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PubMed2005

Retrospective review of the management of simple febrile convulsions at a tertiary paediatric institution.

OBJECTIVES: To review the medical records of children presenting to a tertiary paediatric emergency department (ED) with febrile convulsions over a 3-year period in order to assess quality of clinical practice. METHODS: The medical records of all children presenting to our ED with a discharge diagnosis of 'simple febrile convulsion' during the years 2001-03 were reviewed. Data was extracted based on the parameters of clinical presentation, diagnosis and management. RESULTS: A total of 288 patients were identified. The patients were separated into two groups - those that were discharged from the ED and those that were admitted to the hospital. Two hundred and sixty (84%) of the children were discharged from the ED. A further 28 (15%) patients were admitted to the ward. Of the children discharged from the ED, 78% had not been seen by a medical professional in the previous 24 h, 82% were diagnosed with a viral illness and clinical examination was normal in 88% of cases. A total of 36 out of 527 (6.8%) investigations performed on this group were abnormal. Most children (85%) had no clinical indication to necessitate investigation. Almost all (91%) were treated with antipyretics. The number of inappropriate investigations was directly linked to the inexperience of the treating medical officer. Of the 28 patients admitted to the hospital, 61% were diagnosed with a viral illness. A total of 15 out of 137 (10.9%) investigations were abnormal. Sixty-one per cent of patients were admitted for less than 24 h, a further third of children for 48 h. Twenty of the 28 children had no parental education documented. None were readmitted with a simple febrile convulsion during the same illness. CONCLUSIONS: Although many children who present to the hospital with simple febrile convulsions are managed appropriately, a large number are overinvestigated and overtreated, based on the clinical experience of the treating doctor. In these cases, medical record documentation can be improved. A clinical guideline based on our local fever guideline is suggested.

Analgesics, Non-Narcotic↗

PubMed1979

Status epilepticus in childhood: a retrospective study of initial convulsive status and subsequent epilepsies.

A retrospective study was carried out on 261 patients with various epilepsies who had undergone convulsive status epilepticus prior to the subsequent onset of epileptic seizures. 1. Convulsive status epilepticus was found more in partial epilepsy and secondary generalized epilepsy at about the same rate, and evidently less in primary generalized epilepsy. On the average, three-fourths commenced their convulsive disorders with initial status epilepticus. 2. There were free intervals of years following initial status and preceding subsequent epilepsy. The interval was evidently shorter, less than two years, in a majority of patients with secondary generalized epilepsy, whereas the interval was mostly longer, more than six years, in patients with partial epilepsy. 3. The permanent deficient sequelae resulting from initial status were most closely associated with secondary generalized epilepsy. This was also exemplified by the higher rate of atrophic change on CCT. On the contrary, such permanent sequelae were less marked in partial epilepsy especially of complex seizure. 4. It was concluded that secondary generalized epilepsy resulted in cases with more severe brain damage within a relatively shorter interval, whereas complex partial seizure resulted from less severe damage with an obviously longer interval following convulsive status epilepticus.

Adolescent↗

PubMed1981

The risk of nonfebrile seizures in children who have experienced febrile convulsions.

The frequency of development of nonfebrile seizures in 116 children who had experienced at least one febrile convulsion and were followed for more than five to eight years was 4.3% (5 cases). Of these, three cases had prolonged generalized convulsions of the clonid type. (2) The risk factors identified as nonfebrile seizures after febrile convulsions, were the preexisting neurological abnormality or developmental retardation, focal features and more than a 10-minute duration of the first febrile convulsions, and abnormal paroxysmal discharges at the initial interietal EEG recordings.

Adolescent↗

PubMed1996

Serum and cerebrospinal fluid zinc levels in children with febrile convulsions.

