Acute peripheral nerve compression in the baboon

Abstract

As a model of acute pressure neuropathy (“Saturday night palsy”) in man, a weighted nylon cord lying across the limb has been used to produce local compression of the ulnar and anterior tibial nerves in anaesthetised baboons. Motor nerve conduction studies were carried out 18–24 hr after compression; in some animals they were repeated at intervals for periods of up to 16 weeks. In the ulnar nerve the results were variable, but in the anterior tibial nerve, compression by a 1.5 kg weight for 90 min regularly produced a severe or complete conduction block. In such cases the pressure on the skin over the nerve ranged from 1.6–2.1 kg/cm 2. A pressure of approximately 1.0 kg/cm 2 caused a partial conduction block with a conduction delay in the unblocked fibres. A pressure of 0.75 kg/cm 2 or less caused no conduction defect. When the periods of compression were extended from 90 min to 120, 150 or 180 min, the conduction blocks were accompanied by increasing amounts of Wallerian degeneration. The local blocks produced by the longer periods of compression were also slower to recover. The histological features of the lesions were basically similar to those described previously after nerve compression by a pneumatic tourniquet. In the large myelinated fibres there was displacement of the nodes of Ranvier along the fibres away from the site of pressure. This movement occurred in 2 zones near the edges of the lesion, the nodes at the centre of the lesion being spared. Accompanying the nodal displacement there was stretching of the paranodal myelin on one side of the node and invagination on the other. At the extreme edges of the lesion there was sometimes distension of the paranodal regions with thinning of the myelin. These changes were followed by demyelination and finally by remyelination. In the recovery phase irregular myelin swellings were seen which were similar in appearance to those seen previously in recovering nerves after a pneumatic tourniquet. These results, together with those described previously, indicate that in “Saturday night palsy” and similar pressure lesions of peripheral nerves, the conduction block is due to a direct mechanical effect of the applied pressure on myelinated fibres, and that ischaemia, due to compression of the intra-neural blood vessels, plays little if any part.