Intracerebral hemorrhage is focal bleeding from a blood vessel in the brain parenchyma. The cause is usually hypertension. Typical symptoms include focal neurologic deficits, often with abrupt onset of headache, nausea, and impairment of consciousness. Diagnosis is by CT or MRI. Treatment includes BP control, supportive measures, and, for some patients, surgical evacuation.
Most intracerebral hemorrhages occur in the basal ganglia, cerebral lobes, cerebellum, or pons. Intracerebral hemorrhage may also occur in other parts of the brain stem or in the midbrain.
Intracerebral hemorrhage usually results from rupture of an arteriosclerotic small artery that has been weakened, primarily by chronic arterial hypertension. Such hemorrhages are usually large, single, and catastrophic. Use of cocaine or, occasionally, other sympathomimetic drugs can cause transient severe hypertension leading to hemorrhage. Less often, intracerebral hemorrhage results from congenital aneurysm, arteriovenous or other vascular malformation (see Sidebar 1: Stroke (CVA): Vascular Lesions in the Brain), trauma (see Traumatic Brain Injury (TBI)), mycotic aneurysm, brain infarct (hemorrhagic infarction), primary or metastatic brain tumor, excessive anticoagulation, blood dyscrasia, or a bleeding or vasculitic disorder.
Vascular Lesions in the Brain
Common brain vascular lesions include arteriovenous malformations and aneurysms.
Arteriovenous malformations (AVMs): AVMs are tangled, dilated blood vessels in which arteries flow directly into veins. AVMs occur most often at the junction of cerebral arteries, usually within the parenchyma of the frontal-parietal region, frontal lobe, lateral cerebellum, or overlying occipital lobe. AVMs can bleed or directly compress brain tissue; seizures or ischemia may result.
Neuroimaging may detect them incidentally; contrast or noncontrast CT can usually detect AVMs > 1 cm, but the diagnosis is confirmed with MRI. Occasionally, a cranial bruit suggests an AVM. Conventional angiography is required for definitive diagnosis and determination of whether the lesion is operable.
Superficial AVMs > 3 cm in diameter are usually obliterated by a combination of microsurgery, radiosurgery, and endovascular surgery. AVMs that are deep or < 3 cm in diameter are treated with stereotactic radiosurgery, endovascular therapy (eg, preresection embolization or thrombosis via an intra-arterial catheter), or coagulation with focused proton beams. (See also Recommendations for the management of intracranial arteriovenous malformations from the Stroke Council, American Stroke Association.)
Aneurysms: Aneurysms are focal dilations in arteries. They occur in about 5% of people. Common contributing factors may include arteriosclerosis, hypertension, and hereditary connective tissue disorders (eg, Ehlers-Danlos syndrome, pseudoxanthoma elasticum, autosomal dominant polycystic kidney syndrome). Occasionally, septic emboli cause mycotic aneurysms. Brain aneurysms are most often < 2.5 cm in diameter and saccular (noncircumferential); sometimes they have one or more small, thin-walled, outpouchings (berry aneurysm). Most aneurysms occur along the middle or anterior cerebral arteries or the communicating branches of the circle of Willis, particularly at arterial bifurcations. Mycotic aneurysms usually develop distal to the first bifurcation of the arterial branches of the circle of Willis.
Many aneurysms are asymptomatic, but a few cause symptoms by compressing adjacent structures. Ocular palsies, diplopia, squint, or orbital pain may indicate pressure on the 3rd, 4th, 5th, or 6th cranial nerves. Visual loss and a bitemporal field defect may indicate pressure on the optic chiasm. Aneurysms may bleed into the subarachnoid space, causing subarachnoid hemorrhage. Aneurysms occasionally cause sentinel (warning) headaches before rupture; subarachnoid bleeding may accompany sentinel headaches. Rupture causes a sudden severe headache called a thunderclap headache.
Neuroimaging may detect aneurysms incidentally.
Diagnosis requires angiography, CT angiography, or magnetic resonance angiography.
If 3 cm in diameter may cause midline shift or herniation. Herniation, midbrain or pontine hemorrhage, intraventricular hemorrhage, acute hydrocephalus, or dissection into the brain stem can impair consciousness and cause coma and death.
Symptoms typically begin with sudden headache, often during activity. However, headache may be mild or absent in the elderly. Loss of consciousness is common, often within seconds or a few minutes. Nausea, vomiting, delirium, and focal or generalized seizures are also common. Neurologic deficits are usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause hemiparesis; when located in the posterior fossa, they cause cerebellar or brain stem deficits (eg, conjugate eye deviation or ophthalmoplegia, stertorous breathing, pinpoint pupils, coma). Large hemorrhages are fatal within a few days in about half of patients. In survivors, consciousness returns and neurologic deficits gradually diminish to various degrees as the extravasated blood is resorbed. Some patients have surprisingly few neurologic deficits because hemorrhage is less destructive to brain tissue than infarction.
Small hemorrhages may cause focal deficits without impairment of consciousness and with minimal or no headache and nausea. Small hemorrhages may mimic ischemic stroke.
Bedside glucose measurement
Diagnosis is suggested by sudden onset of headache, focal neurologic deficits, and impaired consciousness, particularly in patients with risk factors. Intracerebral hemorrhage must be distinguished from ischemic stroke, subarachnoid hemorrhage, and other causes of acute neurologic deficits (eg, seizure, hypoglycemia).
Immediate CT or MRI and bedside blood glucose measurement are necessary. Neuroimaging is usually diagnostic. If neuroimaging shows no hemorrhage but subarachnoid hemorrhage is suspected clinically, lumbar puncture is necessary.
Thalamic Intracerebral Hemorrhage
Sometimes surgical evacuation (eg, for many cerebellar hematomas > 3 cm)
Treatment includes supportive measures and control of general medical risk factors. Anticoagulants and antiplatelet drugs are contraindicated. If patients have used anticoagulants, the effects are reversed when possible by giving fresh frozen plasma, vitamin K, or platelet transfusions as indicated. Hypertension should be treated only if mean arterial pressure is > 130 mm Hg or systolic BP is > 185 mm Hg. Nicardipine
2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a
maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Cerebellar hemisphere hematomas that are > 3 cm in diameter may cause midline shift or herniation, so surgical evacuation is often lifesaving. Early evacuation of large lobar cerebral hematomas may also be lifesaving, but rebleeding occurs frequently, sometimes increasing neurologic deficits. Early evacuation of deep cerebral hematomas is seldom indicated because surgical mortality is high and neurologic deficits are usually severe.
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