Neuropsychological assessment in HTLV-1 infection: a comparative study among TSP/HAM, asymptomatic carriers, and healthy controls

Abstract

Background: Human T cell lymphotropic virus type 1 (HTLV-I) can cause tropical spastic paraparesis/ HTLV-1 associated myelopathy (TSP/HAM) and adult T cell leukaemia/lymphoma. More recently other diseases such as isolated peripheral polyneuropathy, myopathy, artropathy, and uveitis have been associated with this retrovirus. Only a few uncontrolled studies, without necessary exclusion criteria, have described mild cognitive deficits among TSP/HAM patients. To further clarify this the authors evaluated, through neuropsychological testing patients with TSP/HAM and asymptomatic infected carriers, comparing both groups with healthy controls. Objectives: To verify the presence of cognitive deficits among TSP/HAM patients and asymptomatic HTLV-1 infected carriers. In addition, the authors aimed to investigate if these deficits correlated with the degree of motor impairment in TSP/HAM patients. Methods: From a cohort of 501 HTLV-1 infected people the authors selected, according to predefined inclusion and exclusion criteria, 40 asymptomatic HTLV-1 carriers and 37 TSP/HAM patients. Neuropsychological testing was blindly performed in both groups and their scores were compared with those obtained from controls. Results: Both the HTLV-1 carrier group and the group of patients with TSP/HAM exhibited a lower performance in neuropsychological tests when compared with controls. Asymptomatic infected carriers and TSP/HAM patients did not differ in their cognitive results. Also, there was no relation between the degree of motor disability and cognitive deficits in the TSP/HAM group. Psychomotor slowing and deficits in the some domains characterised the neuropsychological impairment in HTLV-1 infection: verbal and visual memory, attention and visuomotor abilities. Conclusions: TSP/HAM as well as asymptomatic infection can be associated with mild cognitive deficits. This finding, if confirmed by further studies, will permit the inclusion of cognitive impairment among the neurological manifestations of HTLV-1.

HTLV-1 and neurological conditions: when to suspect and when to order a diagnostic test for HTLV-1 infection?

“…Most of the published papers about cognitive disturbances in HAM/TsP describe psychomotor slowing, attention deficits as well as visual and working memory deficits 16,17 . In the only controlled study using an extensive neuropsychological battery, HTLV-1 infection was associated with mild cognitive deficits characterized by impairments in psychomotor speed, verbal fluency, verbal and visual memory, selective and alternate attention (flexibility), and visuoconstructive abilities 18 .…”

Neurologic abnormalities in HTLV-I– and HTLV-II–infected individuals without overt myelopathy

“…These symptoms and conditions may later progress to HAM or constitute isolated neurologic syndromes associated with HTLV infection. Sensory neuropathy, [6][7][8] gait abnormalities, 9,10 bladder dysfunction, 6,9-12 erectile dysfunction, 13,14 ALS, 15 mild cognitive deficits, 16 and rarely, motor neuropathies 6,8,13,[17][18][19] have all been reported among HTLV-I-infected individuals without HAM. Although less research has focused on HTLV-II, sensory neuropathy has been observed with HTLV-II alone 20 and with HIV coinfection.…”

The motor evoked potential in aids and HAM/TSP State of the evidence

“…Besides the CMCT measurements discussed above, more sophisticated and sensitive TMS measures that detect early changes in thalamocortical-basal ganglia circuitry 20,83,84 such as cortical thresholds, recruitment curves, silent periods, and excitatory and inhibitory phenomena produced by short and long interval stimulation obtained by single and paired magnetic stimulation are worth trying in HIV asymptomatic patients as well as in HTLV-I carriers at times when the fastest corticospinal fibers remain uninvolved 11,12,24,76,[85][86][87][88][89] . This can be done in order to better understand cortico-cortical and neurotransmitter dysfunction early in disease development 90 , and it will also allow the application of more appropriate and effective neuromodulatory measures long before the fatal clinical AIDS or HAM/TSP appears.…”