Intracerebral hemorrhage is characterized by sudden onset of focal neurologic deficit progressing over hours along with headache, nausea, vomiting, altered consciousness, and hypertension. Clinical manifestations depend on hematoma location. Patients with supratentorial hemorrhage often present with contralateral hemiplegia, hemisensory loss, aphasia, neglect, gaze abnormalities, and hemianopia. Infratentorial hemorrhages manifest with signs of brainstem dysfunction, cranial nerve abnormalities, ataxia, nystagmus, and other cerebellar signs.
Conjugate eye deviation frequently occurs in patients with supratentorial intracerebral hemorrhage. Conjugate eye deviation can be evoked by a relatively smaller thalamic hematoma than a putaminal hematoma. In a study, the persistence of conjugate eye deviation was a significant predictor of death (Sato et al 2012).
Seizures occur in approximately 10% of all patients with intracerebral hemorrhage and in almost one half of patients with lobar hemorrhage. Often seizures occur at onset of bleeding or within the first 24 hours of an acute event. Posthemorrhagic seizures, possibly nonconvulsive, have been associated with neurologic worsening on the NIH Stroke Scale and with an increase in midline shift (Vespa et al 2003). In one series, seizures were reported to occur in one third of patients with intracerebral hemorrhage (Claassen et al 2007). In over half of these patients the seizures were purely electrographic. Electrographic seizures were associated with expanding hemorrhages, and periodic discharges were associated with cortical intracerebral hemorrhage and poor outcome. Another study demonstrated that the mean intracerebral hemorrhage volume was independently associated with seizures, and an increase of 1 mm3 in hematoma volume increased the seizure rate by 2.7% (Yang et al 2009).
Blood may rupture into the ventricles and cause hydrocephalus. Rarely, blood may also leak into the subarachnoid space. A large hematoma may compress over adjacent structures such as the brainstem and thalamus, causing herniation and death. There can be rapid rise in intracranial pressure, leading to rapid deterioration of sensorium within a few minutes or hours. Such patients often present with coma, bilateral plantar extensor reflexes, pupillary abnormalities, or Cheyne-Strokes breathing indicating development of brain herniation. If hemorrhage continues worsening, death may result because of compression of vital brainstem centers.
Basal ganglionic capsular hemorrhage. Anatomically, basal ganglia include the putamen, globus pallidus, and caudate nucleus. These structures are supplied by different arteries. Therefore, striatocapsular hemorrhage can be subdivided into specific types according to arterial involvement (Chung et al 2000). Putaminal hemorrhage is the most common type of hemorrhage secondary to hypertension. Contralateral hemiparesis, hemisensory loss, or hemi-inattention is generally present. Aphasia is frequently seen if hemorrhage occurs in the posterior limb of the left internal capsule (Liang et al 2001). Transient conjugate eye deviation to the lesion side can occur if the globus pallidus or medial putamen is involved.
Massive putaminal hemorrhage can extend into the ventricle or herniate onto the brainstem. When deterioration in consciousness occurs in patients with putaminal hemorrhage, hematoma enlargement is more likely to occur than is intraventricular extension (Kase et al 1998). As the lesion enlarges, the ipsilateral pupil first becomes smaller and later larger than a normal pupil; ipsilateral plantar response becomes extensor; and bilateral horizontal gaze palsy develops.
Caudate hemorrhage is frequently associated with intraventricular extension and secondary hydrocephalus. Caudate hemorrhage causes severe headache, nausea, vomiting, and signs of meningeal irritation. Motor focal neurologic deficit develops when the hematoma is large enough to involve the putamen and internal capsule (Kumral et al 1999).
Thalamic hemorrhage. The thalamus is a structure with multiple nuclei and functions. It serves as a relay center for sensory signals prior to their final pathways to the parietal lobe and also contains nuclei that are responsible for wakefulness. Approximately 15% of all hypertensive hemorrhages are thalamic hemorrhages. Hemisensory loss, decreased sensorium, and hemiparesis are usual manifestations of thalamic hemorrhage. Intraventricular extension is more commonly seen than in putaminal hemorrhage and causes obstructive hydrocephalus and, in turn, stupor or coma (Steinke et al 1992). Pure sensory deficits are more commonly seen in thalamic infarction than in hemorrhage. Cognitive dysfunction may include aphasia, neglect, and anosognosia. Vertical gaze abnormalities, upgaze palsy, downward tonic deviation of gaze, small fixed and sluggish pupils, are characteristic neuro-ophthalmological manifestations in thalamic hemorrhage.
Pontine hemorrhage. Pontine hemorrhages typically present with rapid onset of coma, pinpoint pupils, disturbed respiratory patterns, autonomic instability, quadriplegia, and horizontal gaze paralysis. Occasionally, ocular bobbing can also be seen as well as miotic pupils. Damage of the upper pontine reticular formation is responsible for abrupt coma. Quadriparesis is not uncommon especially when hemorrhage occurs at the motor fiber decussation. Although narcotic overdose may present with abrupt coma and miotic pupils mimicking pontine hemorrhage, other cranial nerve function generally remains intact.
