
_______ is caused by a septic embolus that
weakens the wall of the vessel in which it lodges, almost
always at a site in a distal cerebral vessel, well beyond the
circle of Willis.

A

mycotic aneurysm

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57
Q

Fusiform deformities are
also referred to as _________, as they frequently
show atheromatous deposition in their walls, but
it is likely that they are at least partly developmental in
nature.

A

arteriosclerotic aneurysms

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58
Q

MC syndrome of SAH at the onset

A

severe generalized headache develops in the same
instantaneous manner but the patient remains relatively
lucid with varying degrees of stiff neck-the most common
syndrome

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59
Q

Percentage of Sz in SAH

A

Convulsive seizures, usually brief and generalized,

occur in 10 to 25 percent

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60
Q

An aneurysm on the posteroinferior
or anteroinferior cerebellar artery may cause unilateral
______ or _______

A

occipital or cervical pain

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61
Q

approximately_______ percent
of patients with aneurysmal rupture will not have an
aneurysm evident.

A

5 to 10

62
Q

Patients with the typical clinical picture of spontaneous
subarachnoid hemorrhage in whom an aneurysm
or arteriovenous malformation cannot be demonstrated
angiographically have a distinctly _______prognosis than
those in whom the lesion is visualized

A

better

63
Q

T or F

MR1 detects most aneurysms of the basal vessels and
of their first branches but may not yet be of sufficient
sensitivity to replace CT or conventional angiography in
cases where an aneurysm is strongly suspected but too
small to be detected by MRA

A

T

64
Q

Delayed and subacute hydrocephalus as a result of
blockage of the CSF pathways by blood may appear after
_______

A

2 to 4 weeks

65
Q

smoothsurfaced,
sharply outlined collections of blood that cover
the retinal vessels-preretinal or subhyaloid hemorrhages. What is this syndrome?

A

Terson syndrome

66
Q

ECG changes associated with SAH

A

The ECG changes include symmetrically large peaked T waves (“cerebral T waves”) and other alterations, suggesting subendocardial or myocardial ischemia.

67
Q

Reasons of volume contraction in SAH

A

bed rest, but sodium loss, probably
resulting from the release of atrial natriuretic factor
(ANF), a potent oligopeptide stimulator of sodium loss in
renal tubules, may also be a factor

68
Q

In the hands of experienced anesthesiologists and cerebrovascular surgeons, the operative mortality, even in grades III and IV patients, has now been reduced to _________percent

A

2 to 3

69
Q

the International Subarachnoid Aneurysm Trial Group randomly assigned more than 2,000 patients
to surgery or coil deployment; the overall rate of death or
dependence at 1 year was ______percent in the endovascular group and _____ percent in the operated group

A

24

31

70
Q

Risk of rupture for unruptured aneurysm is dependent on:

A

size

71
Q

Size of Giant Cerebral Aneurysm

A

> 2.5cm

72
Q

Mechanism of enlargement of giant aneurysms

A

They grow slowly by accretion of blood clot
within their lumens or by the organization of surface
blood clots from small leaks

73
Q

duration of abx for Mycotic aneurysm

A

6 weeks

74
Q

An___________ consists of a
tangle of dilated vessels that form an abnormal communication
between the arterial and venous systems

A

arteriovenous malformation (AVM)

75
Q

In AVM, blood. The tangled blood vessels
interposed between arteries and veins are abnormally
________

A

thin and do not have the structure of normal arteries or

veins

76
Q

The two lesions-AVM and saccular aneurysm
(on the main feeding artery of the A VM)-are associated in
approximately _______ percent of case

A

5%

77
Q

Onset of sx for AVM

A

between 10 and 30 years

78
Q

When the vein of Galen is enlarged as a
result of drainage from an adjacent AVM,_______
may result, particularly in children

A

hydrocephalus

79
Q

A systolic bruit
heard over the ______ in the neck or over the ______
process or the eyeballs in a young adult is suggestive of
an AVM.

A

carotid

mastoid

80
Q

The summed score gives guidance as to the difficulty in
surgical removal and has a less certain relationship to
the clinical behavior of the lesion. What scoring system for AVM?

