The Use of Sertraline in Patients with Epilepsy: Is It Safe?

Purpose. The purpose of this study was to assess the impact of the selective serotonin-reuptake inhibitor (SSRI) sertraline (SRT) on the severity and frequency of seizures of patients with epilepsy.Methods. We prospectively assessed the seizure frequency of 100 consecutive patients with partial (n = 95) and primary (n = 5) generalized epilepsy during a trial with SRT for the treatment of a depressive (n = 97) or obsessive-compulsive (n = 3) disorder. We compared the monthly seizure frequency recorded while on SRT with those logged during the 3 and 12 months preceding the start of SRT. A definite causality between seizure worsening and SRT was considered in the following circumstances: (1) occurrence of de novo generalized tonic-clonic seizure (GTC); (2) recurrence of a GTC following a period of at least 1 year without this seizure type; and (3) an increase in the monthly seizure frequency beyond the maximal recorded monthly frequency during both 3- and 12-month periods preceding SRT. A probable causality between SRT and seizure worsening was considered in the case of an increase in monthly seizures beyond the maximal frequency recorded during the 3-month, but not the 12-month, period preceding SRT.Results. Six patients (6%) experienced an increase in seizure frequency after starting SRT. One and five patients met criteria for definite and probable causality between SRT and seizure worsening, respectively. Adjustment of antiepileptic drug doses resulted in a return to baseline seizure frequency in the latter five patients; four patients were kept on SRT at the same doses. The SRT dose of these six patients was significantly lower (57.1 +/- 23.8 mg/day vs 111.8 +/- 56.8 mg/day; F = 6.35, P = 0.01) than that of the other 94 patients.Conclusion. SRT can be safely used in the vast majority of patients with epilepsy.     

Is It a Bird? Is It a Plane? Category Use in Problem-solving in Children with Autism Spectrum Disorders

Fourteen children with autism spectrum disorders (ASD) and fourteen age-matched typically-developing (TD) controls were tested on an adapted version of the Twenty Questions Task (Mosher and Hornsby in Studies in cognitive growth. Wiley, New York, pp 86–102, 1966) to examine effects of content, executive and verbal IQ factors on category use in problem-solving (age range 8–17). Across conditions participants with ASD asked questions that focussed on smaller categories than controls. Specific group differences were observed in the handling of abstract content and response to additional working memory demands. In addition, post hoc regression analysis indicated that VIQ predicted performance in ASD but not TD participants. The implications for theories of category processing in autism are discussed.     

Is Cognition Enough to Explain Cognitive Development?

Traditional views separate cognitive processes from sensory–motor processes, seeing cognition as amodal, propositional, and compositional, and thus fundamentally different from the processes that underlie perceiving and acting. These were the ideas on which cognitive science was founded 30 years ago. However, advancing discoveries in neuroscience, cognitive neuroscience, and psychology suggests that cognition may be inseparable from processes of perceiving and acting. From this perspective, this study considers the future of cognitive science with respect to the study of cognitive development.     

A Discrepancy in Comprehension and Production in Early Language Development in ASD: Is it Clinically Relevant?

This study examined the extent to which a discrepant comprehension-production profile (i.e., relatively more delayed comprehension than production) is characteristic of the early language phenotype in autism spectrum disorders (ASD) and tracked the developmental progression of the profile. Our findings indicated that a discrepant comprehension-production profile distinguished toddlers (30 months) with ASD from late talkers without ASD (91% sensitivity, 100% specificity) in groups that were comparable on expressive language, age, and socioeconomic status. Longitudinal data for children with ASD revealed that the discrepant profile steadily decreased from 30 to 44 months until there was no significant comprehension-production difference at 66 months. In conclusion, results suggest that lower comprehension than production may be an age-specific marker of toddlers with ASD.     

Is It Safe to Proceed with Thrombolytic Therapy for Acute Ischemic Stroke in a Patient with Cardiac Myxoma? Case Report and Review of the Literature

No abstract available.     

Is Schizophrenia a Risk Factor for Epilepsy or Acute Symptomatic Seizures?

PURPOSE: The precise prevalence of epilepsies and seizures in patients with schizophrenia remains unclear. METHODS: To assess the prevalence of epilepsy and of acute symptomatic seizures in schizophrenics, we conducted a survey in a urban sector of Marseilles that includes 56,910 inhabitants, among whom 1,154 had been treated for psychiatric disorders, including 460 for schizophrenia or paranoid disorder (PD) (DSM III-R 295 and 297.1, respectively; mean age, 41.9 years; range, 17-79 years; 215 men and 245 women). RESULTS: All 460 patients were receiving long-term neuroleptic drug therapy, and 397 had been hospitalized at least once in the past year, whereas 63 were followed up as outpatients only. Seizures were present in the history of 12 patients: five had various forms of chronic epilepsy (four men, one woman; DSM III-R 295.1, one case; 295.3, two cases; 295.9, two cases), and three of these experienced seizures only after the onset of their psychiatric condition; five had acute symptomatic seizures (four men, one woman; 295.1, two cases; 295.3, 295.9, and 297.1, one case), and two had only pseudoepileptic events (both 295.3). CONCLUSIONS: This survey shows that the prevalence of epilepsy and acute symptomatic seizures is comparatively low in patients with schizophrenia or PD (10.8 per thousand each, respectively), and that the prevalence of a history of seizures (21.7 per thousand in this study) is not particularly increased in this middle-aged population. In contrast to childhood-onset autistic disorders, schizophrenia or PD are not major risk factors for epilepsy or acute symptomatic epileptic seizures.     

