Intraparenchymal hemorrhage is one extension of intracerebral hemorrhage)
with bleeding within brain parenchyma. Intraparenchymal hemorrhage accounts for
approx. 8-13% of all strokes and results from a wide spectrum of disorders. It is
more likely to result in death or major disability than ischemic stroke or
subarachnoid hemorrhage, and therefore constitutes an immediate medical
emergency. Intracerebral hemorrhages and accompanying edema may disrupt or
compress adjacent brain tissue, leading to neurological dysfunction. Substantial
displacement of brain parenchyma may cause elevation of intracranial pressure
and potentially fatal herniation syndromes.
Pathophysiology Nontraumatic intraparenchymal hemorrhage
most commonly results from hypertensive damage to blood vessel walls e.g.: -
hypertension - eclampsia - drug abuse, but it also may be due to autoregulatory
dysfunction with excessive cerebral blood flow e.g.: - reperfusion injury -
hemorrhagic transformation - cold exposure - rupture of an aneurysm or
arteriovenous malformation - arteriopathy - altered hemostasis -
hemorrhagic necrosis - venous outflow obstruction. Nonpenetrating and
penetrating cranial trauma can also be common causes of intracerebral
hemorrhage. Physical Symptoms
Clinical manifestations of intraparenchymal hemorrhage are
determined by the size and location of hemorrhage, but may include the
following: Hypertension, fever, or cardiac
arrhythmias Nuchal rigidity
Subhyaloid retinal hemorrhages Altered level of consciousness
Anisocoria, Nystagmus Focal neurological deficits
Putamen - Contralateral hemiparesis, contralateral sensory loss,
contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia,
neglect, or apraxia Thalamus - Contralateral sensory loss,
contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia,
or confusion Lobar - Contralateral hemiparesis or
sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia,
abulia, aphasia, neglect, or apraxia Caudate nucleus - Contralateral
hemiparesis, contralateral conjugate gaze paresis, or confusion
Brain stem - Tetraparesis, facial weakness, decreased level of
consciousness, gaze paresis, ocular bobbing, miosis, or autonomic
instability Cerebellum - Ataxia, usually beginning
in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze
paresis, skew deviation, miosis, or decreased level of consciousness
Causes Hypertension
Arteriovenous malformation Aneurysm rupture
Cerebral amyloid angiopathy Intracranial neoplasm
Coagulopathy Hemorrhagic transformation of an
ischemic infarct Cerebral venous thrombosis
Sympathomimetic drug abuse Moyamoya
Sickle cell disease Eclampsia or postpartum vasculopathy
Infection Vasculitis
Neonatal intraventricular hemorrhage Trauma
Diagnosis Computed tomography: A CT scan may be
normal if it is done soon after the onset of symptoms. A CT scan is the best
test to look for bleeding in or around your brain. In some hospitals, a
perfusion CT scan may be done to see where the blood is flowing and not
flowing in your brain. Magnetic resonance imaging: A special
MRI technique may show evidence of an ischemic stroke within minutes of
symptom onset. In some hospitals, a perfusion MRI scan may be done to see
where the blood is flowing and not flowing in your brain.
Angiogram: a test that looks at the blood vessels that feed the brain. An
angiogram will show whether the blood vessel is blocked by a clot, the blood
vessel is narrowed, or if there is an abnormality of a blood vessel known as
an aneurysm. Carotid duplex: A carotid duplex is an
ultrasound study that assesses whether or not you have atherosclerosis of the
carotid arteries. These arteries are the large blood vessels in your neck that
feed your brain. Transcranial Doppler: Transcranial
Doppler is an ultrasound study that assesses whether or not you have
atherosclerosis of the blood vessels inside of your brain. It can also be
used to see if you have emboli in your blood vessels.
Treatment Intracerebral hemorrhages is a severe
condition requiring prompt medical attention. Treatment goals include
lifesaving interventions, supportive measures, and control of symptoms.
Treatment depends on the location, extent, and cause of the bleeding.
Often, treatment can reverse the damage that has been done.
A craniotomy is sometimes done to remove blood, abnormal blood vessels, or a
tumor. Medications may be used to reduce swelling, prevent seizures, lower blood
pressure, and control pain. Acute intraparenchymal hemorrhage
Clinical History: An 81-year-old diabetic male presents with a change in
mental status. Findings: Axial CT images through the
brain demonstrate two areas of hyperdensity, one measuring
approximately 2 x 1.5 cm and a second measuring approximately 3 x 4 cm. There
is some surrounding edema with mass effect upon the left ventricle. In
addition, there is extension into the ventricular system.
Diagnosis: Acute intraparenchymal hemorrhage.
Discussion: There are many causes for intraparenchymal hemorrhage. A common
cause is secondary to hypertension. These most commonly occur within the
basal ganglia, subcortical white matter, cerebellum, thalamus and pons.
Hemorrhage into the posterior fossa with mass effect or extension into the
ventricular system carries poor prognosis.
In younger patients, vascular malformations, specifically AVMs and
cavernous angiomas are more common causes for hemorrhage. In addition,
venous malformations are associated with hemorrhage.
In the elderly population, amyloid angiopathy is associated with cerebral
infarcts as well as hemorrhage in superficial locations, rather than deep
white matter or basal ganglia. These are usually described as "lobar". These
bleedings are not associated with systemic amyloidosis.
Hemorrhagic neoplasms are more complex, heterogeneous bleeds often with
associated edema. These hemorrhages are related to tumor necrosis, vascular
invasion and neovascularity. Glioblastomas are the most common
primary malignancies to hemorrhage while thyroid, renal cell carcinoma, melanoma,
and lung cancer are the most common causes of hemorrhage from metastatic
disease. Other causes of intraparenchymal
hemorrhage include hemorrhagic transformation of infarction which is
usually in a classic vascular distribution and is seen in
approximately 24 to 48 hours following the ischemic event. This hemorrhage
rarely extends into the ventricular system.
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