Pathophysiology of nerve compression

Nerve compression lesions remain one of the most puzzling clinical problems in hand surgery. Median nerve compression at the wrist, carpal tunnel syndrome, has a prevalence of around 4% in the population and is more common among diabetic subjects. Nerve compression can induce local changes in the nerve such as impairment of blood flow, oedema formation and inhibition of axonal transport. We are interested in the consequence of the axonal transport blockage and the changes that occur in the neurons. We are particularly interested in the regulation of transcription factors and neuropeptides after nerve compression. Regulation of for example neuropeptides in sensory neurons after compression may be important in pain modulation. Allodynia can be a common symptom after decompression of a nerve trunk particularly if the lesion has been severe. Compression can up-regulate pain related neuropeptides such as PACAP and galanin and particularly the former has a pro-nociceptive role and may play a part in pain sensitisation. Schwann cells also up-regulate different factors and can even undergo apoptosis depending on the magnitude of nerve compression. We are also particularly interested in the response of Schwann cells and neurons in diabetes, which is clinically important due to an observed increased susceptibility of nerves to nerve compression in such conditions.