[A case of sympathotonic orthostatic hypotension following herpes simplex encephalitis].Rinsho Shinkeigaku. 1996 Oct; 36(10):1161-5.RS
The etiology of sympathotonic orthostatic hypotension (SOH) is still unknown. We reported a 50-year-old male case of SOH associated with herpes simplex encephalitis. Eight days before admission to our hospital, he noticed fever, which was followed by intractable hiccup. He was admitted to a local hospital, where nuchal rigidity and mononuclear CSF pleocytosis were noted. On the 9th hospital day, he suddenly developed respiratory arrest, and his consciousness state deteriorated to coma. He was transferred to our hospital with artificial ventilation on the same day. The second CSF examination revealed pleocytosis and positive herpes-simplex-virus antibody. CAT scan showed diffuse high density areas in the bilateral temporal lobes. Intensive anti-herpetic therapy was started. On the 14th hospital day, spontaneous respiration came back and consciousness state was improved from coma to stupor. He gradually recovered to alert state and became ambulatory by the 30th hospital day. Seven weeks after the onset of his illness, he noticed orthostatic dizziness for the first time during his rehabilitation exercises. Blood pressure was 116/78mmHg at supine position and 82/62mmHg at standing position, and the heart rate was 83bpm, and 141bpm, respectively. Plasma noradrenaline concentration was 0.09 ng/ml (within normal range) at supine position, but increased to 0.29ng/ml upon standing. Catecholamine infusion tests revealed hyposensitivity in beta 2-receptors; decrease in blood pressure in response to isoprenaline was blunted, while increase of blood pressure to noradrenaline was not impaired. Nerve conduction studies and sweating tests were normal. When he was discharged from our hospital on the 87th hospital day, he still had orthostatic symptoms. His complete recovery took full one year. Some authors claimed that SOH is an abortive form of acute autonomic neuropathy, while others postulated that it was due to unbalanced cardiovascular alpha- and beta-adrenoceptor functions. SOH of the present case seems to be caused by the central nervous lesions; especially, the brain stem involvement due to herpes simplex encephalitis may well be causing SOH.