The mechanisms underlying febrile convulsions (FC), which have multiple etiological factors, are not yet clear. The aim of the present study was to determine whether there were any changes in serum and cerebrospinal fluid (CSF) zinc (Zn) levels in children with febrile convulsion during seizures. A total of 102 children were included in the study, with four groups formed as follows: group A, 40 children with FC (aged 9 months to 5 years); group B. 20 children having fever without convulsion (aged 6 months to 5 years); group C, 20 children with afebrile convulsion (aged 6 months to 6 years) and group D, 22 healthy children (aged 5 months to 6 years). Serum and CSF zinc levels for groups A, B and C and serum Zn levels only for group D were measured. The serum Zn levels of 17 children in group A were again measured during healthy periods. Serum Zn levels of groups A, B, C and D had a mean of 0.70 +/- 0.10 mg/dL, 1.07 +/- 0.08 mg/dL. 1.26 +/- 0.32 mg/dL and 1.17 +/- 0.21 mg/dL, respectively, and the values of group A were lower than those of the other three groups (P < 0.001). In group B, serum Zn levels were also lower than those of groups C and D (P < 0.05). The CSF Zn levels of groups A, B and C were found to have a mean of 0.07 +/- 0.02 mg/L, 0.12 +/- 0.02 mg/L and 0.14 +/- 0.04 mg/L, respectively. In group A, the CSF Zn levels were lower than those of groups B and C (P < 0.001), and in group B they were lower than those of group C (P < 0.05). For the 17 patients in group A, serum Zn levels during healthy periods (0.87 +/- 0.10 mg/dL) were found to be higher than the values shortly after seizures, but lower than those of groups B, C and D (P < 0.001). We could not observe any relationship between zinc levels of the serum and CSF and the degree and duration of the fever. These findings suggest that serum and CSF Zn levels decreased during infectious diseases, and that this decrease was more significant in patients with FC.

Blood-Brain Barrier↗

PubMed2006

Effects of expectation on amygdala-kindled convulsions and interictal behaviour in rats: confirmation of a Pavlovian mechanism.

We found evidence that the effects of exposure to the stimulation environment on the convulsions and interictal behaviour of basolateral amygdala (BA)-kindled rats are the result of Pavlovian conditioning. In Experiment 1, the rats first received 45 BA stimuli in one environment (CS+) and 45 sham stimuli in another environment (CS-). During this first phase of the experiment, the CS+ and CS- began to exert differential effects on interictal behaviour and convulsions. Then, during the second phase, rats received 45 stimuli and 45 sham stimuli, either as before in their original CS+ and CS- (nonreversal rats) or with their original CS+ and CS- interchanged (reversal rats). During the second phase, the CS+ and CS- continued to exert the same pattern of differential effects on the interictal behaviour and convulsions of the nonreversal rats, whereas the reversal rats began to display the reverse pattern. In Experiment 2, rats received 60 sham stimuli in one environment (CS1). Then, half of the rats received 30 stimuli in a second environment (CS2) and 30 sham stimuli in CS1 (no-pre-exposure rats), whereas the other half (pre-exposure rats) received 30 stimuli and 30 sham stimuli in CS1. Pre-exposure to the stimulation environment attenuated the kindled convulsions. These findings confirm that the conditioned effects of kindling are mediated by a Pavlovian mechanism.

Amygdala↗

PubMed1989

Intention to treat febrile convulsions with rectal diazepam, valproate or phenobarbitone.

One hundred and eighty-six consecutive children aged between six and 72 months admitted to the Manchester Children's Hospitals with a febrile convulsion in the first year of life, a complicated febrile convulsion, or more than one febrile convulsion within two years, were allocated randomly to one of three groups who were offered rectal diazepam in the event of a subsequent prolonged febrile convulsion, or prophylactic treatment with sodium valproate or phenobarbitone. Over-all risk of recurrence was 30 per cent and adequate prophylactic treatment did not lessen this risk. Side-effects in 24 per cent of the valproate group and 61 per cent of the phenobarbitone group did not justify the use of prophylactic treatment.

Administration, Rectal↗

PubMed1992

Convulsions with fever as a presenting feature of bacterial meningitis among preschool children in developing countries.

The authors report 522 infants and young children aged between one month and six years who presented with convulsions and fever as emergencies in Nigeria. 22 had bacterial meningitis, six of whom lacked the usual signs of meningitis. Although features of complex febrile convulsions were significantly associated with bacterial meningitis, it is concluded that, as an aid to the early diagnosis of bacterial meningitis, all preschool children convulsing with fever in developing countries should have a lumbar puncture. This may reduce the contribution of meningitis to chronic neurological disabilities. The necessity for such a policy is illustrated by a case report of a young infant with convulsions and fever caused by meningitis, seen at a general hospital.

Age Factors↗

PubMed1988

Incorporation of glycerol and ethanolamine into glycerophospholipid in rat brain areas during bicuculline-induced convulsive seizures.

