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Socio-affective dysfunction is a risk-factor for sexual offense recidivism. However, it remains unknown whether men who have sexually offended with and without child victims show differences in eye scan paths and autonomic responsivity while viewing facial expressions of emotion. We examined differences in accuracy of emotion recognition, eye movements, and pupil dilation responses between sex offenders with child victims, sex offenders without child victims, and a group of non-offenders living in the community. Sex offenders without child victims looked for longer at the eyes than sex offenders with child victims and non-offenders. Men without child victims also scored higher for psychopathy linked disinhibition, and these traits were associated with looking longer at the eyes of afraid faces. We found no evidence for group differences in accuracy, visual attention to the mouth, or pupil dilation responses. Our findings have implications for understanding the nature of socio-affective dysfunction in sexual offenders.

Substance abuse can be associated with difficulties in emotion regulation. It has been proposed that advantageous emotion regulation is positively associated with heart rate variability , and that ...

The aim of this paper is to outline some of the parts of the brain to increase understanding of the aetiology of criminal behaviours. It goes without saying that any complete answer will encompass:...

Previous reviews exploring facial affect processing among forensic samples have focused on the presence of psychopathy and/or have not distinguished on the basis of offence type. In order to develop understandings about etiological processes implicated in different types of antisocial behavior, the principle aim of this review was to systematically explore facial affect processing in incarcerated violent offenders, relative to other non-violent offenders, sexual offenders, and non-offenders. Following a systematic search of electronic databases and subsequent manual search, eight studies were assessed as meeting inclusion criteria, of which seven obtained a quality score deemed acceptable for review. These studies examined recognition accuracy, sensitivity and response bias for seven emotion categories (including neutral) in incarcerated male offenders with a history of violence. Findings supported the presence of generally impaired facial affect processing among violent offenders, including deficits in fear, anger, and disgust. Overall the findings of the review did not support the presence of a hostile attribution bias among violent offenders. The review also highlights differences in sample composition, stimuli, and study designs in emotion recognition research. Recommendations are made for future work on facial affect processing in clinically relevant groups.

Mindfulness is linked with improved regulatory processes of attention and emotion. The potential benefits of mindfulness are vast, including more positive emotional states and diminished arousal in response to emotional stimuli. This study aims to expand of the current knowledge of the mechanisms of mindfulness by relating the latter to cardiovascular processes. The paper describes two studies which investigated the relationship of trait mindfulness to self-report measures of emotions elicited during a violent video clip and cardiovascular responses to the clip. Both studies recruited male and female participants, mainly university undergraduate students. The clip was 5-min-long and evoked mainly feelings of tension and disgust. In study 1, we found that higher scores for trait mindfulness were associated with increased scores for valence (r = .370, p = .009), indicating a more positive interpretation of the clip. In study 2, the average heart rate during the clip was lower than during the preceding (p

Economics was front and centre during the run-up to the June 2016 referendum on the UK’s membership of the European Union and economists were almost unanimous that leaving would make the UK economically worse off than otherwise. Still, in the 6 months since the referendum, there has been little discernible impact on macroeconomic variables beyond a fall in the value of the pound, and the economics profession has been criticized for being overly gloomy in its predictions. This article offers some immediate reflections on the state of the economy in the run-up to the vote, on the forecasts of economists during the campaign, and on the changes to policy since. The lack of an immediate recession has been taken as evidence that the economics was wrong, but it is not evidence that leaving the EU will be economically harmless. Despite fiscal and monetary loosening most forecasters still expect growth to be slower than otherwise over the medium term. The vote and debate around it does offer some challenges for economics and we conclude with five lessons for the profession.

Psychopathy is characteristically associated with impairments in recognizing others' facial expressions of emotion, and there is some evidence that these difficulties are specific to the callousness features of the disorder. However, it remains unclear whether these difficulties are accompanied by reductions in autonomic reactivity when viewing others' emotional expressions, and whether these impairments are particular to expressions showing another's distress or are more pervasive across different emotional expressions. In this study, 73 adult male prisoners with histories of serious sexual or violent offenses-who ranged across the psychopathy continuum-completed a facial emotion recognition task. For the first time in a convicted offender sample, we used pupillometry techniques to measure changes in the pupil dilation response, a measure of sympathetic autonomic arousal to affective stimuli. We found that the callousness features of psychopathy were related to impaired recognition of fearful faces. Strikingly, we also showed that increasing callousness was associated with a reduction in the pupil dilation response and that this was pervasive across different emotional expressions. Our results highlight a potential role of the locus coeruleus-noradrenaline system in the pathophysiology of psychopathy and demonstrate the potential of the pupillary response as a technique for understanding attention-emotion interactions in psychopathy. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

BACKGROUND Inflammation plays an important role in formation and rupture of intracranial aneurysms. Expression of microsomal prostaglandin E2 (PGE2) synthase type 1 (mPGES-1) is increased in the wall of intracranial aneurysms in humans. PGE2, a by-product of mPGES-1, is associated with inflammation and cerebrovascular dysfunction. OBJECTIVE To test the hypothesis that deletion of mPGES-1 decreases the formation and rupture of intracranial aneurysms in a murine model. METHODS Intracranial aneurysms were induced in wild-type and mPGES-1 knockout (mPGES-1 KO) mice by using a combination of deoxycorticosterone acetate-salt-induced hypertension and intracranial injection of elastase in the basal cistern. Prevalence of aneurysms, subarachnoid hemorrhage, and mortality were assessed. We also tested the effects of administration of aspirin (6 mg/kg/d) by gavage and PGE2 (1 mg/kg/d) by subcutaneous infusion. RESULTS Systolic blood pressure and prevalence of aneurysm were similar in wild-type and mPGES-1 KO mice. However, mortality and the prevalence of subarachnoid hemorrhage were markedly increased in mPGES-1 KO mice (P < .05). Bone marrow reconstitution studies suggest that mPGES-1 derived from leukocytes does not appear to increase rupture of intracranial aneurysms. Aspirin, but not PGE2, attenuated the increased mortality in mPGES-1 KO mice (P < .05). CONCLUSION Vascular mPGES-1 plays a protective role in blood vessels and attenuates rupture of cerebral aneurysms. In contrast to effects on abdominal aneurysms, mPGES-1 deficiency is associated with an increase in rupture of cerebral aneurysms and mortality, which are attenuated by low-dose aspirin.

