Post-traumatic stress disorder: a review of recent findings

This article provides an update on recent findings in post-traumatic stress disorder (PTSD) with reference to pertinent epidemiologic, etiologic, diagnostic, and treatment advances in the past year. New studies serve to confirm high prevalence rates in the general population (7% to 12%), and high rates of secondary mood, anxiety, and substance use disorders. Recent substantive evidence has highlighted 1) the unique pattern of biological alteration in PTSD that distinguishes it from the normative stress response, and 2) the role of constitutional risk factors and trauma-related factors in determining disease expression after trauma exposure. The emergence of consistent data suggesting that medications (selective serotonin reuptake inhibitors) and psychotherapies (cognitive-behavior therapy) are effective in reducing core symptoms and improving quality of life, has reinforced optimism and more widespread use of these interventions in patients with PTSD.     

Parkinson's disease related pain: a review of recent findings

In this review we summarize progress in research on Parkinson's disease-related pain as reported in articles published in the Journal of Neurology in the years 2011 and 2012.     

Lifetime and recent alcohol consumption among male alcoholics. Neuropsychological implications

Alcoholics experience a relatively well-documented pattern of decline in cognitive and motor functions. This decline is likely the result of multiple causal factors that include head injury, malnutrition, and alcohol consumption. Although alcohol consumption per se has been considered a primary causal agent, research has not demonstrated a consistent relationship between levels of alcohol consumption and these neuropsychological deficits. This study explored such relationships within a sample of 40 detoxified male inpatient alcoholics who did not have a history of polydrug abuse, malnutrition, head injury, neurological disease, or non-alcohol-related psychiatric treatment. Increasing lifetime alcohol consumption was associated with increasing age-adjusted impairment on Halstead-Reitan tests that measure such aspects of functioning as concept formation, cognitive flexibility, and perceptual-motor abilities. Alcohol consumption had a linear relationship with test scores and hypothesized interactions with age did not emerge, nor did the effects of recent drinking appear dependent upon total lifetime consumption. The pattern of consumption (e.g., amount consumed per occasion, spree drinking) was also unrelated to impairment, and the critical neuropathological factor appeared to be the total amount of lifetime alcohol consumption.     

Some recent findings on the development of human binocularity: a review

Evidence on the development of binocular function in infancy is reviewed. (1) Visual evoked potentials (VEP) may be recorded from infants in response to dynamic random dot stimuli which alternate between positive and negative binocular correlation. Such responses can only arise in neurones receiving binocular input. (2) Infants' looking behaviour may be shown to depend on the presence of binocular disparity in the stimulus (either random-dot or line stereograms). Results of these techniques agree that binocular function normally develops initially between 2 and 4 months of age. Our own data using VEP show a median age of first binocular response of 13 weeks but with marked individual variations. Binocular development involves the interplay of sensory interaction and oculomotor coordination, but it is unlikely that alignment of the two eyes is the dominant constraint determining the onset of binocular vision. It is possible, but not yet established, that the detection of binocular correlation may precede the ability to discriminate stereoscopic disparities. Infants in the first 3 months of life show an asymmetry of monocular optokinetic nystagmus (MOKN). The response to temporalwards field motion which they lack is driven in cat by a pathway via binocular cortex: thus the development of this response in human infants might depend on development of binocularity. However, the correlation across individual infants between the age of onset of binocularity and the age at which symmetrical MOKN is attained is relatively weak. It is possible that the neuroanatomical basis of MOKN control differs between cat and human.     

Hypnotic action of pentobarbital in mice: a possible mechanism

The effect of GABA receptor agonists (THIP and baclofen) on the hypnotic activity (loss of righting reflex and sleep time) of pentobarbital in mice was investigated. Combinations of either THIP-pentobarbital or baclofen-pentobarbital interacted synergistically by increasing hypnotic activity. The GABAa receptor antagonist, bicuculline, decreased the hypnotic effect of THIP-pentobarbital combinations but not that of baclofen-pentobarbital combinations. These results suggest that the hypnotic activity of pentobarbital involves GABAa receptor function.     

