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Febrile seizures
Author: Marvin A Fishman, MD
Literature review current through: Fev 2012. | This topic last updated: Out 17, 2011. 
INTRODUCTION — Febrile seizures are a common cause of convulsions in young children. They occur in 2 to 4 percent of children younger than five years of age, but the incidence is as high as 15 percent in some populations. This incidence has been attributed to closer living arrangements among family members making detection more likely, but racial and geographic variations may also be important.
The generally accepted criteria for febrile seizures include:
A convulsion associated with an elevated temperature greater than 38°C
A child younger than six years of age
No central nervous system infection or inflammation
No acute systemic metabolic abnormality that may produce convulsions
No history of previous afebrile seizures
Febrile convulsions are divided into two categories, simple (benign), or complex, based upon clinical features. Simple febrile seizures are the most common and are characterized by seizures that last less than 15 minutes, have no focal features, and, if they occur in a series, the total duration is less than 30 minutes. Complex febrile seizures are characterized by episodes that last more than 15 minutes, have focal features or postictal paresis, and occur in a series with a total duration greater than 30 minutes.
ETIOLOGY AND PATHOGENESIS — It is not known how or why seizures are generated in response to fever; it may be that fever-induced factors (eg, interleukin-1beta) are proconvulsant in individuals who are susceptible based upon the stage of brain development and genetic susceptibility. Certain ion channels in the brain are temperature sensitive and may generate fever-associated synchronized neuronal activity. There is also evidence to suggest that hyperthermia-induced hyperventilation and alkalosis may play a role.
Infections — Febrile seizures can occur during both viral and bacterial infections. In one hospital based study, the incidence of febrile seizures was similar with influenza, adenovirus, and parainfluenza infections (6 to 18 percent), and somewhat less common with respiratory syncytial virus and rotavirus (4 to 5 percent). No specific virus was associated with risk of complex febrile seizures or later recurrence. Other studies have reported higher rates of febrile seizures (36 percent) in human herpesvirus (HHV)-6 infections and also a higher rate of complex features and recurrence.
Immunizations — The risk of febrile seizures is increased after administration of diphtheria, tetanus toxoid, and whole-cell pertussis (DTP) and measles, mumps, and rubella (MMR) vaccine. In a large cohort study, febrile seizures were significantly increased on the day of DTP vaccination and 8 to 14 days following MMR vaccination (adjusted relative risks 5.7 and 2.83, respectively). The risk for subsequent seizures or neurodevelopmental disabilities was comparable in children with febrile seizures whether or not they were associated with vaccination; however, because immunization and the clinical onset of neurodevelopmental syndromes occur in early childhood, there may be a perception that the vaccination is causative.
Predisposing factors — Susceptibility to febrile seizures has been linked with abnormalities in neurotransmitters. However, whether observed abnormalities were primary events or were secondary to the convulsions is unclear. As an example, the cerebrospinal fluid (CSF) concentration of gamma-aminobutyric acid (GABA), an inhibitory transmitter, was reduced in one series of children who were studied after their first or second febrile seizure; the samples were obtained after the convulsion and, thus, may be the effect rather than the cause of the seizure. Furthermore, low CSF GABA was not confirmed in other studies of children with febrile seizures.
CSF neopterin concentrations may be elevated in children with febrile seizures. Because neopterin is secreted by activated macrophages, this observation suggests immune activation within the central nervous system.
Iron insufficiency may play a role in pathogenesis. In a prospective study of 150 children, mean ferritin levels were significantly lower in children with a first febrile seizure than in matched controls with febrile illness but no convulsions (29.5 versus 53.3 mcg/L). Plasma ferritin levels ≤30 mcg/L occurred in a significantly greater proportion of children with seizures than controls (65 versus 32 percent). Further studies will be required to confirm this preliminary finding.
