Abstract
Human T-lymphotropic virus type-1 (HTLV-1) is a neglected infection most often associated with an indolent process. However, a subset of HTLV-1 seropositive patients face the risk to develop life-threatening T-cell lymphoma/leukemia, or the highly disabling and incurable HTLV1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Over the years, other complications to HTLV-1 have been proposed and debated intensely. One of these, although rare, associations include cerebellar ataxia occurring most often in Japanese patients with manifest HAM/TSP. Here we present a HTLV-1 seropositive patient from the Middle East featuring a slowly progressive cerebellar syndrome with cerebellar atrophy but not evidence of spastic paraparesis. In addition, this patient suffered from autoimmune conditions such as Sjögren’s syndrome and vitiligo which are putatively associated with HTLV-1.
Highlights
Infection with human T cell lymphotropic virus type 1 (HTLV1) is in most cases indolent; some patients develop adult T cell leukemia, associated with poor prognosis, or the
Onset of neurological symptoms was at age 59, 6 years before Human T-lymphotropic virus type-1 (HTLV-1) infection was diagnosed as a result of contact tracing
Neuroimaging demonstrated cerebellar atrophy (Fig. 1) but not evidence of widespread white matter abnormalities (WMA); lumbar spondylosis was evident, but there were no abnormalities in the spinal cord
Summary
Written consent was obtained for this case report, approved by the Ethics Committee in Stockholm. The patient had brisk patellar reflexes (3+), normal Achilles reflexes, and absence of Babinski’s sign Her muscle tone, strength, and sensation to touch and pin prick were normal. Vibration sense in her malleoli and proprioception were impaired with subsequent abnormal Romberg’s test; the retropulsion test was normal. Her altering hand movements were irregular; bradykinesia was absent. CSF PVL (4 HTLV DNA copies/15 cells), neopterin 3.7 pg/mL (reference 2–3 pg/mL), and CXCL10 249.1 pg/mL (reference 115–160.8 pg/mL) were high Computed tomography of her chest and abdomen showed an enlarged thyroid gland but the patient was euthyroid; a biopsy aspirate demonstrated colloid cells only. Oral steroids were given with chemotherapy, but this did not alleviate the patient’s motor symptoms
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