HTLV-associated myelopathy in a cohort of HTLV-I and HTLV-II-infected blood donors. The REDS investigators.

OBJECTIVE: HTLV-I-associated myelopathy (HAM) is a slowly progressive spastic paraparesis caused by infection with human T-lymphotropic virus type I (HTLV-I). The prevalence of HAM among those infected with HTLV-I is poorly defined, and the association of a similar myelopathy with HTLV-II infection has not been confirmed. DESIGN: Cross-sectional examination of HTLV-I, HTLV-II, and control subjects from the baseline visit of a cohort study. SETTING/ SUBJECTS: Persons testing HTLV seropositive at the time of blood donation at five U.S. blood centers, their seropositive sex partners, and a matched control group of HTLV seronegative blood donors. MEASUREMENTS: HTLV-I and HTLV-II were differentiated by serology and/or polymerase chain reaction. All subjects received systematic neurologic screening examinations. RESULTS: A diagnosis of myelopathy was confirmed in four of 166 HTLV-I subjects (2.4%, 95% confidence interval 0.7%, 6.1%) and in one of 404 HTLV-II subjects (0.25%, 95% confidence interval 0.0%, 0.6%). None of the 798 controls had a similar myelopathy, although one had longstanding typical multiple sclerosis. CONCLUSIONS: Our data also suggest that HAM occurs more frequently among HTLV-I-infected subjects than reported by previous studies. The HTLV-II infected myelopathy patient identified in this cohort, together with three other case reports in the literature, implies a pathogenic role for this human retrovirus. The diagnosis of HTLV-associated myelopathy should be considered in cases of spastic paraparesis or neurogenic bladder when risk factors for HTLV-I or HTLV-II infection are present.

Selective projections from the cat red nucleus to digit motor neurons.

Classical studies of the cat rubrospinal tract describe dense terminations in spinal laminae V-VII and an absence of any significant projection to lamina IX. In contrast, our recent studies, utilizing the anterograde transport of wheat germ agglutinin conjugated with horseradish peroxidase, have demonstrated a consistent and circumscribed area of label in lamina IX at caudal cervical segments. The present study was undertaken to determine the distribution of rubrospinal terminals among motor neurons in lamina IX as well as to identify the likely target muscles of those motor neurons located near rubrospinal terminals. We injected wheat germ agglutinin-horseradish peroxidase into the red nucleus and unconjugated horseradish peroxidase into selected forearm muscles of the same side of the body. The locations of rubrospinal terminals showing anterograde label on one side of the spinal cord could then be compared with the locations of motor neurons showing retrograde label on the opposite side of the cord. The results demonstrated a clear focus of rubrospinal terminals in the lateral and dorsal portions of the ventral horn beginning at C8 and extending through rostral T1. No other segments of the spinal cord showed a focus of rubrospinal terminations in lamina IX. Retrogradely labeled motor neurons from the muscle injections showed that the rubrospinal terminals overlap extensively with motor neuronal pools supplying distal forearm muscles. Several lines of evidence indicate that the terminals are from rubrospinal fibers and are not due to transneuronal transport.

A sensitive low artifact TMB procedure for the demonstration of WGA-HRP in the CNS.

A TMB reaction with increased sensitivity and lower artifact can be obtained by dividing the Mesulam reaction into two stages. Use of the modified reaction with HRP conjugated wheat germ agglutinin (WGA-HRP) yields a powerful technique for anterograde and retrograde tracing.