As noted in Chapter 1, patients with intracerebral (intraparenchymal) hemorrhage (ICH) typically present with relatively abrupt onset of focal neurologic symptoms and signs that may be associated with early decreased level of alertness, severe headache, nausea, and vomiting. In patients with this abrupt onset of symptoms, clinically suspected intracranial hemorrhage should prompt urgent computed tomography (CT) or magnetic resonance imaging (MRI) to determine the location and the size of the hemorrhage (Fig. 15-1) and possibly to reveal other intracranial disease processes (see algorithm for the management of ICH in Appendix E-5). The location of the hemorrhage may guide further evaluation that is necessary to define the mechanism. As noted in the review of the five main locations for intracranial hemorrhage outlined in Chapter 8, the specific location of an ICH may further define the likely mechanism of the hemorrhage. Given that the volume of the hemorrhage is such a strong predictor of outcome, the volume should be estimated from the CT scan using the ellipsoid method. The volume is estimated by measuring the width, length, and height of the hematoma, with multiplication of these measurements in centimeters and division by 2 to provide the very approximate volume in cubic centimeters.

Lobar ICHs are characterized by bleeding into the cortex or subcortical white matter. Common features at the onset include vomiting and localized headache (frontal hemorrhage usually afflicts the forehead area; temporal hemorrhage, the area around or anterior to the ipsilateral ear; parietal hemorrhage, the temple area; and occipital hemorrhage, the area around or over the ipsilateral eye).

In lobar ICHs, unlike deep supratentorial hemorrhages, the neurologic deficits are often more restricted and variable (frontal hematoma usually produces contralateral arm weakness; left temporal hematoma, aphasia and delirium; parietal hematoma, contralateral hemisensory loss; and occipital hematoma, contralateral homonymous hemianopia). Disturbances of the level of consciousness occur later in the clinical course, and a history of hypertension is less frequent. The neurologic deficit appears rapidly, within 1 to several minutes, but not instantaneously as it usually does with an embolus leading to cerebral ischemia. Stiff neck or seizures at the onset are uncommon, and more than half of the patients are drowsy. However, a large lobar ICH may affect two or more lobes and may produce stupor or coma associated with severe neurologic deficit.

Most patients with lobar hematoma require further evaluation with CT angiography (CTA) or MRI/magnetic resonance angiography (MRA) because of the potential for underlying intracranial aneurysm or arteriovenous malformation (AVM). Venous assessment with MR venography or CT venography should be considered in those with hemorrhage appearance suggesting a venous occlusive etiology. If aneurysm is detected on CTA or MRA, then as outlined in Chapter 14, interventional management with either endovascular or surgical
clipping is indicated. If an AVM is detected on CTA or MRA, or is otherwise highly suspected, arteriography is typically performed to characterize the AVM morphology. If no aneurysm is detected and if not performed already, MRI with gadolinium may clarify a cause for the hemorrhage. Use of gradient echo and T2 susceptibility-weighted images may reveal evidence of prior hemorrhages or multiple microhemorrhages, findings that provide additional clues regarding the underlying cause including amyloid angiopathy. In addition to aneurysm, AVM, and amyloid angiopathy, underlying neoplasm, arteriographically occult vascular malformation, bleeding diathesis, and anticoagulant use are other primary considerations for hemorrhage at that site. There has been ongoing debate regarding whether surgical therapy should be considered for lobar hemorrhages. In the International Surgical Trial in Intracerebral Haemorrhage (STICH), 1,033 patients with supratentorial ICH were randomly assigned to early surgery or medical management. The overall outcomes were similar, suggesting that surgery is not indicated for all ICHs. In the subgroup analysis, patients with lobar hemorrhage also were not benefited by surgery. However, hemorrhages that were 1 cm or less from the cortical surface did better with early surgery compared with conservative management. STITCH II then further assessed whether early surgical treatment within 12 hours of study entry may be of benefit in the subgroup of patients with lobar hemorrhages within 1 cm of the cortical surface, 10 to 100 mm³ in volume. In the early surgery group, 41% had a favorable outcome, compared to 38% in those treated with medical management alone. Survival was slightly better in those managed surgically, but the difference was not statistically significant. Adding to the complexity of the interpretation of the results, one in five patients managed medically ended up having a surgical procedure, typically because of neurologic worsening. Whether very selected patients with superficial hemorrhages should be treated surgically with craniotomy remains to be established.

