Biomedical subjects
Publications and source records attributed to C Camfield.
Of 68 children treated with lamotrigine, a new antiepileptic medication, five developed a rash. One child developed Stevens-Johnson syndrome on lamotrigine monotherapy. Of the five patients with the rash, three were admitted to the hospital (two to the intensive care unit). All recovered completely, but one child had a recurrence of the rash within 30 minutes of reexposure to lamotrigine after 6 months.
Using a population-based regional cohort of 479 children with epilepsy, we studied the effect of the number of pretreatment afebrile seizures on seizure control and remission. The number of pretreatment seizures varied from 1 to 20. For the first 10 pretreatment seizures, there was no significant difference or trend in (1) the proportion of children who were seizure free long enough to attempt stopping medication (mean, 70%), (2) the number of breakthrough seizures before control was achieved, or (3) the proportion of children who were seizure free after stopping medication for the first time (mean, 70%). More patients with more than 10 pretreatment seizures had complex partial seizures (59%) than those with 10 or fewer seizures (16%) (p < 0.00001). We conclude that there does not appear to be any penalty for seizure control or early remission of epilepsy if medication is delayed for up to 10 pretreatment seizures.
We studied 97 children who were weaned from antiepileptic drug therapy 1 year after their last seizure. Medication was withdrawn over 4 to 8 weeks, and patients were followed for 12 to 57 months (32.4 +/- 13.1; mean +/- SD) or until seizure recurrence. The overall probability of remaining seizure free was 78% at 3 months, 71% at 6 months, 66% at 12 months, and 61% at 24 months (95% CI, 51, 71), similar to studies that have required longer treatment periods. Factors retained in multivariate analysis were female sex, age at seizure onset over 120 months of age, seizure type, and clinical evidence of neurologic abnormalities. Using these risk factors, a simple method of predicting the 24-month recurrence risk was possible.
BACKGROUND: Based on a follow-up study of 486 children, a scoring system for the long-term outcome for childhood epilepsy has been developed in Nova Scotia, Canada. The scoring system consists of four weighted predictor variables available at the time of diagnosis (ie, age at onset, intelligence, neonatal seizures, and number of seizures before treatment). OBJECTIVE: Validation of the scoring system using long-term follow-up data for childhood epilepsy from a regional cohort in Turku, Finland. DESIGN: Patients were selected from the Turku cohort with the same entry criteria as the Nova Scotia cohort. The scoring system was used to predict their epilepsy outcome. RESULTS: A total of 141 patients were selected from the Finland cohort. After 30 years of follow-up, 60% of the patients were in remission. The Nova Scotia scoring system correctly predicted outcome in 61% of Finnish cases (sensitivity, 43%; specificity, 88%; and positive predictive value, 84%). CONCLUSIONS: Long-term good outcome for childhood epilepsy is well predicted by the Nova Scotia scoring system.
OBJECTIVE: To identify risk factors predictive of sunscreen use in children. DESIGN: Cross-sectional review of convenience sample. SETTING: Emergency department of a regional referral pediatric hospital. SUBJECTS: Nine hundred twenty-five parents of children presenting to the emergency department in August 1993. MAIN OUTCOME MEASURES: Parental risk factors assessed were use of sunscreen, tanning behaviors, previous blistering sunburn, knowledge of cancer risk related to sunburn and sun protection factor definition, education level, and other health-promoting behaviors. The parents were asked about perceived risk for their child's being sunburned in the next month or development of skin cancer in their lifetime, as well as an estimation of safe sun exposure time for their child. Child risk factors included a history of previous painful sunburn and parental assessment of their child's skin type based on susceptibility to sunburn. RESULTS: Eighty-four percent of parents reported that their children had used sunscreen at least once in the previous 2 months. The use of sunscreen in children younger than 1 year was 54%, from 1 to 12 years of age was 91%, and older than 12 years was 68%. Factors associated with increased likelihood of sunscreen use were age of 1 to 12 years, parental use of sunscreen, estimation of safe sun exposure of less than 30 minutes, description of child skin type as burns "sometimes," "easily," or "always," and correct definition of sun protection factor. Application of a multivariate model yielded a sensitivity of 96%, specificity of 36%, and positive predictive value of sunscreen use of 89%. CONCLUSIONS: Sunscreen use in parents is predictive of use in their children and relates more to experience with sunburn than with concerns about future skin cancer risk.
