Disturbances In Social Behavior Research Articles

Epidemiology of cephalalgia in population of central part of India

Introduction: Headache is a major and common neurological problem in worldwide and is a main reason of morbidity, incapacity, absenteeism at work place, interrupted social interaction mood and behavioral disturbances. Yet they are under-recognized, under-diagnosed and under-treated worldwide, only minorities of people with headache disorders are professionally diagnosed. Aim: Given the population load, and the fact that most headaches seen in practice are under diagnosed and undertreated, the burden of headache is significant. The present study was aimed to assess the Epidemiology of chronic headache in population of south eastern Rajasthan India. Materials and Methods: This study was conducted in department of neurosurgery Jhalawar medical college Jhalawar Rajasthan from 15th January 2015 to 15 july2016. Clinical and radiological details of Two thousand Patients of south east Rajasthan and west part of Madhya Pradesh were noted. The data obtained was statistically analyzed using SPSS version 22 and descriptive statistics was used to compare the results obtained. Results: Out of two thousand patients 900(45%) patients were male and 1100(55%) were female. 1760(88%) patients were between 16-60 year age group, there were 1320(66%) patients residing in rural areas and 880(44%) patients were residing in urban areas. Socioeconomic status occupation / income were low in 680(34%) patient’s medium in 1200(60%) patients. Tension type headache occur in1200 (60%), migraine in 400 (20%), cluster headache in 60 (3%), medication overuse headache present in100 (5%) patients. Other cause of headache noted in 240 (12%) as sinusitis, stroke, decrease vision, atypical pain like trigeminal neuralgia brain tumor and abscess. Conclusion: Headache prevalence in central part of India is more in female, adult between 16-60 years age groups, and rural areas with low socioeconomic status / income. Most common cause of headache is tension type headache. Keywords: Cephalalgia, headache, Tens

Neuronal pathways of embarrassment

Abstract Embarrassment is a genuine human emotion that we experience while being publicly exposed in unfavorable situations. The embarrassment we feel informs us how we perform according to prevalent norms and moral values and helps to regulate the impression we make on others. One cornerstone of embarrassment is the capacity to take another’s perspective and reflect on the thoughts, feelings, and intentions of others. On the neural systems level, these processes of perspective taking are linked to neural activation in the medial prefrontal cortex and precuneus. In addition, the mishap and the expected negative evaluation induce affective arousal and activity in the anterior insula and anterior cingulate cortex. Both networks contribute to the experience of embarrassment and it is their orchestrated activity in the (para-) limbic system that accounts for this complex emotional phenomenon. From a conceptual point of view embarrassment thus presupposes the presence of others. This witnessing audience however also reacts to the mishaps of others and embarrassment may also be experienced vicariously. Here, processes of perspective taking also play an important role, while bystanders embody threats to another’s social integrity. Such interpersonal emotional phenomena gain particular relevance in the context of psychiatric disorders. Specifically, autism spectrum disorders and social anxiety disorders have core symptoms in the social domain that manifest in social interactions causing disturbances in social behavior and reduced well-being of affected individuals.

Neuronal pathways of embarrassment

Embarrassment is a genuine human emotion that we experience while being publicly exposed in unfavorable situations. The embarrassment we feel informs us how we perform according to prevalent norms and moral values and helps to regulate the impression we make on others. One cornerstone of embarrassment is the capacity to take another’s perspective and reflect on the thoughts, feelings, and intentions of others. On the neural systems level, these processes of perspective taking are linked to neural activation in the medial prefrontal cortex and precuneus. In addition, the mishap and the expected negative evaluation induce affective arousal and activity in the anterior insula and anterior cingulate cortex. Both networks contribute to the experience of embarrassment and it is their orchestrated activity in the (para-)limbic system that accounts for this complex emotional phenomenon. From a conceptual point of view embarrassment thus presupposes the presence of others. This witnessing audience however also reacts to the mishaps of others and embarrassment may also be experienced vicariously. Here, processes of perspective taking also play an important role, while bystanders embody threats to another’s social integrity. Such interpersonal emotional phenomena gain particular relevance in the context of psychiatric disorders. Specifically, autism spectrum disorders and social anxiety disorders have core symptoms in the social domain that manifest in social interactions causing disturbances in social behavior and reduced well-being of affected individuals.

