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Cerebrovascular disease and risk of stroke
Submitted by Dr. Yasser
Mokhtar, MD. Dept. of internal medicine. School of
medicine, University of South Dakota.
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Stroke is a loss of cerebral
function with symptoms lasting >24 hrs or death due to vascular
disease |
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Causes of stroke
I. Cerebral infarction and ischemia:
Cerebral infarction and ischemia is caused by sudden occlusion of
an artery supplying the brain, or, less often, by low flow distal to an already
occluded or highly stenosed artery. Occlusion or stenosis can be the result of
disease of the arterial wall, embolism from the heart, hematologic disorders and
various rare but sometimes treatable conditions which are proportionately more
common in young stroke patients (where degenerative arterial disease is unusual)
but which can still be a cause of stroke in the elderly. Infarction originates
as a result of an impediment to normal perfusion that usually is caused by
atherosclerosis and coexisting thrombosis. Embolism occurs when a particle of a
thrombus originating from a proximal source (arterial, cardiac or transcardiac)
travels through the vascular system and leads to a distal occlusion.
Ia. Arterial wall disorders:
1. Atherothromboembolism: Atheroma is by far the commonest arterial
disorder and when complicated by thrombosis or embolism, is the most frequent,
but by no means only, cause of cerebral ischemia and infarction. Atheroma mainly
affects large (e.g. aortic arch) and medium sized arteries at places of arterial
branching (e.g. carotid bifurcation), tortuosity (e.g. carotid siphon) and
confluence (e.g. the basilar artery) (Ross et al., 1988 and Amarenco et al.,
1992).
These are sites of hemodynamic sheer stress and thus endothelial trauma,
boundary layer separation and blood stagnation, or turbulence, all of which are
likely to promote thrombosis (Motomiya and Karino 1984 and Reneman et al.,
1985).
Atheroma starts in children, perhaps as a response to endothelial injury
(Ross 1986).
Initial fatty streaks appear first and over many years, smooth muscle cells
proliferate in them, macrophages invade, fibrosis occurs and intra- and
extracellular cholesterol and other lipids are deposited, so forming fibrolipid
plaques. Often there is necrosis and calcification in the advanced lesions.
These plaques invade the media, gradually spread out around and along the
arterial wall, and narrow the lumen. They are complicated by platelet adhesion,
activation and aggregation which initiate blood coagulation and subsequent mural
thrombosis (Verstraete et al., 1985).
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It is likely that atheromatous plaques become active from time to
time as a result of fissuring and cracking of the fibrous cap which covers the
rather rigid lesion, of the ulceration perhaps, or sometimes of hemorrhage
within the plaque rather than the more commonly found hemorrhage entering via a
crack in the endothelial surface of the artery. Any of these events exposes the
thrombogenic depths of the plaque to flowing blood and so causes thrombus to
form and then perhaps to embolize. Thus atherothromboembolism can be regarded as
an acute on chronic disease, at any one time a plaque may be static and
quiescent, slowly growing but asymptomatic or active with ongoing thrombosis and
embolization which may or may not be symptomatic depending on the depth and
duration of the consequent ischemia (Gomez 1990 and Ogata et al., 1990).
2. Intracranial small vessel disease (microatheroma): The small penetrating
arteries of the brain are not supported by a good collateral circulation, i.e.
the lenticulostriate branches of the MCA, the thalamoperforating branches of the
proximal PCA and the perforating arteries to the brain stem. Therefore occlusion
of one of these arteries is rather likely to cause infarction, in a small
restricted area of the brain. Such lacunar infarcts comprise about twenty five
per cent of the first ischemic stroke (Bamford et al., 1987) and perhaps an even
larger proportion of TIAs (Kappelle et al., 1991).
3. Trauma: Penetrating neck injuries are more likely to damage the carotid
artery than the better protected vertebral artery. Laceration, dissection and intimal tears may be complicated by thrombosis and then embolism and therefore
ischemic stroke at the time of, or some days or even weeks after the injury (Pozzati
et al 1989). Non-penetrating neck injury is a more subtle cause of ischemic
stroke because the injury may not be very severe (at least superficially) and
the stroke can be delayed by days or weeks. This can occur at any age but in
young adults it is most frequent identifiable cause of ischemic stroke in some
series (Hilton-Jones and Warlow 1985b).
4. Arterial dissection: is an increasingly recognized but none the less rare
cause of stroke. Sometimes there is a predisposing cause particularly neck
trauma, but often there is no explanation. Blood tracks along a split in the
arterial wall and there may or may not be an intimal tear so that the false
lumen is in communication with the true lumen. The artery may become occluded by
the dissection itself, thrombosis and embolism may complicate occlusive or
non-occlusive dissections and aneurysmal bulging of the weakened arterial wall
may occur (O’Connell et al., 1985).
