Pathogenesis Of Febrile Convulsions Research Articles

Treatment with melatonin ameliorates febrile convulsion via modulating the MEG3/miR‑223/PTEN/AKT signaling pathway.

The PTEN/AKT signaling pathway is involved in the pathogenesis of febrile convulsion (FC), a convulsion caused by abnormal electrical activity in the brain. The objective of the present study was to evaluate the therapeutic effect of melatonin (MT) on FC and the according underlying molecular mechanisms. Reverse transcription‑quantitative PCR and western blot analysis were used to explore the effects of MT on the expression levels of MEG3, microRNA (miRNA/miR)‑223, phosphatase and tensin homolog (PTEN) and protein kinase B (AKT). Luciferase assay was performed to verify the downstream targets of MEG3 and miR‑223. An animal model was established to evaluate the effects of MT on the MEG3/miR‑223/PTEN/AKT pathway. TUNEL staining was carried out to assess the effect of MT on neuronal apoptosis. Finally, the duration of seizure/convulsion was recorded to determine the effect of MT on FC. In both cell and animal models, mRNA levels of MEG3 and PTEN increased in the apoptosis group, while treatment with MT decreased the expression levels of MEG3 and PTEN. miR‑223 expression was decreased in the apoptosis group, whereas treatment with MT increased the expression level of miR‑223. Protein levels of PTEN and cleaved caspase‑3 increased in the apoptosis group, whereas treatment with MT decreased the protein level of PTEN. Phosphorylated (p)‑AKT expression was decreased in the apoptosis group and treatment with MT reversed this effect. miR‑223 could directly bind to MEG3, and PTEN was a direct target of miR‑223. MT could decrease the duration of seizure/convulsion. In all experimental groups, treatment with MT could decrease the ratio of β waves, while increasing the ratios of α, θ and δ waves. Therefore, the results from the present study collectively suggested that treatment with MT alleviated FC via the MEG3/miR‑223/PTEN/AKT pathway, which also indicated that MT could be considered as a novel strategy for the treatment of FC disease.

Changes of HMGB-1 and sTLR4 levels in cerebrospinal fluid of patients with febrile seizures

PurposeFever-induced inflammatory processes and pro-inflammatory cytokines have gained importance in recent years in the pathogenesis of febrile convulsion. Increased levels of HMGB1 (high mobility group box 1), one of the most important pro-inflammatory cytokines, are associated with prolongation of seizure duration, recurrence of seizures and the development of epilepsy. Changes in the sTLR4 level (soluble toll-like receptor 4) in the cerebrospinal fluid (CSF) are thought to be associated with memory and learning functions. In our study, we aimed to evaluate changes in HMGB1 and sTLR4 levels in patients who had febrile seizures between 6 months and 6 years. MethodsForty patients who were admitted to Akdeniz University Medical Faculty Hospital between April 2016 and April 2018 with a complaint of febrile seizure and 45 patients whose CSF samples were taken for complaints other than febrile convulsion (control group) were included in our study. ResultsComparison of the CSF HMGB1 levels of the febrile convulsion group and control group revealed a statistically significant increase in patients with febrile convulsions (p: 0.001). Comparison of the subgroups revealed that the mean value of CSF HMGB1 level was highest in the complex FS group with a mean value of 3363.9 ± 835,47 pg/mL. Comparison of the patient and control groups revealed that the changes in CSF sTLR4 levels were not statistically significant. ConclusionHMGB1 level, a key inflammatory molecule, was significantly higher in the CSF of children with febrile seizures. Our data suggest that the HMGB1 network may contribute to the generation of febrile seizures in children.