In the Minimally Invasive Surgery Plus Recombinant Tissue-Type Plasminogen Activator for ICH Evacuation trials (MISTIE-III) clinical trial, minimally invasive catheter-based hemorrhage evacuation followed by thrombolysis was assessed in patients with nontraumatic supratentorial ICH of more than 30 mL in size, with the goal to reduce the size of the hemorrhage to less than 15 mL. Image-guided treatment included the administration of alteplase every 8 hours for up to 9 doses, compared to standard medical care. The proportion of patients achieving a good outcome (modified Rankin Scale score of ≤3) at 365 days did not differ between those in the surgical group (45%) and those treated with standard medical care (41%). In those whose hematoma size was reduced to less than 15 mL, there was a 10.5% improvement in the proportion of those achieving good functional outcome. The procedure remains under study.

Supratentorial deep hemorrhages in the basal ganglia and internal capsule are usually characterized by sudden onset of headache followed by acute or subacute (as long as 48 hours) loss of consciousness associated with contralateral hemiparesis, hemisensory loss, homonymous hemianopia, and, if the dominant hemisphere is involved, aphasia. Vomiting is common. In comatose patients, signs of uncal herniation (ipsilateral third cranial nerve palsy) or upper brainstem compression may appear (deep, irregular, or intermittent respiration; ipsilaterally dilated and fixed pupil; and decerebrate posturing).

The presence of upward gaze palsy with unreactive miotic pupils, sometimes associated with convergence paralysis, is characteristic of thalamic hemorrhage and helps to differentiate it from putaminal hemorrhage. Besides characteristic oculomotor abnormalities, thalamic hemorrhage often produces contralateral eye deviation, aphasia (dominant hemisphere involvement), neglect (nondominant hemisphere involvement), unilateral hemiplegia or hemiparesis, and unusual sensory syndromes (distressing dysesthesias and spontaneous pain occurring with a latency of days to weeks from onset).

In putaminal hemorrhage, the eyes are conjugately deviated to the side of the lesion, the pupillary size and reactivity are normal unless uncal herniation has occurred, and focal neurologic signs (dense, flaccid hemiplegia or hemiparesis, hemisensory loss, homonymous hemianopia, global aphasia [dominant hemisphere involvement], or hemi-inattention [nondominant hemisphere involvement]) and level of consciousness tend to worsen gradually within minutes to hours.

Caudate hemorrhages are characterized by headache, nausea, vomiting, and various types of behavioral abnormalities (such as disorientation or confusion), occasionally accompanied by prominent short-term memory loss, transient gaze paresis, and contralateral hemiparesis without language disorders.

Basal ganglia hemorrhage is typically caused by chronic hypertension with associated lipohyalinosis and Charcot-Bouchard aneurysms in the small, perforating arteries. In the presence of chronic hypertension, MRI with gadolinium and MRA may be performed to be certain that there is no underlying neoplasm, vascular malformation, or other alternative cause. If there is no history of hypertension, no use of anticoagulants, no history of illicit drug use such as methamphetamine, and patients are younger, it is more likely that a specific underlying cause is present, and MRI/MRA is indicated. Methamphetamine use may also lead to ICH particularly in younger patients, and most commonly in a deep location. Arteriography is typically performed in those with a high clinical suspicion for a vascular malformation or findings suggestive on noninvasive imaging. Hematomas in the putamen with signs of deterioration or progressive neurologic deficit may be amenable to surgical therapy; those in the thalamus
and caudate are rarely operable. When the deficit is stable, hemorrhage in these subcortical locations is typically treated medically. Some data suggest that a minimally invasive surgical approach may have a better short-term neurologic outcome compared to medical management alone in selected patients with a basal ganglia hemorrhage, 25 to 40 mm³ in volume. Adding recombinant tissue-type plasminogen activator to minimally invasive surgery is under ongoing study.