Genetic susceptibility — Genetic and familial factors appear to be important factors in the expression of febrile convulsions and the subsequent development of epilepsy in some children. Among first-degree relatives of children with febrile seizures, 10 to 20 percent of parents and siblings also have had or will have febrile seizures. In addition, monozygotic twins have a much higher concordance rate than do dizygotic twins, in whom the rate is similar to that of other siblings.
Susceptibility to febrile seizures has been linked to several genetic loci in different families, including the long arm of chromosome 8q13-21 (FEB1), chromosome 19p (FEB2), chromosome 2q23-24 (FEB3), chromosome 5q14-15 (FEB4), chromosome 6q22-q24 (FEB5), chromosome 6q16.3-22.31, chromosome 21q22, and perhaps chromosome 18p11.2. The trait is transmitted in an autosomal dominant fashion. However, susceptibility genes have not been identified in most patients with febrile seizures.
Genetic factors are also believed to be important in nonmendelian forms of febrile seizures. One study suggests that common polymorphism in a sodium channel gene (splice site variant SCN1A) is a common risk factor for febrile seizures. However, this finding was not replicated in a follow-up study.
A syndrome of generalized epilepsy with febrile seizures plus (GEFS+) also has been described. The most common phenotype consists of children who had seizures with fever in early childhood that, unlike typical febrile seizures, continued beyond six years of age or were associated with afebrile tonic clonic seizures as well as other seizure types. The epilepsy typically remitted by mid-adolescence. This disorder is usually autosomal dominantly inherited. Family members who inherit the mutation may only have nonfebrile seizures.
Among different families with GEFS+, a variety of gene loci and mutations have been identified, including chromosome 19q with mutations in the beta-1-subunit of the neuronal sodium channel, chromosome 2q with mutations in the alpha-1-subunit of the neuronal sodium channel, chromosome 8p23-p21 and a mutation in the gamma-2 subunit of the GABA-A recepto. A mutation in the last gene has also been identified in a family with febrile seizures without associated epilepsy.
These observations link febrile seizures with afebrile seizures in some families in an autosomal dominant fashion. In addition, previous studies have shown that siblings and parents of patients with febrile seizures have a 4 to 10 percent incidence of epilepsy.
Hippocampal lesions — Another approach linking febrile seizures and epilepsy was suggested from an evaluation of two families with familial febrile convulsions. Magnetic resonance imaging (MRI) was performed in family members who had no seizures, febrile convulsions only, and febrile convulsions with the subsequent development of temporal lobe epilepsy. All subjects with febrile convulsions who did not develop epilepsy and six clinically unaffected relatives showed asymmetry in the size of the hippocampi. In addition to a difference in the size between the right and left hippocampi were changes in the internal architecture of the hippocampal bodies. The authors concluded that a subtle preexisting hippocampal malformation that was present may facilitate febrile convulsions and contribute to the development of subsequent hippocampal sclerosis, which was seen in the patients who developed temporallobe epilepsy. Furthermore, the hippocampal malformation did not appear to be a consequence of the febrile convulsions and, therefore, may have been a predisposing factor associated with the development of epilepsy.
In another study, the effect of prolonged febrile seizures was evaluated in the immature rat. Prolonged hyperthermia-induced seizures did not lead to spontaneous seizures in adult rats. However, the experimental animals, but not control animals, developed hippocampal seizures after systemic administration of a low dose of kainate, a chemical convulsant, indicative of a reduced seizure threshold. An analogous situation may exist in humans. Individuals predisposed to developing epilepsy, by a variety of factors, may become symptomatic in later years after having their thresholds modified by febrile seizures in infancy.
CLINICAL FEATURES — Febrile seizures occur in children between the ages of six months and six years, with the majority occurring in children between 12 to 18 months of age. Febrile seizures have been reported in children over six years of age, but in older children, febrile seizures should be considered a diagnosis of exclusion, as they are more likely than younger children with febrile seizures to have subsequent afebrile seizures.
Simple febrile seizures are the most common type encountered in children. Generalized seizures are mainly clonic, but other forms include atonic and tonic spells. The facial and respiratory muscles are commonly involved. 
