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Post-herpetic neuralgia: post-mortem analysis of a case
C P N Watson1, C Morshead, D Van der Kooy
1Irene Eleanor Smythe Pain Clinic, Toronto General Hospital, Toronto, Ont. M5G 2C4 Canada Neurobiology Research Group, Department of Anatomy, University of Toronto, Toronto, Ont. M5S 1A8 Canada.
Pain
|August 1, 1988
Summary
Severe post-herpetic neuralgia (PHN) pain may stem from damaged nerve fibers. Autopsy revealed spinal cord atrophy and nerve fiber loss, suggesting altered neural signaling causes PHN pain.
Area of Science:
- Neurology
- Pain Medicine
- Pathology
Background:
- Post-herpetic neuralgia (PHN) is characterized by severe neuropathic pain, but its underlying morphological and biochemical mechanisms remain poorly understood.
- Understanding the neurobiological basis of PHN pain is crucial for developing effective therapeutic strategies.
Observation:
- An autopsy study examined the spinal cord and associated ganglia of a 67-year-old male with severe, long-standing PHN affecting the T7-8 dermatomes.
- The study observed significant atrophy in the dorsal horn of the thoracic spinal cord (T4-T8) on the affected side, with substantial loss of both myelin and axons.
Findings:
- While the spinal cord showed widespread axonal and myelin loss, only the T8 dorsal root ganglion exhibited fibrosis and cell loss, with apparent nerve root involvement at that level.
- Key neurochemical markers for unmyelinated afferents, inhibitory neurons, glial cells, and descending pathways showed no significant differences between affected and unaffected spinal cord regions.
Implications:
- The findings suggest that PHN pain may arise from the disinhibition of unmyelinated primary afferents due to the loss of myelinated fibers.
- Hypersensitivity of dorsal horn neurons could also contribute to the persistent, severe pain experienced in PHN.
- This study highlights the complex neuropathology of PHN and suggests potential targets for pain management.