Cannabinoid Transmission in the Hippocampus Activates Nucleus Accumbens Neurons and Modulates Reward and Aversion-Related Emotional Salience

BackgroundCannabinoid receptor transmission strongly influences emotional processing, and disturbances in cannabinoid signaling are associated with various neuropsychiatric disorders. The mammalian ventral hippocampus (vHipp) is a critical neural region controlling mesolimbic activity via glutamatergic projections to the nucleus accumbens. Furthermore, vHipp abnormalities are linked to schizophrenia-related psychopathology. Nevertheless, the mechanisms by which intra-vHipp cannabinoid signaling may modulate mesolimbic activity states and emotional processing are not currently understood. MethodsUsing an integrative combination of in vivo electrophysiological recordings and behavioral pharmacologic assays in rats, we tested whether activation of cannabinoid type 1 receptors (CB1R) in the vHipp may modulate neuronal activity in the shell subregion of the nucleus accumbens (NASh). We next examined how vHipp CB1R signaling may control the salience of rewarding or aversive emotional memory formation and social interaction/recognition behaviors via intra-NASh glutamatergic transmission. ResultsWe demonstrate for the first time that vHipp CB1R transmission can potently modulate NASh neuronal activity and can differentially control the formation of context-dependent and context-independent forms of rewarding or aversion-related emotional associative memories. In addition, we found that activation of vHipp CB1R transmission strongly disrupts normal social behavior and cognition. Finally, we report that these behavioral effects are dependent upon intra-NASh alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission. ConclusionsTogether, these findings demonstrate a critical role for hippocampal cannabinoid signaling in the modulation of mesolimbic neuronal activity states and suggest that dysregulation of CB1R transmission in the vHipp→NASh circuit may underlie hippocampal-mediated affective and social behavioral disturbances present in neuropsychiatric disorders.

Altered social behavior and ultrasonic communication in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy.

BackgroundThe Duchenne and Becker muscular dystrophies (DMD, BMD) show significant comorbid diagnosis for autism, and the genomic sequences encoding the proteins responsible for these diseases, the dystrophin and associated proteins, have been proposed as new candidate risk loci for autism. Dystrophin is expressed not only in muscles but also in central inhibitory synapses in the cerebellum, hippocampus, amygdala, and cerebral cortex, where it contributes to the organization of autism-associated trans-synaptic neurexin-neuroligin complexes and to the clustering of synaptic gamma-aminobutyric acid (GABA)A receptors. While brain defects due to dystrophin loss are associated with deficits in cognitive and executive functions, communication skills and social behavior, only a subpopulation of DMD patients meet the criteria for autism, suggesting that mutations in the dystrophin gene may confer a vulnerability to autism. The loss of dystrophin in the mdx mouse model of DMD has been associated with cognitive and emotional alterations, but social behavior and communication abilities have never been studied in this model.MethodsHere, we carried out the first in-depth analysis of social behavior and ultrasonic communication in dystrophin-deficient mdx mice, using a range of socially relevant paradigms involving various degrees of executive and cognitive demands, from simple presentation of sexual olfactory stimuli to social choice situations and direct encounters with female and male mice of various genotypes.ResultsWe identified context-specific alterations in social behavior and ultrasonic vocal communication in mdx mice during direct encounters in novel environments. Social behavior disturbances depended on intruders’ genotype and behavior, suggesting alterations in executive functions and adaptive behaviors, and were associated with selective alterations of the development, rate, acoustic properties, and use of the ultrasonic vocal repertoire.ConclusionsThis first evidence that a mutation impeding expression of brain dystrophin affects social behavior and communication sheds new light on critical cognitive, emotional, and conative factors contributing to the development of autistic-like traits in this disease model.Electronic supplementary materialThe online version of this article (doi:10.1186/s13229-015-0053-9) contains supplementary material, which is available to authorized users.

Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model.

BackgroundThis study was designed to test a new approach to drug treatment of autism spectrum disorders (ASDs) in the Fragile X (Fmr1) knockout mouse model.MethodsWe used behavioral analysis, mass spectrometry, metabolomics, electron microscopy, and western analysis to test the hypothesis that the disturbances in social behavior, novelty preference, metabolism, and synapse structure are treatable with antipurinergic therapy (APT).ResultsWeekly treatment with the purinergic antagonist suramin (20 mg/kg intraperitoneally), started at 9 weeks of age, restored normal social behavior, and improved metabolism, and brain synaptosomal structure. Abnormalities in synaptosomal glutamate, endocannabinoid, purinergic, and IP3 receptor expression, complement C1q, TDP43, and amyloid β precursor protein (APP) were corrected. Comprehensive metabolomic analysis identified 20 biochemical pathways associated with symptom improvements. Seventeen pathways were shared with human ASD, and 11 were shared with the maternal immune activation (MIA) model of ASD. These metabolic pathways were previously identified as functionally related mediators of the evolutionarily conserved cell danger response (CDR).ConclusionsThe data show that antipurinergic therapy improves the multisystem, ASD-like features of both the environmental MIA, and the genetic Fragile X models. These abnormalities appeared to be traceable to mitochondria and regulated by purinergic signaling.Electronic supplementary materialThe online version of this article (doi:10.1186/2040-2392-6-1) contains supplementary material, which is available to authorized users.