Complex febrile seizures (focal features, longer than 15 minutes or multiple episodes within 24 hours) are unusual; prolonged convulsions occur in fewer than 10 percent and focal features in fewer than 5 percent of children with febrile seizures. An initial simple febrile seizure may be followed by complex seizures, but the majority of children who develop complex febrile seizures do so with their first seizure. However, an initial complex febrile seizure does not necessarily indicate that all subsequent seizures will be complex. In one study of 158 children with a first febrile seizure, prolonged seizures (>10 minutes) occurred in 18 percent and were associated with developmental delay and younger age at first seizure [47]. The findings of this study suggest that 10 rather than 15 minutes might be a more appropriate criterion for complex febrile seizure, particularly for purposes of prognosis.
Some patients present in febrile status epilepticus, ie, continuous seizures or intermittent seizures without neurologic recovery, either lasting for a period of 30 minutes or longer.
The majority of children have their febrile seizures on the first day of illness and, in some cases, it is the first manifestation that the child is ill. The degree of fever associated with febrile convulsions is variable, and approximately 25 percent of events occur when the temperature is between 38ºC and 39ºC. They are often seen as the temperature is increasing rapidly but may develop as the fever is declining. Recurrent febrile seizures do not necessarily occur with the same degree of fever as the first episode and do not occur every time the child has a fever.
DIFFERENTIAL DIAGNOSIS — Involuntary movements can occur in sick children and be confused with seizures. Shaking chills are usually readily distinguished from seizures. Chills are common and are characterized by fine rhythmic oscillatory movements about a joint. They rarely involve facial or respiratory muscles, which frequently occur during febrile seizures. In addition, chills usually involve both sides of the body simultaneously and are not associated with loss of consciousness, in contrast to children with generalized seizures. Thus, bilateral manifestations without apparent unconsciousness strongly suggest that the movements are not convulsive.
An underlying metabolic disorder presenting as a seizure in a febrile child is rare. In such children, the history and physical examination yield clues of an underlying problem. Infants with a history of vomiting, diarrhea, and altered fluid intake may have electrolyte abnormalities (eg, hypernatremia, hyponatremia) that can lead to seizures.
Meningitis and encephalitis are the main concerns in a child presenting with fever and seizures. A thorough evaluation by an experienced clinician almost always will detect the child with meningitis. Although as many as 40 percent, particularly younger infants, who have seizures as an initial manifestation of meningitis do not have meningeal signs, they have other symptoms and findings that strongly suggest the correct diagnosis.
It is exceedingly rare for bacterial meningitis to be detected on the basis of doing a "routine" evaluation of the CSF after a febrile seizure. When the only indication for performing a lumbar puncture is the seizure, meningitis will be found in less than 1 percent of patients and less than one-half of these will have bacterial meningitis.
Children with status epilepticus (SE) and fever are more likely to have bacterial meningitis than those with a short seizure. Meningitis must be considered as a diagnostic possibility in children with SE and fever.
The emergent evaluation and management of the child with suspected meningitis is discussed separately.
DIAGNOSTIC EVALUATION
Lumbar puncture — The need for a lumbar puncture (LP) with CSF examination to exclude meningitis or encephalitis in children with a febrile seizure is uncertain. A retrospective cohort review of 704 patients aged 6 to 18 months who presented with a first simple febrile seizure revealed that 38 percent underwent LP. There were no diagnoses of bacterial meningitis made in children in whom this was not otherwise suspected clinically; leukocytosis was present in 3.8 percent. CSF cultures revealed no pathogens, but in 10 cases (3.8 percent) a contaminant grew. A separate study in children with complex febrile seizures revealed similar findings.
While routine performance of LP in all children with febrile convulsions does not seem warranted, the American Academy of Pediatrics (AAP) recommendations regarding the performance of LP in the setting of febrile seizures are the following:
LP should be performed when there are meningeal signs or symptoms or other clinical features that suggest a possible meningitis or intracranial infection.
LP should be considered in infants between 6 and 12 months if the immunization status for Haemophilus influenzae type B or Streptococcus pneumoniae is deficient or undetermined.
