Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmaco-kinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.

The nonlinear kinetics of phenytoin were evaluated in 54 children by measuring phenytoin concentrations at steady state at three or more doses. There was good correlation between phenytoin doses and concentrations when a nonlinear kinetic model was used (r = 0.896). Increasing age was associated with a reduction in the apparent Vmax. The apparent Km was influenced primarily by drug interactions. Phenobarbital increased the Km and Vmax for phenytoin. Carbamazepine reduced both Km and Vmax. Valproic acid reduced the Km. The low Km (less than 2.6 mg per liter) found in 28% of patients makes titration of the phenytoin dose to therapeutic levels difficult.

A retrospective analysis of quantitative and qualitative immunoglobulin G (IgG) results from 253 children who were either medically and neurologically normal or highly unlikely to have abnormalities of CSF IgG is reported. Normal values in this reference population vary with age for CSF/albumin IgG ratio and CSF/serum IgG index and are significantly different from the adult reference values. The rate of false positivity is lower for quantitative values than for qualitative IgG determinations (oligoclonal bands).

A placebo or methylprednisolone (45-60 mg/M2) was administered in a crossover study as a single morning dose on alternate days to fourteen patients who had a familial progressive polyneuropathy that either began or was maximum in the distribution of the peroneal nerves. Neither the patients nor the examining physician were told whether the patient was taking a placebo or steroid but the steroid side-effects made a double-blind trial impossible. Patients were evaluated at the initiation of the study, the time of crossover, and at the conclusion of the study. Five patients with proven HMSN-I completed the study; eight patients with HMSN-I were placed on a placebo or on steroids for a six-month-period. In neither group was there any evidence of a significant increase in nerve conduction times, a decrease in terminal latencies, an increase in strength or a decrease in sensory loss when evaluated by quantitative methods. These patients were subject to a high incidence of complications from steroids possibly because of root hypertrophy, relative inactivity, and high CSF proteins. These included excessive weight gain, a compression fracture of T-12; cord compression from enlarged nerve roots; myopathy; pseudotumor; and psychiatric disturbances. Considering the lack of benefit of steroids and the high incidence of complications due to the medication further trials of adrenal-corticosteroids in patients who definitely have familial HMSN-I do not seem to be justified.

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