Reversal of autism-like behaviors and metabolism in adult mice with single-dose antipurinergic therapy.

Autism spectrum disorders (ASDs) now affect 1–2% of the children born in the United States. Hundreds of genetic, metabolic and environmental factors are known to increase the risk of ASD. Similar factors are known to influence the risk of schizophrenia and bipolar disorder; however, a unifying mechanistic explanation has remained elusive. Here we used the maternal immune activation (MIA) mouse model of neurodevelopmental and neuropsychiatric disorders to study the effects of a single dose of the antipurinergic drug suramin on the behavior and metabolism of adult animals. We found that disturbances in social behavior, novelty preference and metabolism are not permanent but are treatable with antipurinergic therapy (APT) in this model of ASD and schizophrenia. A single dose of suramin (20 mg kg−1 intraperitoneally (i.p.)) given to 6-month-old adults restored normal social behavior, novelty preference and metabolism. Comprehensive metabolomic analysis identified purine metabolism as the key regulatory pathway. Correction of purine metabolism normalized 17 of 18 metabolic pathways that were disturbed in the MIA model. Two days after treatment, the suramin concentration in the plasma and brainstem was 7.64 μM pmol μl−1 (±0.50) and 5.15 pmol mg−1 (±0.49), respectively. These data show good uptake of suramin into the central nervous system at the level of the brainstem. Most of the improvements associated with APT were lost after 5 weeks of drug washout, consistent with the 1-week plasma half-life of suramin in mice. Our results show that purine metabolism is a master regulator of behavior and metabolism in the MIA model, and that single-dose APT with suramin acutely reverses these abnormalities, even in adults.

Observational themes of social behavioral disturbances in frontotemporal dementia.

ABSTRACT Background: Caregivers report early disturbances in social behavior among patients with behavioral variant frontotemporal dementia (bvFTD); however, there are few direct observational studies of these social behavioral disturbances. This study aimed to identify social behavioral themes in bvFTD by direct observation in naturalistic interactions. The identification of these themes can help caregivers and clinicians manage the social behavioral disturbances of this disease. Methods: Researchers observed 13 bvFTD patients in their homes and community-based settings and recorded field notes on their interpersonal interactions. A qualitative analysis of their social behavior was then conducted using ATLAS.ti application and a constant comparison method. Results: Qualitative analysis revealed the following themes: (1) diminished relational interest and initiation, indicating failure to seek social interactions; (2) lack of social synchrony/intersubjectivity, indicating an inability to establish and maintain interpersonal relationships; and (3) poor awareness and adherence to social boundaries and norms. These themes corresponded with changes from caregiver reports and behavioral scales. Conclusion: This analysis indicates that real-world observation validates the diagnostic criteria for bvFTD and increases understanding of social behavioral disturbances in this disorder. The results of this and future observational studies can highlight key areas for clinical assessment, caregiver education, and targeted interventions that enhance the management of social behavioral disturbances in bvFTD.

Glutamic acid decarboxylase 67 haplodeficiency impairs social behavior in mice

Reduced glutamic acid decarboxylase (GAD)67 expression may be causally involved in the development of social withdrawal in neuropsychiatric states such as autism, schizophrenia and bipolar disorder. In this study, we report disturbance of social behavior in male GAD67 haplodeficient mice. GAD67(+/-) mice, compared to GAD67(+/+) littermates, show reduced sociability and decreased intermale aggression, but normal nest building and urine marking behavior, as well as unchanged locomotor activity and anxiety-like behavior. Moreover, the mutants display a reduced sensitivity to both social and non-social odors, indicating a disturbance in the detection and/or processing of socially relevant olfactory stimuli. Indeed, we observed reduced activation of the lateral septum, medial preoptic area, bed nucleus of the stria terminalis, medial and cortical amygdala upon exposure of GAD67(+/-) mice to social interaction paradigm, as indicated by c-Fos immunohistochemistry. These data suggest a disturbance of stimulus processing in the brain circuitry controlling social behavior in GAD67(+/-) mice, which may provide a useful model for studying the impact of a reduced GAD67 expression on alterations of social behavior related to neuropsychiatric disorders.

