Revisiting personality in epilepsy: Differentiation of personality in two epilepsies starting in adolescence.

PURPOSE: The purpose of this study was to investigate personality characteristics and clinical parameters in two well-defined epilepsies: mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE/HS) and juvenile myoclonic epilepsy (JME) through NEO Revised Personality Inventory (NEO-PI-R) and Neurobehavior Inventory (NBI) standardized instruments. METHODS: One hundred patients undergoing corticoamygdalohippocampectomy (CAH), 100 patients with JME, and 100 control subjects answered the personality measures. Clinical parameters such as psychiatric symptoms, seizure frequency, duration of epilepsy, and side of the lesion in MTLE/HS group were investigated. Statistical analysis consisted of the mean and standard deviation (SD) of each variable. Student's t-test or Fisher exact test were used according to the variable studied. RESULTS: The three groups were within the average range of NEO-PI-R and NBI, although 'tendencies' and differences were demonstrated. The MTLE/HS and control subjects had a similar profile: low scores in Neuroticism and high in Conscientiousness (r = -0.330; p < 0.001/r = -0.567; p < 0.001, respectively) in opposition to what occurred in JME, low in Conscientiousness and high in Neuroticism (r = -0.509; p = 0.005). The NBI 'sense of personal destiny' trait was higher (3.15; p = 0.003) in MTLE/HS than in JME and controls. The JME 'law and order' scores were lower than in other groups (p = 0.024). A tendency towards specific NBI traits differentiates MTLE/HS (Factor 3) from JME (Factor 1) groups. Psychiatric symptoms and seizure frequency were correlated with worse scores in NBI and, especially, in Neuroticism domain of NEO-PI-R. CONCLUSION: Specific personality features were linked to each epileptic disease. These findings highlight the importance of considering unique features linked to epilepsy conditions in daily clinical observation to develop support programmes.

Association between leisure time, physical activity, and mood disorder levels in individuals with epilepsy.

The aim of this study was to investigate the association between physical activity levels (occupational, sports, and leisure time activities), depression, anxiety, and epilepsy. The behavioral outcomes of individuals with epilepsy (E) were also compared with healthy control subjects (C). The sample included 31 individuals with epilepsy (12 with idiopathic generalized epilepsy and 19 with partial epilepsy) and 31 control subjects. Self-rating questionnaires were used to assess mood (State-Trait Anxiety Inventory and Beck Depression Inventory), anxiety, and depression as well as habitual physical activity. Patients with epilepsy were more severely impaired compared to control subjects in both mood questionnaires and presented higher levels of depression (35%), state anxiety (18%), and trait anxiety (12.6%) when compared to the C group. Although physical activity level did not differ significantly between groups, linear regression analyses showed that the physical activity leisure level predicted 31% of depression levels and 26% of anxiety levels in the E group. These data suggest that low levels of physical activity may be considered a risk factor for the development of depression and anxiety and can play an important role in the quality of life of individuals with epilepsy.

Cardiorespiratory and electroencephalographic responses to exhaustive acute physical exercise in people with temporal lobe epilepsy.

We evaluated physiological and electroencephalographic responses during a cardiopulmonary exercise test (CPET) in people with epilepsy. Behavioral outcomes of people with epilepsy were also compared with those of healthy controls. Thirty-eight subjects (19 people with epilepsy and 19 controls) participated in this study. Poor outcomes in the behavioral analyses (habitual level of physical activity and quality of life) were observed in the people with epilepsy. With respect to the CPET, V.O(2max) (14.6%) and V.O(2) at anaerobic threshold (16.1%) were significantly lower in the epilepsy group than in the control group. Although not statistically significant, a decrease in the number of epileptiform discharges was observed between the rest state and exercise (82%) and between the rest state and recovery period (74%). In conclusion, the lower aerobic fitness in people with epilepsy observed may be associated with their sedentary habits. Moreover, our findings reinforce the hypothesis that exhaustive exercise is not a seizure-inducing factor.

Does the lunar phase have an effect on sudden unexpected death in epilepsy?

The incidence of sudden unexpected death in epilepsy (SUDEP) in our epilepsy unit over an 8-year period was analyzed to determine a possible association between phase of the moon and SUDEP. Analysis revealed that the number of SUDEPs was highest in full moon (70%), followed by waxing moon (20%) and new moon (10%). No SUDEPs occurred during the waning cycle. These preliminary findings suggest that the full moon appears to correlate with SUDEP.

The other side of the coin: Beneficiary effect of omega-3 fatty acids in sudden unexpected death in epilepsy.