Primary brainstem hemorrhage usually occurs in the pons and results in early coma, quadriplegia, prominent decerebrate rigidity, pinpoint (1 mm) pupils that react to light, and locked-in syndrome with some persistent ability to move the eyelids and eyes up and down. The eyes are often in midposition and have an impaired or absent response to caloric tests. Hyperpnea, hyperhidrosis, and hyperthermia are common. Primary midbrain and medullary hemorrhages are rare. When midbrain hemorrhage occurs, it often results in homolateral oculomotor paralysis with crossed hemiplegia (Weber’s syndrome). When the hemorrhage enlarges, quadriplegia and coma often occur. Medullary hemorrhage usually produces early coma and rapid death.

Cerebellar hemorrhage usually develops in one of the cerebellar hemispheres (origination in the region of the dentate nucleus is common) within a period of several hours; loss of consciousness at the onset is uncommon. Repeated vomiting, nausea, severe occipital headache, and vertigo with inability to walk or stand (dysequilibrium, limb ataxia) are common early features. Often, some combination of the following signs or symptoms occurs: mild peripheral facial palsy, dizziness, nystagmus, miosis, decreased corneal reflex, paresis of conjugate lateral gaze of the eyes to the side of the hemorrhage, forced deviation of the eyes to the side opposite the lesion, and ipsilateral abducens palsy, which indicates both cerebellar and pontine dysfunction (hemiplegia usually does not occur).

Pontine and cerebellar hemorrhages are commonly a result of chronic hypertension. If the patient does not have a history of hypertension, MRI of the head with gadolinium and MRA should be performed. In younger patients and in those in whom a vascular malformation or other vascular lesion is suggested on the MRI/MRA, arteriography is needed to better detect and characterize an underlying AVM. Hematomas in the brainstem are usually inoperable, but evacuation is occasionally attempted when there is evidence of neurologic deterioration in an otherwise healthy patient with a good life expectancy.

Because moderate to large cerebellar hematomas (2-3 cm or more in diameter) often lead to a life-threatening, downhill course with unpredictable deterioration caused by brainstem compression and/or hydrocephalus, it is important to monitor patients closely and to remove the hematoma before compression causes alteration in the level of consciousness and an unstable clinical situation. Immediate surgical intervention is typically indicated. However, alert patients who have smaller lesions and no signs of brainstem compression may be treated medically under close observation in the neurologic intensive care unit. The same treatment approach applies to a patient who has a stable neurologic course and unimpaired consciousness and is seen later than 1 week after the cerebellar hemorrhage. However, if a patient shows signs of brainstem compression or deterioration, such as a diminution in the level of consciousness, immediate evacuation of the clot is indicated as a potentially life-saving treatment, even if the patient is in a deep coma.

Patients with subarachnoid hemorrhage (SAH) in combination with ICH are likely to have an underlying structural abnormality, such as a saccular aneurysm, and should undergo assessment as outlined for SAH in Chapter 14.
Lumbar puncture (LP) should not be performed in patients who are suspected of having ICH because CT or MRI yields much more information; LP, in the presence of a central nervous system mass lesion, may lead to herniation.

Other laboratory tests are usually performed (as listed for SAH in Table 14-1) to assess further for underlying causes of the hemorrhage and associated complications. In severely impaired patients, the laboratory evaluation is usually not extensive, because 80% to 90% of such patients have a progressive and ultimately fatal clinical course. Specific treatment options relating to identified underlying causes are discussed in Chapter 17.