HEMORRHAGIC STROKES(INTRACEREBRAL AND SUBARACHNOID HEMORRHAGE)
Approximately 15% to 20% of strokes are due to rupture
of blood vessels with intracerebral or subarachnoid
hemorrhage. The three major causes of hemorrhagic stroke
are hypertension, ruptured arterial aneurysms, and
arteriovenous malformations. Intracerebral and subarachnoid
hemorrhage are also very common in head trauma.
HYPERTENSIVE
INTRACEREBRAL HEMORRHAGE
 |
 |
| Hypertensive basal ganglionic hemorrhage |
Hypertensive pontine hemorrhage |
This
hemorrhage results from rupture of small, penetrating
arteries. Hypertensive angiopathy (
small
vessel disease) stiffens vessel walls
and makes them fragile. This, in conjunction with increased
pressure from within the lumen, causes vascular rupture
and hemorrhage. The most frequent sites of hypertensive
intracerebral hemorrhage are the
basal ganglia
and thalamus.
Less commonly, hypertensive intracerebral hemorrhage
involves the cerebellum, the pons, and occasionally
the subcortical white matter. Large intracerebral hemorrhages
cause increased intracranial pressure and carry a high
fatality rate. Improved control of hypertension in
the last 20 years has led to a dramatic reduction in
the incidence of hypertensive intracerebral hemorrhage.
ARTERIAL ANEURYSMS
 |
 |
| Berry aneurysm |
Large aneurysm at the cerebello-pontine angle |
 |
 |
| Subarachnoid hemorrhage |
Intraventricular hemorrhage |
Intracranial aneurysms (IA), also referred to as saccular or berry aneurysms, develop in the walls of major cerebral arteries at branching points, where there are gaps in the media and internal elastica. The majority of them are on the circle of Willis and the first bifurcation of the middle cerebral artery. They are multiple in 20% of the cases. Nonruptured aneurysms are seen in 2% of adult autopsies. The defects in the vessel wall are present since birth but aneurysms are rare in children; they develop later in adulthood, due to gradual weakening of vessels from the constant force of even normal blood pressure and structural changes that occur with advancing age. They are more common in women than men and occur with increased frequency in patients with coarctation of the aorta and polycystic kidney disease. Other risk factors include smoking and alcohol consumption.
Clinical observations have established a familial incidence of IAs. A small proportion are inherited as an autosomal dominant trait and are linked to several genes and chromosomal loci, including some that encode collagen and other structural proteins that are found in vessel walls. There is an increased risk in first degree relatives of patients with aneurysms.
Large IAs can cause symptoms by compressing cranial nerves, vessels, and brain tissue but their most feared complication is rupture. The vessels bearing the aneurysms are in the subarachnoid space. Consequently, their rupture causes subarachnoid
hemorrhage (SAH). Blood spurts out of the ruptured aneurysm with a force that can tear the soft brain. If the stream of blood is directed toward the brain, it may cause intracerebral and intraventricular hemorrhage. The larger the aneurysm, the higher is the likelihood of rupture.
Typically, SAH from
a ruptured IA causes a sudden
severe headache with relative preservation
of consciousness and without focal neurological
deficits. Approximately one week later, vascular
spasm develops, causing additional ischemia. Vasospasm
affects arteries that are surrounded by subarachnoid
blood clots and is triggered by products released
form hemolyzed RBCs. A massive aneurysmal bleed raises
intracranial pressure, resulting in arrest
of cerebral perfusion, unconsciousness, and HIE. Hydrocephalus may
develop due to blockage of CSF flow by subarachnoid
clots and from meningeal fibrosis, which results
from their organization. About half of patients
with aneurysmal bleeds die in six months, some
from the first and most from recurrent bleeds.
Survivors have serious long-term disabilities
and a significant risk of rebleeding.
Fusiform aneurysms are vascular dilatations
due to atherosclerosis. They are seen most commonly in the basilar artery
and are associated with thrombosis and brainstem infarction and less frequently
with rupture and subarachnoid hemorrhage.
ARTERIOVENOUS MALFORMATIONS (AVMs)
 |
 |
| Arteriovenous malformation |
Arteriovenous malformation |
AVMs are developmental abnormalities of cerebral
vessels. They consist of a tangle of abnormal vessels
interposed between a feeding artery and a draining
vein. Most AVMs are in the distribution of the middle
cerebral artery but they may occur anywhere. In addition
to classical AVMs, there are several other related
types of vascular anomalies and hamartomas that have
similar manifestations. The abnormal vessels may be
in brain tissue, in the subarachnoid space, or both.
AVMs and other vascular anomalies cause seizures and
neurologic deficits due to chronic compression and
ischemia of brain tissue. Their most feared outcome
is
intracerebral
and subarachnoid hemorrhage. There may be multiple
episodes of bleeding over many years (sometimes since
childhood) manifested by headaches, a single catastrophic
bleed, or both. Patients with AVMs also have an increased
incidence of aneurysms. A related vascular lesion,
cerebral
cavernous malformation (CCM), consists
of clusters of cavernous vessels without intervening
stroma. CCMs are dominantly inherited and may be
multiple. They cause recurrent hemorrhage and seizures.
OTHER
CAUSES OF HEMORRHAGIC STROKE
 |
 |
| Cerebral amyloid angiopathy |
Lobar hemorrhage |
One of the most frequent causes of intracerebral hemorrhage
is anticoagulants therapy.
The incidence of anticoagulant-associated intracerebral
hemorrhage has increased markedly in recent years,
following the increasing use of warfarin. Less frequently,
intracerebral and subarachnoid hemorrhage is caused
by
cerebral
angiitis (polyarteritis
nodosa, granulomatous arteritis, SLE, bacterial arteritis)
and
cerebral
amyloid angiopathy (CAA). Most
CAA cases are sporadic but there are several familial,
autosomal dominant, forms also. The amyloid peptide
in sporadic CAA is beta amyloid, and most of these
patients also have Alzheimer's disease (AD). Some
of the familial CAAs are caused by mutations of the
beta amyloid precursor protein gene on chromosome
21 and these patients also have beta amyloid deposition
and autosomal dominant AD. Other familial CAAs are
caused by mutations of other genes. These patients
do not have AD and the vascular amyloid has a different
chemical composition. Amyloid deposition
causes leptomeningeal and cortical vessels to become
fragile, resulting in hemorrhages, especially in
the subcortical white matter (
lobar
hemorrhages). CAA also causes ischemic infarcts
and leukoencephalopathy (see also
small
vessel disease).
Other angiopathies (Ehlers-Danlos syndrome,
homocystinuria, amphetamine vasculitis) and genetic or acquired coagulopathies
and platelet disorders may also cause hemorrhagic strokes.
Further reading:
Nahed BV, Bydon M, Ozturk AK,
et al. Genetics of intracranial aneurysms. Neurosurgery.
2007;60:213-25.
PubMed
Flaherty ML, Kissela B, Woo D, et al. The increasing
incidence of anticoagulant-associated intracerebral
hemorrhage. Neurology
2007;68:116-21. PubMed
Updated: December, 2008