In the 1960’s, a new sedative hypnotic, thalidomide, was widely prescribed to pregnant females resulting in the birth of children with limb, organ and neurological abnormalities. One hypothesis for these effects was that thalidomide damaged the neural crest cells and in doing so, disturbed the trophic function of the sensory nerve on the limb (McCredie and Loewenthal, 1978). More recently thalidomide has been used in the treatment of haematological malignancy, its use being limited by the onset of peripheral neuropathy. Subjects exposed in utero to thalidomide were reviewed and assessed clinically and neurophysiologically to determine the aetiology of the new neurological symptoms.
Methods: Sixteen subjects were assessed. Clinical and electrophysiological assessments were tailored to the patients’ symptoms.
Results: The most common cause of new onset upper limb neuropathic symptoms was an entrapment neuropathy at the wrist or “elbow”. Several patients with obvious slowing of median sensory conduction at the wrist had little or no thenar eminence, or innervation of “thenar” muscles was by the ulnar nerve. The radius was absent or rudimentary in these subjects. Patients with symptoms related to the facial muscles had normal, symmetrical blink reflexes despite marked facial asymmetry, and patients with lower limb symptoms appeared to have a radicular distribution of symptoms but without abnormalities of proximal conduction.
Conclusion: New onset limb neurological symptoms in subjects exposed in utero to thalidomide are usually entrapment neuropathies. These neuropathies are often related to abnormal repetitive movements performed or postures adopted to accommodate the effects of the congenital deformity.