Who becomes chronic?

Chronic social disablement is caused by three types of factor: impairment, e.g. slowness in schizophrenia; social disadvantage, e.g. lack of opportunity to develop social or vocational skills; and an underconfidence or unduly low self-esteem which is reactive to impairment and disadvantage. The last of these factors is particularly evident in institutionalism, a condition in which the individual comes to acquire a contentment with institutional life and wishes to lead no other. Many long-stay patients in large mental hospitals used to be well-institutionalized but it became recognized that retraining and rehabilitation could lead to successful resettlement outside hospital. For a time these striking successes suggested to some theorists that abolishing the hospitals would abolish disablement as well but it is now quite clear that this is not the case. Chronic impairments still occur and create a continuing need for sheltered environments. The frequency and type of problems still arising are discussed in the light of recent surveys in England. One small group requires highly-staffed accommodation, others need less supervised day and residential settings; all need long-term care. It is emphasized that some people living at home with relatives also have chronic mental disabilities as have a high proportion of the destitute. Such problems are less frequent than formerly but they still require detailed medical and social attention.     

Cytogenesis in the dentate gyrus after neonatal hyperthermia‐induced seizures: What becomes of surviving cells?

PURPOSE: Febrile seizures (FS) are early-life seizures thought to play a role in epileptogenesis. By labeling cells that were dividing immediately following experimental FS, we previously demonstrated that significantly more of these newborn cells in the dentate gyrus (DG) survived 8 weeks later, relative to animals that did not experience FS. The purpose of the present study was to determine the long-term fate of these newborn cells. METHODS: On postnatal day (PN) 10, hyperthermia-induced seizures (HT, +/-42 degrees C core temperature) were evoked in Sprague-Dawley rats and littermates were used as normothermia controls (NT, +/-35 degrees C core temperature). From PN11 to PN16, rats were injected with bromodeoxyuridine (BrdU) to label dividing cells. At PN66, we evaluated the number of BrdU-labeled cells in the DG that colocalized with the neuronal marker NeuN, glial marker glial fibrillary acidic protein (GFAP), neuronal excitatory amino acid transporter 3 (EAAT3), GABAergic neuronal marker glutamic acid decarboxylase 67 (GAD67) or microglia marker tomato lectin (TL). RESULTS: In all rats, almost all BrdU-labeled cells in the DG, that showed double-labeling, colocalized with NeuN, and rarely with GFAP, GAD67, or TL. In NT controls and HT rats that did not experience seizures ("HT-no seizures"), approximately 23% of BrdU-labeled cells colocalized with EAAT3, which was significantly different from 14% in HT rats that did experience seizures (HT + FS). DISCUSSION: Early-life seizures decrease the population of newborn cells that survive and mature into EAAT3-positive neurons and do not affect the GABAergic cell population. This may affect hippocampal physiology in young adulthood.     

‘What becomes of demented patients referred to a psychogeriatric unit?’ An approach to audit

A 1-year follow-up study was undertaken of a random sample of 40 elderly patients living at home given a diagnosis of "dementia" after referral to the Psychogeriatric Department at St Charles' Hospital, London, W10. Eighteen (45%) patients were admitted to institutional care. There was an association between physical disability and institutionalization. A similar tendency was observed for social disturbance and hospital admission. The 1-year survival rate for the sample was 82.5%. All the seven patients who died were moderately/severely demented. Twenty-three patients (55%) had informal key carers. Half of these showed considerable stress according to the General Health Questionnaire and the Strain Scale scores. All the recommendations made by the psychogeriatric team were carried out without much delay.     

What causes the onset of psychosis?

It has become increasingly clear that the simple neurodevelopmental model fails to explain many aspects of schizophrenia including the timing of the onset, and the nature of the abnormal perceptions. Furthermore, we do not know why some members of the general population have anomalous experiences but remain well, while others enter the prodrome of psychosis, and a minority progress to frank schizophrenia. We suggest that genes or developmental damage result in individuals vulnerable to dopamine deregulation. In contemporary society, this is often compounded by abuse of drugs such as amphetamines and cannabis, which then propel the individual into a state of dopamine-induced misinterpretation of the environment. Certain types of social adversity such as migration and social isolation, as well as affective change can also contribute to this. Thereafter, biased cognitive appraisal processes result in delusional interpretation of the abnormal perceptual experiences. Thus, a plausible model of the onset of psychosis needs to draw not only on neuroscience, but also on the insights of social psychiatry and cognitive psychology.     

