Can emotional stress trigger the onset of epilepsy?

ObjectiveThe aim of this study was to investigate the potential role of an acute adverse stress as “trigger” for the onset of epilepsy.MethodsAmong 4618 consecutive patients, twenty-two reported a major life event within three months before the onset of epilepsy.ResultsAll patients had focal epilepsy except one with idiopathic generalized epilepsy. The temporal lobe was involved in 90% of patients with focal epilepsy. More precisely, 13 patients (62% of patients with focal epilepsy) had medial temporal lobe epilepsy (MTLE), two had lateral temporal lobe epilepsy, four had temporoparietooccipital junction epilepsy, and two patients had central lobe epilepsy. The mean age and the median age at onset of epilepsy for patients with MTLE were both 38 years (range: 9.5–65 years). Ten patients had right and three had left MTLE. Among patients with focal epilepsy, MRI was abnormal in 7 (33%) with hippocampal sclerosis in four, periventricular nodular heterotopia in two, and complex cortical dysgenesis in one. The mean age at onset of epilepsy for patients with brain lesions was 26 years (range: 9.5–49). Twelve patients (54%) reported a death as a triggering factor for the onset of their epilepsy. Seven patients (32%) reported that a relationship of trust had been broken. Three patients (14%) had been subjects of violence. No patient reported sexual abuse as a triggering factor.ConclusionThis study provides evidence that some patients (5/1000 patients) began their seizures in the wake of significant life events. The average age at onset of epilepsy is quite late, around age 30, even in the presence of brain lesions. These patients are emotionally and affectively more prone to have consequences of a stressful life event. The recognition and management of such situations may bring significant relief with improvement of the control of epilepsy.     

Can we manage without the mental hospital?

OBJECTIVES: Many developed countries, having invested massively in psychiatric hospitals in the past 150 years, are in the process of dismantling them. The central question is whether this change in the location of care from the psychiatric hospital to district-based services has benefited the patients. The objectives of this review are to examine the evidence on which an answer to the above question might be based. METHOD: Much of the relevant research comes from the 13-year programme of the Team for the Assessment of Psychiatric Services conducted in London, but other research will be reviewed as appropriate. RESULTS AND CONCLUSIONS: Long-stay, non-demented patients, including the elderly, enjoy a better quality of life in the community homes compared with the psychiatric hospitals. Public attitudes constitute an obstacle to social integration into the healthy community, but can be ameliorated with local educational programmes. The provision of work has been unsatisfactory, but the development of social firms holds some promise. Patients with dementia receive better care in community nursing homes compared with hospital wards, according to their relatives' opinions, backed up by observational studies. The part of the service which is most unsatisfactory is the admission facilities. This is due to a variety of causes, including a failure to plan for the admission needs of discharged long-stay patients, the virtual absence of rehabilitation units in the community and an inadequate provision of a range of sheltered accommodation. However, these problems could be resolved with adequate investment in innovative facilities.     

Can foods influence the onset and progress of neurodegenerative diseases?

Over the course of the last few years, the advertisement and marketing of commercial food products in the European market has seen an increasing focus on the be...     

Can we pass from the experimental to the clinical phase in MS stem cell research?

A crucial point in development of new treatments is the step from the experimental level to the first clinical trials. For stem cell treatments in general, but for stem cell treatment in Multiple Sclerosis specifically, this is the question for the moment. To answer this question a rational analysis of the hypotheses and the suppositions behind the application of stem cells is necessary, as well as a review of the present knowledge, the risks and the gains to be expected. This is a personal analysis of 32 oral presentation and discussions of the European Charcot Foundation Symposium, Taormina 2006. It is the application of the Kenter and Cohen [Kenter MJH, Cohen AF. Establishing risk of human experimentation with drugs: lessons from TGN 1412. Lancet 2006; 368:1387-91] approach, adapted for stem cell treatment in MS. About half of the pertinent issues plead for the start of clinical experiments now. However, the absence of knowledge on deleterious effects and their predictability heavily weights against it. Organisational and funding aspects were discussed to prevent uncritical, uncontrolled clinical approaches.     