The effect of bicuculline-induced convulsive seizures on lipid metabolism has been studied in four brain areas (cerebellum, cerebral cortex, hippocampus, and brainstem) using [2-3H]glycerol and [1,2-14C]ethanolamine as radioactive lipid precursors administered simultaneously with bicuculline. Twelve minutes after the administration, the uptake of radioactivity depended both on brain area and treatment, being generally higher in convulsing rats. The uptake of glycerol was influenced to a larger extent than that of ethanolamine and increased during convulsions, but its incorporation into lipids did not. In contrast, the amount of ethanolamine incorporated into lipids increased during bicuculline-induced seizures. The difference in behavior of glycerol and of ethanolamine is also indicated by the decrease of the 3H/14C ratio of phosphatidyl-ethanolamine in various brain areas during convulsions. It is, therefore, evident that the metabolism of the two precursors is affected differently by seizures.

Animals↗

PubMed1991

Changes in polyamine levels in rat brain after systemic kainic acid administration: relationship to convulsant activity and brain damage.

We have examined the effects of systemic kainic acid (KA) administration (9 mg/kg, i.p.) on rat behavior, brain damage, and polyamine levels and the action of the specific ornithine decarboxylase inhibitor alpha-difluoromethylornithine (DFMO) on these effects. KA elicited convulsant activity in 63% of the animals. In the acute convulsant phase (1-3 h after KA), a rapid decline (-39% at 3 h) of spermidine content in frontal cortex was found. After the acute convulsant phase, levels of hippocampal spermidine and spermine were reduced (-70 and -66%, respectively, at 8 h). A dramatic increase of putrescine content (68.1, 1,382, and 336% at 8 h, 24 h, and 9 days, respectively, after KA) was found, associated with histological signs of cortical brain damage (ischemia and necrosis). There was a close relationship between the concentration of putrescine and signs of delayed toxicity (body weight losses) 24 h and 9 days after KA. DFMO partially antagonized the convulsant activity and reduced the increased putrescine levels to approximately 50% of values in KA-treated animals at 24 h but did not change the pattern of histological damage. The role of polyamines in the early and late phases of KA-induced neurotoxicity is discussed.

Animals↗

PubMed1977

A pharmacological study of the spontaneous convulsive activity induced by 1,2-dihydroxybenzene (catechol) in the anaesthetized mouse.

1. The convulsive activity induced by catechol has been examined in anaesthetized mice either by determining the CD50 for the convulsions in drug-treated and control animals, or by studying the effects of various drugs on the total whole body activity. 2. The results indicate that catecholamines play no part in the mechanism of action of catechol. Drugs which alter cerebral catecholamine levels had no effect on the convulsions, nor did the alpha- and beta-adrenoceptor blocking drugs. 3. 5-Hydroxytryptamine (5-HT) could possibly be important, though results with drugs which either change brain 5-HT levels, or block 5-HT receptors were inconsistent. 4. gamma-Aminobutyric acid also appears not to be involved in the mechanism of action of catechol. 5. The results strongly suggest that catechol primarily activates a central cholinergic system, in that muscarinic and nicotinic receptor blocking drugs inhibit, and anticholinesterases potentiate the convulsions.

Acetylcholine↗

PubMed1987

Inhibition of the rate of GABA synthesis in regions of rat brain following a convulsion.

1 The rate of synthesis of gamma-aminobutyric acid (GABA) in the cortex, hippocampus and striatum of rat brain was assessed by measuring the linear rate of accumulation of GABA following injection of amino-oxyacetic acid (AOAA). 2 Five min after a single electrically induced seizure there was a rise in GABA content in these brain regions and an almost total inhibition of the rate of synthesis. 3 Five min after seizure induced by the inhalant convulsant flurothyl there was no rise in GABA content in these brain regions but a similar marked degree of inhibition of GABA synthesis. 4 Two hours after the convulsion the rate of GABA synthesis had returned to control values in all three brain regions. 5 A single convulsion did not alter the glutamic acid decarboxylase activity in these brain regions either in the absence or presence of added co-factor (pyridoxal phosphate). 6 Evidence for an inhibition of GABA release following a convulsion which may be associated with the inhibition of GABA synthesis is presented in the following paper.

Aminooxyacetic Acid↗

PubMed1991

Convulsive thresholds in mice during the recovery phase from anaesthesia induced by propofol, thiopentone, methohexitone and etomidate.

