In 4 patients with a complete upper limb palsy due to traumatic cervical root avulsion, surgical anastomosis of intercostal to musculocutaneous nerves was performed to restore function in the biceps brachii muscle. Four to 6 months after the operation, motor unit discharges were recorded from the biceps muscle on the operated side during deep breathing and by cortical magnetic stimulation. The motor unit discharges became independent from respirations gradually over 1 to 2 years. The latencies of the motor potentials evoked by cortical and thoracic root magnetic stimulation decreased gradually over 2 to 3 years. Motor cortex mapping of the reinnervated biceps muscle showed a gradual change over 4 to 33 months from the area of the intercostal muscles to that of the arm area, which was more lateral on the motor cortex. These findings suggest that reorganization of the motor cortex to arm flexor muscles occurs following peripheral nerve anastomosis.

To date, three loci for autosomal recessive hereditary spastic paraplegia (ARHSP) linked to chromosomes 8p12‐q13, 16qter, and 15q13–15 have been characterized. We have clinically characterized 13 Japanese ARHSP families and performed genetic linkage analyses. All 13 families were classified as having the “complicated” form, which manifests with mental impairment and thin corpus callosum. Linkage to the 8p12‐q13 and 16qter loci was excluded, although 10 of the 13 families showed marker data consistent with linkage to the 15q13–15 locus. The multipoint LOD score of the 10 families linked to chromosome 15 was above 9.00 in the 3‐centimorgan segment flanked by D15S994 and D15S659, with a maximum multipoint LOD score of 9.68 at a position 1.2 centimorgans telomeric from D15S994 to D15S659. We have shown that ARHSP with thin corpus callosum, a subtype of recessive spastic paraplegia, maps to chromosome 15q13–15. Ann Neurol 2000;48:108–112

To date, three loci for autosomal recessive hereditary spastic paraplegia (ARHSP) linked to chromosomes 8p12-q13, 16qter, and 15q13-15 have been characterized. We have clinically characterized 13 Japanese ARHSP families and performed genetic linkage analyses. All 13 families were classified as having the "complicated" form, which manifests with mental impairment and thin corpus callosum. Linkage to the 8p12-q13 and 16qter loci was excluded, although 10 of the 13 families showed marker data consistent with linkage to the 15q13-15 locus. The multipoint LOD score of the 10 families linked to chromosome 15 was above 9.00 in the 3-centimorgan segment flanked by D15S994 and D15S659, with a maximum multipoint LOD score of 9.68 at a position 1.2 centimorgans telomeric from D15S994 to D15S659. We have shown that ARHSP with thin corpus callosum, a subtype of recessive spastic paraplegia, maps to chromosome 15q13-15.

Sweat function was studied in patients with Parkinson's disease and in normal adults by sympathetic skin response, the bromphenol blue printing method and the silicone mould method. In patients with Parkinson's disease, dysfunction of sweating was classified into two types: one type involved the postganglionic fibres and the other involved the preganglionic fibres or the central nervous system. The latter was observed in patients with milder disease and the former was observed in patients with severe disease. The progressive involvement of sweat function in Parkinson's disease may reflect spread from the central nervous system or preganglionic fibres to postganglionic fibres. In a few patients the results of sweat tests were normal. Ceruletide increased sweating in Parkinson's disease patients, and decreased the prolonged latency of the sympathetic skin response. It is hypothesized that ceruletide facilitates the preserved somatosympathetic reflex of sweating.

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