Cerebellar Hemorrhage in Woman With History of Hypertension

A 65-year-old woman with a long history of hypertension treated with metoprolol and felodipine complained of dizziness, headache, nausea, and vomiting of acute onset. Her blood pressure was 220/110 mm Hg. She was drowsy and unable to stand or walk.

There was no nuchal rigidity, and localizing neurologic signs were absent. The patient exhibited horizontal nystagmus and a positive Romberg sign, with a tendency to fall to the left. A CT scan of the head revealed a hematoma in the right cerebellar lobe.

Drs S. Filis, D. Papaioannides, K. Katte, and D. Sinapidis of Arta, Greece, write that most cerebellar hemorrhages can be attributed to hypertensive vascular disease; less common causes include anticoagulation therapy, arteriovenous malformation, tumors, blood dyscrasia, and trauma. Hypertensive cerebellar hemorrhages usually are located in the deep white matter of the cerebellum and commonly extend into the fourth ventricle.

The clinical presentation ranges from a progressive syndrome that develops over hours or even days to a coma of sudden onset that rapidly progresses to death. The classic clinical picture of hypertensive cerebellar hemorrhage is the sudden onset of a headache that may be accompanied by nausea, vomiting, and vertigo followed by gait ataxia and impaired consciousness, which usually evolves over several hours. The patient's condition may deteriorate quickly, without warning; careful observation and early intervention are paramount.

Typically, the patient's blood pressure is elevated; nuchal rigidity may be present. The pupils are often small and sluggishly reactive. Ipsilateral gaze palsy-with gaze preference away from the side of hemorrhage-and ipsilateral peripheral facial palsy are common. Nystagmus and ipsilateral depression of the corneal reflex may be noted. Dysarthria and dysphagia can occur.

The patient, if alert, exhibits ataxia of stance and gait; limb ataxia is less common. In the late stage of brain stem compression, the legs are spastic and extensor plantar responses (Babinski sign) are present. The cerebrospinal fluid frequently is bloody; however, if cerebellar hemorrhage is suspected, avoid lumbar puncture, which can lead to a herniation syndrome. CT scans or MRI scans can be helpful in confirming the diagnosis.

Surgical decompression may reduce the symptoms dramatically and can be lifesaving. With proper surgical intervention, lethargic or even stuporous patients may survive with minimal or no residual deficits and intact intellect. However, the likelihood that deeply comatose patients can attain this level of recovery is small. This patient's condition was stabilized with cautious control of her blood pressure and medical decompression with mannitol; surgical decompression was not needed. Her recovery was uneventful; there are no residual deficits.