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In Figure 1c, in Little et al’s article on diabetic neuropathy (1), there is a glove and stocking distribution of sensory loss, but with extensive involvement of the upper limbs. This is exactly the distribution of sensory loss in patients with leprosy, demonstrated in 1923 by Monrad-Krohn and shown in the Figure (2). This was a meticulous clinical examination of 63 Norwegian patients. While multiple...
In Figure 1c, in Little et al’s article on diabetic neuropathy (1), there is a glove and stocking distribution of sensory loss, but with extensive involvement of the upper limbs. This is exactly the distribution of sensory loss in patients with leprosy, demonstrated in 1923 by Monrad-Krohn and shown in the Figure (2). This was a meticulous clinical examination of 63 Norwegian patients. While multiple mononeuropathies are well described in leprosy, a sensory polyneuropathy is not recognised by
neurologists, despite a similar pattern of sensory loss being found in a group of leprosy patients in northern Nigeria, in a study carried out without prior knowledge of Monrad-Krohn’s findings (3).
Trophic ulcers, tapering of the heads of the metatarsals and Charcot’s joints are complications which occur in both diabetics and leprosy patients (4). For these reasons, and because of the similarity in the distribution of the sensory loss, an animal autoimmune model of non-lepromatous leprosy using sensory peripheral nerve as antigen (5), could be used to study the pathogenesis of diabetic neuropathy, especially as the ‘characteristic degenerative changes’ in the human disease do not develop in the streptozotocin-diabetic rat (6). There is, however, an important difference between the two disorders, in that postural hypotension is not a feature of leprous polyneuropathy (3) and hence adrenergic function is not impaired.
Little et al. state that the ‘spontaneous shooting and stabbing pains are small fibre sensations due to dysfunction of thinly myelinated A-gamma and unmyelinated C fibres’. (The thinly myelinated fibres are A-delta rather than A-gamma fibres). In the autoimmune peripheral nerve model, the conduction velocity and amplitude of A delta fibres were normal, whereas there was a diminished amplitude in the slower component of C fibres5. As only a highly selective group of neurons are affected in this autoimmune model, depletion of a growth factor may be
implicated, but is unlikely to be nerve growth factor (5,7) as adrenergic function is normal in leprosy polyneuropathy.
1. Little AA, Edwards JL, Feldman EL. Diabetic neuropathies. Pract Neurol2007; 7: 82-92.
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. Harris JR, Brand PW. Patterns of disintegration in the anaestheic foot. J Bone Joint Surg 1966; 48: 4-16.
5. Crawford, C.L. and Hobbs M.J. Neurotrophic factors in diabetic neuropathy. Trends Neurosci. 1995; 18, 15.
6 Thomas PK Growth factors and diabetic neuropathy. Diabetic Medicine 1994; 732-739.
7 Crawford CL, Hardwicke PMD. Animal models of human diabetic polyneuropathy. JAMA 2003; 289: 1779- 1780.
Figure Legend: Horizontal lines: Tactile anaesthesia
Vertical lines: Analgesia