Pediatric seizures have been linked to psychiatric disorders in childhood, but there is a paucity of large-scale population-based studies of psychiatric comorbidity in later life. This study aimed to examine the relation between childhood seizures and the risk of psychiatric disorders in adolescence and early adulthood.

Between Jan 1, 1978, and Dec 31, 2002, 1,291,679 individuals were born in Denmark and followed up in the population cohort (approximately 15 million person-years). 43,148 individuals had a history of febrile seizures, 10,355 had epilepsy, and 1,696 had both these disorders.

83,735 (6%) cohort members were identified with at least one of the psychiatric disorders of interest. The risk of any psychiatric disorder was raised in individuals with a history of febrile seizures (hazard ratio [HR] 1·12, 95% CI 1·08–1·17), epilepsy (1·34, 1·25–1·44), or both disorders (1·50, 1·28–1·75). Excess risk of psychiatric illness associated with childhood seizures was present across a range of different disorders, most notably schizophrenia but also anxiety and mood disorders. Associations did not differ between males and females (p=0·30) but increased with a growing number of admissions for febrile seizures (p<0·0001) and with later onset of childhood epilepsy (p<0·0001).

Children with epilepsy and febrile seizures—with and without concomitant epilepsy—are at increased risk of developing a broad range of psychiatric disorders in later life. Clarification of the underlying mechanisms attributable to these associations is needed to identify potential options for prevention.

Researchers investigated the effectiveness of Diacomit add-on therapy to Depacon (valproate) and Onfi in Dravet syndrome patients carrying known pathogenic (disease-causing) mutations in the SCN1A gene.

Among children with pathogenic SCN1A mutations, Diacomit treatment was more effective in those carrying missense (single nucleotide mutation that alters protein composition) mutations (reduction of 87.50% in seizure frequency), compared to those carrying truncation (mutation that makes proteins shorter) mutations (reduction of 70.50% in seizure frequency).

However, Diacomit treatment was not favorable in children carrying mutations in regions between different domains, or between segments of the same domain of the SCN1A gene, or at splicing sites (regions of the gene that are prone to be removed or shifted to generate different proteins).

Despite “the relative smallness of the sample and it being designed as a retrospective review of clinical data, we were able to demonstrate that STP [stiripentol] has better efficacy in DS [Dravet syndrome] patients with definite SCN1A mutations than in DS patients with VOUS [variants of unknown significance] and benign SCN1A mutations,” researchers wrote.

There is little epidemiological data in the literature on the therapeutic compliance of epileptic children. Yet it is a fundamental issue in the therapeutic education and balance of this pathology. To obtain more epidemiological precision on the observance of epileptic children and to propose, according to the factors involved, the improvement of practices (therapeutic education). Propose an evaluation of the quality of life of their children by a suitable self-questionnaire.

Eligibility

Ages Eligible for Study: 5 Years to 18 Years (Child, Adult)
Sexes Eligible for Study: All
Sampling Method: Non-Probability Sample

Inclusion Criteria:

• Child aged 5 to 17
  • Child who has received complete information on the organization of the research and who has not objected to his participation and the exploitation of his data
  • Holder (s) of the parental authority present (s) having received the complete information on the organization of the research and not being opposed to the participation and the exploitation of the data of his child
  • Epileptic child
  • Follow-up at the neuro pediatric department of CHRU Nancy

Exclusion Criteria:

• Epileptic encephalopathy
• Multiply handicapped child

Objective:
To study associations of the severity of impairment in childhood neurocognition (NC) with long?term mortality and complete seizure remission.

Methods:
A population-based cohort of 245 subjects with childhood onset epilepsy was followed up for 50 years (median = 45, range = 2?50). Childhood NC before age 18 years was assessed as a combination of formal intelligence quotient scores and functional criteria (school achievement, working history, and psychoneurological development). Impaired NC was categorized with respect to definitions of intellectual functioning in International Classification of Diseases, 10th revision (R41.83, F70-F73). The outcome variables, defined as all?cause mortality and 10?year terminal remission with the 5 past years off medication (10YTR), were analyzed with Cox regression models.

Results:
Of the 245 subjects, 119 (49%) had normal childhood NC, whereas 126 (51%) had various degrees of neurocognitive impairment. During the 50?year observation period, 71 (29%) of the subjects died, 13% of those with normal and 44% of those with impaired NC. The hazard of death increased gradually in line with more impaired cognition, reaching significance in moderate, severe, and profound impairment versus normal NC (hazard ratio [Bonferroni corrected 95% confidence interval] = 3.3 [1.2?9.2], 4.2 [1.2?14.2], and 5.5 [2.4?12.3], respectively). The chance for 10YTR was highest among subjects with normal NC (61%), whereas none of those with profound impairment reached 10YTR. In the intermediate categories, the chance was, however, not directly related to the increasing severity of impairment.

Significance:
The severity of neurocognitive impairment during childhood shows a parallel increase in the risk of death. In comparison with normal NC, subjects with lower childhood NC are less likely to enter seizure remission. However, normal NC does not guarantee complete remission or prevent premature death in some individuals with childhood onset epilepsy.