A

Spetzler and Martin

81
Q

Factors increasing risk of bleeding for AVM

A

deep location of the AVM or deep venous drainage channels, and mostly, a previous hemorrhage

82
Q

Rate of re-bleeding in AVM

A

The rate of rebleeding in most series has been

2 to 4 percent per year over decades but may be as high as 6 to 9 percent in the year after a first hemorrhage

83
Q

The combination of a prolonged history of
_____________ in Adams’
series almost always indicated a large malformation

A

headaches, seizures, and a progressive deficit

84
Q

T or F

The weight of evidence
suggests that the risk is raised by pregnancy alone in AVM

A

F

85
Q

Arteriography is usually necessary to establish the diagnosis
with certainty and will demonstrate AVMs larger
than ____ mm in diameter

A

5

86
Q

In AVM,

Grades_____ are generally not resected;

grade ________ lesions may be approached surgically
but often with preceding interventional embolization
of parts of the lesion

A

IV and V

III

87
Q

Some _________percent of AV Ms
are amenable to block dissection, with an operative
mortality rate of 2 to 5 percent and a morbidity of 5 to
10 percent

A

20 to 40

88
Q

This
approach is utilized most often with A VMs of 3 em or
smaller located in an area of the brain in which resection
would be likely to produce a serious neurologic disability.

A

radiosurgery

subnecrotizing stereotactically directed proton radiation

89
Q

The main drawback to “radiosurgery”

is that obliteration of AVMs occurs in ______

A

a delayed manner, usually with a latency of at least 18 to 24 months after treatment, during which the patient is unprotected from rebleeding

90
Q

In radiosurgery,

After 2 years, ________ percent of AV Ms smaller than 2.5 em in diameter have been obliterated

A

75 to 80

91
Q

Cx of RT

A

The first
is delayed radiation necrosis, which is predictable based
on the radiation dose, and the second is venous congestion
that occurs several weeks or months after treatment

92
Q

Radiation necrosis may be reduced
by the administration of ________but the vascular
problem generally is not helped

A

corticosteroids

93
Q

The defining features
are radiologic-a nidus of abnormal arteries and veins
with arteriovenous shunting contained entirely within
the leaflets of the dura.

A

D u ra l Arteriovenous Fistu l a

94
Q

In DAVF,

The lesion is usually fed by dural arterial vessels derived from the internal cranial circulation and often, more prolifically, from the external cranial circulation (_______ and______

A

external carotid artery and muscular

branches of the vertebral artery).

95
Q

The ________ through dural fistulas accounts

for the early opacification of the draining venous structures

A

rapid transit of injected angiographic dye

96
Q

The best-defined examples of acquired
fistulas are those that arise adjacent to a_________ or in association with a ________, most
often of the transverse sigmoid sinus or adjacent to the
cavernous sinus.

A

venous sinus thrombosis

vascular atresia

97
Q

Presentation of DAVF

A

Subdural hemorrhage is an infrequent but dramatic
mode of presentation, sometimes creating a large and
fatal clot; another syndrome is a cerebral-subarachnoid
hemorrhage, although this occurs with not nearly the
same frequency or severity as bleeding from brain
AVMs

98
Q

Tx of DAVF

A

Treatment is by surgical extirpation or endovascular
embolization, at times a painstaking procedure because
of the multitude of potential feeding vessels

99
Q

Cx of high flow DAVF especially in children

A

the high-flow lesions may shunt so much

blood as to cause congestive heart failure, similar to arteriovenous malformations of the vein of Galen.

100
Q

Vascular malformations composed mainly o f clusters
of thin-walled veins without important arterial feeders
and with little or no intervening nervous tissue make
up a significant group, some 7 to 8 percent of AVMs

A

Cavernous Ma lfo rm ations (Cavern o m a )

101
Q

In Cavernomas, The incidence of bleeding is uncertain but is estimated to be __________ per year per lesion but quite often they are multiple lesions so that the cumulative risk in
any one patient is higher

A

less than 1 percent

102
Q

Risk of bleeding in cavernomas

A

0.3 percent annually for
asymptomatic lesions and found that individuals who
had a previous episode of bleeding or had more than
one lesion were 2.5 times more likely to have another
hemorrhage.

103
Q

In Cavernomas,

approximately 10 percent of these lesions
are multiple and _______ percent are familial

A

5

104
Q

MRI of cavernoma

A

which discloses a cluster of vessels surrounded by

a zone of hypodense ferritin in the T1-weighted images

105
Q

About one-half of all cavernous angiomas lie in the
________ and in the past (before the availability of MRI),
many of them were misdiagnosed as multiple sclerosis
because of the stepwise accumulation of neurologic deficits with each hemorrhage

A

brainstem,

106
Q

Cavernous angiomas on the surface of
the brain, within reach of the neurosurgeon, even those
in the brainstem, can be________
with low morbidity and mortality

A

plucked out like blackberries,

107
Q

This i s perhaps the most common cerebral vascular malformation, estimated to occur in almost 3 percent of large autopsy series

A

D e e p ( Deve l o p m e nta l ) Ve n o u s A n o m a l y

108
Q

The defining characteristics are of a caput medusa draining into a small collecting vein. The draining vein itself is often visualized most easily and fills with contrast concurrently with normal cerebral

A

D e e p ( Deve l o p m e nta l ) Ve n o u s A n o m a l y

109
Q

When the bleeding is precipitated
by warfarin therapy, treatment with ________, _________, _________ and similar products, which contains
clotting factors, is recommended.