Intimate partner violence is predominantly viewed as a social problem of men’s violence against women. However, a growing evidence base suggests an equal prevalence rate for male and female perpetrated intimate partner physical aggression. Moreover, female perpetrated intimate partner violence is often assumed to be reactive, yet there is limited evidence to support this notion. In this article, we describe the results of two studies that investigated the prevalence of female perpetrated intimate partner physical aggression, and its correlates in heterosexual female university students. The relationships of personality traits, resting heart rate, and heart rate variability (a correlate of vagal activity) were compared between females who did and did not report having engaged in intimate partner physical aggression. In Study 1, we found that 30.9% of participants reported enacting intimate partner physical aggression during the preceding 12 months. This finding suggests that a considerable number of undergraduate females aggress against their intimate partners. Perpetrators, relative to nonperpetrators, scored higher on secondary psychopathic traits. In Study 2, female intimate partner violence was shown to be associated with low resting heart rate and high heart rate variability. Perpetrators, relative to nonperpetrators, scored higher on psychopathic traits that index emotional resilience and unempathic tendencies, and reported increased proactive and reactive aggression. This raises the possibility that some incidences of female intimate partner physical aggression represent proactive aggressive acts. These findings also support the frequently found association between low resting heart rate and aggression, but raise the prospect that the reported aggressive acts reflect high heart rate variability and strong parasympathetic nervous system activity.

Explanations of aggressive and antisocial behaviour often refer to impairments in self-regulation, or the ability to implement control over ones thoughts, emotions and behaviours. However, the evid...

Oxytocin (OT) plays a critical role in the formation of long lasting social attachments across a range of mammalian species. Raising intracerebral OT levels by intranasal administration of the neuropeptide (inOT) can also have pronounced effects on human sociocognitive functioning. inOT has been associated with increasing altruism, generosity, empathy and trust while decreasing fear, anxiety and stress reactions via neural mechanisms which are yet to be fully elucidated. The observation of the prosocial effects of OT has led to speculation about the role the peptide might play in some psychiatric conditions and debate as to its potential therapeutic uses. Here we note the great similarity in the sociocognitive effects that can be induced by inOT and the effects of acute consumption of modest does of alcohol. We further reflect on how both compounds may act on limbic and prefrontal cortical structures to increase GABAergic transmission, thereby facilitating the release of prepotent responses, that is, more automatic responses which are associated with earlier developmental stages.

Background: Cerebral levels of oxytocin, elevated by intranasal administration, can increase trust, empathy and altruism, and decrease fear. We hypothesised that low levels of these characteristics (found in some personality-disordered forensic patients), would be associated with reduced oxytocin levels. Aims: To assess whether patients, with psychopathic characteristics associated with selfishness, callousness and the remorseless use of others, plus a chronically unstable, antisocial and socially deviant lifestyle, would show depressed levels of oxytocin. Method: Basal urinary oxytocin levels (an indicator of cerebral oxytocin) were assessed in 47 forensic psychiatric patients. Levels were compared with those in 21 non-patient controls, and correlated with psychopathic characteristics. Results: Oxytocin levels were markedly elevated in the patient sample compared to controls. Levels were also strongly correlated with traits associated with a socially deviant lifestyle. Conclusions: The results point to o...

The emotional Stroop task has been used to assess deviant sexual interests of sexual abusers. Two limitations noted in the literature are difficulties surrounding the choice of word stimuli and the task’s inability to elicit significant differences between offender subtypes thus far. The purpose of this study was to examine differences in emotional Stroop bias between three adult groups using new, empirically derived word stimuli intended to reflect sexual interests more specific to sexual abusers. Significant differences were found between sexual abusers and nonoffending controls for affective and sexual word stimuli. The results further support differential processing biases between sexual offenders and nonoffenders; however, difficulties in differentiating between offender groups are still evident. Implications of these findings are discussed and recommendations for future research are made.

Item does not contain fulltext OBJECTIVE: Patients with Parkinson's disease (PD) can perform poorly on tasks involving theory of mind (ToM): the ability to reason about mental states. We investigated whether patients' ToM deficits were independent of executive dysfunction. METHOD: Experiment 1 aimed to establish that ToM deficits were present, and 2 following experiments manipulated the working memory (WM) demands of the ToM task. RESULTS: In Experiment 1, 15 patients with PD performed significantly more poorly than controls on a false belief vignette task but not on a faux pas task. Errors were related to poor verbal fluency. In Experiment 2, 24 patients with PD made fewer errors on shorter false belief vignettes than the original FBT, and errors on the latter were related to WM impairment. In Experiment 3, the FBT was presented as a comic strip visible throughout questioning, reducing WM demands. Patients (n = 24) made memory errors but no false belief errors on the comic strip. They exhibited no verbal fluency or WM impairments, but did exhibit deficits on a black-and-white Stroop task. False belief errors were not correlated with executive performance. CONCLUSIONS: PD patients made very few ToM errors that were independent of errors on memory questions, so in this sample, ToM deficits per se appear unlikely. However, patients still made errors on ToM tasks when associated incidental WM demands were considerably reduced, highlighting the need for future investigations of ToM in PD to account for the role of more general cognitive restrictions exhibited by even some medicated, early stage patients.