1. Convulsive thresholds were measured with intravenous pentylenetetrazol in mice during the recovery phase after intravenous anaesthetic doses of propofol (10 and 20 mg kg-1), thiopentone (30 mg kg-1), methohexitone (10 mg kg-1), and etomidate 3 mg kg-1). 2. The convulsive threshold rose after each agent, indicating an anticonvulsant action for all the drugs tested; this declined to control values with initial half times of: 1.56 min (propofol 10 mg kg-1); 1.03 min (propofol 20 mg kg-1): 1.02 min (methohexitone); 3.35 min (etomidate); 13.7 min (thiopentone). 3. At no time during the recovery phase of any agent did the convulsive threshold fall below control values, which might indicate an epileptogenic effect of the drug. 4. The threshold was depressed below control values by intravenous administration of Ro 15-4513, a partial inverse agonist at the benzodiazepine receptor, thus indicating the ability of this pentylenetetrazol test to demonstrate a proconvulsant effect. 5. We conclude that the abnormal movements or convulsions associated with recovery from anaesthesia with short-acting intravenous anaesthetics may not be the result of an intrinsic proconvulsant action of the drugs.

Anesthesia, Intravenous↗

PubMed1975

Duration and lateralization of febrile convulsions. Etiological factors.

The relationships of certain etiological factors (sex, age, family history of febrile convulsions or epilepsy, term, birth weight, prenatal or perinatal anomalies, temperature, cause of fever) to the duration and localization of the first febrile convulsion (FC) were studied in 402 patients. In patients with prolonged seizures (over 30 min), the mean age was younger, the proportion of girls, common infectious diseases of childhood, and immunization was higher and that of respiratory infections lower than in patients with brief convulsions. In patients with unilateral seizures, the proportion of positive family histories and respiratory infections was lower and that of common infectious diseases of childhood and of immunization was higher than in patients with bilateral convulsions. The association of each of these etiological factors with the duration or lateralization of the first FC was independent of the others.

Age Factors↗

PubMed1984

Effectiveness and toxicity of phenobarbital, primidone, and sodium valproate in the prevention of febrile convulsions, controlled by plasma levels.

The effectiveness and toxicity of phenobarbital (PB), primidone (PRM), and sodium valproate (VPA), used exclusively in monotherapy, were compared in 95 children affected with febrile convulsions. Treatment was restricted to either complicated or simple febrile convulsions with risk factors. The effectiveness and toxicity of each drug were related to the daily dose and the steady-state plasma levels. PB (4.8 +/- 0.7 mg/kg/day) achieved plasma levels of 16.4 +/- 2.8 micrograms/ml and prevented febrile convulsions in 80% of the patients. Side effects were observed in 76.7% of the patients, a change in dose being required only in 13.3%. PRM (17.8 mg/kg/day) yielded PB plasma levels of 14.1 +/- 3.7 micrograms/ml and was effective in 88.2% of the patients. The incidence of side effects was 53%, but no change in treatment was required. VPA (35.2 +/- 5.9 mg/kg/day) achieved plasma levels of 57.2 +/- 15.3 micrograms/ml (measured before the first dose in the morning) and was effective in 91.7% of the patients. Side effects were detected in 45% (significantly lower than after PB, p less than 0.01), and required a change in treatment in 14.3%. No differences in doses and plasma levels were found between patients with or without recurrence of febrile convulsions and with or without side effects; an exception was the higher doses of VPA administered to patients who showed side effects. It is concluded that PRM and VPA were at least as effective and well tolerated as PB. Because the plasma levels of the three drugs were near the lower limit of the therapeutic range, it remains to be elucidated whether higher doses may increase the benefit without adding unacceptable toxicity.

Child↗

PubMed1995

Histamine in cerebrospinal fluid of children with febrile convulsions.