Life events, stress and depression: a review of recent findings

OBJECTIVE: To review recent empirical prospective studies on the relation between life event stressors and depression. METHOD: A systematic literature search focusing on predictive studies was carried out from 1980 to early 2001 using Medline, Embase and PsychInfo. RESULTS: The empirical findings for the most part support clinical impressions of the relation of stressors to depression but at the same time provide some clearer understanding in relation to differences of stressor impact on depression type and on index episode, relapse or recurrence. Twin studies now provide the strongest evidence of the relative magnitude of effect of environmental stressors and genetic factors: the former explains at least as much of the variance in depression as our genes. CONCLUSIONS: Continuing research into life events and depression have been fruitful especially those studies assessing the effect of stressors in combination with other aetiological variables such as genetic factors.     

The contribution of social factors to the development of schizophrenia: a review of recent findings.

OBJECTIVE: To investigate recent evidence suggesting that social factors are causally related to the development of schizophrenia. METHOD: I conducted a sytematic review of MEDLINE to identify possibly relevant studies. The search was limited to peer-reviewed studies and review articles appearing in English-language journals since 1996. Studies were included if they used standardized diagnostic criteria for schizophrenia or standardized assessment instruments for psychotic symptoms. RESULTS: Studies of migrants to western Europe provide compelling support for the notion that social factors contribute to the development of schizophrenia. Findings such as excessively high risk for schizophrenia in second-generation immigrants are difficult to explain solely in terms of biological or genetic factors. A growing number of studies implicate childhood exposure to social adversity as a risk factor for schizophrenia, although few studies have used prospective designs. The increased incidence of schizophrenia risk associated with urban birth and (or) urban upbringing suggests possible social causation, but these findings are more ambiguous. Thus far, no studies have explored actual mechanisms by which exposure to social factors might generate psychotic symptoms, although animal experiments suggest that social defeat or social exclusion may cause dopamine dysregulation or sensitization. CONCLUSIONS: The accumulating evidence suggesting a role for social factors in the development of schizophrenia arises primarily from studies of migrants conducted in Europe. The mechanisms by which social factors exert their influence remain unknown. Future investigations of social causation should clarify the temporal relation between exposure to social defeat and (or) social adversity and the development of psychotic symptoms.     

Ethanol, memory, and hippocampal function: a review of recent findings

For well over a century, ethanol was believed to exert its effects on cognition and behavior by producing a ubiquitous depression of central nervous system activity. A general disruption in brain function was consistent with the belief that ethanol's effects on cognition and behavior were also quite general. Substantial evidence now indicates that ethanol produces a host of selective effects on neural activity, resulting in regional differences in ethanol's effects in the brain. Consistent with such evidence, recent research suggests that ethanol's effects on cognition and behavior are not as global as previously assumed. The present paper discusses evidence that many of ethanol's effects on learning and memory stem from altered cellular activity in the hippocampus and related structures. Potential mechanisms for ethanol's disruption of hippocampal function are reviewed. Evidence suggests that ethanol disrupts activity in the hippocampus by interacting directly with hippocampal neurons and by interacting with critical hippocampal afferents.     

Neuropsychiatric consequences of traumatic brain injury: a review of recent findings