A study of serum zinc levels among children with seizures in comparison with febrile children without seizures

Background: Infants and children are more prone to have seizures than adults. This reflects the greater neuronal excitability at certain ages as the excitatory glutamate system and inhibitory GABA system do not always balance each other. Febrile seizures are the most common type of seizures observed in pediatric age group. Febrile seizures occur in young children at a time in their development when seizure threshold is low. Objective of the study was to determine the levels of zinc in children with febrile seizures when compared to children with fever without seizures.Methods: To determine the levels of zinc in children with febrile seizures when compared to children with fever without seizures. A total of 50 Study subjects were selected into each group. Group 1: Children with Febrile Seizures. Group 2: Children with Fever and Without Febrile Seizures.Results: Among the cases with fever and convulsion Zinc level was found to be low among 72% of the subjects, 22 % of them had normal zinc levels and only 6% had high zinc levels. Among the subjects with Fever and no convulsions nearly 80% of them had normal zinc levels, 16 % had low levels of zinc and 4% had high zinc levels. The association of levels of Zinc between both the groups was found to be statistically significant.Conclusions: This study shows that serum zinc levels are decreased in children with febrile convulsions when compared to children with fever alone without convulsions, thus indicating that zinc deprivation plays significant role in the pathogenesis of febrile convulsions.

A study of serum zinc levels in children with febrile convulsions in comparison with normal and febrile children

Background: A seizure is a paroxysmal time-limited change in motor activity and or behavior that results from abnormal electrical activity in the brain. Seizures are common in the pediatric age group and occur in approximately 10% of children. Most seizures in children are provoked by somatic disorders originating outside the brain such as high fever, infection, syncope, head trauma, hypoxia, or toxins. To determine whether children with febrile convulsion have decreased serum zinc level when compared to normal children and children with fever without convulsions.Methods: The study included children admitted with bronchiolitis in between during the period of September 2018 to January 2019 at Department of Pediatrics, Raja Muthiah Medical College and Hospital. It is a case-control study. A sample size of 50 was selected for each group Totally 3 Groups, 1. Children with febrile convulsions,2. Children with fever without convulsions, 3. Normal Children.Results: The mean serum zinc level in children with febrile convulsions was 42.9 mcg/dl. The serum zinc level in children with fever and normal children was 70 mcg/dl and 71 mcg/dl respectively. On comparing the serum zinc level among the three groups statistical significance was obtained between children with febrile convulsions and the other two groups namely normal children and children with fever alone. Thus, decreased serum zinc level is a significant predisposing factor for febrile convulsions. By using Posthoc Multiple comparisons test we came to know that the Fever convulsion group is significantly different from fever and normal group. There is no significant difference between fever and normal group.Conclusions: This study shows that serum zinc levels are decreased in children with febrile convulsions, thus indicating that zinc deprivation plays a significant role in the pathogenesis of febrile convulsions.

Febrile convulsion: review and update

Febrile convulsions (FCs) are the most frequently occurring epilepsy syndrome experienced in infants/children between 6 months and 6 years of age and occur in 2-4%. It describes any seizure that occurs in response to a febrile stimulus in the absence of meningitis, encephalitis, serum electrolyte imbalance and other acute neurologic illnesses. There have been many recent reports on the molecular genetic and pathogenesis of FC. It has been recognized that there is significant genetic component for susceptibility of FC with different reported mutation. Others have tried to correlate FC to immunologic problem through interleukin, cytokines, immunoglobulin and interferon. Also, reports on correlations between FC and iron deficiency anemia, hypozincemia or to specific infections have been published. Children having first or second degree relatives with a history of FC, neonatal nursery stay of more than 30 days, developmental delay or attendance at a day care center are at increase risk of developing FC. A single simple FC does not seem to increase the risk of epilepsy and there is no causal relationship between FC and subsequent epilepsy. Viruses are the most common cause of illness in children admitted to the hospital with a first FC. Routine laboratory studies, electroencephalogram and neuroimaging are not indicated for patients who have FC, and should be performed only as part of the evaluation for a source of fever and/or in atypical cases. Prognosis is generally good and parents should be counseled about the benign nature of FC. Children with FC are at no greater risk of intellectual impairments than their peers. Maintenance therapy to prevent recurrence has not been shown to prevent later development of epilepsy, and therefore intermittent diazepam or lorazepam are the main drugs to be used. (J Pediatr Neurol 2004; 2(1): 9-14).

