Primary hypertension-induced cerebellar encephalopathy causing obstructive hydrocephalus. Case report.
Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. The parenchyma of the posterior fossa is infrequently involved. The authors report on two cases of isolated edema of the cerebellar hemispheres, which occurred in the setting of hypertensive crisis and led to complete obstruction of or significant impingement on the fourth ventricle and potentially lethal hydrocephalus. To the best of the authors' knowledge, these are the first reported cases of hypertensive encephalopathy centered in the posterior fossa. Two patients presented with profound decreases in neurological status subsequent to development of malignant hypertension. Imaging studies revealed diffusely edematous cerebellar hemispheres with effacement of the fourth ventricle, causing dilation of the lateral and third ventricles. Following emergency placement of external ventricular drains, control of systemic blood pressure was accomplished, and neurological functioning returned to baseline. Although neurological deterioration resolved swiftly following placement of ventricular catheters and administration of diuretic agents, systemic blood pressure did not fluctuate with the release of cerebrospinal fluid and resolution of increased intracranial pressure. Decrease in systemic blood pressure lagged well behind improvement in neurological status; the patients remained morbidly hypertensive until systemic blood pressure was controlled with multiple parenteral medications. The authors hypothesize that the development of hypertension beyond the limits of cerebral autoregulation led to breakdown of the blood-brain barrier in the cerebellum and development of posterior fossa edema secondary to the focal transudation of protein and fluid. Correction of the elevated blood pressure led to amelioration of cerebellar edema. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered.
Verrees
Meg
M
Department of Neurosurgery, Case Western Reserve University, University Hospitals of Cleveland, Ohio 44106, USA. megverrees@yahoo.com
Fernandes Filho
Jose Americo
JA
Suarez
Jose I
JI
Ratcheson
Robert A
RA
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001812:Blood-Brain Barrier / Q000502:physiology; D001929:Brain Edema / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000209:etiology*; D002531:Cerebellum / Q000000981:diagnostic imaging* / Q000503:physiopathology; D003131:Combined Modality Therapy; D003907:Dexamethasone / Q000627:therapeutic use; D004234:Diuretics, Osmotic / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006849:Hydrocephalus / Q000209:etiology* / Q000473:pathology* / Q000601:surgery; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008353:Mannitol / Q000627:therapeutic use; D008875:Middle Aged; D014057:Tomography, X-Ray Computed; D014696:Ventriculostomy / Q000295:instrumentation
D000893:Anti-Inflammatory Agents; D000959:Antihypertensive Agents; D004234:Diuretics, Osmotic; D008353:Mannitol; D003907:Dexamethasone