Male–female differences in left-handedness in Sardinia,Italy

Males were consistently found to be more likely than females to report left-hand preference in single-hand tasks, but the literature reports negative results too. Using data from a large sample in Sardinia, we aimed at testing the links of left-handedness with sex, age, residence, and seasonality of birth. A total of 4239 participants (males = 1589; females = 2650) were recruited in public places such as high schools, university classes, or gyms in one of the major islands of Italy. Hand preference was established with the question: Which hand do you normally use to write legibly? The monthly distribution of births was studied with the Rayleigh test. In the sample, 270 female participants reported left-hand preference in writing (10.2%) versus 161 male participants (10.1%). Left-hand preference in writing was negatively related to age, with increasing left-hand preference in the younger generations. Left-hand preference in writing was not more common in urban than in suburban or rural settings. The month of birth was found to have a seasonal effect on the left-handed (p=.031) but not on the right-handed (p=.80) participants, and this seasonal effect was more evident in males (p=.04) than in females (p =.26). In our sample males were not more likely to report left-hand preference in writing than females. On the other hand, left-hand preference does vary by age and, in all likelihood, this is an effect of the reduced cultural pressure to write with the right hand in the younger generations.     

“When are we going to move?”

Recent reports have indicated that many rehousing projects, moving people out of hospitals large and small, suffer periods of delay. This article relates the frustrations and delays experienced by one such project and, in particular, the effects on five people who were the first due to move into a home of their own within the project. The article argues that staff working on such schemes should acknowledge that such delays are very likely and do all they can to minimise the effects on the residents involved.     

μ‐Opioid receptor desensitization: homologous or heterologous?

There is considerable controversy over whether μ‐opioid receptor (MOPr) desensitization is homologous or heterologous and over the mechanisms underlying such desensitization. In different cell types MOPr desensitization has been reported to involve receptor phosphorylation by various kinases, including G‐protein‐coupled receptor kinases (GRKs), second messenger and other kinases as well as perturbation of the MOPr effector pathway by GRK sequestration of G protein βγ subunits or ion channel modulation. Here we report that in brainstem locus coeruleus (LC) neurons prepared from relatively mature rats (5–8 weeks old) rapid MOPr desensitization induced by the high‐efficacy opioid peptides methionine enkephalin and DAMGO was homologous and not heterologous to α₂‐adrenoceptors and somatostatin SST₂ receptors. Given that these receptors all couple through G proteins to the same set of G‐protein inwardly rectifying (GIRK) channels it is unlikely therefore that in mature neurons MOPr desensitization involves G protein βγ subunit sequestration or ion channel modulation. In contrast, in slices from immature animals (less than postnatal day 20), MOPr desensitization was observed to be heterologous and could be downstream of the receptor. Heterologous MOPr desensitization was not dependent on protein kinase C or c‐Jun N‐terminal kinase activity, but the change from heterologous to homologous desensitization with age was correlated with a decrease in the expression levels of GRK2 in the LC and other brain regions. The observation that the mechanisms underlying MOPr desensitization change with neuronal development is important when extrapolating to the mature brain results obtained from experiments on expression systems, cell lines and immature neuronal preparations.     

‘No evidence of disease activity’ – is it an appropriate surrogate in multiple sclerosis?

The increasing number of disease‐modifying treatments available for multiple sclerosis has broadened treatment options for patients, but also challenges clinicians to select the best therapy for each individual at the appropriate stage of the disease. Early prediction of treatment response still remains one of the main difficulties in the management of multiple sclerosis patients. The concept of ‘no evidence of disease activity’ (NEDA) has been proposed as a surrogate for treatment response based on the absence of relapses, disability progression and radiological activity. Although there are several apparently logical arguments for the NEDA approach, there are also some major concerns that have to be considered and that are not sufficiently addressed yet. Amongst others, each parameter's limitations are not eliminated solely by its use within a composite score, and the contribution of each parameter to NEDA is not well balanced, as the detection of, for example, a single new magnetic resonance imaging lesion is considered as significant as the occurrence of a severely disabling relapse. NEDA in its current form also neglects underlying pathophysiology of the disease, has not been shown to fulfil formal criteria of a surrogate marker and its prognostic value has not been sufficiently evidenced yet. From a clinical point of view, ‘evidence of disease activity’ seems the more relevant surrogate; however, its implications are even less clear than those of NEDA. Here, existing literature on NEDA is critically reviewed and improvements are discussed that value its potential use in clinical trials and, even more importantly, treatment decision making in daily routine.     

What is ‘early onset dementia’?

There are two types of dementia with early onset: (i) presenile dementias; and (ii) senile dementias with early onset. Most patients who develop dementia before 65 years of age have Alzheimer's disease (AD). The remainder are likely to have vascular dementia (VaD), frontotemporal dementia, head injury, alcohol intoxication, or metabolic disorder. Presenile dementias, caused by frontotemporal lobar degeneration, progressive supranuclear palsy, and corticobasal degeneration, usually occur in patients of presenile and are rarely seen in patients of senile age. Although the factors responsible for the accelarted onset of the illness are not fully known, genetic abnormalities appear to be important in some types of presenile dementia, such as frontotemporal dementia with parkinsonism linked to chromosome 17. Conversely, senile dementias such as sporadic AD and VaD commonly occur in patients of senile age. These disorders may also occur in patients of presenile age, although less frequently. Alzheimer's disease was originally classified as a ‘presenile dementia’. Since the 1980s, ‘senile dementia of Alzheimer type’ (SDAT) and ‘Alzheimer's disease’ have been considered to belong to the same pathological entity and both are now known as ‘dementia of Alzheimer's type (DAT)’ or merely ‘Alzheimer's disease’. Rapid progression of cognitive impairment with neuropsychological syndromes and neurological symptoms has been considered a characteristic of early onset AD. However, recently, neurological symptoms such as spastic paraparesis, seizures, and myoclonic convulsions have been reported to occur infrequently in early onset AD, although language problems and visuospatial dysfunctions are common. There are at least three dominant genes that have been identified in cases of familial Alzheimer's disease with early onset, namely the amyloid precursor gene (APP), and the genes encoding presenilin 1 (PSEN1) and presenilin 2 (PSEN2). Therefore, genetic abnormalities are important factors contributing to the earlier onset of the illness. It is also important to investigate the pathophysiological mechanism in relation to genetic abnormalities, environmental factors, physical illnesses, and metabolic disturbances to understand the processes underlying the development of dementia with early onset.     

