Clinical Pearls & Morning Reports
Published October 26, 2022
Spontaneous intracerebral hemorrhage accounts for approximately 10 to 15% of all strokes. Read the NEJM Review Article here.
Q: What are some of the causes of intracerebral hemorrhage?
A: Excluding traumatic hemorrhage, rupture of cerebral aneurysms or malformations, and hemorrhagic transformation of ischemic stroke, the main inciting causes of intracerebral hemorrhage in adults are hypertension, cerebral amyloid angiopathy, and anticoagulation. Older age is associated with an increased frequency of intracerebral hemorrhage, owing in part to the association of advanced age with cerebral amyloid angiopathy and with conditions such as atrial fibrillation that result in exposure to anticoagulation therapy.
Q: Where does typical spontaneous intracerebral hemorrhage occur?
A: Typical spontaneous intracerebral hemorrhage occurs in deep brain structures as a consequence of damage to the walls of small cerebral blood vessels that traverse these regions. These small arteries and arterioles are in most cases branches of large vessels of the circle of Willis that supply the basal ganglia, thalamus, pons, and deep portions of the cerebellum. Lobar intracerebral hemorrhage, in which the hematoma is located in the white matter of the frontal, parietal, temporal, or occipital lobe, is more common in recent series than deep intracerebral hemorrhage.
A: Patients with intracerebral hemorrhage present with focal neurologic signs that are abrupt in onset but not instantaneous, as occurs with embolic ischemic stroke. The evolution is typically over minutes. Further differentiating hemorrhagic from ischemic stroke are headache, nausea or vomiting, and, in many cases, a depressed level of consciousness. A reduced level of consciousness usually indicates compression of the arousal nuclei and pathways of the upper brain stem; alternatively, intraventricular hemorrhage with hydrocephalus can cause stupor. Focal neurologic deficits with intracerebral hemorrhage in the cerebral hemispheres correspond to the location of the hemorrhage and its transection of white-matter tracts; these deficits include hemiparesis, hemisensory loss, and gaze preference. Hemorrhage in the brain stem is usually located in the pons and causes an impaired level of consciousness, cranial nerve palsies, pinpoint (but reactive) pupils, absent or impaired horizontal gaze, ocular bobbing (a sign in which the eyes rapidly and conjugately deviate downward and then slowly upward to midposition), and facial weakness.
A: Intraventricular hemorrhage occurs in 30 to 50% of patients with intracerebral hemorrhage, and the resultant hydrocephalus owing to the added volume to the ventricular space, obstruction of cerebrospinal fluid (CSF) flow and inflammation-stimulated secretion of CSF leads to a decreased level of arousal and poor outcome. Hydrocephalus that results in decreased wakefulness usually is treated by the placement of an external ventricular drain to divert CSF and reduce intracranial pressure. In the Clot Lysis Evaluation of Accelerated Resolution of Intraventricular Hemorrhage (CLEAR III) trial, which evaluated 500 patients with hydrocephalus after intracerebral hemorrhage, intraventricular administration of alteplase was used to dissolve the ventricular clot. Although the overall comparison between groups showed no difference in functional outcomes, thrombolysis might have been associated with improved survival. Patients who survive intraventricular hemorrhage typically have substantial disability at 6 months.