Serum Zinc Level in Children With Simple Febrile Convulsions

Dear Editor, Febrile convulsions are the most common convulsive seizures in infants and preschool children (1, 2). Such events, have great impact on the parents and are a leading cause of parental anxiety and family disruption (3). Pathophysiology of febrile convulsions has not been known.2 Genetics and environment have been implicated in their generation (4). Trace elements have been hypothesised to involve in the pathophysiology of febrile convulsions. Recent studies have shown lower post ictal serum zinc levels in children with febrile convulsions (5). Considering the importance of febrile convulsions in our province (south west of Iran) and the theorised implication of hypozincemia in their occurrence, we carried out a case-control study to determine post ictal serum zinc level in a group of children with simple febrile convulsions comparing by those of a control group of febrile children with the same age. To be enrolled children had to be between 6 months and 5 years old and had to meet the diagnostic criteria of simple febrile convulsions according to the International League against Epilepsy definition (6). Excluded were those who received zinc supplements. The control group was comprised of children less than 5 years who were seen in the outpatient clinic or emergency department because of a febrile illness other than central nervous system infection. Informed consent was obtained from the parents of all children before enrolment into the study. Blood samples (2 ml) were drawn by venipuncture from the antecubital vein using a disposal plastic syringe with a 23 gauge needle in the morning between 8:00 and 10:00 am. All children with febrile convulsions were at least 24 hours seizure-free from the sampling time. Blood samples were centrifuged at 1500 RPM for 10 min, and the serum was stored at -86oC until the time of analysis. Serum zinc concentration was measured by the graphite furnace flame atomic absorption spectrophotometry (AAS; SpectrAA 220, GTA 110, Varian, Australia) technique. Serum zinc concentration was reported as microgr/dl. Statistical analysis was performed using SPSS version 16.0 statistical software (SPSS, Inc, Chicago, IL). Categorical variables were analysed using the χ2 test. Continuous variables were analysed using independent sample t-test, or Mann-Whitney Rank Sum test when appropriate. A P 0.05). In both groups the most frequent cause of fever was otitis media and other upper respiratory tract infections. No significant difference was found between two groups in terms of aetiology of fever. In the patients’ group, serum zinc level (median; 70 microgr/dl) was significantly lower than the control group (median; 90 microgr/dl) (P < 0.001) (Figure 1). Figure 1. Serum Zinc Level Was Significantly Lower in Children With Febrile Convulsion (40) Than Children With Fever (40) (P < 0.001) In both groups, no relation was found between serum zinc level and age. In both groups, no relation was found between serum zinc level and aetiology of fever. Our results indicate that low or reduced postictal serum zinc level in children with febrile convulsion is a reproducible finding in different geographical regions of the world. Moreover, no relation was found between aetiology of fever and serum zinc level. Recently, hypozincemia and reduced levels of CSF zinc have been reported in children who had febrile convulsions (5). However, exact role of the zinc in the pathogenesis of febrile convulsions is still unknown. Previous studies have been proposed a theory about induction of febrile convulsions with a reduced level of serum zinc level. Based on this theory, hypozincemia activates the NMDA receptor, one of the glutamate families of receptors, which may play an important role in inducting epileptic discharge.5 Moreover, zinc has a regulatory effect on glutamic acid decarboxylase and this enzyme is the core in the synthesis of GABA. Decreased function of the mentioned enzyme has been hypothesized in hypozincemia. Therefore, hypozincemia could lead to reduced levels of GABA in the brain and finally seizure threshold could be reduced in conditions with hypozincemia. The major limit of this study was that we only measured serum zinc level during a febrile illness; therefore we could not compare the serum zinc level of our participants during illness and healthy states. Few studies with the same methods were conducted in different countries to measure the serum zinc level in children with febrile convulsions. In all of these studies, results were shown that children with simple febrile convulsions had serum zinc levels lower than that of febrile children with the same age (7, 8). In conclusion, a considerable body of evidence now exists that shows hypozincemia in children with febrile convulsions during an episode of seizure. We think it is valuable to design large prospective trials to assess the serum zinc level in children at risk for the occurrence of febrile convulsions during healthy states and before a seizure occurrence.