LP should be considered when the patient is on antibiotics because antibiotic treatment can mask the signs and symptoms of meningitis.
Once a decision to perform an LP has been made, blood culture and serum glucose testing should be performed concurrently.
LP should also be considered when febrile seizures occur after the second day of illness, or when, based on history or examination, the clinician remains concerned about possible central nervous system infection. Based on case series, but not included in the AAP guidelines, febrile status epilepticus may be another possible indication for lumbar puncture.
Other tests — A complete blood count and measurement of serum electrolytes, blood sugar, calcium, and urea nitrogen is of very low yield; these parameters should be measured only when the patient has a history of vomiting, diarrhea, and abnormal fluid intake, or when physical findings of dehydration or edema exist.
Neuroimaging with computed tomography (CT) or MRI is not required for children with simple febrile seizures. Urgent neuroimaging (CT with contrast or MRI) should be done in children with abnormally large heads, a persistently abnormal neurologic examination, particularly with focal features, or signs and symptoms of increased intracranial pressure.
Routine electroencephalography (EEG) is not warranted, particularly in the setting of a neurologically healthy child with a simple partial febrile seizure. Abnormalities are more likely to be found when the test is performed shortly afterthe seizure and when convulsions are of long duration and have focal features. An abnormal EEG cannot predict the likelihood of recurrent febrile seizures or the development of afebrile seizures.
TREATMENT OPTIONS
General considerations — Febrile seizures that continue for more than five minutes should be treated. Airway, respiratory status, and circulatory status are continuously assessed in patients with active seizures. Blood should be obtained for electrolytes and glucose determination, if indicated. Antiepileptic drugs should be administered intravenously, if possible, starting with a short-acting benzodiazepine such as lorazepam (0.05 to 0.1 mg/kg). If the seizure persists, an additional dose may be given. The child's respiratory status needs to be monitored carefully and intubation undertaken if the ventilatory status becomes inadequate.
Persistence of the seizure is rare. When it does, the child can be treated with fosphenytoin (15 to 20 mg/kg IV). If intravenous access is not possible or if the child is being treated at home, diazepam rectal gel may be used (0.5 mg/kg).
The fever should be treated as the seizures are controlled. 
Recurrent febrile seizures — One strategy for the treatment of a recurrent febrile seizure is the use of rectal diazepam gel if the episode lasts longer than five minutes. Parents can be taught to safely give the medication at home, and one dose administered rectally will not lead to respiratory depression.
One factor helpful in predicting a prolonged febrile seizure is focality. A strong correlation appears to exist between focality and a prolonged duration of both first and recurrent febrile seizures. In children with recurrent febrile seizures, those with long duration, defined as lasting longer than 10 minutes, tend to have similar features in repeat episodes. Similarly, children who have multiple risk factors for recurrent febrile seizures (focal onset, multiple seizures during the episode) and have a prolonged febrile seizure often have prolonged recurrent febrile seizures [59]. This may be a group of children for whom rectal therapy at the time of occurrence should be strongly considered.
PROGNOSIS — The prognosis for children with febrile seizures is favorable. While early reports had suggested that febrile seizures were associated with sudden death, the results from a large population-based study indicate that the small excess in mortality among children with febrile seizures is restricted to those with complex febrile seizures. Furthermore, the increased risk in those patients is explained, at least in part, by pre-existing neurologic abnormalities and subsequent epilepsy.
Recurrent febrile seizures — Children with febrile seizures are at risk for developing recurrent febrile seizures. The overall recurrence rate is approximately 30 to 35 percent [61,62]. However, the values vary with age from as high as 50 to 65 percent in children who are younger than one year of age at the time of the first seizure to as low as 20 percent in older children. A major factor influencing the recurrence rate is the age of the infant at the time of the first seizure. 
