Brain Damage after Febrile Convulsions

Abstract

Despite the suggestions of several writers on the importance of convulsive seizures in infancy as an aetiological factor in the development of cerebral palsies, little attention is given to this association in the standard texts in general medicine and pathology, or even in the more special treatises on diseases of the nervous system. It is not altogether surprising, therefore, that convulsions occurring in the course of febrile illnesses are often not treated with the gravity and urgency they deserve. Because convulsions are so frequent an accompaniment of relatively innocuous infections and in most cases leave the patient apparently normal, the paediatrician may regard both a convulsion of purely febrile origin and the resulting signs of nervous disease as common manifestations of some other intracranial process.The following five cases are presented in the hope that the potentially lethal nature of convulsions will be more widely acknowledged. Materials and MethodsThe pathological material was obtained from necropsies performed at the Adelaide Children's Hospital during the years 1954 to 1956 inclusive. Before immersion of the intact brain pieces were removed for fixation in formolammonium bromide, and in two cases samples were kept for animal inoculation. After prolonged fixation complete coronal slices of the cerebral hemispheres and smaller pieces of brain-stem and cerebellum were embedded in celloidin and paraffin, and stained by Weil's method for myelin sheaths, with Nissl's stain, and by haematoxylin, counterstaining with both eosin and van Gieson's mixture. Frozen sections were used for the metallic impregnation of neurofibrils and astrocytes using Bielschowsky's and Cajal's methods, respectively.Case Reports Case 1. The patient, previously a healthy boy of 2 years, developed measles two days before admission. He had not been very sick but had been coughing a lot. On the day of admission he was found in his cot at 7.45 a.m. in a convulsive attack, blue and frothing at the mouth. This continued until 9.30 a.m. when the convulsion was controlled by ether anaesthesia in the Casualty Department of the Adelaide Children's Hospital where his colour was described by the Admitting Officer as 'almost black'.On examination in the ward his temperature was 103°F., he was slightly cyanosed, with a cold skin on which there was a fading measles rash. The pupils were equal and reacted sluggishly to light. The fundi oculorum were normal. The fauces were moderately reddened, the right tympanic membrane was dull and slightly bulging. Air entry into the lungs was good but there were many rhonchi. The abdomen was normal. Reflexes were absent in the limbs. Slight neck stiffness was present for an hour after the convulsions had ceased. SPECIAL INvEsTIGAIoNs. The cerebrospinal fluid was under a pressure of 100 mm. of water, contained 28 mg. protein per 100 ml. and no cells. The white blood count was 24,000 per c.mm., of which 81% were polymorphonuclear leucocytes. COURSE. In the evening of admission he went pale, with a blood...

Outcome of childhood status epilepticus and lengthy febrile convulsions: findings of national cohort study.

“…In Aicardi and Chevrie's 1970 study children with encephalitis were classified separately from those with "cryptogenic" febrile status epilepticus, although the authors agreed that it was difficult to differentiate.2 Fowler applied the term "febrile convulsion" to attacks lasting from one to six hours that occurred in five children, four of whom remained unconscious after the attacks until they died. 16 The evidence presented in this and previous papers7-0 suggests that such catastrophic attacks are rare. Apart from the children with encephalitis and the child who became hyperthermic, probably due to mis-management of a febrile convulsion, there were no cases in this study in which permanent new neurological signs were documented after status epilepticus or lengthy febrile convulsions.…”

“…The first studies were conducted by an external research team at HM Prison Saughton, Edinburgh, in August 1991 and October 1992.12 In 1992 surveillance was extended to Polmont Young Offenders' Institution, which is Scotland's largest establishment for young male offenders (aged [16][17][18][19][20][21]. Prisoners in Polmont were invited to participate in a study of HIV prevalence, risk behaviours, and uptake of HIV tests by young males in the communities served by Polmont.…”

Do seizures damage the brain? The epidemiological evidence

“…In 1950 Ekholm and Niemineva reported a mortality rate of 11% in a group of children in hospital with “infection convulsions.”24 Fowler25 and Meldrum26 described neuronal necrosis in the cerebral cortex, the hippocampi, and the cerebellum of children who died after prolonged “febrile convulsions.” These necropsy studies were of extreme cases that were not typical of the majority of febrile convulsions (see below).…”

Short report: Mesial temporal haemorrhage, consequence of status epilepticus

“…Acute haemorrhagic lesions were observed in the brain, involving symmetrically both amygdala and cornu Ammonis. The sequential occurrence of these lesions with status epilepticus are discussed in the light of data from the literature.Numerous reports have delineated the pathological findings in status epilepticus (Fowler, 1957;Scholz, 1959;Norman, 1964): ischaemic lesions and glial reactions are observed in selectively vulnerable regions. These lesions are commonly held to be the consequence and not the cause of the convulsive status (Meldrum, 1976).…”

“…Numerous reports have delineated the pathological findings in status epilepticus (Fowler, 1957;Scholz, 1959;Norman, 1964): ischaemic lesions and glial reactions are observed in selectively vulnerable regions. These lesions are commonly held to be the consequence and not the cause of the convulsive status (Meldrum, 1976).…”