The widespread but silent cerebral mineralization: a case report.

We present a sporadic infantile case of primary cerebral mineralization with unexpected asymptomatic clinical course. An 11 months old boy with negative familial and gestational data developed normally. He died after two days of fever and rapid course of cardiorespiratory failure due to pneumonia. Parathyroid dysfunction and somatic abnormalities were not evident clinically. Neuropathological examination revealed bilateral, diffuse or pericapillary calcifications in the striatum, cerebral and cerebellar cortex, dentate nucleus and brain stem. The mineralizations were less prominent in the cerebral hemispheres than in cerebellum. A diffuse demyelination was seen in the cerebellum where calcifications were numerous. We suggest that the intracerebral calcifications progressed gradually through a disease course and probably started in the cerebellum. We discuss the lack of clinico-pathological correlations and the nosologic position of the observed syndrome.

Treatment of post-intubation laryngotracheal stenosis.

Post-intubation laryngotracheal stenosis in children is an important therapeutic problem in pediatric otolaryngology. The numbers of children treated by prolonged intubation and resuscitated children are increasing. In the Department of Pediatric Otolaryngology in Warsaw, 6 children were treated for post-intubation laryngotracheal stenosis. In the treatment the method of longitudinal intralaryngotracheal incisions was applied; in 3 cases with tracheotomy followed by cellophane separation and in 3 cases without the use of separator and without tracheotomy. There were no complications connected directly with the operation. Pneumonia was a frequent later complication making treatment difficult. Good therapeutic results were obtained.

[Neuropathological analysis of 8 cases of clinically diagnosed Reye syndrome]. / Analiza neuropatologiczna w 8 przypadkach klinicznie rozpoznanego zespolu Reye'a.

Authors discuss the possible etiopathogenesis of Reye syndrome (RS) on the base of eight own cases presented in this paper and others previously described. The febrile infection was observed on the beginning of the disease in all actually analysed cases and was followed by symptoms of acute damage of liver and brain. The central nervous system lesions present the changes increasing with time from brain oedema to the necrosis of nerve tissue. The oedematous changes could be recognized as a principal cause of unconsciousness and even of coma in RS. When the etiology of RS remain unknown the clinico-pathological observations of such cases incline to formulate three questions: Is an genetically conditioned background necessary which facilitate toxic or infectious factors to induce the RS? Is the etiology of RS only genetically conditioned? Is an specific viral infection the cause of RS?