Trace Elements in Febrile Seizure Compared to Febrile Children Admitted to an Academic Hospital in Iran, 2011

Pathogenesis of Febrile Convulsion (FC) is unknown but some elements and genetic predispositions have been considered in the top list. This case-control study was designed to compare some trace elements in paediatrics who were admitted with FC and those in febrile ones without seizure attacks at an academic hospital in northeast of Iran. This case-control study was done from June 2010 to July 2011 on 160 paediatrics (6-months to 5-years old) who were diagnosed with FC and on 160 age-matched febrile children as control group. Data on the age, gender, past history of fever and convulsion, age at the first episode of seizure and family history of FC were gathered by using a designed checklist. Complete Blood Count (CBC), serum iron, Total Iron Binding Capacity (TIBC), zinc, magnesium and calcium were tested after taking informed consents from the parents. Serum levels of trace elements were measured by a photometric method. Independent t-test or non-parametric Mann-Whitney test were used to compare means between two groups. There were no significant differences between the cases and controls with regards to the gender or age. TIBC and magnesium were lower in FC, but calcium, iron and zinc were higher in FC as compared to those in the other group (not significant). So, it could be said that deficiency of trace elements was not significantly related to febrile convulsion in our study and it seemed that these tests were not necessary in FC cases. But further investigations on other trace elements are needed.

Serum Trace Element Levels in Febrile Convulsion

Febrile convulsion is the most common disorder in childhood with good prognosis. There are different hypotheses about neurotransmitters and trace element changes in biological fluids which can have a role in pathogenesis of febrile convulsion. In this study, serum selenium, zinc, and copper were measured by atomic absorption spectrometry in the children with febrile convulsion (n = 30) and in the control group (n = 30). The age and sex of the subjects were registered. Selenium and zinc were found to be significantly lower in febrile convulsion cases than in the control group (p < 0.0001 and p < 0.0001, respectively). There was no significant difference in the value of copper between the two groups (p = 0.16). While selenium and zinc levels were 44.92 +/- 10.93 microg/l and 66.13 +/- 18.97 microg/dl in febrile convulsion, they were found to be 62.98 +/- 9.80 microg/l and 107.87 +/- 28.79 microg/dl in healthy children. Meanwhile, copper levels were 146.40 +/- 23.51 microg/dl in the patients and 137.63 +/- 24.19 microg/dl in the control group, respectively. This study shows that selenium and zinc play an important role in the pathogenesis of febrile convulsion.

LYMPHOCYTES SUBSETS IN CHILDREN WITH FEBRILE CONVULSIONS

In this study, lymphocytes subsets including blood CD3, CD4, CD8, CD16, CD19, and CD56 values were analyzed in children with febrile convulsion (FC) to determine whether there was the association of lymphocytes subsets in the pathogenesis of FC. The study includes 48 children with FC, and 55 healthy age matched control subjects, followed in Yüzüncü Yıl University, Faculty of Medicine, Department of Pediatrics between October 2003 and June 2004. Blood CD3, CD4, CD8, CD16, CD19, and CD56 values were examined in the study and control groups. The analyses were performed in the Hematology Laboratory, Yüzüncü Yıl University Faculty of Medicine, with flow cytometer device (Coulter Epics XL2, Flow Cytometer). A total of 48 children [17 girls (35.5%) and 31 boys (64.5%)], aged 6 months to 60 months (mean 22.20 ± 13.75 months) with FC and 55 healthy children [28 girls (51%) and 27 boys (49%)], aged 6 months to 60 months (mean 28.87 ± 17.04 months) were included in the study. When compared with the control group, the study found significantly decreased blood CD3 and CD4 values in the study group (p <.05). However, there was not significant difference in CD8, CD16, CD19, and CD56 values between the control and study groups (p >.05). When comparing the children with and without positive family history for FC, the study did not find any difference for all CD values between the groups (p >.05). Similarly, there was not significant difference in CD values between the children with simple and complex FC (p >.05). The findings suggested that decreased blood CD3 and CD4 values might be responsible for the infections connected with FC or that they might be related to the pathogenesis of FC in some children.

