Head trauma and neuroprotection.

Traumatic brain injury is a serious clinical problem connected with high mortality rate and long-term neurobehavioral and socioeconomic consequences. Pathomechanism of such insult is complex and not clear in all aspects as yet. Thus, a primary mechanistic insult to the brain initiates metabolic and inflammatory processes which exacerbate the primary traumatic injury to neurons, leading to secondary brain damage. In this paper we present the main components of destructive cascade with relevant theoretical strategy for neuroprotection. It should be emphasized that pathological processes involved in secondary brain damage are complex and interrelated. It makes blockade of a single mechanism unlikely to prevent either early or delayed cellular death.

[Convulsive status epilepticus--clinical analysis of patients treated iin the Neurological Clinics, Medical Academy in Lublin in the years 1986-1995]. / Stan padaczkowy napadów drgawkowych--analiza kliniczna chorych leczonych w Klinice Neurologii AM w Lublinie w latach 1986-1995.

The authors reviewed clinical records of 57 consecutive adults (age: 17-78, 63%--men) treated in the intensive care unit to convulsive SE that was refractory to first-line medication (BDZ,PB). They were divided into three groups: up to 30 (mean 21 years, 28%), between 31-50 (43 y, 32%) and above 50 (59 y, 40%), 58% had previously had epilepsy with prevalence in the youngest (85%). Among the oldest in whom epilepsy occurred de novo as much as 42% experienced it in the form of convulsive SE. Generalized SE was observed in 83% of cases; exclusively in patients up to 50 and in 61% of the oldest. The identifiable precipitating causes of SE were determined in 72% cases but in 25% there were two or more of them. Among previously epileptics leading etiologies for SE were: alcohol abuse, infection or drug withdrawal. Recent brain injury (stroke, neuro-infection, trauma) accelerated refractory seizures in epilepsy-free cases. Time to recovery varied from 0.5-2 (6%) to 2-6 or above 6 hrs (46% each) after continuous i.v. administration of BZD or chlormethiazole (53%) when ineffective. No side effects were noted. The commonest complications during SE were hyperthermia and transient dysregulation of circulatory or/and respiratory systems. Everyone was led out of SE. Overall mortality amounted to 12%. Among the deceased 71% were in the oldest group and everyone with recent brain lesion. This study highlights differences in the course of convulsive SE according to age and underlying etiology and the importance of intense care in therapeutic schedule. A more common chlormethiazole administration, a useful therapeutic tool in management of convulsive SE in adults had been discussed.