Correlated nerve conduction, somatosensory evoked potential and neuropathological studies in clioquinol and 2,5-hexanedione neurotoxicity in the baboon.

Observations have been made on 10 baboons receiving a high-dose regimen of clioquinol administered orally, 6 receiving a low-dose regimen and 6 treated with 2,5-hexanedione. The results were compared with those obtained from 10 control animals. Motor and sensory nerve conduction velocity was markedly reduced in the hexanedione-treated animals but only very minor abnormalities were detected in the clioquinol-treated baboons. Cervical and Rolandic somatosensory evoked potentials to lower and upper limb stimulation were delayed in both the high-dose clioquinol-treated and the hexanedione-treated animals, particularly in the latter. Histopathological studies in the low-dose clioquinol-treated group showed no abnormalities. In the high-dose group; axonal degeneration was confined to the spinal cord, cerebellar vermis and optic tract. It was most marked in the rostral portions of the dorsal spinal columns and the caudal parts of the direct and crossed corticospinal tracts. Occasional dorsal column fibres had degenerated back to the root entry zone in the cord. The distribution was that of a selective central distal axonopathy. There appeared to be no correlation with estimated blood levels of unaltered clioquinol. In hexanedione-treated animals there was also degeneration in the distal optic tracts and peripheral nerves in a pattern of central-peripheral distal axonopathy.

Intracellularly studied excitability changes in coronal-pericruciate neurons following low frequency stimulation of the corticobulbar tract.

Direct intracellular measurements of excitability changes to injected current were made in 116 cortical neurons of awake cats following antidromic or orthodromic activation by repetitive, 1-6 Hz stimulation of the pes pedunculi. The predominant effect seen in antidromically activated cells was a transient decrease in excitability and input resistance. The predominant effect seen in orthodromically (transsynaptically) activated cells was a transient increase in excitability and input resistance. In the absence of accompanying change in rates of spontaneous spike activity, the above results suggest that adaptations supporting the changes in excitability and resistance occur locally to these cells.

Amino acid uptake by dorsal root ganglia from streptozotocin-diabetic rats.

Dorsal root ganglia from streptozotocin-diabetic rats and age- and weight-matched control animals were incubated with 4-amino 3H-butyric acid. A significant reduction in uptake was observed in the diabetic animals. The incorporation of 3H-leucine into protein was also significantly reduced but the results did not allow a conclusion as to whether this was a secondary or an independent effect. These findings are discussed in relation both to the abnormalities known to develop in diabetic rats and to the causation of human diabetic neuropathy.

Developmental characteristics of histamine methyltransferase and phenylethanolamine-N-methyl-transferase of rat brain.

The specific activity of histamine methyltransferase of rat brain increases rapidly from the 16th until the 25th day of gestation (7 days after birth). The specific activity of phenylethanolamine-N-methyl-transferase shows a rapid increase during the 1st and the 2nd week after birth, the adult values being obtained by the end of the 2nd week.

Peripheral neuropathy in patients with beta-thalassaemia.

As some patients with beta-thalassaemia manifested neurological signs, clinical and electrophysiological investigations were carried out on 53 thalassaemic patients and 29 healthy control subjects. Twenty per cent of the patients showed clinical and electrophysiological findings of a mild peripheral sensorimotor neuropathy, mainly of the lower limbs. The clinical symptoms were numbness, pins and needles sensations, muscular cramps, myalgia and muscle weakness. The electrophysiological abnormalities were manifested by decreased motor conduction velocity (MCV) and prolonged F-wave latencies of the tibial and the peroneal nerves. Borderline increase in the latencies of the sensory potentials of the median nerve was also observed. The electromyographic findings of the patients with diminished MCVs were compatible with a predominantly motor peripheral neuropathy. This neuropathy appears during the second and third decade of life.