Fear of the unknown: One fear to rule them all?

The current review and synthesis was designed to provocatively develop and evaluate the proposition that “fear of the unknown may be a, or possibly the, fundamental fear” (Carleton, 2016) underlying anxiety and therein neuroticism. Identifying fundamental transdiagnostic elements is a priority for clinical theory and practice. Historical criteria for identifying fundamental components of anxiety are described and revised criteria are offered. The revised criteria are based on logical rhetorical arguments using a constituent reductionist postpositivist approach supported by the available empirical data. The revised criteria are then used to assess several fears posited as fundamental, including fear of the unknown. The review and synthesis concludes with brief recommendations for future theoretical discourse as well as clinical and non-clinical research.     

What lies beneath the face of aggression?

Recent evidence indicates that a sexually dimorphic feature of humans, the facial width-to-height ratio (FWHR), is positively correlated with reactive aggression, particularly in men. Also, predictions about the aggressive tendencies of others faithfully map onto FWHR in the absence of explicit awareness of this metric. Here, we provide the first evidence that amygdala reactivity to social signals of interpersonal challenge may underlie the link between aggression and the FWHR. Specifically, amygdala reactivity to angry faces was positively correlated with aggression, but only among men with relatively large FWHRs. The patterns of association were specific to angry facial expressions and unique to men. These links may reflect the common influence of pubertal testosterone on craniofacial growth and development of neural circuitry underlying aggression. Amygdala reactivity may also represent a plausible pathway through which FWHR may have evolved to represent an honest indicator of conspecific threat, namely by reflecting the responsiveness of neural circuitry mediating aggressive behavior.     

What should animal models of depression model?

In this article, we discuss what animal models of depression should be attempting to 'model'. One must first determine if the goal is to model the regulatory mechanisms by which antidepressant treatments alleviate the various symptoms of depression, or to model the dysregulatory mechanisms underlying the etiology of those symptoms. When modeling the mechanisms of antidepressant effects, a key feature that is often overlooked is the time course required for behavioral efficacy. Even in the clinical literature, there is considerable confusion and inconsistency in defining and identifying 'time of onset' of clinical effect. Although the 'therapeutic lag' may not be as long as has been commonly believed, it does occur. Observable improvement in either global symptomatology or specific symptoms becomes evident after 7-14 days of treatment, and more complete recovery takes considerably longer. Thus, any model addressing potential mechanisms of antidepressant action should exhibit a similar time-dependency. Second, whether attempting to address mechanisms underlying behavioral effects of antidepressants, or the neurobiological substrates underlying the development and manifestation of depression, it is essential to recognize that the syndrome of depression is a diagnostic construct that includes a variety of disparate symptoms, some of which may be related mechanistically, and others that may not be specific to depression, but may cut across categorical diagnostic schemes. Further, it is critical to recognize the close relationship of depression and anxiety. Psychological studies have suggested that the myriad symptoms of depression and anxiety may be subsumed within a more limited number of distinct behavioral dimensions, such as negative affect (neuroticism), positive affect, or physiologic hyperarousal. These dimensions may be related to the functioning of specific neurobiological systems. Thus, rather than trying to recreate or mimic the entire spectrum of symptoms comprising the syndrome of depression, it may be more informative to develop animal models for these behavioral dimensions. Such models may then provide access not only to the neural regulatory mechanisms underlying effective antidepressant treatment, but may also provide clues to the processes underlying the development and manifestation of depression.     

What kind of illness is anorexia nervosa?

With the best will in the world, it is difficult not to become disillusioned with the diagnostic system for eating disorders. Although repeatedly revised, diagnostic criteria such as those of DSM-IV or ICD10 are inadequate to describe the patient's condition. This essay critically appraises the historical development of eating disorders and challenges the widely held notion that bulimia nervosa and anorexia nervosa share a common psychopathology. It further argues that the time has arrived to think about anorexia nervosa and the eating disorders in a way different to the current stereotyping. It suggests that anorexia nervosa like neoplasia is a disease that requires staging and a model for such staging is presented.