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Brain, Vol. 114, No. 2, 867-892, 1991
© 1991 Oxford University Press


research-article

SURAL NERVE MORPHOMETRY IN DIABETIC AUTONOMIC AND PAINFUL SENSORY NEUROPATHY

A CLINICOPATHOLOGICAL STUDY

J. G. LLEWELYN1,*, S. G. GILBEY2,**, P. K. THOMAS1,, R. H. M. KING1, J. R. MUDDLE1 and P. J. WATKINS2

1Department of Neurological Science, Royal Free Hospital School of Medicine London, UK 2Diabetic Department, King's College Hospital London, UK

Correspondence to: Correspondence to: Professor P. K. Thomas, Department of Neurological Science, Royal Free Hospital School of Medicine, London NW3 2PF, UK

Observations have been made on a selected series of insulin-dependent patients with neuropathy, subdivided into three groups: (1) severe autonomic neuropathy with an accompanying painless sensory neuropathy; (2) severe autonomic neuropathy with a chronic painful sensory neuropathy, and (3) chronic or acute painful sensory neuropathy with no autonomic neuropathy. All three groups showed a loss of large and small myelinated nerve fibres in sural nerve biopsy specimens which was greater in Groups 1 and 2. Regenerative activity was prominent in all three groups, but least in Group 3. Teased fibre studies showed evidence both of axonal regeneration and remyelination. Active fibre degeneration was rare. Measurements of gratio (axon diameter:total fibre diameter) gave no indication of axonal atrophy. The density of unmyelinated axons was reduced in all three groups, as was their median diameter.

Vibration sense threshold was positively correlated with the total number of myelinated fibres and thermal sensory threshold with median unmyelinated axon diameter but not with total unmyelinated axon numbers. No correlation between the occurrence of pain and active degeneration of myelinated fibres or with regenerative activity either in myelinated or unmyelinated axons was detectable. Assessment of differential loss of large or small myelinated nerve fibres was difficult because of the presence of large numbers of small regenerating myelinated axons.

The results are discussed in relation to the concept of ‘diabetic small fibre neuropathy’ and the causation of pain in diabetic neuropathy.

.

Received February 7, 1990. Revised May 25, 1990. Accepted May 30, 1990.


*Present address: Department of Neurology, King's College Hospital and Institute of Psychiatry, Denmark Hill, London SE5.

**Present address: Department of Endocrinology, Royal Postgraduate Medical School, Hammersmith Hospital, DuCane Road, London W12.


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