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Post-traumatic anosmia. Ultrastructural correlates.

B W Jafek1, P M Eller, B A Esses

  • 1Department of Otolaryngology/Head and Neck Surgery, University of Colorado School of Medicine, Denver 80262.

Archives of Neurology
|March 1, 1989
PubMed
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Head trauma can disrupt olfactory epithelium regeneration, preventing axons from reaching the olfactory bulb. This study investigates the cellular basis of post-traumatic anosmia in five patients.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Otorhinolaryngology

Background:

  • Post-traumatic anosmia, or loss of smell after head injury, is a common clinical problem.
  • The underlying cellular mechanisms of olfactory dysfunction following trauma remain incompletely understood.

Purpose of the Study:

  • To investigate the ultrastructural changes in the olfactory epithelium of patients with post-traumatic anosmia.
  • To elucidate the cellular basis for the failure of olfactory nerve regeneration after head trauma.

Main Methods:

  • Olfactory biopsy specimens from five patients with post-traumatic anosmia were obtained.
  • Biopsies underwent detailed ultrastructural examination using electron microscopy.
  • Psychophysical testing and clinical evaluation were performed for each patient.

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Main Results:

  • Olfactory epithelium showed disrupted architecture with distorted olfactory receptor cells.
  • Axons were frequently observed near the basement membrane and within the epithelium, but olfactory cilia were rare.
  • Bald olfactory vesicles, containing basal bodies, were commonly identified, suggesting attempted regeneration.

Conclusions:

  • Head trauma leads to significant disruption of the olfactory epithelium.
  • Regenerating axons appear unable to penetrate the fibrotically healed cribriform plate.
  • This blockage prevents re-innervation of the olfactory bulb, causing persistent anosmia.