PURPOSE OF REVIEW: Behavioral and psychiatric disturbances are the more frequent consequences of traumatic brain injury and major determinants of the quality of life of patients. This review was designed to familiarize the reader with the more recent work published in this field. RECENT FINDINGS: We have now a more consistent view of the epidemiology of post-traumatic brain injury psychiatric disorders both in adult and pediatric populations. Mood disorders, anxiety disorders and substance use disorders are the more prevalent psychiatric diagnoses among traumatic brain injury patients. The phenomenological characteristics and clinical correlates of major depression, post-traumatic stress disorder, alcohol use disorders, and post-traumatic brain injury attention deficit hyperactivity disorder have been studied in more detail. Newer structural, metabolic and functional neuroimaging techniques help to clarify the pathogenesis of these disorders. In turn, this knowledge may lead to the implementation of more efficient therapeutic interventions. Unfortunately, controlled treatment studies have been the exception in the field, and treatment decisions usually lack adequate empirical support. SUMMARY: Recent advances in the basic neuroscience of traumatic brain injury as well as in behavioral genetics, social science and neuroimaging techniques should contribute to a better understanding of the pathophysiology of the psychiatric disorders occurring after the injury. There is a great need for randomized, double-blind, placebo-controlled trials to establish the most effective treatments for these disorders.     

Imipramine and children: a review and some speculations about the mechanism of drug action.

Although the FDA recommends imipramine hydrochloride (IMI) only for temporary relief of symptoms of enuresis nocturna (EN), the drug has been applied to a number of other pediatric situations, including the Hyperkinetic Syndrome (HS), childhood depression, somnambulism and pavor nocturnus, school phobia, petit mal epilepsy, allergies, autism, encorpresis and head-banging. We have reviewed the literature, with particular attention to the pharmacokinetics of IMI in children, and its putative mechanisms of action. The drug probably works through a number of different actions, and the futher delineation of these will be of considerable heuristic value. We review the toxic effects of IMI treatment and IMI poisoning in children, and the pediatric literature concerning other antidepressant drugs and lithium carbonate (Li).     

Suicide prevention is possible: A review of recent studies

Because of a dearth of randomised controlled trials demonstrating the efficacy of suicide prevention programs, some commentators have been pessimistic about our ability to influence suicidal behavior. However, such research methodology is probably not achievable because of the low base rate of suicide. Nevertheless, an examination of interventions using alternative research methodologies provides persuasive evidence of the effectiveness of a number of different management approaches. Far from being pessimistic about research into suicide prevention, the present review suggests that by introducing a number of these interventions we can be optimistic that the unacceptable rate of suicide world wide can be reduced.     

Regulation of blood L-glutamate levels by stress as a possible brain defense mechanism

Isoflurane-anesthetized rats submitted to a closed head injury (CHI) display a significant decrease of their blood glutamate levels. Having demonstrated that a decrease of blood L-glutamate (glutamate) causes an increase of the driving force for a spontaneous brain-to-blood glutamate efflux, and consequently affords brain neuroprotection, we investigated here the possible mechanisms which can affect blood glutamate levels. Reasoning that the spontaneous decrease of blood glutamate levels post CHI could be part of a stress response, we observed that the stress involved in tail artery catheterization under isoflurane anesthesia does not affect blood glutamate levels. Investigating in naïve rats the stress effectors, we found that corticotropin-releasing factor (CRF) significantly decreased blood glutamate levels. Pretreatment with antalarmine (a selective type-1 CRF receptor antagonist) occludes the CRF-mediated decrease in blood glutamate levels. In contrast, the adrenocorticotrophic hormone (ACTH) did not affect blood glutamate levels. Investigating the effectors of the sympathetic/adrenomedullary system, we observed that in naïve rats, adrenaline but not noradrenaline decreased blood glutamate levels. Confirming the role of adrenaline, propranolol pretreatment (a non-selective β-antagonist) prevented the spontaneous decrease of blood glutamate observed post CHI. On the strength of these results, we further observed that isoproterenol (a β_1/2-selective adrenoreceptor agonist) produced a marked sustained decrease in blood glutamate levels. These results suggest that stress induces a decrease of blood glutamate levels partly via the activation of peripheral CRF receptors and the activation of the β-adrenoreceptors. We propose that this newly identified component of the stress response could be a peripherally mediated defense mechanism of the injured brain against the deleterious effects of excess glutamate.     