A prospective cohort study of 428 children with a first febrile seizure defined other features and factors influencing recurrences. Approximately one-third of the children had at least one recurrence, 17 percent had one recurrence, 9 percent had two recurrences, and approximately 6 percent had three or more recurrences. The majority of recurrences (50 to 75 percent) took place within one year of the initial seizure and almost all occurred within two years [64]. Four factors in the prospective cohort study increased the recurrence risk:
Young age at onset
History of febrile seizures in a first-degree relative
Low degree of fever while in the emergency department
Brief duration between the onset of fever and the initial seizure
Children who had all four factors were much more likely to have a recurrent febrile seizure than were those with none (≥70 versus ≤20 percent). Complex features were not associated with the risk of recurrence. These findings were confirmed in another prospective study.
Other factors identified in different studies have been abnormal development before the first febrile seizure, a history of afebrile seizures in parents and siblings, recurrence of seizures within the same illness, and the number of subsequent febrile illnesses. Among children who have had one recurrence, younger age at the time of the first recurrence and a family history of epilepsy are predictors of subsequent recurrences [61,65]. Another risk factor is an unprovoked seizure after a febrile seizure; such children are at substantial risk for further seizures with fever (rate ratio 3.47 after adjusting for the above risk factors, p = 0.0015).
Neurologic sequelae — Neurologic sequelae, including new neurologic deficits, intellectual impairment, and behavioral disorder, are rare following febrile convulsions.
Most reports documenting neurologic complications have been anecdotal and derived from biased populations consisting of children assessed in hospitals or clinics; in some cases, they may reflect preexisting abnormalities. When new deficits were reported, they occurred only after complex or prolonged febrile seizures.
In general, population-based studies do not corroborate anecdotal reports of neurologic complications. In the National Collaborative Perinatal Project, approximately 5 percent of children had febrile seizures lasting longer than 30 minutes. None of these children sustained permanent motor deficits and none had impaired mental development unless they developed afebrile seizures. Similar findings were noted in a population-based study of 381 children with febrile convulsions in the United Kingdom. The children were assessed when they were ten years old, and children who had neurologic and developmental problems prior to the first febrile seizure were excluded. No difference was found in measurements of academic progress in children with febrile convulsions, whether simple, complex, or recurrent, compared to a controlled cohort. There was also no difference in behavior between the two groups. Finally, among 18 thousand Danish conscripts aged 18 to 20 years, there was no association found between febrile seizures and cognitive function.
Subsequent epilepsy — Epilepsy occurs more frequently in children who have had febrile seizures than in the general population. In a normal child with a simple febrile seizure, the risk is only slightly above that of the general population. Epidemiologic studies have identified risk factors for epilepsy among children with febrile seizures:
In the National Collaborative Perinatal Project, children with abnormal neurologic development and whose first seizure was complex (focal, multiple, or longer than 15 minutes) had a 9.2 percent incidence of afebrile seizures by seven years of age; a risk 18 times higher than that in children with no history of febrile seizures (0.5 percent) and more than eight times higher than that in normal children with a noncomplex first febrile seizure (1.1 percent).
In Rochester, Minnesota, 687 children with a history of febrile seizures were observed into adulthood. Three risk factors for developing epilepsy were identified: focal seizures, prolonged seizures, and repeated episodes within 24 hours during the same illness. The risk of developing epilepsy was 2.4, 6 to 8, 17 to 22, and 49 percent in children with no, one, two, or three of these risk factors, respectively.
A population-based study in Denmark also followed children with febrile seizures into adulthood. The cumulative incidence of epilepsy was 6.9 percent at 23 years, and the relative risk associated with febrile seizures was 5.4. The risk of epilepsy was higher in those with a family history of epilepsy, cerebral palsy, or low Apgar scores at five minutes.
Subsequent temporal lobe epilepsy — Although a variety of seizure types follow febrile convulsions, whether prolongedfebrile convulsions lead to the development of temporal lobe epilepsy is controversial. Reports of patients with refractory temporal lobe epilepsy considered for surgery often find an association with febrile convulsions in infancy, particularly prolonged seizures. In addition, studies assessing hippocampal volume in adults with epilepsy have found an association between a smaller hippocampus and a history of febrile seizures. Data are conflicting as to whether a correlation exists between the duration of epilepsy and a reduction in hippocampal volume. As noted above, hippocampal abnormalities have also been associated with familial febrile seizures.