5. Fibromuscular dysplasia (FMD): is a rare segmental disorder of small and
medium sized arteries (Luscher et al., 1987). Patients are of any age, females
are affected more than males and the cause is unknown. It usually affects more
than one artery in the same individual. The mid cervical portion of the ICA is
the most commonly affected artery to the brain. Histologically, there is
fibrosis and thickening of the arterial wall alternating with atrophy, so that
the typical angiographic appearance is likened to a string of beads. In rare
cases, there is concentric tubular narrowing of the affected segments, or
sometimes just a web at proximal ICA. FMD of some arteries to the brain may be
found in up to one per cent of routine postmortems so that any association with
cerebral ischemia or infarction may be no more than a coincidence. Occasionally,
however, it may indeed be complicated by thrombosis and embolism (Morgenlander
and Goldstein 1991).
6. Congenital arterial anomalies: Congenital arterial loops may be associated
with aneurysm formation leading to a pulsatile neck swelling, intracavitary
thrombosis and embolism (Desai and Toole 1975). Some inherited disorders of
connective tissue can present with or be complicated by arterial dissection or
even rupture, aneurysm formation and mitral leaflet prolapse e.g. Ehlers-Danlos
syndrome (Schievink et al., 1990).
7. Moyamoya syndrome: In japanese, moyamoya means haze, like a puff of smoke and
the term describes a characteristic but rare radiologically defined consequence
of stenosis or occlusion of one, or more often both, distal ICAs, frequently
with additional involvement of parts of the circle of Willis and sometimes of
the proximal cerebral and basilar arteries (Chen et al., 1988). The disorder
seems to be almost confined to the Japanese and other Asians and in most cases
the cause is unknown (Bruno et al., 1988). The syndrome presents in infancy with
recurrent episodes of cerebral ischemia and infarction, mental retardation,
headache, seizures and occasionally involuntary movements (Ikeda et al., 1991).
8. Embolism from arterial aneurysm: Embolism from thrombus within the cavity of
aneurysms must be rare and is difficult to prove in an individual case (Maruyama
et al., 1989). Of course, aneurysms may be coincidental with atherothrombosis or
a cardiac source of embolism, thus making any cause and effect relationship for
ischemic stroke something of a guess. It is far more common for intracranial
aneurysm to present with rupture and SAH (Hommel et al., 1984).
9. Binswanger’ s disease: The radiological appearance of Binswanger’ s disease
on computed tomography of the brain is more or less symmetrical periventricular
hypodensity, with or without ventricular dilatation and focal white matter
hypodensities (Inzitari et al., 1990 and Calcedo et al., 1991). It is more
frequent in hypertensive patients and in those with other vascular risk factors
(Hijdra et al., 1990 and van Swieten et al., 1991). The radiological appearance
is due to demyelination, axonal loss and gliosis, probably a consequence of
diffuse rather than focal ischemia in the distribution of the long perforating
arteries presumably rendered sclerotic by chronic hypertension, perhaps also
exacerbated by periods of hypotension as a result of cardiac failure, etc. (van
Swieten et al., 1991).
10. Inflammatory vascular disease: There are a number of inflammatory disorders
of the arterial (or venous) wall. The inflammation may provoke enough cellular
proliferation, necrosis and fibrosis to occlude the lumen, precipitate
thrombosis and then embolism, or promote aneurysm formation, dissection and even
rupture of the vessel. These vasculitic disorders may present with, or be
complicated during their course by, ischemic stroke, intracranial hemorrhage,
intracranial venous thrombosis and most often a generalized ischemic
encephalopathy (Sigal 1987). Inflammatory vascular diseases include giant cell
arteritis (Castelli et al., 1988), Takayasu’s disease (Hall et al., 1985),
systemic lupus erythematosus causing either generalized encephalopathy with
underlying vascular pathology appearing to be intimal proliferation rather than
vasculitis (Kitagawa 1990) or embolism from the heart (Libman-Sacks endocarditis)
(Devinski et al., 1988), systemic vasculitis (Ford and Sickert 1985), rheumatoid
disease (Howell and Molyneux 1988), Behcet’s disease (Sevdaroglu et al., 1989)
and isolated angiitis of the central nervous system (Hankey et al., 1991).
11. Irradiation: Excessive irradiation of the head and neck can damage intra- and extracranial arteries. Later a localized stenotic and sometimes apparently
atheromatous lesion may become symptomatic (Loftus et al., 1987).
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