Innovations In Clinical Neuroscience

JAN-FEB 2018

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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C A S E R E P O R T 34 ICNS Innovations in Clinical Neuroscience • January–February 2018 • Volume 15 • Number 1–2 a CD4 count of less than 50 cells/mm 3 at the time. Neurosyphilis, HIV-related opportunistic infections, and underlying cognitive disorders were considered in narrowing the diagnosis. To further assess the status of the patient, the infectious disease department was consulted, and a physical exam revealed oral candidiasis and a new left upper-extremity (LUE) weakness. MRI of the brain demonstrated abnormal hyperintensities and hyperenhancement on fluid-attenuated inversion recovery (FLAIR) sequences and contrast-enhanced T1-weighted imaging. After the exclusion of differentials, the treatment team diagnosed the patient with progressive multifocal leukoencephalopathy (PML) (Figure 1A). After two weeks of hospitalization, the patient remained disoriented to date, year, place, and location. In addition, she had significant motor retardation, inability to use full sentences, lack of insight, and poor abstraction. Due to the severity of the diagnosis and with recovery being unlikely, hospice and home care options were discussed with the family, and the patient was discharged from the hospital. A month later, the patient presented for follow-up at our outpatient clinic. She had improved, had no recollection of her hospital admission, and reported reintroduction of HAART therapy at a local treatment center. The patient took the Montreal Cognitive Assessment (MoCA), a screening instrument for cognitive dysfunction, and received 16/30 points, suggesting cognitive impairment. A score of 26 and above is considered normal. The patient continued her follow-up appointments with the psychiatric clinic. She expressed symptoms of depressed mood, poor sleep, decreased energy and appetite, and a persistent LUE weakness. Two months after the reintroduction of HAART, the serotonergic 5HT 2A receptor antagonist mirtazapine 15mg was added to the patient's therapy regimen as an antidepressant and as empirical treatment for PML. Mirtazapine targets the 5HT 2A receptor, resulting not only in antidepressant properties but also in the medication's ability to positively impact treatment of PML, likely due to targeting the same receptor that mediates the JC virus infection of the central nervous system (CNS). Over the following seven months, the patient remained adherent with HAART and mirtazapine, and showed improvement in LUE weakness and quantifiable progress in her cognitive function (MoCA 22/30 [previously 16/30]). Corresponding follow-up MRIs of the brain demonstrated near resolution of the pre- existing findings (Figure 1B). The patient was able to perform daily tasks, played an active role in taking care of her child, and enjoyed writing and listening to music. DISCUSSION PML is a JC virus-mediated, opportunistic infection of the CNS that predominantly targets FIGURE 1: (A) Initial magnetic resonance imaging (MRI) of the brain axial in fluid-attenuated inversion recovery (FLAIR) (top row) and corresponding contrast enhanced T1-weighted images (bottom row) show multifocal, bilateral and asymmetric areas of hyperintensities and enhancement of the subcortical white matter of the right frontal, right parietal and left temporal lobes (arrows). (B) Follow-up MRI after introduction of highly active antiretroviral therapy (HAART) and mirtazapine demonstrates near resolution of preexisting findings and interval development of multifocal encephalomalacia and supratentorial volume loss (arrows)

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