OBJECTIVE: To assess the reliability of interictal spike discharge in routine electroencephalography (EEG) testing in children. METHOD: EEG results of all children diagnosed in Nova Scotia with epilepsy onset between 1977-85 (excluding myoclonic, akinetic-atonic and absence) were reviewed. The results of the EEG at time of diagnosis (EEG1) were compared with those of a second EEG (EEG2) within 6 months. RESULTS: Of 504 children with epilepsy, 159 had both EEG1 and EEG2. EEG2 was more likely ordered if EEG1 was normal or showed focal slowing but less likely if EEG1 contained sleep (p < 0.05). EEG1 and EEG2 were both normal in 23%. If EEG1 was abnormal, there was a 40-70% discordance for the type of abnormality on EEG2. Abnormalities were present on both EEG1 and EEG2 in 67 cases. Of the 42/67 with major focal abnormalities on EEG1, 7 had only generalized spike wave on EEG2. Of the 17/67 with only generalized spike wave on EEG1, 7 showed only major focal abnormalities on EEG2. Statistical testing showed low Kappa scores indicating low reliability. CONCLUSIONS: The interictal EEG in childhood epilepsy appears to be an unstable test. A repeat EEG within 6 months of a first EEG may yield different and sometimes conflicting information.
Acute and chronic toxicity complicates all antiepileptic medications (AED) and is idiosyncratic. Acute toxicity can be categorized into 1) acute brain dysfunction or 2) acute organ dysfunction when AED's are started. Despite promising in vitro lymphocyte testing, anticipation of acute reactions cannot be offered. Furthermore, screening for AED toxicity by routine blood and urine tests in asymptomatic patients is of doubtful value and should be abandoned. Patients should be informed of possible reactions and immediately report early symptoms. Treatment for acute reactions is largely unstudied. It is unclear how to reintroduce AED's following acute reactions. Often patients are sensitive to drugs with a similar chemical structure. The "desensitization" protocol of Purvis may be of merit. Three major chronic toxicities of AED's have been noted--soft tissue and gum hypertrophy, progressive ataxia, and peripheral neuropathy. New AED's require careful post-marketing surveillance since long term toxicity data are not yet available.
In a population of 850,000, the authors studied afebrile seizures that follow febrile seizures. Review of all paediatric EEGs identified 504 children with epilepsy beginning between 1977 and 1985. Follow-up averaged 85 months. 14.9 per cent had preceding febrile seizures: 13 per cent complex partial, 13 per cent partial/secondary generalized and 22 per cent generalized tonic-clonic. The rate of preceding febrile seizures did not vary with the cause of epilepsy. Prolonged febrile seizures were not associated with any particular afebrile seizure type. Of 17 with preceding prolonged febrile seizures, seven developed intractable epilepsy: 17.9 per cent of the total intractable cases. Only two developed idiopathic intractable complex partial seizures after prolonged febrile seizures. The authors conclude that febrile seizures most often precede generalized tonic-clonic afebrile seizures. Prolonged febrile seizures rarely precede idiopathic intractable complex partial seizures. The febrile seizure tendency may be a fundamental marker of an individual's seizure threshold.
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OBJECTIVE: To identify risk factors predictive of a first febrile seizure. DESIGN: Case-control study. SETTING: Regional referral pediatric hospital emergency department. PATIENTS: Seventy-five patients aged 6 months to 4 years presenting with a first febrile seizure were age-matched to two febrile and two afebrile noninfectious controls who had never had a seizure. METHODS: Telephone interview of parents. MAIN OUTCOME MEASURES: Risk factors assessed included family history of febrile or afebrile seizures, neurodevelopmental abnormality, and child-care arrangement. Analysis was done by matched case-control and logistic regression. RESULTS: Factors associated with a significant increase in risk of a first febrile seizure were febrile seizures in first-degree relative (odds ratio [OR], 4.5) or second-degree relative (OR, 3.5); neonatal discharge at 28 days or later (OR, 5.6); parental report of "slow" development (OR, 4.9); and day-care attendance (OR, 3.1). For children with two risk factors (an estimated 3% of the population), the risk of developing febrile seizures is approximately 28% (assuming a population incidence of febrile seizures of 4%).
A population-based study was conducted in an attempt to predict which child's epilepsy will remit. Use of data from a regional electroencephalography laboratory allowed identification of all children in Nova Scotia with epilepsy onset from 1977 through 1985 (excluding those with absence and "minor motor" seizures). Children were followed for an average of 7 years. On the basis of clinical characteristics, a multivariate analysis was used to develop a scoring scheme to predict remission (defined as off medication at the end of the follow-up period). Survival curve methods were used to estimate the duration of medication treatment for those with remission. Of the 504 eligible patients, approximately 70% became seizure free long enough to discontinue medication. Approximately 70% of those stopping medication a first time remained seizure free. At the end of follow-up, 55% of the total cohort were in remission. At diagnosis, the best predictors of remission were age < 12 years at onset, normal intelligence, no prior neonatal seizures, and fewer than 21 seizures before treatment. If predicted to have a remission, then, on the basis of survival curve analysis, 80% were without medication 100 months after diagnosis. After 12 months of treatment, prediction was enhanced by including a score for the number of seizures between 6 and 12 months on treatment. We conclude that approximately 55% of childhood epilepsy will remit. Our scoring system predicts reasonably accurately who will have a remission and when medication is likely to be discontinued.