Why Is There Still Doubt to Cut It Out?

Surgical treatment for epilepsy has made tremendous strides in the past few decades as a result of advances in neurodiagnostics—particularly structural and functional neuroimaging—and improved surgical techniques. This has not only resulted in better outcomes with respect to epileptic seizures and quality of life, and reduced surgical morbidity and mortality, but it has also increased the population of patients now considered as surgical candidates, particularly in the pediatric age range, and enhanced cost-effectiveness sufficient to make surgical treatment available to countries with limited resources. Yet surgical treatment for epilepsy remains arguably the most underutilized of all accepted medical interventions. In the United States, less than 1% of patients with pharmacoresistant epilepsy are referred to epilepsy centers.Although the number of epilepsy surgery centers has increased appreciably over the past two decades, the number of therapeutic surgical procedures performed for epilepsy has not increased at all. For patients who are referred, the average delay from onset of epilepsy to surgery is more than 20 years—too late for many to avoid a lifetime of disability or premature death. Not only has there been no consistent message to convince neurologists and primary care physicians to refer patients for surgery, but the increase in epilepsy surgery centers in the United States has appeared to result in a divergence of approaches to surgical treatment. Efforts are still needed to further improve the safety and efficacy of surgical treatment, including the identification of biomarkers that can reliably determine the extent of the epileptogenic region; however, the greatest benefits would derive from increasing access for potential surgical candidates to epilepsy surgery facilities. Information is needed to determine why appropriate surgical referrals are not being made. Consensus conferences are necessary to resolve controversies that still exist regarding presurgical evaluation and surgical approaches. Standards should be established for certifying epilepsy centers as recommended by the Institute of Medicine''s report on epilepsy. Finally, the epilepsy community should not be promoting epilepsy surgery per se but instead emphasize that epilepsy centers do more than epilepsy surgery, promoting the message: All patients with disabling pharmacoresistant seizures deserve evaluation by specialists at epilepsy centers who can provide a variety of advanced diagnostic and therapeutic services.The modern era of surgical treatment for epilepsy began in the late nineteenth century. The epileptogenic region was originally localized on the basis of seizure semiology and identification of a structural lesion, which was then superseded by the advent of EEG in the mid-twentieth century (1). Introduction of advanced neuroimaging by the end of the twentieth century—first PET and then MRI—returned presurgical evaluation to a more lesion-directed approach, with EEG often playing a confirmatory role. SPECT, MEG, and fMRI also contribute to the identification of previously invisible lesions, such as hippocampal sclerosis in patients with mesial temporal lobe epilepsy (MTLE), as well as malformations of cortical development (MCD), particularly in infants and young children. Advances in operative techniques have greatly improved the safety, as well as the efficacy, of epilepsy surgery. As a result, not only are we achieving better outcomes today, but many patients are receiving surgery who would not have been considered surgical candidates a decade ago. Furthermore, procedures are now sufficiently cost-effective to permit establishment of epilepsy surgery programs in countries with limited resources (2). A major remaining challenge is establishment of biomarkers that reliably localize and determine the extent of the epileptogenic region, particularly in patients without obvious structural lesions (3).     

Is inadequate family history a barrier to diagnosis in CADASIL?

OBJECTIVES: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) has typical clinical features that include stroke, migraine, mood disturbances and cognitive decline. However, misdiagnosis is common. We hypothesized that family history is poorly elicited in individuals presenting with features of CADASIL and that enquiry into family history of all four cardinal manifestations of CADASIL is superior to elicitation of family history of premature stroke alone in raising the diagnostic possibility of CADASIL. MATERIALS AND METHODS: Retrospective review of family histories at presentation in 40 individuals with confirmed CADASIL was performed through structured interview in a Neurovascular Genetics clinic (182 first-degree and 242 second-degree relatives identified). Family history obtained from structured interview was compared to family history initially documented at presentation. RESULTS: At initial presentation, 30% of individuals were inaccurately documented to have no family history of significant neurological illness. Thirty-five per cent of patients had an initial alternative diagnosis. Initial inaccurate documentation of negative family history was more frequent in individuals with an initial alternative diagnosis. After structured interviews, 34% of 182 first-degree and 35% of 242 second-degree relatives of CADASIL patients had history of stroke (16% of first-degree relatives had stroke before the age of 50 years). Forty-three per cent of first-degree and 28% of second-degree relatives had migraine, mood disturbance or cognitive decline. CONCLUSIONS: A false-negative family history was commonly documented in individuals presenting with features of CADASIL and was associated with initial misdiagnosis. Restriction of family history to premature stroke alone is probably inadequate to identify affected CADASIL pedigrees.