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Letter to the Editor
September 1999

Human T-Cell Lymphotropic Virus Type 1–Associated Neurologic Disorder Without Spastic Paraparesis

Author Affiliations

Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999

Arch Neurol. 1999;56(9):1167. doi:10.1001/archneur.56.9.1167

In a recent article, Douen and colleagues1 described a neurologic complication of human T-cell lymphotropic virus type 1 (HTLV-1) infection in the absence of spastic paraparesis. We read the article with interest because we have reported a similar case.2 A 63-year-old Japanese woman complained of flaccid paraplegia for 13 years. Tendon reflexes were hypoactive in the legs, and a Babinski sign was observed. Vibratory sense was diminished distally in the legs. Motor nerve conduction velocity was low borderline. Sensory nerve conduction velocity was normal, but sensory evoked potentials revealed delayed N9 potentials (11.1 and 10.7 milliseconds) with normal spinal and central responses. The H and F waves were normal. Needle electromyography showed myogenic changes in the upper limb and paraspinal muscles and neurogenic changes in the lower limbs. Serum creatine kinase and myoglobin levels were mildly elevated. Antibodies for HTLV-1 were found in both the serum (titre, 1:131,072) and cerebrospinal fluid (titre, 1:512) by particle agglutination, and this was confirmed by Western blot. Histologic examination verified mild myogenic changes in the biopsy specimen from the deltoid muscle and both neurogenic and myogenic changes in the quadriceps femoris muscle. A spastic bladder was observed by cystometry, without any complaint of urinary dysfunction. We therefore believed that this patient had a myelopathy, as suggested by the Babinski sign and spastic bladder, but the patient did not show spastic paraparesis because of a coexisting myopathy, neuropathy, or anterior horn involvement, which also can be associated with HTLV-1 infection.

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