How does the ‘environment’ come to the person? The ‘ecology of the person’ and addiction

Currently, psychiatry lacks a field that can be called “theoretical psychiatry”, which uses theoretical concepts and explanatory models: The main stream of research is to collect data of all kinds in the hope that the computational Big Data approach will shed a bright light on the black box of mental disorders. Accordingly, the biology-based Research Domain Criteria of the National Institute of Mental Health have been established. However, as philosophical analyses of concepts and methods have shown, several epistemological gaps stand in the way of a consistent multilevel understanding of mental disorders. Also, the implicit ontological problems in the biological reduction of the psychosocial level and in the integration of so-called hard and soft disciplines are mostly left out. As a consequence, a non-reductive psychological theory of mental disorders is sought that also integrates correlating biological and sociological issues. In this context, one example of promising nonreductive psychiatric research is the option of systems/network psychopathology. The possibilities for integrating different psychological perspectives are highlighted for the field of addiction research and treatment, where pragmatic behaviorist approaches dominate over the theory-based practice of psychoanalysis. In comparing the theoretical constructs of these two approaches, the relevance of the concept of “(social) environment” as the wealth of influential sociocultural factors is discussed at levels superior to the interpersonal micro-level, namely the organizational meso- and societal macro level, which is not sufficiently considered in current biopsychiatry. On this basis of argumentation, the usefulness of grounding and framing psychiatry through the field of ecological sciences, especially human ecology, is demonstrated. Finally, to this end, an outline of an ecological model of mental health and illness is presented.     

14‐3‐3 Proteins in Pineal Photoneuroendocrine Transduction: How Many Roles?

Recent studies suggest that a common theme links the diverse elements of pineal photoneuroendocrine transduction--regulation via binding to 14-3-3 proteins. The elements include photoreception, neurotransmission, signal transduction and the synthesis of melatonin from tryptophan. We review general aspects of 14-3-3 proteins and their biological function as binding partners, and also focus on their roles in pineal photoneuroendocrine transduction.     

COMMUNICATION — can microelectronics help?

SUMMARY. Many children, particularly those with cerebral palsy, are not able to speak or speak with difficulty. Some, who have no intellectual deficits, are considered to be physically handicapped and, once they have mastered reading, they can take advantage of Possum machines. Those with mental handicap as well as cerebral palsy may be helped to communicate by means of an electronic speaking aide which has simple, specific controls. Young children with physical handicaps only could also benefit from this type of device.     

‘Why are my friends changing?’ Explaining dementia to people with learning disabilities

There are many publications that seek to explain the causes and effects of dementia for the non‐learning disabled population and there is evidence of the benefit of supporting carers and of establishing support groups. However, there is much less published material aimed at people with learning disabilities, and little focus on the specific needs of people who share their homes and lives with other people with learning disabilities who develop dementia. This article is based on group work with residents who had expressed bewilderment at the gradual changes they were witnessing in two of their housemates with dementia with whom they had shared a home and friendships over many years. Employing a wide range of visual aids, equipment, role plays and exercises, we sought to make the explanation of dementia as accessible and concrete as possible. The group also provided a forum for the residents to talk about the effects of living with others who develop dementia. Evaluation showed how a relatively short intervention can result in positive changes for both the people with learning disabilities who develop dementia and their peers.     

vCJD – predicting the future?

The recent emergence of variant Creutzfeldt-Jakob disease (vCJD) in the UK, and demonstration that vCJD is caused by the same prion strain that causes bovine spongiform encephalopathy, have led to concerns about the possibility of a human epidemic. Although only 79 cases of vCJD have occurred to date, it is likely that hundreds of thousands of infected cattle entered the human food chain in the late 1980s and early 1990s, and the average incubation period of vCJD is unknown. Mathematical models have not yet been able to give useful predictions of future numbers of cases, and in the absence of a blood test for vCJD, current attempts to reduce uncertainties about future numbers of cases are based on the accumulation of PrPSc in lymphoreticular tissues. Extensive lymphoreticular PrPSc accumulation has been seen in all cases of symptomatic vCJD so far examined, and in one case 8 months prior to the onset of symptoms. Animal models of prion disease suggest that lymphoreticular involvement occurs early in the incubation period and reliably predicts future neurological disease. Based on these data, large scale anonymous studies looking for PrP accumulation in surgically removed tonsillectomy and appendicectomy specimens are underway. Examination of the first 3000 specimens has not revealed any positive samples, but at the moment the significance of negative findings is uncertain. It is anticipated that by the time these studies are complete more data will be available on how early PrP can be demonstrated in lymphoreticular tissue in vCJD, which together with the results from examination of further samples, will allow some comment as to the likelihood of a large human vCJD epidemic.