Background and Purpose— Angiotensin II produces oxidative stress and endothelial dysfunction in cerebral arteries, and angiotensin II type I receptors may play a role in longevity and vascular aging. Angiotensin-converting enzyme type 2 (ACE2) converts angiotensin II to angiotensin (1–7) and thus, may protect against effects of angiotensin II. We hypothesized that ACE2 deficiency increases oxidative stress and endothelial dysfunction in cerebral arteries and examined the role of ACE2 in age-related cerebrovascular dysfunction. Methods— Endothelial function, expression of angiotensin system components, NADPH oxidase subunits, and proinflammatory cytokines were examined in cerebral arteries from adult (12 months old) and old (24 months old) ACE2 knockout (KO) and wild-type (WT) mice. The superoxide scavenger tempol was used to examine the role of oxidative stress on endothelial function. Results— Vasodilatation to acetylcholine was impaired in adult ACE2 KO (24±6% [mean±SE]) compared with WT mice (52±7%; P phox , and Regulator of calcineurin 1 in both ACE2 KO and WT mice. mRNA levels of angiotensin system components did not change during aging. Conclusions— ACE2 deficiency impaired endothelial function in cerebral arteries from adult mice and augmented endothelial dysfunction during aging. Oxidative stress plays a critical role in cerebrovascular dysfunction induced by ACE2 deficiency and aging.

Research with developmental and adult samples has shown a relationship of psychopathic traits with reduced eye gaze. However, these relationships remained to be investigated among forensic samples. Here we examined the eye movements of male violent offenders during an emotion recognition task. Violent offenders performed similar to non-offending controls, and their eye movements varied with the emotion and intensity of the facial expression. In the violent offender group Boldness psychopathic traits, but not Meanness or Disinhibition, were associated with reduced dwell time and fixation counts, and slower first fixation latencies, on the eyes compared with the mouth. These results are the first to show a relationship of psychopathic traits with reduced attention to the eyes in a forensic sample, and suggest that Boldness is associated with difficulties in orienting attention toward emotionally salient aspects of the face.

On 23 June 2016, the UK public voted in favour of leaving the European Union. However, important decisions remain about the model for the UK's relationship with Europe outside of the EU, not least whether the UK seeks to remain a "member" of the Single Market or only seeks (tariff-free) "access". This report looks at exactly what the Single Market is and distinguishes between "membership" and "access", including the impact on the financial services sector. It also considers the potential for new trade deals beyond the EU and assesses the economic and public finance implications of the various options. This should inform the likely trade-offs between the level of access to the Single Market and other negotiating objectives such as control of immigration and budgetary contributions.

Adolescent sexual abusers are a heterogeneous group of offenders that often receive generic assessment and treatment services that are modeled on research findings from adult sex offender samples. The emotional Stroop task has been used to measure deviant sexual interest in adult samples. The purpose of the present study was to test whether the emotional Stroop task could also be used to assess deviant sexual interest in adolescent samples. Three groups of adolescents (a) sexual abusers ( n = 24); (b) offending controls ( n = 21); and (c) nonoffending controls ( n = 21) completed two emotional Stroop tasks related to deviant sexual interest and tests of executive function. Adolescent sexual abusers were significantly slower to color-name some word stimuli than both adolescent offending controls and adolescent nonoffending controls. However, the task was unable to differentiate between the groups on most of the Stroop word categories. Very little research has been conducted with adolescent offender samples and the emotional Stroop task. Reaction time (RT) and Stroop bias outcome data for adolescent samples appear to be more unsystematic and weaker than has been observed in previous adult data. Based on potential difficulties with reading and development, the emotional Stroop task may not be a task suitable for measuring deviant sexual interest in adolescent samples.

If the result of the referendum on 23 June leads to the UK leaving the EU, there will be impacts on the UK public finances. This report aims to set out the possible impacts, focusing particularly on the short run, given that the Chancellor wishes to achieve a budget balance by the end of this parliament. We also look at possible long-run consequences. The overall impact on the public finances will depend on two distinct components, each of which is uncertain to some degree: - The mechanical effect. As a net contributor to the EU, leaving the EU would strengthen the public finances because our net contribution would fall. But given uncertainty over the form of any subsequent arrangement with the EU, it might not necessarily fall to zero. - The national income effect. Any effect of leaving the EU on UK national income would affect the public finances. A rise in national income would strengthen the public finances, a fall would weaken them ...

It has been noted that some offenders are characterized by problems in the appropriate regulation of emotional states. Deficits in emotional regulation are particularly pertinent in sexual offenders. Therefore, therapeutic programs should, in part, focus on the development of effective strategies for the control of emotional arousal. In this review, we will provide an outline of how anatomical structures including the amygdala and regions of the prefrontal cortex (PFC) are involved in the appropriate regulation of emotion. It is argued in this paper that the effective control of emotional states may be helped through the adoption of a group of meditational practices, known as mindfulness techniques, which have emerged from Buddhist philosophy. These techniques involve slow, deep breathing and have been shown to affect vagal modulation of the heart and the functioning of specific neural circuits which are critically involved in emotional regulation.

