Magnesio en líquido cefalorraquídeo en la isquemia cerebral aguda: relación con la neurotoxicidad por el glutamato
Introduction. In animal models it has been shown that there is an increase in tissue magnesium concentration during cerebral ischemia. We studied the changes in magnesium levels in the cerebrospinal fluid (CSF) during the acute phase of cerebral ischemia. Material and methods. We included 95 patients with first ischemic cerebral infarcts admitted to hospital within the first 24 hours and also 37 controls. CT scan was done on admission and between four and seven days later (when the volume of the infarct was determined). The neurological defect was evaluated on the Canadian scale on admission, after 48 hours, on the seventh day and after three months. The CSF magnesium concentration was determined using a colorimetric method and the glutamate by HPLC. Results. The CSF magnesium concentrations were significantly higher in the patients than in the controls (2.6 +/- 0.6 mmol/l vs 2.2 +/- 0.6 mmol/l p= 0.0001). The magnesium concentration was higher in the larger infarcts (Pearson’s coefficient = 0.2901, p= o.0043), and in those presenting greater neurological defects after 48 hours (Spearman’s coefficient = -0.4649, p< 0.0001). The magnesium concentration was not related to the presence of early signs on the initial CT scan and the Canadian scale rating on admission.The concentration of magnesium was significantly correlated with that of glutamate (Pearson coefficient = 0.7735, p< 0.0001). Conclusions. The levels of magnesium in the CSF were satisfactorily related to the volumes of the infarct and the intensity of the neurological defect. However, this association was late, occurring more than 48 hours after onset of the condition
Resultados La concentración de magnesio en el LCR fue significativamente más elevada en los pacientes respecto a los controles (2,6 ± 0,6 mmol/l vs 2,2 ± 0,6 mmol/l, p= 0,0001). La concentración de magnesio fue mayor en los infartos más grandes (coeficiente de Pearson= 0,2901, p= 0,0043) y en los que presentaron mayor déficit neurológico a las 48 horas (coeficiente de Spearman= -0,4649, p< 0,0001). La concentración de magnesio fue independiente de la presencia de signos precoces en la TC inicial y con la escala Canadiense al ingreso. La concentración de magnesio se correlacionó significativamente con la de glutamato (coeficiente de Pearson= 0,7735, p< 0,0001).
Conclusiones Los niveles de magnesio en el LCR se relacionan adecuadamente con el volumen del infarto y con la intensidad del déficit neurológico, pero esta asociación no es precoz y tiene lugar después de las primeras 48 horas de iniciado el cuadro clínico