A

fresh-frozen
plasma and vitamin K, sometimes prothrombin complex
concentrate (PCC)

110
Q

In the elderly, ________ appears to be a
major cause of lobar bleeding, especially if hemorrhages
appear in succession or are multiple

A

amyloid angiopathy

111
Q

Greenberg and colleagues found that _________
the same marker that is overrepresented in Alzheimer
disease, is associated with severe amyloid angiopathy
and a risk of intracerebral hemorrhage, but others have
found an association with the E2 allele

A

apolipoprotein E4,

112
Q

Primary intraventricular
hemorrhage, a rare event in adults, can sometimes
be traced to a __________ and _________ or one of the choroidal arteries

A

vascular malformation or neoplasm of

the choroid plexus

113
Q

Multiple small hemorrhages, brain “microbleeds,”
are most commonly considered to be the result of _________ , but may
also be associated with_____

A

vascular amyloid

chronic hypertension

114
Q

The pathologic entity called brain purpura (pericapillary
encephalorrhagia), incorrectly referred to as _____________consists of multiple petechial
hemorrhages scattered throughout the white matter

A

“hemorrhagic

encephalitis,”

115
Q

In hemorrhagic encephalitis

The lesions in brain purpura are
small, 0.1 to 2.0 mm in diameter, and are confined to the
white matter, particularly the ____,________,______

A

corpus callosum, centrum

ovale, and middle cerebellar peduncles

116
Q

This angiopathy consists of the deposition of amyloid in
the media and adventitia of small vessels, predominantly
in the meninges, cortex, and cortical penetrating vessels

A

CAA

117
Q

There is a separate familial amyloidotic condition of
diffuse white matter degeneration with dementia, associated
in some families with calcification in the occipital
lobes, and the aforementioned mutations in the _______
gene cause a disruption of the small vessel wall that can
cause small cerebral hemorrhages that are similar to those
of cerebrovascular amyloid

A

COL4A

118
Q

_________ is the term applied to a relatively
rapidly evolving syndrome of severe hypertension
in association with headache, nausea and vomiting, visual disturbances, confusion, and-in advanced cases-stupor and coma.

A

Hypertensive encephalopathy

119
Q

MRI findings of HPN encephalopathy

A

bilateral increase in T2 signal intensity in the
white matter on .MRI and a corresponding reduced density
on CT, usually concentrated in the posterior part of
the hemispheres

120
Q

Hypertensive encephalopathy and eclampsia may
cause _________. Most such cases are
not caused by the rupture of an intracranial aneurysm

A

subarachnoid hemorrhage

121
Q

Pathophysio of brain edema in HPN encephalopathy

A

The brain edema is the result of active exocytosis of water rather than simply a passive leak from vessels subjected to high pressures

122
Q

Target BP for HPN Enceph

A

a safe target is a pressure of 150 / 1 00 mm Hg

or a 20 percent reduction in mean pressure

123
Q

Anti-HPN for HPN enceph

A

intravenous sodium nitroprusside, 0.5 to 0.8 mg/kg/min;
a calcium channel blocker such as nifedipine, 10 to 20 mg
sublingually;
or intravenous beta-adrenergic blockers (labetalol, 20 to 40 mg intravenously followed by an infusion at 2 mg/min, or esmolol are favored)

124
Q

This type of vasculopathy is produced by sympathomimetic
drugs alone, such as ephedra in health food
supplements, phenylpropanolamine, pseudoephedrine,
methamphetamine, and cocaine

A

DIFFUSE CEREBRA L VASOSPASM
( R EVERSIBLE CERE BRAL
VASOCONSTRICTIO N SYN DROM E [RCVS],
CALL-FLE M I N G SYN DROM E)

125
Q

Most feared cx of Giant Cell Arteritis

A

Occlusion of branches of the ophthalmic
artery (mainly those to the posterior ciliary artery
and the choroidal circulation that supply the anterior
optic nerve) results in blindness in one or both eyes, is the most feared complication, often unpredictably

126
Q

In Giant Cell Arteritis, The administration of prednisone, ____________provides striking relief of the headache and polymyalgic symptoms within days and sometimes within hours, and also prevents blindness.

