Elevated plasma concentrations of lipoprotein(a) in medicated epileptic patients.

Lipoprotein(a) [Lp(a)] has been identified as an independent risk factor for vascular diseases. There are no data on Lp(a) levels in patients on long-term medication with carbamazepine, phenytoin, phenobarbital, or valproate. To investigate the effects of such treatment on Lp(a) levels and common carotid artery intima media thickness we studied 51 epileptic outpatients on long-term antiepileptic medication and 51 age-and sex-matched controls. Lp(a) levels above 45 mg/dl were found in 11 of 50 patients, but in only 4 of 51 controls (P < 0.05). The mean serum concentration of Lp(a) was 33.0+/-7.0 mg/dl in patients and 16.9+/-2.7 mg/dl in controls (P < 0.05). Epileptic patients also had a thicker intima media of the common carotid artery (0.79+/-0.04 mm) than controls (0.69+/-0.02 mm, P < 0.05) as measured by B-mode ultrasonography. Our results suggest an untoward effect of long-term antiepileptic medication on Lp(a) serum concentrations. Elevated Lp(a) levels might be a risk factor for arteriosclerosis in epileptic patients.

Recent infection as a risk factor for intracerebral and subarachnoid hemorrhages.

Previous infection has been shown to be a risk factor for acute cerebral ischemia. We tested the hypothesis that recent infection is also a risk factor for intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). We performed a case-control study with 56 consecutive patients with ICH, 44 consecutive patients with SAH, and 56 and 44 neurological control patients, respectively. Infection within 4 weeks was associated with SAH independently of hypertension and smoking (p = 0.049). There was no significant association between infection and ICH. Recent infection, primarily upper respiratory tract infection, may be a risk factor for SAH by contributing to the formation and rupture of aneurysms.

Neurochemical monitoring of fatal middle cerebral artery infarction.

BACKGROUND: Microdialysis is a method for neurochemical monitoring that has been applied more frequently over the past few years in patients suffering from subarachnoid hemorrhage, acute brain injury, and stroke. It is used to study the course of extracellular molecules of low molecular weight, such as excitatory amino acids or metabolic end products. CASE DESCRIPTION: We report the case of a 43-year-old patient suffering from left hemispheric stroke with a space-occupying postischemic edema leading to a considerable mass effect on the contralateral side. For treatment of severe edema, hypothermia was initiated. The microdialysis and intracranial pressure probe were placed into the noninfarcted hemisphere. A massive increase in levels of glutamate, glycerine, and the lactate-pyruvate ratio was measured 24 hours before intracranial pressure elevation was observed and brain death occurred. CONCLUSIONS: Monitoring excitatory amino acids, glycerine as a membrane component, and lactate-pyruvate ratio as an energy marker by microdialysis is a useful tool to increase our understanding of biochemical events in secondary brain damage. For future prevention of secondary ischemia in patients with massive stroke, close neurochemical monitoring might be valuable to improve therapy, particularly in the critically ill.