Spontaneous intracerebral hemorrhage (sICH) is defined as bleeding within the brain parenchyma, and occurs twice as commonly as subarachnoid hemorrhage, but is equally as deadly. Risk factors for sICH include hypertension, advanced age, leukoaraiosis, prior ICH, renal failure, use of anticoagulant drugs, and cerebral amyloid angiopathy. Leukoaraiosis, also known as small vessel ischemia, is often referred to as unidentified bright objects (UBOs) on brain scans.
The abrupt onset of focal neurological symptoms is presumed to be vascular in origin until proven otherwise. Vomiting, systolic BP >220 mm Hg, severe headache, coma or decreased level of consciousness, and progression over minutes or hours all suggest ICH, although none of these findings are specific. The clinical features will depend on the location, size, direction of spread, and rate of development of the sICH.
Spontaneous intracerebral hemorrhages are generally categorized as primary or secondary. Primary sICH accounting for 80% of cases is often attributed to hypertensive vasculopathy and cerebral amyloid angiopathy (CAA). CAA is seen in 40–60% of patients older than 70, and is considered responsible for the majority of primary lobar ICH occurring in the elderly population.
Secondary sICH is due to arteriovenous malformations (AVMs), ruptured aneurysms, anticoagulation, hemorrhage into neoplasm, and hemorrhagic transformation of ischemic infarction.
Supratentorial spontaneous intracerebral haemorrhage (sICH) accounts for 20% of all stroke-related sudden neurological deficits, has the highest morbidity and mortality of all stroke, and the role of surgery remains controversial1. Spontaneous supratentorial intracerebral haemorrhage is a heterogeneous disorder with clinical manifestations that range from none to rapid death. It affects 4 million patients worldwide each year and median case fatality at 1 month is 40%.
When a patient is clinically suspected of having sICH, Computed Tomography (head) scan is very sensitive for identifying acute hemorrhage and is considered the gold standard. Gradient echo and T2*susceptibility weighted MRI are as sensitive as CT for detection of acute blood and are more sensitive for identification of prior hemorrhage.
A 56 year old hypertensive man on irregular treatment presented with sudden onset of altered consciousness and speech difficulty. An urgent Magnetic Resonance Imaging was requested.
MR Imaging confirmed a large left Temporal sICH with mass effect.
The earlier time from symptom onset to first neuroimage, the more likely subsequent neuroimages will demonstrate hematoma expansion. Hematoma expansion, primarily during the first few hours is highly predictive of neurological deterioration, poor functional outcome, and mortality. It is estimated that for each 10% increase in ICH size, there is a 5% increase in mortality. Intravenous recombinant factor VIIa within 4 hours of sICH onset has been shown to significantly reduce hematoma growth.
Contrast extravasation seen on CT Angiography (CTA), MRI, and digital subtraction angiography correlates with hematoma growth, indicating ongoing bleeding. Contrast extravasation on the arterial phase of a CTA has been coined the CTA Spot Sign. Spot Sign demonstrable in one-third of sICH is defined as an increase in size of more than 30% of the initial volume or an absolute increase of 6 ml.
Preoperative MR Angiography (Image above) could not convincingly demonstrate a left MCA aneurysm.
A catheter angiogram may be considered if clinical suspicion is high or noninvasive studies are suggestive of an underlying vascular cause.
MR signal intensities in relation to age of hematoma
|Time||Dominant blood component||Signal on
|6-24 hrs||Intracellular oxyhemoglobin||Decreased||Increased|
|1-3 days||Intracellular deoxyhemoglobin||Isointense or
|3-7 days||Intracellular methemoglobin||Increased||Increased|
|30 days||Extracellular methemoglobin & hemosiderin||Increased||Decreased|
In view of the altered consciousness and speech difficulties (Aphasia), with the MRI Scan revealing a large intracerebral hematoma in the left Temporal lobe, the patient was treated with a Left Frontotemporal craniotomy with evacuation of a 40 ml clot through a small opening in the cortex (‘corticectomy’). His consciousness improved in the postoperative period. He is undergoing speech assessment for ‘fluent’ dysphasia.
Many survivors remain severely disabled and therefore are an enormous burden on stroke services with only a quarter having a good outcome.