Delayed decrement of the nerve impulse propagation during induced limb ischaemia in chronic hepatic failure.

Abstract

SYNOPSIS Sensory thresholds for vibrations and electrical shocks and the sensory nerve conduction velocity (median nerve) were measured during 30 minutes of induced limb ischaemia in 10 normal subjects and 15 patients with chronic hepatic failure. Sensory action potentials were recorded simultaneously at the wrist and the elbow. Seven patients (group A) had a normal perception time for vibrations. As in normal subjects, the potential amplitude decreased from the onset of ischaemia, more pronounced at the elbow than at the wrist, and the conduction velocity became reduced more rapidly in the wrist-elbow than in the first digit-wrist segment, indicating impulse propagation with decrement. Eight patients (group B) had a markedly prolonged perception time for vibrations. The reduction of potential amplitude and conduction velocity was considerably delayed, and the impulse propagation showed no evidence of decrement for 20-25 minutes of ischaemia. A rise of the threshold for electrical shocks was absent or very delayed. As in the two other groups, the rise was abrupt and occurred at the moment when the potential below the occluding cuff (elbow) was extinct. In both groups of patients there was an increasing temporal dispersion of action potentials and in patient group A a desynchronization of the late phase of the potential took place early in the course of ischaemia. Differences between groups A and B could not be predicted from the pre-ischaemic nerve conduction data.Peripheral nerve function during ischaemia is sometimes better preserved in patients with certain metabolic disorders than in normal subjects. This was shown in diabetic patients for vibratory perception (Steiness, 1959), and has later been demonstrated for touch and pain as well (Gregersen, 1968). The phenomenon has also been demonstrated in patients with uraemia (Christensen and 0rskov, 1969), chronic hepatic failure 1970), and hypercalcaemia (Gregersen and Pilgaard, 1971). In a previous study, we reported that vibratory perception was abnormally preserved during ischaemia in 18 out of 33 patients (540 %) with severe hepatic failure . The present paper further extends this study by an

Is resistance to ischaemic conduction failure induced by hypoxia?

“…RICF has been associated with diabetes for many years [4], and although this abnormality is more pronounced in those with established neuropathy [6], the question of whether this is also associated with causative factors of neuropathy remains unclear. RICF has also been reported in other metabolic conditions such as uraemia and hepatic failure [16,17] and there may be more than one mechanism responsible for producing the effect. However, although much recent work studying the pathogenesis of diabetic neuropathy has been associated with metabolic theories of aetiology, Jaramillo et al were unable to demonstrate any association between RICF and the aldose reductase pathway [10].…”