Ischemic Conditions
- Transient
Ischemic Attacks (TIAs)
- reversible
episodic focal neurologic deficit of less than 24 hours duration
- Usually
represents embolic disease
- Sources:
- Carotid
disease, AFIB, cardiac clot, cardiac valve vegetations, atrial nyxoma
- Diagnosis:
- Carotid
doppler studies frequently show stenosis
- Cerebral
angiogram remains definitive study
- ECHO to
r/o cardiac disease
- Recommend
a contrasted head CT to r/o acute stroke
- Treatment:
- Patients
with clear evidence of ongoing embolic episodes must be anticoagulated
and volume expanded to prevent further episodes while work-up
progressing (goal PTT 45-50)
- Anticoagulation
has been shown to be effective in preventing strokes in patients with
AFIB
- If long-term
anticoagulation is treatment, coumadin is given to attain PT 18-20
- In
patients with carotid disease, treatment is carotid endarterectomy vs.
anticoagulation
- CEA
provides significant protection against subsequent ipsilateral cerebral
ischemia in patients with high-grade stenosis, the benefits of which are
realized early and persist over extended periods of time
- Atherosclerotic
stenosis –
usually at ICA bifurcation or distal basilar
- Carotid
endarterectomy should be done if stenosis greater than 70% in symptomatic
patient; if ACA/AComm/PCA open, no need for shunt
- Most
patients undergoing CEA ultimately die of MI
- Venous
Thrombosis
– most frequently affects SSS, followed by transverse sinus; also sigmoid,
cavernous
- 25%
mortality
- causes
changes in white matter
- associated
with dehydration, pregnancy, infection, hypercoagulable state (such as
tumor, contraceptives, lupus anticoagulant, etc.)
- Moya
moya – due
to stenosis and eventual occlusion of distal ICA/proximal MCA (intimal
thickening/fibrosis)
- Disease of
occlusions of the vessels of the circle of Willis
- Enlarged
lenticulostriate and thalamoperforating collaterals
- Most
have stroke and cerebral atrophy
- Two
peaks in age of presentation: <10 years (juvenile form) and 3rd
decade (adult form)
- 3:2
female to male predominance
- Some
cases are congenital (12% Japanese cases have strong familial tendency)
- Presentation:
- Hemorrhagic,
epileptic, ischemic with infarction, and transient ischemic attacks
(TIAs)
- Juvenile
form typically presents with ischemic symptoms (weakness)
- Adult
form typically presents with intracranial hemorrhage (SAH)
- Diagnosis:
- Angiogram
shows stenosis or occlusion at the termination of the internal carotid
at origin of MCA/ACA with appearance of an abnormal vascular network (“puff
of smoke”) due to dilatation of collateral sin the basal ganglion region
and transdural anastomosis formation (rete mirabile)
- Treatment:
- Surgical
revascularization if progressive symptoms
- Encephalomyogynangiosis,
superficial temporal – MCA anastomosis
- Encephaloduroarteriosynangiosis
– superficial temporal artery attached to dura, forms perforators
- Prognosis:
- Juvenile
form – 3% mortality
- Adult
form – 11% mortality (mainly due to ICH)
- Sickle
cell disease
– stroke (endothelial injury leads to vascular degeneration); aneurysms in
unusual locations
- Marfan’s
syndrome –
large vessel vasculopathy
- Ehlers-Danlos – vascular fragility (CCF,
arterial narrowing)
- Fibromuscular
dysplasia
– segmental noninflammatory narrowing of arteries due to degeneration of
elastin/muscle in wall of artery and replacement with fibrous tissue
- F>M,
middle age
- 75%
involve anterior circulation, 25% posterior; 75% bilateral; 20% risk of
aneurysm
- 2nd
most frequent angiographic carotid lesion
- Incidence
is approximately 3%
- Location:
- Internal
carotid artery, typically 2-2.5 cm. above bifurcation
- 65% of
cases are bilateral
- Occasionally
occurs in vertebral or intracranial circulation
- Diagnosis:
- Angiogram
shows alternating areas of narrowing and outpouchings, focal or tubular
narrowing, and occasional diverticulum (“string of beads” appearance)
- Treatment:
- No
intervention unless symptomatic
- Appears
to have a benign natural history
- Vasculitis
- Infection
– H.flu, TB, actinomycosis, HSV, syphilis, endocarditis (10% risk due to
mycotic aneurysms)
- Immune
complex vasculitis
- Polyarteritis
nodosa (most common in CNS) – small to medium vessels (obliteration of
vaso vasorum); sometimes produces mononeuropathy multiplex;
microaneurysms, stenosis, skin purpura, renal dysfunction
- Lupus –
75% involve nervous system (myopathy, peripheral neuropathy, strokes
from antiphospholipid antibody, hemorrhage from coagulopathy,
Liebman-Sachs endocarditis) – lupus vasculitis is rare
- Cell
mediated vasculitis
- temporal
arteritis (elderly, M>F); extracranial circulation (ophthalmic);
giant cells seen in all three layers; resorption of internal elastic
lamina
- Takayasu
(occlusive giant cell arteritis, pulseless disease) – fever, weight
loss, increased ESR
- Wegener’s
– M>F, respiratory/renal problems, peripheral/central neuropathy,
anti-neutrophil antibody
- Chemical
– ergot drugs, pseudoephedrine, contraceptives
- Sarcoid
- Kawasaki – fusiform ectasia/aneurysm
- Bueger’s
disease (thromboangiitis obliterans) – small to medium vessels
- Behçet's
disease – involves veins as well as arteries; also oral/genital ulcers,
uveitis, ulcerative colitis, erythema nodosum, polyarteritis,
thrombophlebitis; arterial occlusions and aneurysms seen
- TTP –
small vessels
- Hypertensive
disease
- Acute –
endothelial pinocytosis, breakdown of blood brain barrier
- Chronic
– dilated perivascular spaces in centrum ovale/basal ganglia;
lipohyalinosis
- Binswanger’s
disease –
hypertensive dementia; lacunae in centrum ovale
- Preeclampsia – hypertension and
proteinuria; seen in 5-10% of pregnancies; 1% of these have eclampsia (cerebral
edema/seizures/deep hemorrhage/white matter changes)