Expression of Hsp72 in Lymphocytes in Patients with Febrile Convulsion

The pathophysiology of febrile convulsion, the most common childhood neurologic disease, remains unclear. In this study, we investigated what role a heat shock protein plays in this disease. We enrolled eight boys and two girls with febrile convulsion and 10 age-matched healthy controls. We did a biosynthetic evaluation of both groups by separating lymphocytes and measuring the expression of heat shock protein 72 before and after heat shock treatment. Before the treatment, both groups were found to have small amounts of constitutive heat shock protein 72. Afterwards, its expression increased in both groups, and no statistical difference was found between the increases in the two groups. In addition, there was no obvious difference in the susceptibility to produce heat shock proteins. However, the febrile convulsion group was found to have a significant decrease in phosphorylation of heat shock protein 72. These results suggest the possible involvement of post-translational modification of heat shock proteins, most likely phosphorylation, in the pathogenesis of febrile convulsion.

Hypercalciuria in children with febrile convulsions.

The purpose of the present study was to investigate whether idiopathic hypercalciuria may be implicated in the pathogenesis of febrile convulsions. We studied 38 children (22 boys) with febrile convulsions (mean (+/- SD) age 3.25 +/- 1.09 years) and 45 healthy children (28 boys) of similar age who served as controls. Twenty-four hour urine calcium and phosphate, as well as serum calcium, phosphate, alkaline phosphatase and intact parathyroid hormone (PTH) concentrations were determined. Hypercalciuria (urine Ca >4.0 mg/kg bodyweight per 24 h) was found in nine children with febrile convulsions (23.7%) and in three controls (6.7%). Hypercalciuric children excreted significantly more phosphate in their urine (37.0 +/- 11.6 mg/kg bodyweight per 24 h) than normocalciuric children (18.7 +/- 8.7 mg/kg bodyweight per 24 h) and controls (20.2 +/- 7.6 mg/kg bodyweight per 24 h). They also had higher serum intact PTH concentrations (49.87 +/- 15.36 pg/mL) than normocalciuric (35.39 +/- 15.67 pg/mL) and control children (28.21 +/- 14.00 pg/mL). According to the calcium-loading test, eight of nine children with hypercalciuria had the renal type of the disorder. Furthermore, hypercalciuric children had significantly more convulsive episodes (2.77 +/- 1.98) than normocalciuric children (1.86 +/- 1.24). Our results suggest that renal hypercalciuria may be implicated in the pathogenesis of febrile convulsions.

Do recurrent febrile convulsions decrease the threshold for pilocarpine-induced seizures?: Effects of nitric oxide

The aim of the study was to determine whether (1) number of febrile convulsions is a predictor of development of temporal lobe epilepsy, (2) the susceptibility of rats to pilocarpine-induced seizures is increased due to febrile convulsions and (3) nitric oxide is a mediator in the pathogenesis of febrile convulsions. Rat pups were exposed to single or multiple hyperthermic seizures. Subconvulsant doses of pilocarpine (100 mg/kg and 150 mg/kg) were injected intraperitoneally to these rats at 60–70 days of age. Also l-arginine was applied to some rats before a single hyperthermic seizure. We found that risk of future epilepsy increases parallel to the number of febrile convulsions and nitric oxide does not have a pathogenetic role at given doses.

Hypozincaemia in febrile convulsion.