Child molesters are frequently uncomfortable in adult company but show high emotional congruence with children. It was hypothesized that these emotional problems may be mirrored by physical intimacy problems such that child molesters would show exaggerated disgust reactions to the thought of coming into physical contact with adults, but not children. It was demonstrated that the discomfort shown by both offenders and non-offenders at the prospect of coming into contact with the bodily fluids of another person increases in relation to the age of the person that the bodily fluid came from. Furthermore, child molesters, in comparison to non-offenders and violent offenders, showed excessive concern at the thought of being touched on the lips or tongue with a re-sterilized surgical swab. These exaggerated anxieties combined withthe implicit belief that children are less contaminating than adults could add to the drive for child molesters to seek physical intimacy with children.

Psychopathic traits are linked with impairments in emotional facial expression recognition. These impairments may, in part, reflect reduced attention to the eyes of emotional faces. Although reduced attention to the eyes has been noted among children with conduct problems and callous-unemotional traits, similar findings are yet to be found in relation to psychopathic traits among adult male participants. Here we investigated the relationship of primary (selfish, uncaring) and secondary (impulsive, antisocial) psychopathic traits with attention to the eyes among adult male non-offenders during an emotion recognition task. We measured the number of fixations, and overall dwell time, on the eyes, and the mouth of male and female faces showing the six basic emotions at varying levels of intensity. We found no relationship of primary or secondary psychopathic traits with recognition accuracy. However, primary psychopathic traits were associated with a reduced number of fixations, and lower overall dwell time, on the eyes relative to the mouth across expressions, intensity, and sex. Furthermore, the relationship of primary psychopathic traits with attention to the eyes of angry and fearful faces was influenced by the sex and intensity of the expression. We also showed that a greater number of fixations on the eyes, relative to the mouth, were associated with increased accuracy for angry and fearful expression recognition. These results are the first to show effects of psychopathic traits on attention to the eyes of emotional faces in an adult male sample, and may support amygdala based accounts of psychopathy. These findings may also have methodological implications for clinical studies of emotion recognition.

Objective: To investigate theory of mind and the understanding of nonliteral language in patients with Tourette syndrome (TS). Background: In TS, striatal dysfunction could affect the functioning of the frontal cortex. Changes in frontal functioning could lead to impairments in theory of mind: the understanding of mental states, such as beliefs, emotions, and intentions. Poor understanding of a speaker's mental state may also impair interpretation of their nonliteral remarks. Method: In this study, patients with TS and healthy controls completed tasks to assess their understanding of sarcasm, metaphor, indirect requests, and theory of mind. These tasks were the Pragmatic Story Comprehension Task, the Hinting task, and a faux pas task. Inhibitory ability was also assessed through the use of the Hayling task and a black and white Stroop test. Results: Patients with TS exhibited significant impairment on the faux pas task and Pragmatic Story Comprehension Task despite limited evidence of inhibitory impairment. Conclusion: TS may be associated with changes in theory of mind.

The mechanisms by which acute alcohol intoxication results in increased violent behaviours are not fully understood. Pro-violent attitudes can act as a predictor of aggressive behaviour. It was hypothesised that alcohol intake would lead to shifts in attitudes to violence such that participants would express more pro-violent attitudes when drunk. This hypothesis was tested in two separate experiments with undergraduate students who were drinking in a familiar social setting. Results were the converse of what was predicted, in that the intake of alcohol resulted in decreased positive attitudes to violence. This attitudinal shift was accompanied by a significant increase in interference on an emotional Stroop test in response to words associated with conviviality implying that alcohol consumption did indeed result in an increase in pro-social feelings. These findings add support to the view that the effects of alcohol on behaviour are strongly influenced by situational and individual factors.

Psychopathy and metacognitive difficulties have been associated with the occurrence of violence in schizophrenia. However, evidence suggests that nonschizophrenic psychopaths match or even outperform healthy controls on tests of metacognition. We hypothesize that the metacognitive difficulties associated with schizophrenia may be ameliorated by comorbid psychopathy. To this end, metacognition (using the Metacognition Assessment Scale-Abbreviated [MAS-A]) and psychopathy (using the Hare Psychopathy Checklist-Revised [PCL-R]) are assessed in 79 patients with schizophrenia with a history of criminal offending. Piecewise regression reveals that the association between metacognition and psychopathy changes from a negative to a positive association at a breakpoint corresponding to a score of 24 on the PCL-R. This score is within the range of the cut-off point used for the diagnosis of psychopathy in Europe, which corresponds to a score of 26 on the PCL-R. The patients scoring above 24 on the PCL-R demonstrated better overall metacognitive abilities, suggesting that these patients constitute a specific group in which schizophrenia has an attenuated impairing effect on metacognition. However, this effect was absent for the Mastery subscale of the MAS-A, which refers to the ability to use one's own mental states to solve social and psychological dilemmas. Our results suggest that the relative preservation of metacognitive abilities in schizophrenic patients with extreme levels of psychopathy may contribute to their offending behavior as it may enable them to understand how to manipulate and extort their victims. However, enhancing the Mastery domain of metacognition in these patients may attenuate this offending behavior.

