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Immunological and endocrinological disturbances in patients after prolonged coma following head injury

Formisano1, Grelli, Matteucci

  • 1I.R.C.C.S. S. Lucia, Rome, Italy.

European Journal of Neurology
|April 22, 1999
PubMed

Insights

Severe brain damage can cause temporary immune system deficits and neuroendocrine changes, particularly in the early recovery phase. These effects, including reduced interleukin-2 (IL-2) production and natural killer (NK) cell activity, may indicate a prolonged stress response.

Area of Science:

  • Neuroscience
  • Immunology
  • Endocrinology

Background:

  • Severe brain damage can lead to early deficits in cellular immunity.
  • Long-term immunological and neuroendocrine changes following severe brain injury require further investigation.

Purpose of the Study:

  • To investigate the long-term effects of severe brain damage on immunological and neuroendocrine parameters in patients recovering from prolonged coma.
  • To compare these changes with those in spinal cord injury patients and healthy individuals.

Main Methods:

  • Cross-sectional study comparing post-comatose (PC) patients with spinal cord injury (SCI) patients and healthy controls.
  • Assessed lymphomonocyte subsets, interleukin-2 (IL-2) production, natural killer (NK) activity, and serum levels of ACTH, cortisol, FSH, LH, prolactin, T3, and T4.

Main Results:

  • Patients 3-6 months post-injury (PC1 subgroup) showed decreased IL-2 production, NK activity, and CD25+ lymphocytes compared to controls.
  • Similar immune disturbances were noted in SCI patients.
  • PC1 patients exhibited elevated serum cortisol and prolactin (PRL) levels.

Conclusions:

  • Early post-severe brain injury (3-6 months) is associated with transient but prolonged immunological disturbances.
  • These changes, along with elevated cortisol and prolactin, suggest a chronic stress or alarm reaction state.

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