Een patiënt met asbestose, chorea en neuropsychiatrische symptomen

A patient with known asbestosis and a recent chorea was admitted for analysis of increasing disturbances of mobility, memory and social unacceptable behavior. At physical examination only minor neurological signs were seen. Additional investigations (among others CT-brain and PET-scan) suggested early M. Alzheimer. Two months later, the patient was readmitted with pneumonia and delirium. A literature review revealed some reports of vague neurological symptoms. An association between asbestos and the disorders in this patient was considered unlikely . An approach is proposed for asbestosis patients with vague neurological and/or psychiatric symptoms.

Alterations in social behavior of Japanese medaka (Oryzias latipes) in response to sublethal chlorpyrifos exposure

The behavioral and biochemical responses of Japanese medaka (Oryzias latipes) to acute and subacute (sublethal) levels of chlorpyrifos were studied. In the acute exposure test, medaka were exposed to 0.018, 0.055, 0.166, or 0.500mgL−1 chlorpyrifos for 4d. As a result, fish showed hypoactivity compared to the control (at 0.018, 0.055, and 0.166mgL−1, swimming speeds were 55.6%, 39.0%, and 27.3% those of the control), Brain acetylcholinesterase activity and swimming speed were significantly correlated. In the subacute toxicity test, medaka were exposed to 0.012mgL−1 chlorpyrifos (10% of LC50) for 8d. On day 4, there were no significant differences in behavioral and biochemical endpoints in exposed fish as compared to the control. On day 8, exposed fish became hyperactive, and the swimming speed of the social group increased to 2times that of the control, whereas acetylcholinesterase activity was decreased to 68% that of the control. In addition, fish exhibited significant alterations in social behavior (schooling duration increased to 2.6times and solitary duration decreased to 28% that of the control). Our findings clearly demonstrate a subacute effect of chlorpyrifos on the social behavior of medaka, which may pose a risk at population level because of the disturbance of social behavior. In addition, the recorded behavioral alterations may provide a useful tool for assessing the toxicity of organophosphorous pesticides to aquatic organisms.

Originalarbeiten: Multifamilientherapie in Deutschland

Multi-family therapy, common group therapy with several families per one index patient, has been gaining popularity recently. This has occasioned an exploratory study of the status of implementation and common factors in all multi-family therapy programs in Germany. In a survey conducted across Germany, all providers of multi-family therapy interventions were requested to give a detailed description of their intervention. Quantitative data were analyzed with descriptive statistics, and verbal data were summarized categorically with qualitative content analysis. Of the 25 intervention programs examined 21 are directed at emotionally disturbed children and young people and their families; mainly with disturbances in social behavior. Over 4,000 families per year are treated in multi-family therapy, and five programs were systematically evaluated. MFT is characterized by systematically oriented group therapy methods. Those surveyed traced the effect of this form of intervention back to activating problems in the group, activating resources, changing perspective, learning models, experiencing self-efficacy, and the therapeutic relationship. Systematic studies of multi-family therapy in evaluations and in random controlled study designs are recommended.

CPB-K mice a mouse model of schizophrenia? Differences in dopaminergic, serotonergic and behavioral markers compared to BALB/cJ mice

Schizophrenia is characterized by disturbances in social behavior, sensorimotor gating and cognitive function, that are discussed to be caused by a termination of different transmitter systems. Beside morphological alterations in cortical and subcortical areas reduced AMPA- NMDA-, 5-HT2-receptor densities and increased 5-HT1-receptor densities are found in the hippocampus.The two inbred mouse strains CPB-K and BALB/cJ are known to display considerable differences in cognitive function and prepulse inhibition, a stable marker of sensorimotor gating. Furthermore, CPB-K mice exhibit lower NMDA-, AMPA- and increased 5-HT-receptor densities in the hippocampus as compared to BALB/cJ mice. We investigated both mouse strains in social interaction test for differences in social behavior and with immuncytochemical approaches for alterations of dopaminergic and serotonergic parameters. Our results can be summarized as follows: compared to BALB/cJ, CPB-K mice showed: (1) significantly reduced traveling distance and number of contacts in social interaction test, (2) differences in the number of serotonin transporter-immunoreactive neurons and volume of raphe nuclei and a lower serotonergic fiber density in the ventral and dorsal hippocampal subfields CA1 and CA3, (3) no alterations of dopaminergic markers like neuron number, neuron density and volume in subregions of substantia nigra and ventral tegmental area, but a significantly higher dopaminergic fiber density in the dorsal hippocampus, the ventral hippocampus of CA1 and gyrus dentatus, (4) no significant differences in serotonergic and dopaminergic fiber densities in the amygdala.Based on our results and previous studies, CPB-K mice compared to BALB/cJ may serve as an important model to understand the interaction of the serotonergic and dopaminergic system and their impact on sensorimotor gating and cognitive function as related to neuropsychiatric disorders like schizophrenia.