Research with violent offenders has consistently shown impaired recognition of other’s facial expressions of emotion. However, the extent to which similar problems can be observed among sexual offenders remains unknown. Using a computerized task, we presented sexual and violent offenders, and non-offenders, with male and female expressions of anger, disgust, fear, happiness, sadness, and surprise, morphed with neutral expressions at varying levels of intensity (10%, 55%, and 90% expressive). Based on signal detection theory, we used hit rates and false alarms to calculate the sensitivity index d-prime (d’) and criterion (c) for each emotional expression. Overall, sexual offenders showed reduced sensitivity to emotional expressions across intensity, sex, and type of expression, compared with non-offenders, while both sexual and violent offenders showed particular reduced sensitivity to fearful expressions. We also observed specific effects for high (90%) intensity female faces, with sexual offenders showing reduced sensitivity to anger compared with non-offenders and violent offenders, and reduced sensitivity to disgust compared with non-offenders. Furthermore, both sexual and violent offenders showed impaired sensitivity to high intensity female fearful expressions compared with non-offenders. Violent offenders also showed a higher criterion for classifying moderate and high intensity male expressions as fearful, indicative of a more conservative response style, compared with angry, happy, or sad. These results suggest that both types of offender show problems in emotion recognition, and may have implications for understanding the inhibition of violent and sexually violent behaviors.

Purpose: This paper combines material from domestic violence, animal aggression and neuropsychology research to construct a model to account for some domestic violence offending. The basic hypothesis is that some incidents of domestic violence can be understood in terms of the operation of primitive defence mechanisms, which are also implicated in panic attack. Perceptions of threat from an intimate partner could potentially trigger these same neuronal circuits thus releasing violent and emotionally charged responses at the spouse. Arguments: The hypothesis is based on:(a) the marked anatomical/physiological overlap of the neural substrates underlying defensive aggression and those implicated in panic attack, (b) reports of panic attack-like symptoms experienced by perpetrators during domestic violence assaults, (c) experimental evidence that demonstrates that standard physiological challenges can elicit panic/anger attacks in some domestic violence offenders (George et al., 2000). Conclusions: Panic/anger attack represents inappropriate activation of affective defensive responses due to inappropriate control of critical midbrain sites by the amygdala and/or prefrontal cortex. Panic attacks could be potentially suppressed by increasing the capacity of the prefrontal cortex to inhibit the midbrain affective defence mechanisms. However, learnt associations between stimuli and panic responses are difficult to extinguish and panic responses typically show sensitization overtime. The same may be true of the behaviour of domestic violence offenders. There is a need to establish the typology of the subgroup of offenders who perpetrate panic attack related domestic violence. (PsycINFO Database Record (c) 2010 APA, all rights reserved) (journal abstract)

Inflammation plays a key role in formation and rupture of intracranial aneurysms. Because hepatocyte growth factor (HGF) protects against vascular inflammation, we sought to assess the role of endogenous HGF in the pathogenesis of intracranial aneurysms. Circulating HGF concentrations in blood samples drawn from the lumen of human intracranial aneurysms or femoral arteries were compared in 16 patients. Tissue from superficial temporal arteries and ruptured or unruptured intracranial aneurysms collected from patients undergoing clipping (n=10) were immunostained with antibodies to HGF and its receptor c-Met. Intracranial aneurysms were induced in mice treated with PF-04217903 (a c-Met antagonist) or vehicle. Expression of inflammatory molecules was also measured in cultured human endothelial, smooth muscle cells and monocytes treated with lipopolysaccharides in presence or absence of HGF and PF-04217903. We found that HGF concentrations were significantly higher in blood collected from human intracranial aneurysms (1076±656 pg/mL) than in femoral arteries (196±436 pg/mL; P P >0.05), but significantly increased the prevalence of subarachnoid hemorrhage and decreased survival in mice ( P P P

This paper describes what is currently known about attachment from the development, social-cognitive and biological literatures and outlines the impact on organisms given adverse development experiences that can have an effect upon attachment formation in childhood across these three literatures. We then describe the effects that 'insecure' attachment styles arising in childhood can affect brain chemistry and brain function and subsequently adult social/romantic relationships. In the paper, we note that a number of sexual offenders report adverse childhood experiences and that they possess attachment styles that, taken together, make it likely that they will either seek out intimate attachments in ways where they will have sex with children, perhaps confusing sex with intimacy or in aggressive ways as particularly happens with men who sexually assault adult women. The last section of the paper describes chemical treatment for sexual offenders, focusing on the use of selective serotonin re-uptake inhibitors (SSRIs). We note evidence for the role of SSRIs in promoting more social/affiliative behaviors and speculate on the effects that SSRIs have in the treatment of sexual offenders by targeting areas of the social brain. Here, we would argue that it would be useful to carry out treatment where there is a combination of SSRI treatment (to promote more prosocial feelings and behaviors) in conjunction with therapy that typically addresses thoughts and behaviors, i.e., cognitive-behavioral therapy/schema-focused therapy.

Recent successes in identifying the genes and associated proteins underlying several familial neurodegenerative conditions have not always resulted in accounts as to why the associated patterns of neuronal damage are so specific and limited. Here, with reference to Huntington's disease, we present a general scheme to show how the mutant protein could interact with associated proteins to form an aggregation product. This could lead to neuronal death by direct actions on caspases, or by raising the levels of intracellular calcium ions and reactive oxygen species above a threshold that cannot be resisted by the protection normally conferred by endogenous factors such as calcium binding proteins, free radical scavengers and trophic factors. The local distributions of vulnerability and protective factors could ultimately dictate the pattern of damage induced by the mutant gene. IUBMB Life, 55: 293-298, 2003

