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The influence of long-term corticosteroid and ACTH therapy in two sisters was followed up. The periods of observation were 4 and 2 years. The high levels of corticosteroids obviously reversed the fatal progress of the disease. The relapses in the elder sister occurred during longer periods of discontinued corticosteroid therapy. In the younger the therapy was continuous. There was no relapse except for a short one appearing after the tooth extraction and discontinuation of the therapy for 10 days. Some correlation between neurological signs and symptoms and porphobilinogen androporphyrin levels were found. The question arises how it is possible to influence the genetically determined disease by corticosteroids or ACTH.

Three cases were observed with the same substantial clinical features: flexion contracture of the third, fourth, and fifth finger and less extensive of the wrist. The contracture appeared after a mechanical injury not related to the involved muscles. In two cases the lesion was situated above or in the elbow region, in the third on the ulnar border of the forearm. In all cases there were some ulnar nerve signs and symptoms but the contracture involved flexor muscles which were co-innervated by the median nerve. The signs and symptoms improved or disappeared entirely after neurolysis. The question is raised, whether the contracture is due to peripheral nerves damage.

In our investigation 119 patients suffering from carpal tunnel syndrome, and 45 suffering from cubital tunnel syndrome have been analyzed. The above mentioned syndromes belong to compressive mononeuropathies and are the result of the narrowing of the anatomical channel, through which the nerve passes, causing direct or indirect pressure on the nerve and difficulties in the flow of particles and nerve impulses towards the periphery. The aim of our work was to study the influence of the compressive lesion, primarily on the distal motor and sensory latencies. To achieve a better precision, the distal motor latency is expressed as a quotient of terminal latency. It is obtained by dividing the distance between the stimulation and the recording point in centimeters with the latency of response expressed in miliseconds. Sensory latencies are obtained by orthodromic stimulation of the finger and the detection of the neural potential at the wrist. According to our results, the proximal pathological process, besides causing the localized slowing down of conduction velocity, affects the conduction velocity of the distal sensory fibers in a higher degree than of the distal motor fibers. In any case the distal motor latencies are in a higher percentage prolonged by the distal lesion, such as carpal channel syndrome, in comparison with the proximal lesion (cubital tunnel syndrome). The less pronounced prolongation of the distal latencies, especially of sensory ones, must not be proclaimed as a consequence of a local compression without additional plurisegmental analysis.