Neuropsychological Evidence of Impaired Cognitive Empathy in Euthymic Bipolar Disorder

The empathic abilities have never been examined in bipolar disorder patients, despite frequent observations of impaired social behavior. To examine the neuropsychological processes that underlie the affective and cognitive empathic ability in bipolar disorder, the authors compared affective and cognitive empathic abilities, as well as theory of mind and executive functions, of euthymic bipolar disorder patients and healthy comparison subjects. Significant deficits in cognitive empathy and theory of mind were observed, while affective empathy was elevated in bipolar disorder. Patients showed impaired cognitive flexibility (shifting and reversal learning) but intact planning behavior. Impaired cognitive empathy was related with performance in neurocognitive tasks of cognitive flexibility, suggesting that prefrontal cortical dysfunction may account for impaired cognitive empathy in bipolar disorder.

PRECLINICAL STUDY: Acute and chronic cannabinoid treatment differentially affects recognition memory and social behavior in pubertal and adult rats

Although cannabis belongs to the most widely used drugs among adolescents, little is known about its acute and lasting neurobehavioral effects during critical developmental periods. In the present study we investigated acute and long-term behavioral effects of the cannabinoid agonist WIN 55,212-2 (WIN) in pubertal and adult rats. Chronic WIN (1.2 mg/kg)/vehicle treatment was extended over 25 days throughout puberty, from postnatal day (pd) 40 to pd 65, or for a similar time period in adult rats (> pd 80). All animals were tested at three time points for object/social recognition memory, social interaction and spontaneous social behavior. First, acute cannabinoid effects were investigated directly after the first injection. Additionally, behavioral performance was retested 24 hours and 15 days after cessation of WIN treatment. Chronic pubertal WIN treatment induced persistent object/social recognition deficits, indicating a general impairment in short-term information processing. Lasting disturbances in social behavior, social play and self-grooming were also found. Furthermore, behavioral deficits seen after acute WIN administration were more pronounced in pubertal than in adult rats. These results confirm our recent findings that chronic pubertal cannabinoid treatment leads to lasting behavioral alterations in adulthood, and they show that acute cannabinoid administration induces more severe behavioral deficits in pubertal rats than in mature animals. We therefore conclude that an immature brain is more susceptible to the acute and chronic effects of exogenous cannabinoids than an adult organism, which might be explained by an overactive endocannabinoid system and concomittant maturational disturbances in further neurotransmitter systems during pubertal development.

Stereotypies and hyperactivity in rhesus monkeys exposed to IgG from mothers of children with autism

Autism together with Asperger syndrome and pervasive developmental disorder not otherwise specified form a spectrum of conditions (autism spectrum disorders or ASD) that is characterized by disturbances in social behavior, impaired communication and the presence of stereotyped behaviors or circumscribed interests. Recent estimates indicate a prevalence of ASD of 1 per 150 ( Kuehn, 2007). The cause(s) of most cases of ASD are unknown but there is an emerging consensus that ASD have multiple etiologies. One proposed cause of ASD is exposure of the fetal brain to maternal autoantibodies during pregnancy [Dalton, P., Deacon, R., Blamire, A., Pike, M., McKinlay, I., Stein, J., Styles, P., Vincent, A., 2003. Maternal neuronal antibodies associated with autism and a language disorder. Ann. Neurol. 53, 533–537]. To provide evidence for this hypothesis, four rhesus monkeys were exposed prenatally to human IgG collected from mothers of multiple children diagnosed with ASD. Four control rhesus monkeys were exposed to human IgG collected from mothers of multiple typically developing children. Five additional monkeys were untreated controls. Monkeys were observed in a variety of behavioral paradigms involving unique social situations. Behaviors were scored by trained observers and overall activity was monitored with actimeters. Rhesus monkeys gestationally exposed to IgG class antibodies from mothers of children with ASD consistently demonstrated increased whole-body stereotypies across multiple testing paradigms. These monkeys were also hyperactive compared to controls. Treatment with IgG purified from mothers of typically developing children did not induce stereotypical or hyperactive behaviors. These findings support the potential for an autoimmune etiology in a subgroup of patients with neurodevelopmental disorders. This research raises the prospect of prenatal evaluation for neurodevelopmental risk factors and the potential for preventative therapeutics.

