Hello, my name is Lane and I'm a PGI 3 at Rush University Medical Center. Today, I am presenting on progressive lower extremity weakness and spasticity due to HTLV-1 associated myelopathy, tropical spastic parapheresis, a case report. HTLV-1 is a retrovirus that infects 10 to 20M people worldwide and is largely asymptomatic, leading to disease in less than 5% of cases. HTLV-1 is associated with adult T cell leukemia lymphoma and HTLV-1 associated myelopathy, otherwise known as tropical spastic parapheresis. HTLV-1 associated myelopathy is more common in females and affects less than 2% of HTLV-1 carriers. The onset can range from 4 months to 30 years after infection. The disease is characterized by slow onset of progressive weakness and spasticity in the lower extremities, hyperreflexia, ankle clonus, and lumbar pain. Diagnosis involves evaluation of blood or CSF for HTLV-1 antibodies. CSF may also have increased protein and mild lymphocyte pleocytosis. Lobulated lymphocytes may be present in the blood and or CSF as well. MRI can be normal or have atrophy of the cervical or thoracic cord and or white matter lesions in the subcortical and periventricular regions. This case report is about a 50-year-old female with history of stroke without any residual deficits who originally presented after suffering lower extremity weakness and spasticity following a motor vehicle accident. The patient underwent extensive workup, including infectious serological tests, MRI-MRA brain, MRI of the spine, EMG, EEG, and HTLV-1 antibody testing. EMG was abnormal with spontaneous activity in the right lower lumbar paraspinal muscles, thought to be due to nonspecific right lumbosacral radiculopathy. Additional workup was notable for MRI brain with hyperintensity in the subcortical and deep white matter and positive HTLV-1 antibodies. While the multifocal white matter lesions seen can be a manifestation of HTLV-1-associated myelopathy, the enhancing lesions are not and could possibly represent lymphoma. It was recommended that the patient undergo CSF workup. However, she refused. During her admission, she underwent intrathecal baclofen trial. However, the results were inconclusive as the patient became lethargic and drowsy, which limited the ability to perform a functional exam. She was ultimately discharged on baclofen 10 mg nightly to subacute rehab. On follow-up, the baclofen dose was increased to 10 mg BID with notable improvement in spasticity and function with continued outpatient therapy. The treatment for spastic parapheresis due to HTLV-1 infection is supportive care, including pain relief and physical therapy. However, few studies have shown systemic corticosteroids can be used to slow progression and reduce neurologic disability. Preliminary trials with monoclonal antibody treatment resulted in improvement in spasticity and reduced motor disability. This patient did not receive steroids or monoclonal antibody treatment. As previously stated, her spasticity was treated with nightly oral baclofen as intrathecal baclofen trial was discontinued due to significant lethargy. Additionally, the patient developed urinary retention, for which she was educated on clean intermittent catheterization. But she reported performing Q3 hours while awake on follow-up. The patient's early participation in therapy improved her functional ability, allowing her to ambulate with a rolling walker and perform most ADLs independently. In conclusion, HTLV-1 associated myelopathy is characterized by slow onset of progressive weakness and spasticity in the lower extremities, hyperreflexia, ankle clonus, and lumbar pain. Treatment is focused on supportive care with pain management and therapy interventions, which can potentially reduce disability. Thank you for your time.

HTLV-1 associated myelopathy

tropical spastic parapheresis

retrovirus

lower extremity weakness

spasticity