A 52-year-old human immunodeficiency virus type 1-seropositive bisexual black man was evaluated at UCLA because of the recent onset of progressive lower-extremity weakness. Initial neurologic examination showed that the patient's distal weakness was greater than his proximal weakness, with bilateral
foot drop and electrophysiologic evidence of
denervation in the distal lower extremities. Magnetic resonance imaging of the brain and spinal cord disclosed no abnormalities. Subsequent neurologic evaluation 8 months later showed a
myelopathy, with progression of lower-extremity weakness, spasticity, and flexor
spasms, and
urinary incontinence, as well as the
peripheral neuropathy noted previously. A second magnetic resonance imaging scan of the brain showed patchy foci of increased signal intensity in white matter and cortex, with mild generalized cerebral and cerebellar
atrophy and no lesions in the spinal cord. Specimens of the patient's serum and cerebrospinal fluid contained
antibodies to human immunodeficiency virus type 1. Additionally, specimens of his serum and cerebrospinal fluid were tested for antibody to human
T-cell leukemia virus type I by Western blotting and radioimmunoprecipitation, and found to be positive for human
T-cell leukemia virus type I gag, env, and tax
antibodies. The primary cause of severe
myelopathy in this patient may be
infection with human
T-cell leukemia virus type I rather than with human immunodeficiency virus type 1. Treatment with
prednisolone resulted in improvement of the lower-extremity weakness, reduction in flexor
spasms, and slower but significant improvement in urinary symptoms. Patients who are infected with human immunodeficiency virus type 1 and have unusual motor findings should be tested for concomitant human
T-cell leukemia virus type I
infection.