Can we relate MeCP2 deficiency to the structural and chemical abnormalities in the Rett brain?

The mutated gene for Rett syndrome, MECP2, has now been identified in ninety percent of cases. Molecular biologists are immersed in the study of this gene's biology determining how its mutation could be responsible for such an enigmatic phenotype. In this paper the same question is considered, re-examining the structural phenotype of the Rett brain and asking; is MeCP2 present at the appropriate time and place in brain development to influence the structural and chemical abnormalities which characterize the Rett brain? Data from the literature and previous research suggest that MeCP2 is expressed during critical periods of brain development at several sites and in different neurons. It supports the idea that inadequate functioning of MeCP2 alters trophic factors and raises the possibility that replacement of these factors might improve brain function. The availability of mouse models now makes it possible to test such ideas.     

Can we share the joy of others? Empathic neural responses to distress vs joy

The neural bases of empathy have been examined mainly in the context of reacting to others’ distress, while almost no attention has been paid to the mechanisms by which we share others’ joy. Using functional magnetic resonance imaging, we demonstrated that the same neural network mediates judgment of the emotional state of the other in response to both negative and positive events through empathy-related structures, such as the medial prefrontal cortex (MPFC), the insula, the superior temporal sulcus (STS) and the inferior frontal gyrus (IFG). However, the responses of the MPFC, bilateral insula and the right IFG to negative experiences occurring to the other (but not to the self) were found to be much more intense than the responses to positive experiences, indicating that humans have a remarkable ability to share the distress of others, but may react less to the joy of others.     

Toe temperature change: a measure of sleep onset?

In an attempt to provide a more "physiological" measure of sleep onset, temperature of the great toe was monitored for 166 sleeper-nights in both insomniac and control groups. All subjects were women between 21 and 45 years of age. Earlier published reports had suggested that toe temperature elevation was the result of lowered sympathetic tone and marked a "vegetative preparedness for sleep." More recently, elevation of the toe temperature has been used to denote a level of chemical anesthesia sufficient for major surgery. In this study, however, the mean latency of the time course of the temperature elevation of the toe was uncorrelated with sleep onset determined by EEG criteria. Temperature elevations were frequently of large magnitude but were not uniformly observed across all subjects and all nights. It is suggested that the toe temperature elevation is reflective of metabolic adjustments which coincide with the onset of the night's first period of slow wave sleep.     

Can we use peripheral tissue biopsies to diagnose Parkinson's disease? A review of the literature

Phosphorylated α‐synuclein (phosαSYN) containing inclusions in neurons (Lewy bodies, LB) and nerve terminals (Lewy neurites, LN), the pathological hallmark of Parkinson's disease (PD), are not confined to the central nervous system, but have also been reported in peripheral tissues. However, the usefulness of αSYN/phosαSYN detection in tissues accessible to biopsies as a reliable biomarker for prodromal PD remains unclear. A systematic review of studies using biopsies of skin, olfactory and gastrointestinal (GI) tissues was conducted to evaluate the sensitivity and specificity of both αSYN and phosαSYN staining in PD patients. Data analysis was hampered by the diversity of the methods used, e.g. choice of biopsy sites, tissue processing, staining protocols and evaluation of the findings. Tissue obtained from GI tract/salivary glands (13 post‐mortem, 13 in vivo studies) yielded the highest overall sensitivity and specificity compared to skin (three post‐mortem, eight in vivo studies) and olfactory mucosa/bulb (six post‐mortem studies, one in vivo study). In contrast to phosαSYN, αSYN was more consistently detectable in peripheral tissues of healthy controls. GI tract/salivary glands appear to be the most promising candidate tissue for peripheral biopsy‐taking. phosαSYN is considered as the marker of choice to delineate pathological aggregates from normal αSYN regularly found in peripheral neural tissues. However, the sensitivity and specificity of phosαSYN are not yet acceptable for using phosαSYN as a reliable peripheral biomarker for PD in clinical routine. Further refinement regarding the interpretation of the peripheral αSYN/phosαSYN burden and the phenotypical definition of peripheral LB/LN is needed to optimize screening methods for prodromal PD.