Spinal somatosensory evoked potentials to stimulation of the peroneal nerves in the popliteal fossa were recorded from 46 insulin-dependent neurologically normal patients with juvenile diabetes. Conduction velocities of these potentials were determined over proximal peroneal nerve, cauda equina, and spinal cord and were compared with those obtained from 46 age-matched control subjects. Mean values for overall spinal conduction velocity (L3-C7 spines) and conduction velocity over rostral spinal cord (T6-C7 spines) and peroneal nerve-cauda equina (stimulus to L3 spine) were lower in the diabetic group (p less than 0.001). Peripheral nerve conduction velocity alone was slow in 5 patients, and spinal conduction velocity was slow in 8; in 2 patients both peripheral and spinal velocities were slow. This study suggests that in addition to impairment of peripheral nerve function, patients with juvenile diabetes without clinical evidence of neurological involvement can have a defect in spinal afferent transmission.

The relationships between growth retardation and metabolic and hormonal parameters were studied in 7 children with fetal alcohol syndrome (FAS). Fasting blood concentrations of TSH, T(4), T(3), FSH and LH were normal. Plasma prolactin concentrations after chlorpromazine stimulation were normal. 3 children had abnormal oral glucose tolerance tests with increased plasma insulin response. Peak plasma growth hormone responses to insulin-induced hypoglycemia were elevated in 5 patients. Fasting bioassayable serum somatomedin activity, determined in 6 patients, was elevated in 3 patients and normal in 3 patients. Administration of hGH to 3 patients with FAS had little effect upon nitrogen retention and did not increase plasma insulin concentrations, although serum somatomedin activity sharply increased in 1 patient evaluated for somatomedin response. The data indicate that the growth defect in FAS is not due to deficiency of growthpromoting hormones, but rather to peripheral unresponsiveness.

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