The epilepsies are the most common serious neurological condition. People with epilepsy have a two- to threefold increased risk of dying prematurely than those without epilepsy, and the most common epilepsy-related category of death is sudden unexpected death in epilepsy (SUDEP). The exact pathophysiological causes of SUDEP remain unknown, but it is very probable that cardiac arrhythmia during and between seizures plays a potential role. Although the pharmacological treatments available for the epilepsies have expanded, antiepileptic drugs are still limited in clinical efficacy. In this regard, several factors such as genetic, environmental, and social can contribute to the inefficacy of therapeutic outcome in patients with epilepsy. Among these factors, nutritional aspects, that is, omega-3 fatty acid deficiency, have an interesting role in this scenario. Animal and clinical studies have demonstrated that omega-3 fatty acids may be useful in the prevention and treatment of epilepsy. Moreover, as omega-3 fatty acids per se have been shown to reduce cardiac arrhythmias and sudden cardiac deaths, it has been proposed that omega-3 fatty acid supplementation in patients with refractory seizures may reduce seizures and seizure-associated cardiac arrhythmias and, hence, SUDEP. Given their relative safety and general health benefits, our update article summarizes the knowledge of the role of dietary omega-3 fatty acids in epilepsy.

Evaluation of physical activity habits in patients with posttraumatic stress disorder.

OBJECTIVE: In this study, we present data from a survey that aimed to assess the physical activity habits of adult Brazilian patients with Posttraumatic Stress Disorder. METHOD: Fifty male and female patients with Posttraumatic Stress Disorder participated in this study. The mean age at onset was 37+/-12 years, and the mean time between diagnosis and follow-up was 3.6+/-4.2 years. RESULTS: Substantial changes in physical activity habits were observed following the onset of PTSD. While more than half of the patients participated in physical activities prior to Posttraumatic Stress Disorder onset, there was a significant reduction in their participation afterwards. The justifications for stopping physical activities or sport participation were lack of time and lack of motivation. DISCUSSION: Several studies have shown that physical exercise decreases reverts symptoms of psychiatric disorders such as depression, anxiety and social isolation. We could therefore hypothesize that patients with Posttraumatic Stress Disorder who exercise should experience the same benefits. CONCLUSION: Our findings demonstrated that patients with Posttraumatic Stress Disorder have low levels of participation in sports or physical activities.

Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results.

OBJECTIVE: To further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced status epilepticus (SE) METHOD: Adult male Wistar rats were divided into four groups: (A) control rats, received neither pilocarpine nor lovastatin (n=5); (B) control rats, received just lovastatin (n=5); (C) rats that received just pilocarpine (n=5); (D) rats that received pilocarpine and lovastatin (n=5). After pilocarpine injection (350 mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20 mg/kg via an oesophagic probe immediately and 24 hours after SE induction. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl method. RESULTS: The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1=26.8 +/- 13.67; CA3=38.1 +/- 7.2; hilus=43.8 +/- 3.95) when compared with control group animals (Group A: CA1=53.2 +/- 9.63; CA3=63.5 +/- 13.35; hilus=59.08 +/- 10.24; Group B: CA1=74.3 +/- 8.16; CA3=70.1 +/- 3.83; hilus=70.6 +/- 5.10). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 +/- 17.88) was statically significant increased when compared with animals that just presented SE. CONCLUSION: Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE.

[Analysis of cardiac parameters in animals with epilepsy: possible cause of sudden death?]. / Avaliação de parâmetros cardíacos em animais com epilepsia: possível causa de morte súbita?

Among the causes for sudden death in epilepsy, cardiac dysfunction has been an area of interest. Based on this, the aim of our study was to evaluate the heart rate (in vivo and in vitro) and ventricular pressure in vitro of rats with epilepsy induced by pilocarpine. Adult male Wistar rats (n=6) were given pilocarpine hydrochloride to induce status epilepticus. Control rats (n=6) received saline solution instead pilocarpine. Our results showed significant differences in the mean of heart rate in vivo between the groups. In contrast, we did not find differences during in vitro experiments. Our results suggest a central nervous system modulation on the heart, which could explain the sudden unexpected death in epilepsy.

[Qualitative study of hippocampal formation in hypertensive rats with epilepsy]. / Estudo qualitativo da formação hipocampal de animais hipertensos com epilepsia.

