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• Leprosy
  Colin L. Crawford
  Published on: 23 February 2009

• Published on: 23 February 2009

  Leprosy

  • Colin L. Crawford, Retired

  Dear Editor,

  Richard Hughes does not include leprosy in his list of peripheral nerve disorders.(1) While it is true that new cases of leprosy are declining rapidly , as a result of effective anti-bacterial therapy, there are still frequent numbers with residual disabilities in endemic countries.

  In neurological text books, a mononeuropathy or multiple mononeuropathy is regarded as the sole neurolog...

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  Dear Editor,

  Richard Hughes does not include leprosy in his list of peripheral nerve disorders.(1) While it is true that new cases of leprosy are declining rapidly , as a result of effective anti-bacterial therapy, there are still frequent numbers with residual disabilities in endemic countries.

  In neurological text books, a mononeuropathy or multiple mononeuropathy is regarded as the sole neurological lesion in leprosy. In 1923, Monrad-Krohn described a sensory polyneuropathy involving superficial sensory modalities in patients with leprosy.(2) A similar pattern of sensory loss was found in a group of northern Nigerian leprosy patients, without prior knowledge of Monrad-Krohn’s observations.(3) There are still no references to Monrad-Krohn’s findings in neurological text books. This omission is serious because a patient with this sensory polyneuropathy can develop trophic ulcers, mutilation of the extremities and Charcot’s joints. Moreover, this polyneuropathy, because of the distribution of the sensory loss, cannot be caused by direct invasion of the peripheral nerves by Mycobacterium leprae

  Sensory loss in leprosy can be acute in onset with simultaneous involvement of all four limbs(3) and could be an autoimmune response to an antigen in sensory peripheral nerve rather than a direct response to M.leprae . In order to test this hypothesis, rabbits were injected with a homogenate of human sensory peripheral nerve plus adjuvant and electrophysiological recordings were made from the hind limb. It was found there was a diminished amplitude in the slower component of C fibres but the conduction velocity and amplitude of A delta fibres were normal.(4) An animal model of diabetic neuropathy could be developed as a result of these experiments.(5) Some of the rabbits previously injected with sensory nerve developed a state of granulomatous hypersensitivity. ie. Skin testing in sensitised rabbits results in the formation of a granuloma,(6) with invasion of mononuclear cells into the endoneurium of dermal nerves, together with axonal damage.(7) The antigen involved is a non-myelin membrane fraction.(8) A similar antigen in the central nervous system could be used to induce tolerance, which if successful could lead to a vaccine against multiple sclerosis.(9)

  The observations on the clinical aspects of leprosy may therefore lead to a greater understanding of the pathogenesis of diabetic neuropathy and multiple sclerosis, in which case it will reinforce the maxim that there is no substitute for precise clinical examination, with no need for auxiliary aids, apart from a pin and a piece of cotton wool.

  REFERENCES

  1. Hughes R.
  Peripheral nerve diseases.
  Pract Neurol 2008; 8: 396-405.

  2. Monrad-Krohn GH.
  The neurological aspect of leprosy.
  Christiania; Jacob Dybwad, 1923.

  3. Crawford CL.
  Neurological lesions in leprosy.
  Lepr Rev 1968; 39: 9-13.

  4. Crawford CL, Hobbs MJ.
  Neurotrophic factors in diabetic neuropathy.
  Trends Neurosci 1995; 18: 15.

  5. Crawford CL.
  Diabetic Neuropathies.
  Available at http://pn.bmj.com/cgi/eletters/7/2/ 82 Accessed 22 January 2009.

  6. Crawford CL, Hardwicke PMD, Evans DHL, Evans EM.
  Granulomatous hypersensitivity induced by sensory peripheral nerve.
  Nature 1977; 265: 457-459.

  7. Crawford CL, Hardwicke PMD.
  Somatic unmyelinated degeneration in rabbits with granulomatous hypersensitivity produced by a non-myelin antigen sensory peripheral nerve.
  Acta Neuropath 1979; 45: 1-7.

  8. Hardwicke PMD, Crawford CL.
  Nature of the antigen of human sensory nerve that induces granulomatous hypersensitivity.
  J Neurochem 1978; 30: 1609-1611.

  9. Crawford CL.
  Is it possible to induce oral tolerance using a non-myelin peripheral nerve antigen?
  Available at http://www.jci.org/eletters/view/32132 Accessed 22 January 2009.

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  Conflict of Interest:
  None declared.

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