A

50 to 75 mg/ d,

127
Q

This i s a nonspecific chronic arteritis involving mainly
the aorta and the large arteries arising from its arch. It
is similar in some ways to giant cell arteritis except for
its propensity to involve the proximal rather than the
distal branches of the aorta.

A

Ta kayasu D i sease ( “ P u l se l ess D i sease “ )

128
Q

Mechanism of Takayasu

A

The etiology has never been ascertained

but an autoimmune mechanism is suspected

129
Q

Arteries involved in Takayasu

A

brachiocephalic, subclavian, carotid, vertebral,
and other arteries that may be asymptomatic or
cause neurologic ischemic symptoms

130
Q

Pathology of Takayasu

A

periarteritis
of the large vessels, often with giant cells and reparative
fibrosis.

131
Q

_______when injected intravenously more so than when
used intranasally, is prone to cause cerebral hemorrhage
as a result of acute hypertension, similar to the bleeding
that may be precipitated by other sympathomimetic
drugs such as amphetamine and phenylpropanolamine

A 
cocaine hydrochloride (the usual form of ingestible
cocaine)
132
Q

The strokes

with crack cocaine, however, are more often _______

A

ischemic,

typically involving the territory of a large vessel

133
Q

Crack cocaine may also cause a _____________ not unlike that associated with
antiphospholipid antibody but generalized rather than
focal

A

choreiform disorder

(“crack dancing”),

134
Q

This i s yet another poorly understood form of vasculitis,
consisting of a microangiopathy affecting mainly the brain
and retina. Psychiatric symptoms, headache, dementia,
sensorineural deafness, vertigo, and impairments of vision
are the clinical manifestations

A

S u sac Sy n d ro m e

135
Q

In Susac syndrome, The MRI may show characteristic white

matter lesions, particularly in the ____

A

corpus callosum

136
Q

The administration of drugs such as _____, ________, and _______ and even the hypercoagulable
reaction to heparin that is associated with
thrombocytopenia have all been cited as risks for cerebral venous thrombosis

A

tamoxifen,

bevacizumab, and erythropoietin,

137
Q

Thrombosis of the vein
of Labbe causes infarction of the underlying________ and occlusion of the vein of Trolard implicates
the _______

A

superior temporal lobe,

parietal cortex

138
Q

Increased intracranial pressure without ventricular

dilatation occurs with thrombosis of the :

A

superior sagittal
sinus, the main jugular vein, and the transverse sinus or
the confluence of the sinuses

139
Q

Once a venous thrombosis
becomes established for several days or longer, the tributary
surface veins take on a ________appearance that is
appreciated on the venous phase of an angiogram

A

“corkscrew”

140
Q

In Cavernous sinus thrombosis, Also involvement of the _________
may be accompanied by a fifth nerve palsy

A

superior petrosal sinus

141
Q

Occlusion of the ______ and ______ is the least common and clinically most obscure of
the venous syndromes

A

vein of Galen and of the internal cerebral

veins

142
Q

the overall mortality rate
remains high, with large hemorrhagic venous infarctions
found in ______ percent of cases

A

10 to 20

143
Q

Sterile vegetations, referred to also as ___________, consist of fibrin and platelets and are loosely attached to the mitral and aortic valves and contiguous endocardium

A

nonbacterial thrombotic endocarditis

144
Q

The essential pathologic change in ______ is the occurrence
of widespread fibrin thrombi in small vessels,
resulting in numerous small infarctions of many organs,
including the brain

A

DIC

145
Q

Ab associated with APAS

A

l upus an ticoagulant and

anticardiolipin

146
Q

The most frequent neurologic abnormality in APAS is a TIA,
often taking the form of ________`, with or without retinal arteriolar or
venous occlusion

A 
amaurosis fugax (transient monocular
blindness)
147
Q

The _______`is an arteriopathy producing
deep blue-red skin lesions of livedo reticularis and
livedo racemosa in association with multiple ischemic
strokes. Many, but not all, patients have high titers of
antiphospholipid antibodies

A

Sneddon syndrome

148
Q

In APAS asscoiated strokes, Warfarin, the definitive therapy, alters the testing for antibodies and several guidelines recommend confirming the presence of antibodies after_______ before starting treatment

INR must be maintained close to _______for
effective prevention of stroke

A

an interval of two weeks

3

149
Q

T or F

in APAS

Aspirin, on uncertain grounds, is thought
not to confer protection for stroke

A

T

150
Q

T or F

in APAS

In “catastrophic” cases
with repetitive strokes, intravenous immunoglobulin and
plasma exchange have been used with some effect

A

T

Neurology - Physiology (44 decks)

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