Nontraumatic Intracranial Hemorrhage
Key Point
Nontraumatic intracranial hemorrhage is defined as a spontaneous hemorrhage into the brain parenchyma (intracerebral hemorrhage) or the CSF space (subarachnoid hemorrhage). Intracerebral hemorrhages cause acute signs and symptoms resembling those of cerebral ischemia and account for approximately 10% of strokes. One of the more common forms of intracerebral hemorrhage is hypertensive hemorrhage. The main symptom of subarachnoid hemorrhage is headache; its most common source is a ruptured aneurysm.
General manifestations of intracranial hemorrhage Though the manifestations of intracranial hemorrhage and cerebral ischemia are similar, generally speaking (sudden onset of focal neurologic deficits), there are several clinical signs and symptoms that are more characteristic of hemorrhage than of ischemia. These include:
Acute headache.
Often, vomiting.
Rapidly or very rapidly progressive neurologic deficits (whose type depends on the site of hemorrhage).
Progressive impairment of consciousness, possibly leading to coma.
In many patients, epileptic seizures.
If these manifestations are present, an intracranial hemorrhage is the probable cause. The definitive diagnosis, however, can only be made with neuroimaging.
6.6.1 Intracerebral Hemorrhage
Etiology and pathogenesis Most cases of intracerebral hemorrhage are due to the rupture of vascular lesions of hypertensive origin (“rhexis hemorrhages” of pseudoaneurysms of lipohyalinotic arterioles, generally in older patients) or of vascular malformations (aneurysms, arteriovenous malformations, and angiomas, which may affect younger patients) ( ▶ Fig. 6.34, ▶ Fig. 6.35). Intracerebral hemorrhage may also be a complication of therapeutic (over-) anticoagulation. Smaller hemorrhages, particularly those that are near the cortical surface, are often due to amyloid angiopathy ( ▶ Fig. 6.35). There can also be bleeding into an infarct, a primary brain tumor, a metastasis, or a cavernoma. Multifocal bleeding should arouse suspicion of amyloid angiopathy ( ▶ Fig. 6.38), a bleeding diathesis (anticoagulation, sepsis, leukemia), venous or venous sinus thrombosis, endocarditis, vasculitis, or trauma.
The more common etiologies of intracerebral hemorrhage are listed in ▶ Table 6.18.
Cause | Examples, remarks |
Chronic arterial hypertension | Hypertension leads to microangiopathy with fibrinoid necrosis, pseudoaneurysms, and vascular leakage. When hemorrhage occurs, neighboring arterioles are torn, leading to further extension of the hemorrhage. Typical sites of hypertensive hemorrhage are the thalamus, basal ganglia, subcortical white matter, and pons |
Aneurysm rupture | Typical sites are shown in ▶ Fig. 6.40. Aneurysms can rupture into the brain parenchyma as well as into the subarachnoid space |
Hemorrhage into a preexisting lesion | For example, infarct, tumor |
Vascular malformation | For example, cavernoma, arteriovenous malformation |
Vascular fragility due to vasculopathy | For example, cranial arteritis, amyloid angiopathy |
Bleeding diathesis | For example, hematologic disease, sepsis, therapeutic anticoagulation |
Cerebral venous thrombosis and venous sinus thrombosis | Diapedetic hemorrhage |
Drug abuse | Rare, e.g., cocaine |
Acute hypertension (hypertensive crisis) | Rare |
Fig. 6.34 Arteriovenous malformation and cavernoma. (a) Arteriovenous malformation in the left temporal lobe of a 68-year-old man with epileptic seizures. (b) Cavernoma in the right hippocampus of another patient (T2-weighted image).
Fig. 6.35 Arteriovenous malformation. (a) The T2-weighted spin-echo image reveals the feeding and draining vessels as signal-free areas (“flow voids”). (b) Analogous finding in a sagittal image. (c) The right carotid angiogram shows that the malformation is fed by branches of the right middle cerebral and pericallosal arteries. (d) The left carotid angiogram shows that it also derives part of its blood supply across the midline from the left pericallosal artery.
The effects of intracranial hemorrhage include:
Direct destruction of brain tissue at the site of the hemorrhage.
Compression and possible damage of surrounding brain tissue.
Elevation of ICP.
Brain edema that additionally raises the ICP, possibly leading to a vicious circle of edema and intracranial hypertension (see Section ▶ 6.3 and ▶ Table 6.9).
Clinical features The clinical picture mainly depends on the site and extent of the hemorrhage and to a much lesser extent on etiologic factors. Certain aspects of the clinical course can, however, suggest that one etiology is more likely than another:
Chronic arterial hypertension and advanced age (typically 60–70 years) make a rhexis hemorrhage more likely. These hemorrhages are ultimately caused by hypertension and are usually very large. Common sites are the basal ganglia (pallidum, putamen) and internal capsule ( ▶ Fig. 6.36), with the corresponding clinical manifestations: contralateral usually dense, hemiparesis or hemiplegia, horizontal gaze palsy, and initially, in many cases, déviation conjuguée and deviation of the head to the side of the lesion. Less common sites are the subcortical white matter, brainstem, thalamus ( ▶ Fig. 6.37), and cerebellum. Very large hemorrhages, particularly if located in the posterior fossa, can rapidly elevate the ICP, causing brainstem compression and, in turn, impairment of consciousness and coma.
Acute worsening of more or less severe preexisting signs and symptoms, perhaps accompanied by additional impairment of consciousness, suggests hemorrhage into an infarct or tumor.
Focal or generalized epileptic seizures preceding the acute event point toward a tumor, vascular malformation, or other structural lesion of the brain as the likely cause of hemorrhage.
Fig. 6.36 A basal ganglionic hemorrhage that is a few days old. The MRI typically shows a heterogeneous signal, partly hyperintense, partly hypointense. (a) T2-weighted MR image. (b) T1-weighted MR image. (c) T1-weighted MR image after contrast administration; contrast enhancement at the edge of the hematoma.
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