To understand further the role role of trace elements in pathogenesis of febrile convulsions, serum zinc (Zn), copper (Cu), magnesium (Mg) and CSF An, Cu, Mg and protein levels were measured by spectrometry in patients with febrile convulsion (n = 19), bacterial meningitis (n = 9), viral CNS infection (n = 16) and in the control group (n = 10) which consisted of children with signs of meningeal irritation due to upper respiratory tract infection but normal CSF findings. Samples were obtained within 6 h after admission to hospital. Mean serum and CSF Zn levels in the febrile convulsion group were significantly lower than in the other groups (for serum Zn: 0.66 +/- 0.03 mg/1 vs 0.98 +/- 0.07 mg/1, 1.06 +/- 0.08 mg/1, 1.05 +/- 0.09 mg/1 P < 0.05; for CSF Zn: 22.96 +/- 1.62 micrograms/1 vs 75.47 +/- 6.9 micrograms/1, 50.32 +/- 5.235 micrograms/1, 39.85 +/- 2.81 micrograms/1 P < 0.05). A linear relationship was established between serum Zn and CSF Zn levels (P < 0.001). Mean CSF Zn, Cu and protein levels in the bacterial meningitis group were significantly higher than in the other groups (for CSF Cu 63.94 +/- 6.33 micrograms/1 vs 38.77 +/- 2.70 micrograms/1, 35.84 +/- 3.48 micrograms/1, 33.86 +/- 2.88 micrograms/1 P < 0.05; for CSF protein 0.80 +/- 0.12 g/1 vs 0.22 +/- 0.02 g/1, 0.53 +/- 0.08 g/1, 0.19 +/- 0.01 g/1 P < 0.05). In children with meningitis, the elevation of the mean CSF Zn and Cu levels may result from the breakdown of the blood-brain barrier and subsequent leakage of trace elements and protein from serum to CSF. There was no significant difference between the four groups in terms of mean serum Mg and mean CSF Mg levels. Serum and CSF Zn levels are decreased in children with febrile seizures. Zinc deprivation may play a role in the pathogenesis of febrile seizures.

The role of vasopressin, somatostatin and gaba in febrile convulsion in rat pups

In order to further elucidate a possible role of neuropeptides and GABA in the pathogenesis of febrile convulsions, we studied changes of immunoreactive-arginine vasopressin (IR-AVP), IR-somatostatin (IR-SRIF) and gammaaminobutyric acid (GABA) in the rat brain after febrile convulsions induced by ultra-red light (UR). Male Wistar rats at 16 days of age irradiated with UR developed generalized convulsions after 4.9 ± 0.5 min irradiation. Six rats were killed by microwave irradiation 3 min after UR irradiation prior to convulsion development, and 29 rats were killed either 0 min, 2 h, 6 h, 24 h or 48 h after febrile convulsions. Non-irradiated rats served as controls. The rat brain was dissected into 4 regions; amygdala, hypothalamus, cortex and hippocampus, and subjected to radioimmunoassays. IR-AVP levels in hypothalamus were increased 3 min after UR and decreased at 2 h and 6 h after the convulsions. IR-SRIF levels were increased in cortex and hippocampus at 3 min after UR and 0 min after the convulsions. The GABA content increased in all regions tested at 2 h and 6 h after the convulsions. These results suggest that AVP, SRIF and GABA may be involved in the pathogenesis of febrile convulsions in different ways.

Increased Interleukin‐1 (IL‐1) Production from LPS‐Stimulated Peripheral Blood Monocytes in Children with Febrile Convulsions

Peripheral blood mononuclear cells (MNC) from 27 children with a febrile convulsion were tested for production of interleukin-1 (IL-1) in culture. MNC stimulated with lipopolysaccharide (LPS) showed a significantly increased production of IL-1 when compared to MNC from children without convulsions but with bacterial infections (p less than 0.001), viral infections (p less than 0.005) or no infection (p less than 0.005). Children who had experienced a febrile convulsion were retested several months later; this time the IL-1 production from LPS-stimulated MNC was not different from controls. These results demonstrate that MNC at the time of febrile convulsions have increased sensitivity to LPS and possibly to other IL-1 inducers; the resulting enhanced IL-1 response from sensitized MNC may have a role in the pathogenesis of febrile convulsions.

Genetic EEG patterns in febrile convulsions--a multivariate analysis.