Chronic administration of typical neuroleptics is associated with tardive dyskinesia in some patients. This dyskinetic syndrome has been associated with loss of GABAergic markers in the basal ganglia but the cause of these GABAergic depletions remains uncertain. Haloperidol, a commonly prescribed typical neuroleptic, is known to be toxic in vitro , possibly as a consequence of its conversion to pyridinium-based metabolites and potentially by raising glutamate-mediated transmission. We report here that the in vivo , acute administration of a large dose of haloperidol resulted in a microglial response indicative of neuronal damage. This was accompanied by an increase in the number of apoptotic cells in the striatum (especially in the dorsomedial caudate putamen) and in the substantia nigra pars reticulata. These apoptotic cells were characterised by the stereotaxic injection of a retrograde neuroanatomical tracer into the projection targets of the striatum and substantia nigra pars reticulata prior to the systemic injection of haloperidol. This procedure confirmed that the dying cells were neurones and demonstrated that within the striatum the majority were striatopallidal neurones though relatively high levels of apoptotic striatoentopeduncular neurones were also seen. The possibility that chronic administration of haloperidol could induce cumulative neuronal loss in the substantia nigra pars reticulata and thereby induce the pathological changes which lead to tardive dyskinesia is discussed.

Angiotensin II (Ang II) stimulates vascular inflammation, oxidative stress, and formation and rupture of intracranial aneurysms in mice. Because Ang 1–7 acts on Mas receptors and generally counteracts deleterious effects of Ang II, we tested the hypothesis that Ang 1–7 attenuates formation and rupture of intracranial aneurysms. Intracranial aneurysms were induced in wild-type and Mas receptor–deficient mice using a combination of Ang II–induced hypertension and intracranial injection of elastase in the basal cistern. Mice received elastase+Ang II alone or a combination of elastase+Ang II+Ang 1–7. Aneurysm formation, prevalence of subarachnoid hemorrhage, mortality, and expression of molecules involved in vascular injury were assessed. Systolic blood pressure was similar in mice receiving elastase+Ang II (mean±SE, 148±5 mm Hg) or elastase+Ang II+Ang 1–7 (144±5 mm Hg). Aneurysm formation was also similar in mice receiving elastase+Ang II (89%) or elastase+Ang II+Ang 1–7 (84%). However, mice that received elastase+Ang II+Ang 1–7 had reduced mortality (from 64% to 36%; P P P P >0.05) in groups treated with elastase+Ang II or elastase+Ang II+Ang 1–7. The expression of Mas receptor was detected by immunohistochemistry in samples of human intracranial arteries and aneurysms. In conclusion, without attenuating Ang II–induced hypertension, Ang 1–7 decreased mortality and rupture of intracranial aneurysms in mice through a Mas receptor–dependent pathway.

Phencyclidine (PCP), a non-competitive antagonist of the NMDA subtype of glutamate receptor, which also acts as an indirect dopamine agonist and at sigma sites, can induce a long lasting psychotic state when taken acutely. It is well established that PCP is toxic to specific limbic structures and we have recently demonstrated that it induces apoptosis of a subpopulation of striatal neurons. These neurons lie predominantly in the dorsomedial striatum and project to the globus pallidus. The mechanisms mediating this neuronal death are unclear though manipulations of dopamine transmission can induce striatal c-fos expression and continuous c-fos expression has been implicated in the molecular cascades controlling apoptosis. We accordingly undertook a series of experiments to determine the action of PCP on striatal Fos-like immunoreactivity (FLI). PCP (80 mg/kg, s.c.) elicited FLI in three distinct striatal areas, namely dorsomedial, dorsolateral and the nucleus accumbens. The level of PCP-induced FLI was consistently attenuated by the co-administration of the D-1 antagonist, SCH 23390. Vehicle injections also induced modest levels of FLI in the dorsomedial striatum and the nucleus accumbens which again were attenuated by SCH 23390. The type of striatal neuron in which PCP-induced FLI was determined by the use of a retrograde anatomical tracer. A colloidal gold tracer was thus injected into the major areas of termination of striatal projection neurons prior to the administration of PCP. This procedure demonstrated that the majority of the FLI positive striatal cells were striatopallidal neurons, though some FLI positive striatoentopeduncular neurons were also seen. The potential pharmacological mechanisms underlying the results are discussed. It is argued that the complex pattern of PCP-induced striatal FLI might be accounted for by a differential action upon extracellular dopamine levels whereby they are elevated in some striatal areas and simultaneously reduced in others.

Phencyclidine, a non-competitive N-methyl-D-aspartate receptor antagonist and indirect dopamine agonist, has neuroprotective properties. Phencyclidine, however, can also exert toxic effects and causes degeneration of neurons in the retrosplenial cortex. In this paper we demonstrate that acute administration of a high dose of phencyclidine to rats, (80 mg/kg), also causes death of a subpopulation of striatal neurons. The dying cells exhibited many of the morphological and biochemical features of cells undergoing apoptosis as revealed by a silver methenamine stain, propidium iodide fluorescence histochemistry and a TUNEL procedure. The majority of the dying cells tended to be clustered within the dorsomedial aspect of the striatum. The type of striatal cell undergoing apoptosis was determined by stereotaxically injecting a colloidal gold retrograde anatomical tracer into the major areas of striatal termination prior to the administration of phencyclidine. This procedure demonstrated that phencyclidine induced striatal apoptosis is almost exclusively limited to striatopallidal neurons. A similar series of experiments was conducted to determine whether the synthetic corticosteroid, dexamethasone, also induces apoptosis of striatal neurons. Corticosteroids are known to be toxic to hippocampal neurons and interact with striatal dopamine transmission. Acute administration of dexamethasone, (20 mg/kg), induced apoptosis of a subpopulation of striatal cells. As was the case with phencyclidine, most of the dexamethasone-induced apoptotic striatal cells were striatopallidal neurons located within the dorsomedial striatum. The pathology during the early stages of Huntington's disease is restricted to an equivalent subpopulation of striatal neurons. Many Huntington's patients are extremely psychotic during this stage in the progression of the disease. Psychosis is also associated with the acute administration of both phencyclidine and dexamethasone to humans. We accordingly speculate that the selective loss of striatopallidal neurons in the dorsomedial striatum may represent the neural substrate of many forms of psychosis.