UNLABELLED: The aim of our study was to investigate the hippocampus and dentate gyrus neuropathological features of spontaneous hypertensive rats (SHR) with epilepsy. METHODS: Animals were randomly divided into 4 groups: control Wistar, Wistar with epilepsy, control SHR and SHR with epilepsy. The pilocarpine model of epilepsy was used in this experiement. After spontaneous recurrent seizures, all animals were perfused and their brains processed for histological analysis through Nissl and neo-Timm methods. RESULTS: In the Wistar rats with epilepsy we observed cell loss in hippocampal subfields CA1, CA3 and hilus of the dentate gyrus when compared with control animals. In the SHR with epilepsy we observed hippocampal formation atrophy with ventricular dilatation. No morphological alterations were observed in SHR and Wistar control rats. The neo-Timm staining of hippocampal formation has shown supragranular sprouting in Wistar and SHR with epilepsy. CONCLUSION We found neuropathological alterations in hippocampal formation in Wistar with epilepsy and SHR with epilepsy, suggesting that epilepsy per se or associated to hypertention are able to cause neuronal damage.

The effects of alcohol intake and withdrawal on the seizures frequency and hippocampal morphology in rats with epilepsy.

The aim of our study, using the pilocarpine model of epilepsy, was to investigate the effects of alcohol administration and withdrawal on the spontaneous recurrent seizures (SRSs). Four groups of adult, male Wistar rats were studied: (A). control rats (n=10), received neither pilocarpine nor alcohol, (B). alcohol-treated rats (n=10), received a daily dose of 3.0 g x kg(-1) of a 30% alcohol solution via an oesophagic probe for 30 days, (C). rats with epilepsy (n=10), (D). rats with epilepsy with alcohol intake (n=10). SRSs were induced by a single dose of pilocarpine (i.p.) and the basal frequency of SRSs was video monitored (24h per day) for 30 days. Following this period, the animals of group D received a daily dose of alcohol solution as described above and at the end of this period, alcohol administration was stopped and the seizure frequency was assessed for more 30 days. The basal seizure frequency observed in groups C and D during the first 30 days was 2.2+/-1.8 seizures per week per animal. In group D, it was observed an increase to 12.2+/-5.8 during the first 2 weeks of alcohol administration. During the last 2 weeks of alcohol administration, the number of SRSs returned to the previous basal level. During alcohol withdrawal the seizure frequency increased to 14.3+/-7.4 seizures per week per animal for the first 2 weeks, and returned to the basal level in the remaining period of observation. The Neo-Timm and Nissl staining of hippocampal formation and of the dentate gyrus in rats with epilepsy showed a cell loss in the hippocampal subfield CA1 and in the hillus of dentate gyrus. In rats with epilepsy with alcohol intake, we observed a cell loss in hippocampal subfields CA3 and hillus of the dentate gyrus, with significant neuronal death in subfield CA1, when compared with control animals. The alcohol withdrawal syndrome is a crucial event for the development of functional and neuropathological alterations associated with epilepsy.

Thyroid gland and cerebella lesions: New risk factors for sudden cardiac death in schizophrenia?

People with schizophrenia show a two to threefold increased risk to die prematurely than those without schizophrenia. Patients' life style, suicide, premature development of cardiovascular disease, high prevalence of metabolic syndrome and sudden cardiac death are well-known causes of the excess mortality. The exact pathophysiological cause of sudden death in schizophrenia is unknown, but it is likely that cardiac arrhythmia and respiratory abnormalities play potential role. Some antipsychotics may be associated with cardiovascular adverse events (e.g., QT interval prolongation) and lesions in specific brain regions, such as cerebella may be associated with respiratory abnormalities, suggesting that metabolic and brain dysfunction could lead to sudden cardiac death in patients with schizophrenia. However, exact knowledge regarding the association of these findings and schizophrenia is lacking. As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.

Sudden unexpected death in epilepsy: an important concern.

Epilepsy is one of the most common neurologic problems worldwide. Unfortunately, individuals with epilepsy are at higher risk of death than the general population, and sudden unexpected death in epilepsy is the most important direct epilepsy-related cause of death. In this review article, our research group focused on the risk factors, mechanisms and preventative measures obtained from clinical and experimental studies on sudden unexpected death in epilepsy.

Mothers of children with cerebral palsy with or without epilepsy: a quality of life perspective.

PURPOSE: Disability in a child affects not only the child's life but also the family's life. The aim of our study is to verify the quality of life (QOL) of mothers of disabled children with cerebral palsy (CP) with epilepsy compared with non-epilepsy children evaluated in a Brazilian center. METHODS: Thirty mothers of disabled children participated in the study. The control group comprised of 18 healthy mothers of children without disabilities. All mothers agreed to participate in the study. They completed the evaluation forms of the SF-36 health survey, a well-documented, self-administered QOL scoring system. RESULTS: The results of our study support the premise that mothers of children with CP, as a group, have poorer QOL than mothers of not disabled children. CONCLUSIONS: We also observed that mothers of children with CP and epilepsy have poorer QOL than mothers of children with CP without epilepsy.