Sudden unexplained death in children with epilepsy: a cohort study with an eighteen-year follow-up.

Aim: Sudden unexplained death is a significant cause of mortality in adults with epilepsy. Only a few data exist about this risk in childhood.

Methods: Cases of sudden unexplained death in epilepsy (SUDEP) up to the age of 18 y occurring at our hospital between 1984 and 2001 were identified.

[Myoclonic-astatic epilepsy in early childhood: review of clinical signs, EEG features, etiology, and therapy].

Myoclonic-astatic epilepsy in early childhood: review of topical knowledge of clinical signs, electroencephalographic characteristics, etiology and therapy. The classification of epilepsy in childhood is discussed continuously. On the basis of some selected cases, the clinical and electrophysiological characteristics of myoclonic-astatic epilepsy in early childhood are described.

Tula virus infection associated with fever and exanthema after a wild rodent bite.

Reported here is the first case of human acute infection with Tula virus, which occurred in a 12-year-old boy in Switzerland. This hantavirus had been considered apathogenic to humans, and in Switzerland only TULV-genome sequences have been demonstrated in wild rodents to date. In this case, paronychia, fever and exanthema occurred after the patient was bitten by a wild rodent, indicating an unusual route of hantavirus transmission.

Biotinidase deficiency: a cause of subacute necrotizing encephalomyelopathy (Leigh syndrome). Report of a case with lethal outcome.

An unusual clinical course of a patient with biotinidase deficiency, causing Leigh syndrome, is reported. Laryngeal stridor was the major presenting symptom followed by progressive neurologic deterioration and death at the age of 21.5 mo.

The hemodynamic effect of STA-MCA bypass.

rCBF was measured by 133Xenon inhalation at rest and during pCO2 manipulation in 19 patients prior to and at various times after STA-MCA bypass surgery. The resting flow increased gradually postoperatively, seemingly more due to progressive clinical recovery from the original neurologic disability than due to the surgical intervention. CO2 reactivity increased in some patients, more in those who preoperatively had the poorest reactivity.