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Diminished nocturnal lipolysis in cluster headache

A sign of central sympathetic dysregulation?

From the Department of Neurology (Drs. Meyer and Waldenlind) and Department of Clinical Science Pediatric Endocrine Research Laboratory (Dr. Marcus), Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.

Address correspondence and reprint requests to Dr. E. Laudon Meyer, Department of Neurology, Karolinska Institutet R54, Huddinge University Hospital, S-141 86 Huddinge, Sweden; e-mail: eva.laudon-meyer{at}hs.se

Background: It is unclear whether the autonomic symptoms during cluster headache (CH) attacks are of central or peripheral origin. A metabolic change such as altered lipolysis would reflect a central autonomic dysfunction.

Objective: To study nocturnal lipolysis in CH patients and healthy control subjects.

Methods: Microdialysis technique was used to measure glycerol levels, the end-product of lipolysis, in subcutaneous adipose tissue. Ten CH patients participated, of whom six were studied in remission as well as during symptomatic periods but between headache attacks. Fifteen healthy control subjects were studied. Mean glycerol, glucose, and lactate concentrations were calculated for three 2-hour intervals between 2400 and 0600 hours.

Results: Compared with healthy control subjects, symptomatic CH patients had lower glycerol levels during all three intervals (69, 61, and 73% of control levels; p < 0.05). CH patients in remission showed lower glycerol levels from 0200 to 0600 hours (68 and 63% of control levels; p < 0.05). There were no significant differences between the CH groups. Compared with healthy control subjects, patients in remission also showed a significantly different nocturnal temporal pattern, demonstrating declining glycerol levels during the first part of the night.

Conclusions: Altered lipolysis was found in patients with CH, both in symptomatic periods and in remission. The altered lipolysis may be due to a reduced nocturnal sympathetic activity and consequently an indication of central sympathetic dysregulation and hypothalamic dysfunction.

Received November 4, 2002. Accepted in final form July 29, 2003.

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