The possibility of hippocampal injury induced by febrile seizures was assessed by MRI in infants who had had complex febrile seizures. Abnormalities were found in the children with focal and prolonged complex febrile seizures but not in those with generalized febrile convulsions. In a few children who had significantly longer seizures, MRI suggested acute edema of the hippocampus, a finding noted in other case series as well. Follow-up imaging studies in these children may show hippocampal atrophy or abnormal apparent diffusion coefficient measurements. Another study found that hippocampal atrophy and other MRI characteristic of hippocampal sclerosis were more common in adults with a history of febrile seizures in childhood than those without. Although these observations suggest acute injury to the hippocampus during a febrile seizure, the possibility of preexisting lesions leading to susceptibility to injury is not excluded.
Studies based mainly upon imaging results and patients being considered for epilepsy surgery suggest an association between febrile seizures and temporal lobe epilepsy. Some clinical studies reached a similar conclusion. In one, patients presenting to an epilepsy clinic because of a previous diagnosis of epilepsy or recent onset of seizures were prospectively questioned about febrile convulsions and their characteristics. Febrile convulsions were reported by 13.2 percent of the patients. Temporal lobe epilepsy was more likely to be preceded by febrile convulsions than by other types of epilepsy (25.2 percent versus 5.6 percent, respectively). Prolonged duration was the most common feature of the complex febrile seizure associated with temporal lobe epilepsy, although patients with generalized epilepsy were more likely to have had simple febrile convulsions.
However, carefully performed community-based epidemiologic studies have not been able to confirm this association. In one, the characteristics of epilepsy were evaluated in 524 children who were one year of age or older at the onset of epilepsy. Febrile seizures were present in 14 percent of the patients. Complex febrile seizures were associated with a younger age at onset of the epilepsy, but there was no specific association with localization-related forms of epilepsy. No evidence that focal or prolonged febrile seizures were associated with temporal lobe epilepsy was found; three children had hippocampal atrophy demonstrated on their initial MRI, but none had a history of febrile seizures.
In summary, febrile seizures do not appear to cause temporal lobe epilepsy. The association may represent an inherent susceptibility in some children who are predisposed to prolonged febrile seizures and epilepsy simultaneously.
FEBRILE STATUS EPILEPTICUS — A prolonged febrile seizure (febrile status epilepticus [FSE]) is a concern for both physicians and parents. A multicenter prospective cohort study described the characteristics of prolonged (>30 minutes) febrile seizures in 119 children, aged one month through five years. The following findings were noted:
The median duration was 68 minutes
The seizures were convulsive in all but one child
The seizures were continuous in 52 percent and intermittent in 48 percent
Two-thirds of seizures were partial
This was the first febrile seizure in 76 percent of children
Chart reviews suggested that status epilepticus was often not recognized by the emergency department staff, perhaps contributing to the long duration of the seizures.
The clinical setting in which FSE is not clearly different than shorter febrile seizures. In the multicenter cohort described above, the median peak temperature was 103ºF (39.4ºC), most patients had a defined viral or bacterial illness, and there was a higher than expected family history of epilepsy.
In another series, patients with FSE were more likely to have a family history of epilepsy than children who presented with briefer febrile seizures; they also had a higher prevalence of baseline neurologic disease and a personal history of epilepsy.
Some reports suggest that children with status epileptics and fever are more likely to have bacterial meningitis than those with a short seizure. A group of 24 children with status epilepticus in the setting of fever were identified over a six month period through a British surveillance study of children with SE. Lumbar puncture was performed in nine patients, four of whom had findings characteristic of bacterial meningitis. The incidence of bacterial meningitis in this report is quite high and may be due, in part, to the small sample size. In another series 11 of 95 children with status epilepticus and fever (11.6 percent) had acute bacterial meningitis. Thus, meningitis must be considered as a diagnostic possibility in children with presumed FSE.