Febrile convulsions (FC) are frequent acute neurologic disturbances of childhood. The cellular and neurochemical mechanisms causing FC are unclear. Among other mechanisms, the CNS histamine (HA) has been suggested to participate in seizure control and thermoregulation. We evaluated the possible role of HA in regulation of FC by measuring HA and tele-methylhistamine (t-MH) concentrations in the cerebrospinal fluid (CSF) of children with FC. The study group consisted of 35 children treated for acute FC in the hospital. The control groups consisted of (a) feverish children without seizures (n = 23), (b) convulsive children without fever (n = 7), and (c) children with neither fever nor convulsions (n = 21). HA was assayed by high-performance liquid chromatography (HPLC) with fluorescence detection, and t-MH was measured by gas chromatography-mass spectrometry. CSF HA concentration in the group of febrile children without seizures was significantly higher (0.69 +/- 0.16 pmol/ml, mean +/- SE) than in children with FC (0.36 +/- 0.07 pmol/ml, p < 0.05, analysis of variance, ANOVA). HA concentration was 0.37 +/- 0.18 pmol/ml in the group of nonfebrile convulsive children and 0.36 +/- 0.08 pmol/ml in the nonfebrile nonconvulsive group. No statistical differences in t-MH were detected between groups. The increased susceptibility to seizures during fever may be connected to the lack of increase in CSF HA in the FC group. The data support the hypothesis that the central histaminergic neuron system may be involved in inhibition of seizures associated with febrile illnesses in childhood.

Child↗

PubMed2005

Long-term effect of convulsive behavior on the density of adenosine A1 and A 2A receptors in the rat cerebral cortex.

PURPOSE: Adenosine is a neuromodulator that has been proposed to act as an anticonvulsant mainly via inhibitory A1 receptors, but recent data show that genetic deletion of facilitatory A 2A receptors might also attenuate convulsions. Since both A1 and A 2A receptors are prone to down- and upregulation in different stressful situations, we investigated if convulsive behavior leads to a long-term change in A1 and A 2A receptor density in the rat cerebral cortex. METHODS: Stage 4-5 convulsions (Racine's scale) were induced in adult Wistar rats either through amygdala stimulation (kindling) or by intraperitoneal injection of kainate (10 mg/ml). Rats were killed after 4 weeks to evaluate adenosine A1 and A 2A receptor density in the cerebral cortex using both Western blot and membrane binding assays. RESULTS: The binding density of the A1 antagonist, 3H-DPCPX, decreased by 40. +/- 4.4% and by 20.7 +/- 0.5% after kindling or kainate injection. Likewise, A1 receptor immunoreactivity in cortical membranes from kindled or kainate-injected rats decreased by 19.1 +/- 3.3% and 12.7 +/- 5.7%, respectively. In contrast, the binding density of the A 2A receptor antagonist 3H-SCH 58261 increased by 293 +/- 34% and by 159 +/- 32% in cortical membranes from kindled or kainate-injected rats, and A 2A receptor immunoreactivity also increased by 151 +/- 12% and 79.6 +/- 7.0%. CONCLUSIONS: This indicates that after convulsive behavior there is a long-term decrease of A1 receptors accompanied by an increased density of A 2A receptors, suggesting that A 2A antagonists rather than A1 agonists may be more promising anticonvulsive drugs.

Amygdala↗

PubMed1982

Serum vitamin D metabolites in epileptic patients treated with 2 different anti-convulsants.

The serum concentrations of the vitamin D metabolites 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D (24,25(OH)2D), and 1,25-dihydroxyvitamin D (1,25(OH)2D) were measured in 18 epileptic patients and 10 controls. The patients were divided according to the anti-convulsant treatment they had been receiving for at least 1 year: 9 patients had received phenytoin and 9 patients carbamazepine, as the sole anti-convulsant therapy. The serum 25OHD was decreased in the patients on phenytoin (P less than 0.01), whereas the other serum vitamin D metabolites were normal. Moreover, serum alkaline phosphatase was increased (P less than 0.001) and serum calcium was decreased (P less than 0.001) in this patient group. In the patient group treated with carbamazepine (a negligible, liver inductor), changes in serum 25OHD and serum alkaline phosphatase were less pronounced (P less than 0.05), but the same degree of hypocalcaemia (P less than 0.001) was present. Our data suggest that liver induction in epileptic patients on anti-convulsant drugs cannot explain the pathophysiology behind anti-convulsant osteomalacia.

24,25-Dihydroxyvitamin D 3↗

PubMed1984

Changes in response to metrazole during fever in juvenile rats; a new model for febrile convulsions?

Previous models for febrile convulsions have used environmentally induced hyperthermia as the stimulus to induce convulsions. Changes in response to metrazole during yeast-induced fever in juvenile rats are reported here. Animals were more susceptible to metrazole during the rising phase of fever but showed some resistance to its convulsant effects once the fever was established and following defervescence. It is suggested that this may form the basis of a physiologically more appropriate model for the study of the pathogenesis of febrile convulsions.

Animals↗