Benign febrile convulsions with amoebiasis

Answer 1

The pathophysiology of febrile seizures remains unclear.[17] It is generally believed that an FS is an age-dependent response of the immature brain to fever.[17] This postulation is supported by the fact that most (80-85%) febrile seizures occur between 6 months and 3 years of age, with the peak incidence at 18 months.[6,7,8] Although the mechanism of this increased susceptibility is unclear, animal models suggest that there is enhanced neuronal excitability during the normal brain maturation.[17] It is well known that febrile seizures tend to occur in families, and this genetic susceptibility can be transmitted through both parents.[18,19] A positive family history for febrile seizures can be elicited in 25-40% of children with febrile seizures, and the reported frequency in their siblings ranges from 9-22%.[18] Familial clustering studies indicate a doubling of risk in children when both parents, rather than one parent, had febrile seizures.[19] Studies show a higher concordance rate in monozygotic as compared to dizygotic twins.[20] Although there is clear evidence for a genetic basis, the precise mode of inheritance is unclear.[20,21] Most studies suggest that the mode of inheritance of susceptibility to febrile seizures is mostly polygenic and rarely autosomal dominant.[20,21] No single human leukocyte antigen (HLA) haplotype has been found to be statistically more frequent among pooled FS subjects because of the considerable genetic heterogeneity of proneness to febrile seizures.[20,21] In recent times, linkage studies in several large families in Japan have mapped the FS susceptibility genes to two putative loci, FEB1 (chromosome 8q13-q21) and FEB2 (chromosome 19p13.3), indicating an autosomal dominant pattern with reduced penetrance.[21] Preliminary studies in children suggest that the cytokine network is activated and may have a role in the pathogenesis of febrile seizures.[22] Children with febrile seizures have been reported to have significantly low levels of plasma ferritin, suggesting a possible role of iron insufficiency.[23] The incidence of febrile seizures in thalassemic children is significantly lower, and iron overload may be a major factor that prevents their occurrence.[24] Also, significantly lower levels of zinc have been reported in the serum and cerebrospinal fluid of children with febrile seizures.[25,26] However, the precise clinical significance of these observations remains unclear. The systemic effects of CSE are initially dominated by the body's attempt to maintain homeostasis.9 Blood pressure and central venous pressure increase, blood glucose increases, and the patient becomes tachycardic.9 10 CSE may also result in electrolyte imbalance and hyperthermia.11 Cerebral blood flow, blood glucose, and oxygen utilisation increase in the initial phases of a seizure to maintain cerebral homeostasis. After 30 minutes homeostatic failure begins and the patient may need systemic support.9 Cerebral blood flow, brain glucose, and parenchymal oxygenation all decrease and potentially play a part in the cell damage associated with CSE.9 10 Respiratory and metabolic acidosis, electrolyte imbalance (for example, hyperkalaemia), hyperthermia, and rhabdomyolysis may all occur (table 1).Treatment with drugs with depressant cardiorespiratory side effects (for example, benzodiazepines and barbiturates) may worsen the systemic complications of CSE.

Golda Meir Ruiz