Genetically determined EEG patterns being found during a longterm follow-up of children with febrile convulsions are subjected to a multivariate statistical analysis. The study is mainly concerned with the examination of interrelationships between spikes and waves, theta-rhythms, and photosensitivity. The three patterns form two-categorial variables (occurrence yes, no) and enter a three-way contingency table. Associations between the variables are examined by fitting a log-linear model to the data. Three effects in the structure of the contingency table are statistically significant: the main effect of theta-rhythms which are relatively frequent in the group, and the two-variable-interactions of spikes and waves with theta-rhythms and photosensitivity respectively. The results of the study emphasize that combinations of different genetic factors are important in the pathogenesis of febrile convulsions.

Parental age and birth order effects in children with febrile convulsions.

This is a study of the parental age and birth order of 100 Chinese children with febrile convulsions compared with 100 controls. The birth order of children with febrile convulsions (1.6 +/- 0.8) was found to be lower than that of the controls (2.1 +/- 1.0), a difference significant at P less than 0.001, whereas there was no significant difference for both paternal and maternal age. Using multiple regression analysis, it was found that the birth order effect was significant at P less than 0.0001. This finding suggests that perinatal factors may play a role in the pathogenesis of febrile convulsions.

Central nervous system mediators of vasopressin release.

articleCentral nervous system mediators of vasopressin releaseA. H. Sklar, and R. W. SchrierA. H. Sklar, and R. W. SchrierPublished Online:01 Oct 1983https://doi.org/10.1152/physrev.1983.63.4.1243MoreSectionsPDF (6 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAngiotensin AT1A receptors expressed in vasopressin-producing cells of the supraoptic nucleus contribute to osmotic control of vasopressinJeremy A. Sandgren, Danny W. Linggonegoro, Shao Yang Zhang, Sarah A. Sapouckey, Kristin E. Claflin, Nicole A. Pearson, Mariah R. Leidinger, Gary L. Pierce, Mark K. Santillan, Katherine N. Gibson-Corley, Curt D. Sigmund, and Justin L. 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ventrolateral medulla in ratsNeuroscience Letters, Vol. 51, No. 2 More from this issue > Volume 63Issue 4October 1983Pages 1243-1280 Copyright & PermissionsCopyright © 1983 the American Physiological Societyhttps://doi.org/10.1152/physrev.1983.63.4.1243PubMed6197715History Published online 1 October 1983 Published in print 1 October 1983 Metrics

EEG longitudinal studies in febrile convulsions. Genetic aspects.

It was the purpose of the study to obtain viewpoints on the genetics of febrile convulsions and their relationship to epilepsy by EEG long term follow up. 89 children with febrile convulsions could be followed up to the age of 11 to 13 years (in total 1046 EEG records). The study was concentrated on genetically determined EEG patterns: bilaterally synchronous spikes and waves, photosensitivity and 4-7 cps rhythms. The statistical evaluation was based on standards derived from known strict age dependence of the different patterns. Theta rhythms were found in 54%, spikes and waves of the resting record in 49% and photosensitivity in 42%. In total, genetically determined EEG patterns were found in 81% of the cases which were sufficiently investigated according to given standards. Spikes and waves are strongly age dependent with a maximum at the age of 5-6 years and appear very inconstantly. Theta rhythms and spikes and waves are closely correlated. Spikes and waves are a heterogeneous phenomenon. The type described here must be interpreted as a facultative symptom of the same functional anomaly which forms the basis of 4-7 cps rhythms. The possible pathophysiological basis of the pattern is discussed.--Photosensitivity is interpreted as the symptom of a genetically independent pathogenetic mechanism, which can lead to additive effects by interaction with other genetic abnormalities as well as exogenous factors.--The pathogenesis of febrile convulsions is multifactorial in the strict sense. While the exogenous pathogenetic factors are rather uniform, the genetic predisposition apparently is not. It is based on different genetic anomalies. Each of them is polygenically determined. In the individual case one or different factors can be involved. The genetic predisposition to febrile convulsions is definitely not only polygenic, but of heterogeneous nature. Finally the genetic relationship between febrile convulsions and epilepsy is discussed.