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The aim of this study was to compare the effect of treatment with lamotrigine (LTG) or carbamazepine (CBZ) on health-related quality of life (HRQOL) and to demonstrate the use of the SEALS Inventory as a comparative tool in clinical trials. Two hundred and sixty patients with newly diagnosed epilepsy were randomized to 48 weeks of treatment with LTG (n = 131) or CBZ (n = 129). HRQOL was measured at baseline and weeks 4, 12, 24, and 48 using the modified Side Effect and Life Satisfaction (SEALS) Inventory-a 38-item questionnaire divided into five subscales: Worry, Temper, Cognition, Dysphoria, and Tiredness. Overall, SEALS scores in the LTG group decreased (improved) significantly from baseline (P = 0.001). The LTG group had improvement in all five subscales over the 48 weeks of the study. CBZ patients had significantly worse SEALS scores than LTG patients at week 4 (P < 0.038). There was no significant change (positive or negative) in subsequent SEALS assessments. Analysis of SEALS data by subscale showed that the the CBZ group experienced more cognitive side-effects in general and more general changes in energy levels and affect during the first 4 weeks of treatment. These changes may help explain the difference in study completion rate: LTG 65%, CBZ 51% (P = 0.018). LTG offers the patient with newly diagnosed epilepsy significant benefits of greater tolerability and better health-related quality of life compared with CBZ. The SEALS Inventory is an effective tool for use in clinical trials of AEDs; it was a better predictor of trial completion than seizure counts, and used as a covariate enabled better detection of treatment effects. In general practice, the use of the SEALS Inventory to assess HRQOL has the potential to improve quality of care for people with epilepsy.

SUMMARY A battery of psychometric tests was administered to 85 patients with epilepsy, of whom 26 were untreated, 40 received carbamazepine monotherapy and 19 took carbamazepine with another anticonvulsant. Carbamazepine alone had little effect on performance, but carbamazepine polypharmacy produced significant impairment. Increasing concentrations of carbamazepine (four tests) and its active metabolite, carbamazepine 10,1 1 epoxide (seven tests), correlated with decreasing performance in the monotherapy patients.Since the epidemiological studies of the 1950s, an association has been established between seizure disorders and neuropsychological deficit.' 2 The complex relationship between fits, cognitive impairment, psychosocial difficulties and underlying cerebral pathology has been the subject of several recent investigations.3 The tangle of causality between these four factors has not been fully unravelled. Since the first controlled study of Reynolds and Travers,6 there has been a growing body of evidence that a fifth factor, the presence of antiepileptic drugs in the brain, contributes independently to disruption of intellectual functioning. Thompson and Trimble7 and Ludgate and his colleagues8 have shown that patients receiving multiple anticonvulsants function less well on cognitive testing than those treated with monotherapy and that reducing the number ofcirculating drugs can lead to improvement in performance without producing a deterioration in seizure control.Patients taking carbamazepine appear to show less evidence of cerebral impairment than those treated with older agents such as phenytoin or phenobarbitone.9Y'1 However, Macphee and co-workers, in a recent series of studies using a battery of simple psychomotor tests, have demonstrated that subtle derangement can be produced in naive subjects

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Two groups of adult outpatients (n = 19 and n = 21) with poorly controlled epilepsy and significant psychological disorder, assessed in terms of rating scales, received two psychological treatments in a balanced cross-over design after stable baseline seizure frequency had been established. A third group (n = 19), who had poorly controlled epilepsy but no significant psychological disturbance received one type of psychological treatment after a stable baseline. The treatments were educational and were designed to improve coping skills. Weekly seizure frequency was monitored for 42 weeks, and self-rating measures of anxiety and depression were obtained before treatment and at the end of follow-up. All three groups showed a significant reduction in seizure frequency that was maintained at 6-month follow-up. The two groups with psychological symptoms showed a significant improvement in scores on the self-rating scales. We concluded that routine use of psychological intervention may be helpful in outpatient management of epilepsy.

Twenty-four patients with refractory epilepsy on one or more antiepileptic drugs were given additional vigabatrin (1 g twice daily for six weeks, followed by 1-5 g twice daily for a further six weeks) and matched placebo in a double blind, randomised, crossover study. A battery of neuropsychological tests was administered at baseline and at weeks two, six and 12 of both treatment periods. No significant differences were found between vigabatrin and placebo at any time point for any of the objective tests of cognitive function. Patients, however, reported a greater degree of sedation after two and six weeks on vigabatrin than during the equivalent placebo phase (p < 0 01), although no such difference was apparent at 12 weeks. Follow up over a mean of 14-75 months in 12 responders, who continued on vigabatrin, revealed a significant improvement (all p < 001) on each of three composite scales (three psychomotor tests, four memory tests, three self rating scales) compared with their scores during the double blind trial.

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