Circadian rhythm of the plasma cortisol level in cases of prolonged coma.

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  • OKUYAMA HIDEYA
    Division of clinical Neurology, Institute of Brain Diseases, Tohoku University School of Medicine
  • ENDO MINORU
    Division of clinical Neurology, Institute of Brain Diseases, Tohoku University School of Medicine
  • OHARA YOSHIRO
    Division of clinical Neurology, Institute of Brain Diseases, Tohoku University School of Medicine
  • TAKASE SADAO
    Division of clinical Neurology, Institute of Brain Diseases, Tohoku University School of Medicine
  • ITAHARA KATSUYA
    Division of clinical Neurology, Institute of Brain Diseases, Tohoku University School of Medicine

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  • Circadian Rhythm of the Plasma Cortisol

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Circadian variations of plasma cortisol were studied in four different groups of subjects; 17 patients with prolonged coma, 3 patient with tetraplegia with alert consciousness and without body movement, 4 patients with stabilized chronic infection with alert consciousness and with normal body movement, and control subjects consisting of 7 healthy volunteers and 5 patients with various neuromuscular disease without disturbance of con-sciousness, motor dysfunction or infection. The maximum level of plasma cortisol attained during the circadian variations was low in prolonged coma, whereas the minimum level was high in prolonged coma, as compared to other three groups. The amplitudes between the maximum and the minimum level were significantly smaller in prolonged coma than in control (p<0.005). The tendency that the maximum level appeared at early morning and the minimum at late evening was similarly observed in both prolonged coma and control groups suggesting that there is no phase shift of the circadian rhythm of cortisol in prolonged coma. The responses of plasma TSH to synthetic TSH-releasing hormone or those of plasma cortisol to ACTH were not different between prolonged coma and control, suggesting that the reduced amplitude in prolonged coma is not attributed to the function of the patients' pituitary and/or adrenal cortex. Also, there were no differences in diurnal variations in plasma glucose or non-esterified fatty acid between the prolonged coma and control, nevertheless the former was fed with liquid food via a _??_ asal tube. Therefore, highly significant reduction of the amplitude of circadian variation of cortisol in prolonged coma may not be due to exogenous factors, such as a poverty of body movement, complications due to chronic infection, or tube feeding. The results seem to suggest that the reduced amplitude of the circadian variations in plasma cortisol may have relation to the unconsciousness of prolonged coma due to severe damage to the central nervous system.

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