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Absence of Detectable Melatonin and Preservation of Cortisol and Thyrotropin Rhythms in Tetraplegia¹

Program in Neuroscience, Harvard Medical School (J.M.Z., C.A.C.), and Circadian, Neuroendocrine, and Sleep Disorders Section, Endocrine Division, Department of Medicine, Harvard Medical School, Brigham and Women’s Hospital (J.M.Z., S.A.S., C.A.C.), Boston, Massachusetts 02115; and Pulmonary and Critical Care Medicine Section, Spinal Cord Injury Service, Brockton/West Roxbury Veterans Administration Medical Center (N.T.A., R.B.), West Roxbury, Massachusetts 02132

Address all correspondence and requests for reprints to: Dr. Charles A. Czeisler, Circadian, Neuroendocrine, and Sleep Disorders Section, Endocrine Division, Department of Medicine, Harvard Medical School, Brigham and Women’s Hospital, 221 Longwood Avenue, Room 438A, Boston, Massachusetts 02115. E-mail: caczeisler{at}gcrc.bwh.harvard.edu

The human circadian timing system regulates the temporal organization of several endocrine functions, including the production of melatonin (via a neural pathway that includes the spinal cord), TSH, and cortisol. In traumatic spinal cord injury, afferent and efferent circuits that influence the basal production of these hormones may be disrupted. We studied five subjects with chronic spinal cord injury (three tetraplegic and two paraplegic, all neurologically complete injuries) under stringent conditions in which the underlying circadian rhythmicity of these hormones could be examined. Melatonin production was absent in the three tetraplegic subjects with injury to their lower cervical spinal cord and was of normal amplitude and timing in the two paraplegic subjects with injury to their upper thoracic spinal cord. The amplitude and the timing of TSH and cortisol rhythms were robust in the paraplegics and in the tetraplegics. Our results indicate that neurologically complete cervical spinal injury results in the complete loss of pineal melatonin production and that neither the loss of melatonin nor the loss of spinal afferent information disrupts the rhythmicity of cortisol or TSH secretion.

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