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NEUROLOGY 1987;37:1050
© 1987 American Academy of Neurology

CSF somatostatin in multiple sclerosis

Reversible loss of diurnal oscillation in relapses

K. V. Søarensen, MD, T. Alslev, MD, S. E. Christensen, MD, N. B. Jensen, MD and H. Ørskov, MD

University Department of Neurology (Dr. Sørensen), Kommunehospitalet, Aarhus C; the Neuromedical Institute (Drs. Sørensen and Alslev), University of Odense, Odense; the Neurological Department (Drs. Sørensen and Jensen), Central Hospital, Viborg, the Second University Clinic of Internal Medicine (Dr. Christensen), Aarhus Kommunehospital, Aarhus C; and the Institute of Experimental Clinical Research (Dr. Ørskov), University of Aarhus, Aarhus C, Denmark.

CSF and venous blood were sampled hourly during 24 hours in 6 control subjects and in 12 patients with MS, 5 of whom were in stable phase and 7 in relapse. CSF somatostatin immunoreactivity was 166 ± 5.3 (SEM) pg/ml in controls at noon and rose around midnight to 208 ± 3.8 pg/ml, then decreased to basal levels at about 5 hours and exhibited another small peak 3 hours later. Almost identical patterns were found in patients with MS during stable phase. During relapse, CSF somatostatin was reduced to 99 ± 9.2 pg/ml and showed no variation from this value. CSF albumin was similar in the three groups and exhibited no fluctuations. Diurnal patterns of serum growth hormone were similar and unrelated to the oscillations in CSF somatostatin, indicating that hypothalamic release was insignificant in the overall production and in variations. The observation that the CNS releases somatostatin at lower levels during relapse in MS and that these do not oscillate may suggest that the constant low contents represent passive spillover from somatostatin-containing neurons, while the undulating levels above them are representative of active, yet unknown neurophysiologic (eg, neurotransmitter) functions which become reversibly extinct in relapse.

Address correspondence and reprint requests to Dr. Sørensen, Neurological Department, Central Hospital, DK-8800 Viborg, Denmark.

Supported by The Danish Medical Research Council, The Sclerosis Foundation, Aarhus University Research Council, P. Carl Petersen Foundation, Fonden til Laegevidenskahne Fremme and Institute of Experimental Research.

Received April 2, 1986. Accepted for publication in final form September 19, 1986.




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