In this review we systematically assess our currently available knowledge about psychogenic non-epileptic seizures (PNES) with an emphasis on the psychological mechanisms that underlie PNES, possibilities for psychological treatment as well as prognosis. Relevant studies were identified by searching the electronic databases. Case reports were not considered. 93 papers were identified; 65 of which were studies. An open non-randomized design, comparing patients with PNES to patients with epilepsy is the dominant design. A working definition for PNES is proposed. With respect to psychological etiology, a heterogeneous set of factors have been identified. Not all factors have a similar impact, though. On the basis of this review we propose a model with several factors that may interact in both the development and prolongation of PNES. These factors involve psychological etiology, vulnerability, shaping, as well as triggering and prolongation factors. A necessary first step of intervention in patients with PNES seems to be explaining the diagnosis with care. Although the evidence for the efficacy of additional treatment strategies is limited, variants of cognitive (behavioural) therapy showed to be the preferred type of treatment for most patients. The exact choice of treatment should be based on individual differences in the underlying factors. Outcome can be measured in terms of seizure occurrence (frequency, severity), but other measures might be of greater importance for the patient. Prognosis is unclear but studies consistently report that 1/3rd to 1/4th of the patients become chronic.

Summary: Purpose: This study compares the cognitive effects of topiramate (TPM) with those of valproate (VPA) using efficacious doses of each drug when used as adjunctive therapy to carbamazepine (CBZ). A key question of the study is to what extent a more gradual introduction of TPM improves tolerabil‐ity and prevents cognitive impairment. Methods: The study is a multicenter, randomized, observer‐blinded, parallel‐group clinical trial with VPA or TPM given as first‐line add‐on therapy to steady‐state treatment with CBZ. TPM is introduced at 25 mg and increased with weekly 25‐mg/d increments to a minimum dosage of 200 mg/d. The target dosage ranges from 200 to 400 mg/d for TPM and is 1800 mg/d for VPA. The study evaluates cognitive function changes from baseline to end point (after 20 weeks of treatment) and during titration (after 8 weeks of treatment). The primary outcome measure is the difference between the treatments (TPM versus VPA) in change from baseline to end point and change from baseline to titration, using a 95% confidence interval approach. Results: For the 10 baseline‐to‐end point comparisons, one test measuring short‐term verbal memory (Rey Auditory Verbal Learning Test) yields a statistically significant difference between the treatments (p = 0.02), showing worsening for TPM and improvement of scores for VPA. The 10 baseline‐to‐titration comparisons also show one statistically significant difference, again for a test measuring short‐term memory (Recognition of Words; p = 0.04), showing a larger change in the negative direction for TPM. None of the mood tests or the test for subjective complaints shows statistically significant differences between the treatments, although more scores are in the negative direction for TPM during titration. Conclusion: Although the pattern of changes in the negative direction seems consistent with clinical information, the differences found between the treatments are small. An important finding of our study is that, when the results are compared with those of other studies, it is clear that gradual introduction of TPM can reduce the extent of cognitive impairment (with a maximum of about 0.6 SD).

The diagnosis of pseudo-epileptic seizures (PES) is confirmed in 7-10% of the patients that are considered to suffer from 'refractory epilepsies'. As yet no consistent model is available to explain the development of PES in individual patients. This open non-randomized clinical study aimed at assessing behavioural mechanisms that trigger PES, independent of the underlying personality characteristics. Twenty-four patients with PES were compared with pairwise matched patients that suffered exclusively from genuine epileptic seizures (ES). The patients were assessed with two personality inventories that measured potential important behavioural mechanisms: the 19 PF-form B of the Cattell IPAT Anxiety Scale and the Dutch ABV-scale, largely based on Eysenck's Maudsley Personality Inventory. This assessment was complemented with individual history taking and psychiatric examination. The results are presented in a model in which three factors are involved that have a combined effect on the development of PES in individual patients: personality disorders (of heterogeneous origin), the behavioural mechanism of somatization and a familiarity with epilepsy as a modifying factor.

Cognitive effects of lamotrigine as first-line add-on in patients with localization-related (partial) epilepsy Aldenkamp, A.P.; Mulder, O.G.; Overweg, J.