Cerebellar hemorrhage. Like other hypertension-related hemorrhages, cerebellar hemorrhage is typically located in the area of the dentate nucleus, which is supplied by small penetrating vessels with microscopic hypertensive changes. The most common symptoms of cerebellar hemorrhage are vertigo, severe nausea and vomiting, and ataxia. Headache may be severe. Patients with cerebellar hemorrhage can rapidly become comatose within hours after the onset. Alteration of mental status can be secondary to damage to the pons or midbrain or abrupt obstructive hydrocephalus. Occasionally, peripheral facial weakness and horizontal gaze impairment can also occur, representing herniation onto the pons. Cerebellar clots greater than 3 cm in diameter have a poor prognosis if left untreated.
Lobar hemorrhage. This is one of the most clinically silent hemorrhages; brain imaging is of utmost importance in making the diagnosis. Clinical presentations depend on the location and size of the hematoma, varying from no symptoms at all to focal neurologic deficits corresponding to the area of the brain being damaged. Hematoma in the frontal lobe may present as abulia, aphasia, contralateral hemiplegia, and conjugate eye deviation toward the side of the hemorrhage. Parietal hematoma manifests as hemisensory loss, visual inattention, and abnormalities of visuospatial functions. If hematoma involves the inferior parietal region, the patient may have abnormalities of reading, writing, and calculation. Occipital hematoma presents with hemianopia. Temporal hematoma manifests as delirium and Wernicke aphasia. Large hematomas may produce coma if they compress over the midbrain and thalamus. In patients with cerebral amyloid angiopathy-related lobar intracerebral hemorrhage, the parietal lobes are the most frequently affected site (Hirohata et al 2010). Recurrence of lobar intracerebral hemorrhage is associated with previous microbleeds or macrobleeds and posterior CT white matter hypodensity, which may be markers of severity for underlying cerebral amyloid angiopathy. Use of an antiplatelet agent following lobar intracerebral hemorrhage may also increase recurrence risk (Biffi et al 2010).
Intraventricular hemorrhage. Primary intraventricular hemorrhage is a rare form of intracerebral hemorrhage characterized by direct bleeding into the ventricular system of the brain. Primary intraventricular hemorrhage accounts for only 3% of all spontaneous intracerebral hemorrhages. Hypertension is a major cause of primary intraventricular hemorrhage. Short-term outcomes depend on patient age and the extent of intraventricular hemorrhage. The yield of diagnostic cerebral angiography in the setting of primary intraventricular hemorrhage is very high. The 2 most common causes identified on angiography are arteriovenous malformations and aneurysms (Flint et al 2008).
Intraventricular hemorrhage can occur following rupture of parenchymal hemorrhage into the ventricular system or can result from primary diseases of the ventricular system of the brain or structures just beneath the ventricular wall. Thalamic and caudate locations had the highest intraventricular hemorrhage frequency (69% and 100%) (Hallevi et al 2008). This condition is clinically characterized by sudden onset of severe headache, vomiting, progressive deterioration in consciousness, and signs of meningeal irritation. If the hemorrhage is massive, signs of brainstem herniation are present. Most of these patients have associated hydrocephalus, and some may require ventricular drainage. The 2 most common causes of primary intraventricular hemorrhage identified by angiography are arteriovenous malformations and aneurysms (Flint et al 2008). Anticoagulant administration increases intraventricular hemorrhage volume and risk of intraventricular extension in lobar and deep intracerebral hemorrhage (Biffi et al 2011b). Patients with intraventricular hemorrhage are twice as likely to have a poor outcome when compared to patients without intraventricular hemorrhage. Caudate location has been associated with a good outcome despite 100% incidence of intraventricular hemorrhage (Hallevi et al 2008). Approximately one third of patients with primary intraventricular hemorrhage do not survive hospital discharge. Patient age and amount of intraventricular hemorrhage independently predict in-hospital mortality (Flint et al 2008). Intraventricular thrombolysis in patients with intraventricular hemorrhage may be associated with better outcome (Dunatov et al 2011).
Multiple intracerebral hemorrhages. Simultaneous occurrence of multiple intracerebral hemorrhages in different arterial territories is a rare clinical event. Multiple simultaneous intracerebral hemorrhages account for 5.6% of all spontaneous intracerebral hemorrhage (Stemer et al 2010). Causes of multiple intracerebral hemorrhages include cerebral amyloid angiopathy, venous sinus thrombosis, coagulopathy, vasculitis, hemorrhagic transformation of cerebral infarcts, and multiple intracranial pathologies such as vascular anomalies or tumors. Although hypertension is the most common etiological factor for the development of spontaneous single intracerebral bleeding, its role in simultaneous multiple intracerebral hemorrhages is not clear (Yen et al 2005).
Hemorrhagic infarct. Pregnancy and the puerperium can be associated with cerebral hemorrhage due to cerebral venous thrombosis and eclampsia. In cerebral venous thrombosis, the affected cortex and underlying white matter becomes congested, swollen, and hemorrhagic, leading to venous infarction. Hemorrhage in the venous infarct range from a large hematoma to petechial hemorrhages within the infarct.