Cardiocerebral Infarction: A Single Institutional Series.

OBJECTIVES: Cardiocerebral infarction (CCI) is the rare occurrence of acute ischemic stroke (AIS) and acute myocardial infarction (AMI), either at the same time (simultaneous or synchronous) or one after the other (metachronous). The aim of this study is to describe the clinical profile, management and treatment outcomes of patients with CCI. MATERIALS AND METHODS: This is a 3-year cross-sectional study of patients with CCI describing their clinical presentation, management, and outcomes. The primary outcome measures were all-cause mortality and functional outcome measured with the modified Rankin Scale score (mRS) at discharge and at 30 days post-CCI. We also described the frequency of major and minor hemorrhagic events. RESULTS: Out of 1683 AIS patients and 1983 AMI patients admitted during our time period, 29 patients fulfilled the inclusion criteria (mean age 60 ±12, 79% males, median admission NIHSS 16 [range 1-26]). Of these, 20 (69%) had metachronous CCI while 9 (31%) had synchronous CCI. Most of the patients were given antithrombotics and only 14% were given reperfusion therapies. The all-cause mortality is 45% and 69% of which were cardiovascular deaths. Seventeen and 21% of CCI patients had a good functional outcome on discharge and at 30 days from CCI onset respectively. A total of 8 (28%) patients had hemorrhagic events. CONCLUSIONS: We present the largest single institutional series showing the prevalence rate of cardiocerebral infarction to be 0.79% (0.55% for metachronous, 0.25% for synchronous), with patients presenting as moderate-severe acute ischemic strokes and high-risk acute myocardial infarction. These patients have a high mortality rate with a significant proportion having cardiovascular deaths.

Neurologic Wilson disease: case series on a diagnostic and therapeutic emergency.

Wilson disease is a rare genetic disease causing pathologic deposition of copper in the liver, brain, cornea, kidney, and cardiac muscles. Presented are two cases of neurologic Wilson disease with progressive movement disorder and Kayser-Fleischer rings with low serum copper, low ceruloplasmin, and increased 24-hour urine copper against a background of normal transaminases. Cranial imaging revealed symmetric basal ganglia hyperintensities in T2/FLAIR. More often than not, these cases go unnoticed and misdiagnosed because of its rarity and varied presentation. Extensive workup is necessary to confirm the diagnosis. As for management, the earlier the intervention is initiated, the better prognosis would be for recovery. There are several treatment options which should be tailored to every patient with neurologic Wilson disease. Neurologic Wilson disease is considered as a copper toxicity; immediate diagnostic evaluation and early treatment initiation is a must.

La Enfermedad de Wilson es una enfermedad genética rara provocada por un depósito patológico de cobre en el hígado, cerebro, córnea, riñón y músculo cardíaco. Se presentan dos casos de Enfermedad de Wilson neurológica con trastorno progresivo del movimiento y anillos de Kayser-Fleischer con cobre y ceruloplasmina séricos bajos, y aumento de cobre en orina de 24 horas, con transaminasas normales. Las imágenes craneales revelan hiperintensidad simétrica en T2/FLAIR de los ganglios basales. Lo más frecuente es que estos casos pasen inadvertidos o no se realice el diagnóstico correcto debido a la rareza y variedad de sus presentaciones. Se require de un completo trabajo para poder precisar el diagnóstico. Respecto al manejo, cuanto antes se inicie la intervención, mejor será el pronóstico para la recuperación. Existen diversas opciones terapéuticas y deben adaptarse a cada paciente con Enfermedad de Wilson neurológica. La Enfermedad de Wilson neurológica se considera una toxicidad al cobre, por lo que es una necesidad la evaluación diagnóstica inmediata y el tratamiento precoz.

La maladie de Wilson est une maladie génétique rare qui provoque un dépôt de cuivre pathologique dans le foie, le cerveau, la cornée, le rein et le muscle cardiaque. Nous présentons deux cas de maladie de Wilson dans sa forme neurologique avec un trouble kinétique progressif et des anneaux de Kayser-Fleischer, avec une hypocuprémie, une hypocéruloplasminémie et une hypercuprurie des 24 h, les transaminases étant normales. L'IRM cérébrale montre des hypersignaux symétriques en FLAIR et T2 des ganglions de la base. Le plus souvent ces cas ne sont pas diagnostiqués et passent inaperçus en raison de la rareté et de la présentation variée de la maladie. Un bilan approfondi est nécessaire pour établir le diagnostic. De même que pour la prise en charge, plus tôt le traitement est instauré, meilleur est le pronostic de guérison. Plusieurs options de traitement sont disponibles qui doivent être adaptées à chaque patient atteint de la maladie de Wilson. La maladie de Wilson sous sa forme neurologique est considérée comme une toxicité au cuivre ; elle nécessite une évaluation diagnostique immédiate et un traitement précoce.