Several relationships have been obtained between cognitive impairment and epilepsy-related or treatment related factors. One of these factors is treatment-related: the central cognitive side effects of the antiepileptic drugs (AEDs). The second and third factors are disease-related factors , i.e., the effect of the seizures and underlying epileptiform discharges in the brain and the localization of the epilepto-genic focus in specific areas of the brain. Although most cog-nitive problems have a multifactorial origin and often several factors combined are responsible for the "make-up" of a cog-nitive problem, we have attempted to isolate one factor: the effect of seizures and epileptiform EEG discharges on cog-nitive function. Several studies show the impact of ictal activity , but special attention is required for the postictal and interictal effects of epilepsy on cognitive functions. This may explain substantial cognitive impairments in children with subclinical epileptiform discharges or with infrequent subtle seizures. Cognition can be defined as the capacity of the brain to process information accurately and to program adaptive behavior (1). Cognition involves the ability to solve problems, to memorize information, or to focus attention. On a higher level, it involves dealing with complex situations creatively by transcending from the immediate circumstances to anticipate future acting (2). Epilepsy is a symptom of ictal and intenctal brain dysfunction, and the possibility that cognitive impairment may develop as a secondary symptom is therefore obvious. A considerable body of research exists with regard to the general issue of cognitive functioning in epilepsy. Speed of information processing, memory, vigilance, alertness, sustained and focused attention, and motor fluency appear to be particularly vulnerable areas of functioning in epilepsy (3-9). Although the complex relationships between daily life function, underlying cognitive impairment, and epilepsy-related or treatment-related factors have not been fully explored, the existing literature clearly shows the impact of several factors. One factor is treatment-related: the central cognitive side effects of antiepileptic Address correspondence and reprint requests to Dr. A. Aldenkamp at Epilepsiecentrum Kempenhaeghe, PO Box 6 I , NL-5590 AB Heeze, The Netherlands. drugs (AEDs). The second and third factors are disease-related, i.e., the effect of the seizures and underlying epileptiform discharges in the brain and the localization of the epileptogenic focus in specific brain areas. This article highlights one of these factors, the effect of seizures and epileptiform EEG discharges on cognitive function. In evaluating this factor, it is imperative to realize that, in practice, most cognitive problems have a multifactorial origin and the three factors combined are usually responsible for the characteristics of a cog-nitive problem. IMPACT OF SEIZURES AND EPILEPTIFORM EEG DISCHARGES ON COGNITIVE FUNCTION Seizures Diurnal seizures are reported to directly ef...

Millions of healthy people participate in sport on a regular basis. Moreover, in the last decade patients with chronic disorders have been encouraged to take part in sporting activities as a part of their rehabilitation. Can epileptic patients freely participate in sport or whether they are restricted to a certain extent by their disorder? An important factor is freedom from seizures. If seizures have been controlled for over 2 years the risk of relapse is the same as the risk of a first seizure. The risk of patients drowning or falling, or their epilepsy worsening because they are engaged in sport is thought to be low. Clinical data suggest that the incidence of seizures during sports and exercise is reduced. In the cooling down period, however, seizures tend to occur more frequently. Physicians should encourage epileptic patients to participate in sporting activities to enhance their physical fitness, self-esteem, and social integration. Before giving advice about the most suitable type of sport, the physician should known the patient's medical history, have a good insight into the different types of sport and be able to judge the role and function of sport to the particular patient. With certain precautions virtually all sports are suitable for most epileptic patients and should therefore be encouraged. However, a small minority of hospitalised patients with severe epilepsy need the supervision of qualified trainers, coaches and volunteers.

We explored factors that may predispose patients to adverse mood effects during treatment with vigabatrin (gamma-vinyl GABA; VGB): mood disorders before VGB treatment, type of epilepsy, seizure type and seizure frequency, type and number of comedication, and VGB dose. The clinical relevance of such a study is that it may help identify circumstances in which VGB should be administered with caution. Seventy-three patients (40 males, 33 females), all with refractory epilepsies, who received VGB as add-on therapy, were assessed by the Amsterdamse Stemmingslyst (ASL), a mood-rating scale, before the start of treatment, and demographic and clinical data were recorded. The patients were followed for 6 months after the start of VGB treatment. Treatment with VGB had to be discontinued in 38 patients (52% of the total sample). Mood problems were the main reason for discontinuation in 9 (12.3% of the total sample). In 6 other patients, mood problems were mentioned as the reason for discontinuing treatment, in combination with lack of drug efficacy. Development of adverse mood effects could not be predicted by a specific mood profile on the ASL. Before treatment, the "mood problems discontinuation group" did not show extreme scores for any assessed areas of mood and no significant differences from other patients were noted on the mood scales. Neither did clinical or demographic data show statistically confirmed specific characteristics for the mood problems discontinuation group, though the patients tended to use more antiepileptic drugs (AEDs) as cotherapy, to have a slightly lower daily dose of VGB, to be slightly older, and were mostly female.(ABSTRACT TRUNCATED AT 250 WORDS)

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