The distribution of seizure durations suggests that the longer a febrile seizure continues the less likely is it to stop without treatment. Patients with FSE should be treated with anticonvulsant medication as are other patients with status epilepticus and efforts should be made to lower fever using antipyretics and a cooling blanket.
The long term consequences of FSE have not been defined. Clinical follow-up of the above mentioned cohort is in progress. Another study followed 44 children with FSE, most of whom were identified prospectively. After a mean follow-up of 28 months, the risk of recurrent seizures (febrile and afebrile) was increased only in those who had prior neurologic abnormalities. This finding is similar to that seen in patients with febrile seizures without status. Other case series have found that EEG studies, performed within one week after FSE, show focal slowing in one-third. While some have found that this is associated with a higher risk of epilepsy, this association has not been consistently reported and requires further study.
ROLE OF PREVENTIVE THERAPY
Antiepileptic therapy — Children with febrile seizures are at increased risk for recurrent febrile as well as the development of afebrile seizures, suggesting a role for prophylactic treatment with chronic antiepileptic medications (AEDs). However, there is increasing consensus that risks of AED treatment outweigh potential benefits for most patients.
The effectiveness of AEDs was evaluated in a meta-analysis of studies for the prevention of recurrent febrile seizures; treatment with either phenobarbital or valproate were associated with reduced odds of recurrent febrile seizures (OR 0.54 and 0.09, respectively). There was no benefit for the use of intermittent diazepam. The latter finding is in contrast to a controlled trial in which oral diazepam (0.33 mg/kg every eight hours during the first few days of a febrile illness) was as effective as was the continuous administration of phenobarbital in reducing episodes of recurrent febrile seizures. Another observational study found that diazepam PR was associated with a reduced incidence of recurrent febrile seizures (2 versus 15 percent) compared with patients not so-treated.
The potential benefit of AED prophylaxis in reducing the usually benign recurrence of febrile seizures within the same illness must be balanced with the potential adverse effects of treatment, which include ataxia, lethargy, irritability, and others occurring in as many as 40 percent of patients.
There is no availableevidence that the use of chronic AEDs or the prevention of recurrent febrile seizures is associated with a reduced risk of epilepsy.
The Committee on Quality Improvement, Subcommittee on Febrile Seizures of the AAP concluded that "Based on the risk and benefits of effective therapies, neither continuous nor intermittent anticonvulsive therapy is recommended for children with one or more simple febrile seizures. The American Academy of Pediatrics recognizes that recurrent episodes of febrile seizures can create anxiety in some parents and their children and as such appropriate educational and emotional support should be provided".
There is no data upon which to base a recommendation regarding AED prophylaxis in children with complex febrile seizures. Treatment in such cases is individualized based upon underlying risk factors.
Antipyresis — For children who have had febrile seizures, treatment with antipyretics at the time of a febrile illness may be helpful in overall management but does not appear to affect the recurrence rate of febrile seizures:
A study in which low dose acetaminophen or a placebo was administered for fever failed to demonstrate a decrease in febrile seizures. However, the fact that the patients also received diazepam or a placebo and the fact that all patients apparently received acetaminophen if temperature reached 40 C (104 F) makes the data difficult to interpret.
A systematic review of 12 trials (1,509 patients) of acetaminophen versus placebo or sponging for treatment of fever concluded that there was insufficient evidence to show whether or not acetaminophen influenced the risk of febrile convulsions.
A subsequently published clinical trial randomly assigned 231 children with febrile seizures to receive either rectal diclofenac or placebo at onset of a subsequent febrile episode; patients were simultaneously randomized into one of three subsequent treatment groups (oral placebo versus acetaminophen versus ibuprofen) to begin eight hours after initial treatment. In this study, antipyretics were not effective at lowering body temperature or preventing the recurrence of febrile seizures (overall incidence 23 percent).
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