Prevalence of alcohol consumption, abuse and dependence in a country with high per capita consumption: findings from the German TACOS study

  Background: The aim of the Transitions in Alcohol Consumption and Smoking (TACOS) project is to investigate substance use and use disorders in the adult general population in a region of the under-researched north of Germany, focussing on smoking and alcohol consumption. In this study, the design and quality assurance provisions of the baseline cross-section of the longitudinal project are described. Prevalence rates of alcohol use disorders, consumption pattern, and the nature of their association are also analysed with regard to preventive strategies. Method: A random sample of 4075 participants, aged 18 to 64 and drawn from residents registration office files, was interviewed with a DSM-IV adapted version of WHO CIDI. Fieldwork resulted in a response rate of 70.2% and an unbiased database with regard to demographic characteristics. Results: Low lifetime prevalence of alcohol use disorders (4.5% abuse, 3.8% dependence) and hazardous consumption (13.2% lifetime; 6.0% 12-month) was found compared to southern regions of Germany and US American data. In contrast, we found a comparatively high percentage of moderate alcohol uses. Male subjects are more affected by lifetime alcohol use disorders (abuse OR 8.3, 95% CI 5.3–13.2; dependence OR 4.3, 95% CI 2.8–6.4). The association between alcohol use disorders and alcohol consumption pattern revealed a weaker relation for alcohol abuse compared to dependence. Conclusion: National and regional drinking habits and norms have to be considered as a significant source of variance, supporting the need for European epidemiological research on substance use in addition to US American activities, and emphasising the advantages of community-based preventive measures. An evaluation of public recommendations for safe limits of alcohol consumption and prevention targets referring to average consumption is indicated. There is also a need for a clear distinction between alcohol abuse and dependence. Accepted: 27 October 2000     

Progesterone alters GABA and glutamate responsiveness: a possible mechanism for its anxiolytic action

In this study, the neuromodulatory effects of progesterone were tested in an intact neuronal circuit of a model extrahypothalamic CNS area. Spontaneous discharge and responses of single cerebellar Purkinje neurons to microiontophoretically applied γ-aminobutyric acid (GABA) and glutamate were monitored before, during and after either systemic injection, at physiologic doses, or local application of the steroid. By both means of administration, progesterone significantly enhanced inhibitory responses of Purkinje cells to GABA and suppressed glutamate excitation within 3–10 min post-steroid. These results are consistent with the anxiolytic actions of the steroid.     

The pharmacologic treatment of alcohol and cocaine abuse. Integration of recent findings into clinical practice.

The clinical evidence available to date does not yet support the routine use of pharmacologic interventions in the majority of cases of alcohol or cocaine abuse. The available data suggest, however, that interventions should be considered, especially in patients who relapse or drop out of treatment, in more difficult cases, and in instances in which there are associated psychiatric disorders. Education and prevention should be reconsidered as the important "treatments" they are today.     

Autistic-like symptomatology in Prader-Willi syndrome: A review of recent findings

Prader-Willi syndrome (PWS) is caused by either the structural loss of material or the absence of gene expression from the paternally inherited copy of chromosome 15 in the q11-q13 region. In addition to a well-described behavioral phenotype that includes hyperphagia, obsessive-compulsive symptoms, disruptive behavior, and an increased risk for mood disorders, recent evidence also suggests that some individuals with PWS have repetitive behavior and social deficits reminiscent of autism spectrum disorders. In particular, it appears as if those with maternal uniparental disomy (UPD) as the cause of PWS are at greater risk for autistic symptomatology than those with paternal deletions of 15q11-q13. These findings are particularly intriguing in light of data implicating maternal duplications and triplications of the same chromosomal interval in idiopathic autism, as well as evidence that functional alterations of genes in this region are associated with social deficits found in a variety of neurodevelopmental disorders. This paper will review the recent evidence for phenotypic similarities between autism and PWS and the risk of symptomatology for the UPD subtype.