Research Article

Progressive neurological dysfunction during latent HIV infection.

BMJ 1989; 299 doi: (Published 22 July 1989) Cite this as: BMJ 1989;299:225
  1. J. Jakobsen,
  2. T. Smith,
  3. J. Gaub,
  4. S. Helweg-Larsen,
  5. W. Trojaborg
  1. Department of Clinical Neurophysiology, University Hospital of Copenhagen, Rigshospitalet, Denmark.


OBJECTIVE--To determine whether the delayed conduction through the spinal cord and peripheral nerves seen in patients with AIDS is related to infection with HIV or to the presence of an immunodeficient state. DESIGN--Two year prospective follow up study of electrophysiological measurements in subjects positive for HIV antibody but without AIDS. SETTING--HIV screening clinic and clinical departments in a university hospital in Copenhagen, Denmark. SUBJECTS--Twelve homosexual men positive for HIV antibody who had not developed AIDS. RESULTS--Eight latencies were measured: from the ankle to T12, the wrist to C7, T12 to the cerebral cortex, C7 to the cerebral cortex, the ankle to the gluteal crease (tibial nerve), the gluteal crease to T12, the wrist to Erb's point (median nerve), and Erb's point to C7. Spinal latencies increased in all subjects at C7 by a mean of 4.2% (SE 0.9%) and in all except one at T12 by a mean of 5.5% (1.0%). The conduction time from the gluteal crease to T12 was increased by a mean of 32.0% (5.0%) whereas that in the median and tibial nerves by only 5.6% (1.0%) and 2.2% (2.2%) respectively. CONCLUSIONS--A mild and slowly progressive peripheral neuropathy of the axonal type and a more severe progressive myelopathy or myeloradiculopathy occur concomitantly with early HIV infection, possibly as the result of a direct neurotropic action of HIV.