We studied social outcome for all the normally intelligent children in our province with onset of epilepsy between 1977 and 1985 (excluding absence and "minor motor" seizures). After follow-up averaging 7 1/2 years, the 337 patients were 7 to 28 years of age. Outcome measures were age dependent. Of those old enough to be at risk, the percentage with each unfavorable outcome was as follows: school failure 34%, use of special educational resources 34%, mental health consultation 22%, psychotropic medication 5%, unemployment 20%, social isolation 27%, inadvertent pregnancy 12%, and criminal conviction 2%. In social isolation 27%, inadvertent pregnancy 12%, and criminal conviction 2%. In a multivariate model correcting for number of potential unfavorable outcomes (based on age at end of follow-up), many variables related to epilepsy, seizure control, and electroencephalographic findings were not associated with social outcome. Only two variables were associated with at least one unfavorable outcome--learning disorder (p < 0.001) and more than 21 seizures before treatment was begun (p < 0.03). The only variable with no unfavorable outcome was simple partial seizures (p < 0.003). Sensitivity and specificity of this model were 54% and 68%, respectively, indicating that social outcome for these children was often not related to biologic factors reflected by the medical details and clinical course of their disorder.
We report the first comparison of Chewable and Regular Carbamazepine (CBZ) tablets in children with epilepsy. Forty-four children receiving chronic monotherapy CBZ participated. In month 1 children received regular CBZ; in month 2, the same dose of Chewable CBZ. Once per week fasting predose CBZ and CBZ epoxide serum levels were determined. In a subset of 15 children, at the end of each month serum levels were obtained every 2 hours for 12 hours beginning pre-dose. Standards for CBZ and CBZ epoxide were tested in each centre. Overall, weekly levels showed no consistent differences between the month on chewable CBZ and regular CBZ. Seizure control and rates of reported side effects were similar. In five patients chewable CBZ produced higher peak CBZ levels while five had higher peaks with regular CBZ. In conclusion, regular and chewable CBZ often have unpredictable differences in peak but not trough levels of CBZ suggesting that peak level side effects with one form of CBZ might be alleviated by changing to the other.
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Severe or fatal reactions to anticonvulsant agents are fortunately rare. We examined the value of routine screening of blood and urine to detect early signs of such reactions in asymptomatic patients. The basic assumptions of this type of screening program have been faulty or unproven, and the results of studies, although not definitive, have not supported the value of such programs. Our recommendations, approved by the Canadian Association for Child Neurology, suggest that asymptomatic patients not undergo routine screening of blood and urine but, rather, be informed of the early symptoms of severe toxic reactions and be asked to report them immediately to a physician.
We randomized 31 children with a 1st afebrile unprovoked seizure to receive carbamazepine (CBZ) or no medication for 1 year or until the time of a 2nd seizure. All seizures had a focal onset or were generalized tonic-clonic. Overall, 2/14 randomized to CBZ and 9/17 with no medication had a recurrent afebrile seizure. Compliance with CBZ was excellent in 12/14, but noncompliance may have contributed to 1 of the recurrences with CBZ. Four discontinued CBZ because of side effects. Two additional children taking CBZ had a febrile seizure. Thus, only 6/14 taking CBZ had a year completely seizure-free with no unacceptable medication side effects. Of those taking no medication, 2 had a febrile recurrence, and 7/17 had a year completely-seizure free. Side effects and febrile recurrences may limit the value of CBZ for some children, although CBZ appears to reduce significantly recurrences after a 1st afebrile seizure.
Clobazam is a new benzodiazepine recently introduced in Canada on an experimental basis. We report our experience with 27 children (average age 9.1 years) with severe intractable seizure disorders. All had mixed seizures (41% focal plus generalized, 59% mixed generalized) and 93% were mentally retarded. Eighty-five percent had multiple daily seizures and all had been on an average of 6 other anticonvulsants in the past. Forty-one percent of our patients responded to clobazam with a reduction of greater than 75% in seizure frequency and 15% had no further seizures. Tolerance to clobazam which could not be overcome by dose increases developed in 26% of patients. Forty-four percent of non-responders had exacerbations of their seizures shortly after starting clobazam, however 43% of these patients had reductions in comedications simultaneously. Side effects of clobazam in responders were minimal. We conclude that clobazam shows sufficient promise to warrant further trials in more benign seizure disorders in children.