Parkinson’s disease results from degeneration of dopaminergic neurons within the substantia nigra. The treatment of the disease was revolutionised by the introduction of dopamine replacement therapy. However, it has become increasingly clear that prolonged administration of dopamine agonists results in the onset of a spectrum of serious adverse effects, including dyskinesias. Accordingly, there is great interest in alternative strategies for the treatment of this condition. It is now realised that the loss of nigral dopamine cells and subsequent lowering of striatal dopamine levels causes a chain of pathophysiological events within the basal ganglia. One of the most prominent of these events is an elevation in the level of glutamate-mediated transmission within the striatum and the output structures of the basal ganglia. A range of glutamate antagonists has been shown to alleviate symptoms in animal models of Parkinson’s disease. Antagonists of both the N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtypes of the glutamate receptor result in an improvement in motor behaviour in experimental animal models. However, systemic administration of NMDA antagonists is also associated with several adverse effects, the most common being ataxia, sedation and cognitive impairments. These problems can potentially be overcome by the use of antagonists that are selective for the subtypes of NMDA receptors which are preferentially expressed in the critical parts of the pathophysiological circuitry. Glutamate antagonists are also known to have strong neuroprotective effects. Consequently, administration of glutamate antagonists may slow the rate of loss of nigral dopaminergic neurons and thus slow the progression of Parkinson’s disease.

MITCHELL, I.J. AND C.B. CARROLL. Reversal of parkinsonian symptoms in primates by antagonism of excitatory amino acid transmission: potential mechanisms of action. NEUROSCI BIOBEHAV REV 21(4) 469-475,1997-Pxkinsonism is charactetised by overactive glutamatergic transmission in the cortico-striatal and subtbalamo-medial pallidal pathways. Local blockade of glutamatergic transmission in these pathways can alleviate parkinsonian symptoms. The effectiveness of the treatment, however, is often limited by the simultaneous appearrmce of unwanted side-effects. These side-effects, including ataxia and dissociative anaesthesia, are particularly problematic when N-methyl-o-aspartate (NMDA) antagonists are used. In an attempt to overcome these problems we have attempted to manipulate excitatory iamino acid (EAA)-mediated neurotransmission indirectly by targeting the NMDA receptor associated modulatory sites. We review evidence which demonstrates that antagonists for both the NMDA associated glycine and polyamine sites can reverse parkinsonian symptoms when injected intra-cerebrally in both MPTP-treated and bilateral 6-OHDA lesioned marmosets without eliciting unwanted side-effects. We further review preliminary data which suggest that ifenprodil, a polyamine site antagonist, has striking anti-parkinsonian actions in the marmoset. Potential mechanisms of action underlying these effects are discussed in terms of NMDA receptor subtypes and the neuroanatomical locus of action. The anti-parkinsonian efficacy of intra-striatally administered EAA antagonists leads us to question the view of dopamine acting in the striatum as a simple neuromodulator. 0 1997 Elsevier Science Ltd. Parkinsonism glutamate excitatory amino acid NMDA striatum globus pallidus glycine (R)-HA-966 polyamine ifenprodil kappa opiate primate

Inflammation has been linked to progression and rupture of intracranial aneurysms in humans and animal models. Angiotensin II drives vascular inflammation in several models of vascular disease. Angiotensin 1-7, the product of metabolism of angiotensin II by ACE2, acts on Mas receptors and counteracts the deleterious effects of angiotensin II. We previously demonstrated that ACE2 deficiency is associated with cerebrovascular dysfunction. We now explore the hypothesis that angiotensin 1-7 attenuates formation and rupture of intracranial aneurysms in mice. In wild type (WT) C57Bl/6 mice an intracranial injection of elastase was made, and then angiotensin II (Ang II) or angiotensin II + angiotensin 1-7 (Ang II + Ang 1-7) were infused for 3 weeks. Increase in systolic pressure was similar in mice receiving Ang II (146±5 mmHg, mean ±SE) or Ang II + Ang 1-7 (147±5 mmHg). Mortality was higher in Ang II-treated mice (64% (16/25)) than in Ang II + Ang 1-7-infused mice (33% (7/21) p0.05). In conclusion, angiotensin 1-7 does not attenuate the increase in systolic blood pressure induced by Ang II in WT or Mas-KO mice. Angiotensin 1-7 does not affect the incidence of aneurysm formation in this mouse model of intracranial aneurysms. Importantly, angiotensin 1-7 decreases mortality and intracranial aneurysm rupture. Protective effects of angiotensin 1-7 on aneurysm rupture are not seen in Mas-KO mice, confirming that these effects of angiotensin 1-7 are mediated by its receptor Mas. We speculate that angiotensin 1-7 may be of therapeutic value for prevention of rupture of intracranial aneurysms.