Social behavior phenotypes in fragile X syndrome, autism, and the Fmr1 knockout mouse: Theoretical comment on McNaughton et al. (2008).

Comments on the article by C. H. McNaughton et al.. Individuals with fragile X syndrome (FXS) show varying degrees of social behavior disturbances, from social anxiety to autism. This variability of social behavior phenotypes in FXS is likely to be due to interactions of Fmr1 with other gene variants and environmental factors during brain development, although very little is known about the specific genetic and neural mechanisms involved. The Fmr1 knockout mouse is an important experimental resource for elucidating the neural mechanisms of social anxiety, social reward, and social cognition. However, studies of social behavior phenotypes in the Fmr1 knockout mouse are still in early stages. McNaughton et al provide important new information on these phenotypes in the Fmr1 knockout mouse through their use of novel, detailed behavioral analysis to identify signs of increased social anxiety and social cognition deficits. Their significant refinements in measurement of social behavior phenotypes will help to advance future efforts to elucidate the genetic and neural mechanisms underlying social behavior disturbances in FXS and autism.

Theory of mind and the frontal lobes

Theory of mind (ToM) is the ability to attribute mental states to other individuals. Its cerebral organization is not enough established, even though the literature suggests the relevant role of the frontal lobes.To evaluate frontal lobe patients and controls in ToM tests.We studied 20 patients with lesions limited to the frontal lobes (as shown by CT or MRI), and 10 normal control subjects by means of ToM tests (recognizing himself in mirrors, false belief, first and second order ToM tasks), as well as tests of other cognitive functions (counter-proofs).Patients and controls performed similarly in ToM tests. There was significant difference between frontal subgroups (left, right, bifrontal) in the double-bluff task (second order ToM) (p=0.021), without relation to verbal fluency (p=0.302) or delayed recall ability (p=0.159). The only two patients with deficits in ToM tasks had impairment of social behavior.Frontal lesions do not necessarily implicate in ToM deficits, which may occur when such lesions are associated to disturbance of social behavior.

Impaired social interaction and reduced anxiety-related behavior in vasopressin V1a receptor knockout mice

The arginine vasopressin (AVP) system plays an important role in social behavior. Autism, with its hallmark disturbances in social behavior, has been associated with the V1a receptor (V1aR) gene. Furthermore, impairments of social function are often observed in symptoms of schizophrenia. Subchronic phencyclidine (PCP) produces behaviors relating to certain aspects of schizophrenic symptoms such as impairing social interaction in animals and it reduces the density of V1aR binding sites in several brain regions. Here, we report that V1aR knockout (KO) mice exhibited impairment of social behavior in a social interaction test, and showed reduced anxiety-related behavior in elevated plus-maze and marble-burying behavior tests. Given the current findings, the V1aR may be involved in the regulation of social interaction, and V1aR KO mice could be used as an animal model of psychiatric disorders associated with social behavior deficits, such as autism and schizophrenia.

Theory of mind and the frontal lobes

Theory of mind (ToM) is the ability to attribute mental states to other individuals. Its cerebral organization is not enough established, even though the literature suggests the relevant role of the frontal lobes. To evaluate frontal lobe patients and controls in ToM tests. We studied 20 patients with lesions limited to the frontal lobes (as shown by CT or MRI), and 10 normal control subjects by means of ToM tests (recognizing himself in mirrors, false belief, first and second order ToM tasks), as well as tests of other cognitive functions (counter-proofs). Patients and controls performed similarly in ToM tests. There was significant difference between frontal subgroups (left, right, bifrontal) in the double-bluff task (second order ToM) (p=0.021), without relation to verbal fluency (p=0.302) or delayed recall ability (p=0.159). The only two patients with deficits in ToM tasks had impairment of social behavior. Frontal lesions do not necessarily implicate in ToM deficits, which may occur when such lesions are associated to disturbance of social behavior.