Opsoclonus-myoclonus-ataxia syndrome associated with central nervous system HIV-1 escape phenomenon. / Síndrome opsoclono-mioclono-ataxia asociado a fenómeno de escape viral por virus de la inmunodeficiencia humana en el sistema nervioso central.

INTRODUCTION: Opsoclonus-myoclonus-ataxia (OMA) syndrome is a rare neurological disorder characterized by involuntary conjugate saccadic eye movements, myoclonus, and ataxia. Few reports exist on patients with HIV and OMA. CASE REPORT: A 41-year-old man diagnosed with HIV-1 infection in 1997 coursed with multiple anti-retroviral schemes as a consequence of poor adherence. In 2008 he presented an HIV-1 viral load of 100,000 copies/mL and a CD4+ T cell count of 10 cells/mm3. In 2013 our patient arrived with an 11-month history of progressive opsoclonus and ataxia. He had undetectable plasma HIV-1 RNA load and CD4+ of 606 cells/mm3. No opportunistic infections were found. Cerebrospinal fluid analysis showed mildly elevated protein concentration and HIV-1 viral load of 534 copies/mL. Cerebrospinal fluid co-receptor tropism test showed selective CCR5 usage. A brain magnetic resonance imaging showed hippocampal atrophy and T2-weighted hyperintensities. Our patient exhibited a dramatic recovery and cerebrospinal fluid HIV clearance after adjustment of anti-retroviral treatment based on genotyping resistance and tropism analyses. CONCLUSIONS: In patients with HIV presenting cengral nervous system dysfunction without opportunistic infections, cerebro-spinal fluid and plasma HIV-1 viral load, resistance and tropism tests should be performed to assess a potential viral escape and to design the appropriate anti-retroviral therapy in an individual patient basis.

TITLE: Síndrome opsoclono-mioclono-ataxia asociado a fenómeno de escape viral por virus de la inmunodeficiencia humana en el sistema nervioso central.Introducción. El síndrome opsoclono-mioclono-ataxia (OMA) es un trastorno neurológico infrecuente caracterizado por movimientos oculares conjugados sacádicos involuntarios, mioclonías y ataxia. Existen pocos casos en la bibliografía de pacientes con virus de la inmunodeficiencia humana (VIH) y OMA. Caso clínico. Varón de 41 años y diagnóstico de infección por el VIH-1 desde 1997, que cursó con múltiples esquemas antirretrovirales debido a una pobre adhesión al tratamiento. En 2008 presentó una carga viral de 100.000 copias/mL y una cuenta linfocitaria CD4+ de 10 células/mm3. En 2013 sufrió un cuadro progresivo de 11 meses de evolución caracterizado por opsoclonía y ataxia. En ese momento, su carga viral era indetectable, y la cuenta de CD4+, de 606 células/mm3. Se descartaron infecciones oportunistas. El examen del líquido cefalorraquídeo demostró hiperproteinorraquia leve y una carga viral de 534 copias/mL. El examen del tropismo de correceptor en el líquido cefalorraquídeo demostró un uso selectivo de CCR5. La resonancia magnética cerebral objetivó atrofia hipocámpica e hiperintensidades en las secuencias ponderadas en T2. El paciente mostró una recuperación clínica franca y un aclaramiento de la carga viral en el líquido cefalorraquídeo tras el ajuste de antirretrovirales basado en la resistencia de genotipo y el análisis de tropismo. Conclusiones. En pacientes con infección por el VIH y disfunción del sistema nervioso central sin infecciones oportunistas, debería llevarse a cabo una determinación de la carga viral en el plasma y el líquido cefalorraquídeo para descartar un potencial fenómeno de escape viral, así como exámenes de resistencia y tropismo para diseñar el tratamiento antirretroviral adecuado.

Association of neurologic manifestations and CEA levels with the diagnosis of brain metastases in lung cancer patients.

PURPOSE: Lung cancer (LC) is the most common source of brain metastases (BM). Because of the difficulty in predicting LC patients who will develop BM, we aimed to identify the clinical and serologic markers that could predict the presence of BM in LC patients. METHODS: We analyzed a cohort of LC patients sent for neurooncological consultation for any neurologic symptom at a cancer center from June 2013 to July 2017. INCLUSION CRITERIA: histologically confirmed LC, age ≥ 18 years and complete clinical records. EXCLUSION CRITERIA: BM diagnosis before our consultation and absence of MRI. Oncologic history, clinical symptoms and comorbidities were analyzed. RESULTS: From 199 patients, most (70%) had > 1 neurological symptom. The most common was headache (n = 46, 21%), followed by seizures (17%), altered mental status (16%) and focal motor weakness (13%). BM was found in 74% of the patients during follow-up. Multivariate logistic regression analysis showed factors associated with a higher frequency of BM: age < 65 years [OR 3.15, 95% CI 1.3-7.5], headache (OR 3.8, 95% CI 1.2-11.8), seizures (OR 3.2, 95% CI 1.1-9.3) and CEA ≥ 15 ng/mL (OR 5.5, 95% CI 2.2-13.8). Focal sensory deficit was associated with a lower frequency of BM (OR 0.2, 95% CI 0.06-0.92). The presence of certain clinical neurologic symptoms, together with CEA level, was associated with a higher risk of BM in LC patients. CONCLUSION: The clinical manifestations of patients with LC should not be overlooked because some may have a substantial correlation with BM.