Psychopathic personality traits are linked with selfish and non-cooperative responses during economical decision making games. However, the possibility that these responses may vary when responding to members of the in-group and the out-group has not yet been explored. We aimed to examine the effects of primary (selfish, uncaring) and secondary (impulsive, irresponsible) psychopathic personality traits on the responses of non-offending participants to the in-group and the out-group (defined in terms of affiliation to a UK University) across a series of economical decision making games. We asked a total of 60 participants to act as the proposer in both the dictator game and the ultimatum game. We found that across both tasks, those who scored highly for secondary psychopathic traits showed an elevated intergroup bias, making more generous offers toward members of the in-group relative to the out-group. An exaggerated intergroup bias may therefore represent a motivational factor for the antisocial behavior of those with elevated secondary psychopathic traits.

It is often assumed that if physical differences exist between the brains of people with schizophrenia and normal people then those biological differences will have caused the psychological abnormalities to occur. In this article, we challenge this view. First, we argue that the reverse case is also plausible, namely, that it is possible for the physiological differences associated with the condition to be the result of the condition and not the cause. Less contentiously, we propose that the relationship between the psychological problems and the physiology should be viewed not as a simple billiard-ball style cause-and-effect relationship but more as a reciprocal and iterative relationship where psychological effects can affect the physiology that can in turn affect the psychology. The evidence for the various physiological differences between people with schizophrenia and normals is assessed and it is concluded that these differences exist but that there is little evidence to demonstrate that all (or indeed even any), of them precede the onset of schizophrenic symptoms. Similarly, current information-processing theories can also be considered as descriptive of a psychotic state rather than causal to it. Similarities between traumatic shock and schizophrenia are discussed and it is argued that phenomena associated with trauma might need to be considered as an integral part of the psychotic's experience. It is also concluded that no psychological theory can deny the importance of the physiological level in schizophrenia.

Drug-induced dyskinesias are a major drawback of the dopaminergic therapies currently employed to treat Parkinson's disease. It is commonly speculated that these dyskinesias may be mediated by functional changes within the striatum. Recent research has, therefore, focused on finding new modes of therapy which will alleviate parkinsonian symptoms without directly altering neurotransmission in the striatum. It has recently been demonstrated that the behavioural symptoms observed in dopamine-depleted rodents can be alleviated by blockade of excitatory neurotransmission in the entopeduncular nucleus. A series of experiments was conducted in order to determine whether this manipulation affected the pattern of Fos immunoreactivity in the basal ganglia elicited by dopamine depletion. The results demonstrated that the most striking change in Fos levels was found in the subthalamic nucleus, indicating that reversal of parkinsonian symptoms in this manner cannot be considered as a simple redress in the balance of activity in the output structures of the basal ganglia.

Pharmacological manipulations which result in abnormal levels of excitatory amino acid (EAA) mediated neurotransmission can result in neuronal apoptosis. We accordingly hypothesised that manipulations of the external environment which induce prolonged EAA-mediated transmission in sensory neurons may also induce apoptosis. This hypothesis was tested by placing groups of adult mice, housed in their home cage, on a turntable which slowly rotated (0.8 rev./min). This non-invasive manipulation will have resulted in abnormal discharge patterns in the vestibular nuclei. Significantly greater levels of neuronal apoptosis were seen in the vestibular complex after rotation for 48 h compared with non-rotated controls. This finding was also predicted independently from a computational approach.

The glutamatergic cortico-striatal and subthalamo-entopeduncular pathways are both overactive in parkinsonism. Previous behavioural investigations have shown that intra-entopeduncular injection of either NMDA-site or glycine-site antagonists results in alleviation of parkinsonian symptoms, although injection of the former is associated with the appearance of anaesthetic-like side effects. These behavioural differences may be mediated by action on different NMDA receptor subtypes. Recent neurochemical and molecular pharmacological studies have indicated the existence of NMDA receptor subtypes which display differential modulation by glycine. In the present study, three potential modes of NMDA antagonism were differentiated in vitro by effects on [3H]-glycine binding to striatal sections. Specific [3H]-glycine binding was totally displaced by the glycine partial agonist (R)-HA-966; the NMDA-site antagonist D-CPP had no effect; and the NMDA-site antagonist D-AP5 displaced [3H]-glycine binding in a subpopulation of glycine sites. The anti-parkinsonian effects of (R)-HA-966, D-CPP and D-AP5 were assessed by intra-striatal injection in reserpine-treated rats and 6-OHDA-lesioned rats. Injection of (R)-HA-966 and D-CPP resulted in alleviation of parkinsonian akinesia, although the latter elicited anaesthetic-like side effects; D-AP5 was ineffective as an anti-parkinsonian agent. (R)-HA-966 was also effective as an anti-parkinsonian agent when administered systemically in the reserpine-treated rat. These data suggest that different classes of NMDA antagonist mediate different behavioural responses within the parkinsonian striatum. The behavioural response produced may depend on the exact nature of the conformational change induced by the antagonist and the location of the subtype most sensitive to that class of compound. Selection of a specific mode of NMDA receptor antagonism or targeting of striatal NMDA receptor subtypes may form the basis of a novel therapeutic approach to Parkinson's disease.

Assessing the implicit attitudes and beliefs of offenders has proved difficult over decades of work and research with offender samples. The purpose of this paper is to outline the research related to the use of the emotional Stroop task and to encourage researchers and practitioners to use it as a measure to assess the implicit attitudes of offenders within their assessments. We consider the factors that may influence Stroop results along with the research considerations that need to be taken into account when using an emotional Stroop paradigm. Currently, a significant limitation of the emotional Stroop task is a lack of standard word stimulus sets that are able to distinguish between offender types. This limitation could seriously impede further development of this tool. Suggestions for future research are proposed. © 2012 Copyright National Organisation for the Treatment of Abusers.