Personality profile of male adolescents with Tourette syndrome:a controlled study

Tourette syndrome is a neurodevelopmental disorder characterized by multiple tics and commonly associated with behavioral problems, especially obsessive-compulsive disorder and attention-deficit hyperactivity disorder (ADHD). The presence of specific personality traits has been documented in adult clinical populations with Tourette syndrome but has been underresearched in younger patients. We assessed the personality profiles of 17 male adolescents with Tourette syndrome and 51 age- and gender-matched healthy controls using the Minnesota Multiphasic Personality Inventory-Adolescent version, along with a standardized psychometric battery. All participants scored within the normal range across all Minnesota Multiphasic Personality Inventory-Adolescent version scales. Patients with Tourette syndrome scored significantly higher than healthy controls on the Obsessiveness Content Scale only (P = .046). Our findings indicate that younger male patients with Tourette syndrome do not report abnormal personality traits and have similar personality profiles to healthy peers, with the exception of obsessionality traits, which are likely to be related to the presence of comorbid obsessive compulsive symptoms rather than tics.

Differential moderating effect of locus of control on effect of driving experience in young male and female drivers

Investigations of relationships between the specific personality variable, locus of control (LOC, Rotter, 1966) and driver behaviour or accidents have returned contrasting results. Review suggests dependence on gender or experience characteristics of participants, suggesting these factors interact with LOC to influence driving. Relationships were investigated in terms of influence on the eight driving styles of the Multidimensional Driving Style Inventory (MDSI, Taubman-Ben-Ari, Mikulincer & Gillarth, 2004) in young drivers (18-29 years). Gender and LOC differences in driving styles previously related to accidents were proposed. It was also proposed that driving experience influences driving style, and LOC influences effect of driving experience. Gender differences were found for dissociative, anxious, patient, risky, angry and high velocity styles. Women had more external LOC than men, and driver stress styles increased with more external LOC, but reduced with increased driving experience, but so did patient style. High velocity style increased with experience. Controlling for LOC revealed important gender differences in effect of experience: positive effects for men (reducing angry and high velocity, increasing carefulness) and negative effects for women (increasing angry and higher velocity, reducing carefulness). Findings suggest negative influence of high internal LOC on young men in terms of its interaction with experience.

Childhood auditory processing disorder as a developmental disorder:the case for a multi-professional approach to diagnosis and management

Auditory processing disorder (APD) is diagnosed when a patient presents with listening difficulties which can not be explained by a peripheral hearing impairment or higher-order cognitive or language problems. This review explores the association between auditory processing disorder (APD) and other specific developmental disorders such as dyslexia and attention-deficit hyperactivity disorder. The diagnosis and aetiology of APD are similar to those of other developmental disorders and it is well established that APD often co-occurs with impairments of language, literacy, and attention. The genetic and neurological causes of APD are poorly understood, but developmental and behavioural genetic research with other disorders suggests that clinicians should expect APD to co-occur with other symptoms frequently. The clinical implications of co-occurring symptoms of other developmental disorders are considered and the review concludes that a multi-professional approach to the diagnosis and management of APD, involving speech and language therapy and psychology as well as audiology, is essential to ensure that children have access to the most appropriate range of support and interventions.

Nonprofit leaders and for-profit entrepreneurs:similar people with different motivation

Today's market conditions require nonprofit leaders to act in an increasingly business-like fashion. This study asks whether NPO leaders have a similar disposition to act entrepreneurially as for-profit entrepreneurs, but hold different underlying motives. For this purpose, the study contrasts a sample of 72 leaders of nonprofit organizations with 117 entrepreneurs on their personality traits and explicit motives using standard personality tests and interviews. Both groups exhibit similar general and entrepreneurship-specific personality traits but differ significantly regarding their motivation. While nonprofit leaders' motivation stems primarily from the meaningfulness of their work; entrepreneurs are mainly motivated by the independence as well as by the income and profit provided by their work. This paper helps us understand who leaders of nonprofit organizations are.

Brand personality perception - regional or country specific

Brand personality is a key determinant of brand equity. Consumers seek brands with congruent personalities and use brands’ personality to define their sense of self. However, far from being universal, previous researches found that European (Spanish) brand personality dimensions differ from those in America and Asia (Japan). Are these typical of the region or do they reflect national variations? This study examines brand personality dimensions among Chinese consumers with consumers responding to 10 different commercial brands. This shows perceptions of brand personality are country specific, due to the differences found between Japanese’ and Chinese’. Implications of these findings are discussed.

Impaired sustained attention and executive dysfunction:bipolar disorder versus depression-specific markers of affective disorders

Objective - To identify neurocognitive measures that could be used as objective markers of bipolar disorder. Methods - We examined executive function, sustained attention and short-term memory as neurocognitive domains in 18 participants with bipolar disorder in euthymic state (Beuth), 14 in depressed state (Bdep), 20 with unipolar depression (Udep) and 28 healthy control participants (HC). We conducted four-group comparisons followed by relevant post hoc analyses. Results - Udep and Bdep, but not Beuth showed impaired executive function (p = 0.045 and p = 0.046, respectively). Both Bdep and Beuth, but not Udep, showed impaired sustained attention (p = 0.001 and p = 0.045, respectively). The four groups did not differ significantly on short-term memory. Impaired sustained attention and executive dysfunction were not associated with depression severity, duration of illness and age of illness onset. Only a small number of abnormal neurocognitive measures were associated with medication in Bdep and Beuth. Conclusion - Impaired sustained attention appears specific to bipolar disorder and present in both Beuth and Bdep; it may represent an objective marker of bipolar disorder. Executive dysfunction by contrast, appears to be present in Udep and Bdep and likely represents a marker of depression.

Overlap between neurodegenerative disorders

Neurodegenerative disorders are characterized by the formation of distinct pathological changes in the brain, including extracellular protein deposits, cellular inclusions, and changes in cell morphology. Since the earliest published descriptions of these disorders, diagnosis has been based on clinicopathological features, namely, the coexistence of a specific clinical profile together with the presence or absence of particular types of lesion. In addition, the molecular profile of lesions has become an increasingly important feature both in the diagnosis of existing disorders and in the description of new disease entities. Recent studies, however, have reported considerable overlap between the clinicopathological features of many disorders leading to difficulties in the diagnosis of individual cases and to calls for a new classification of neurodegenerative disease. This article discusses: (i) the nature and degree of the overlap between different neurodegenerative disorders and includes a discussion of Alzheimer's disease, dementia with Lewy bodies, the fronto-temporal dementias, and prion disease; (ii) the factors that contribute to disease overlap, including historical factors, the presence of disease heterogeneity, age-related changes, the problem of apolipoprotein genotype, and the co-occurrence of common diseases; and (iii) whether the current nosological status of disorders should be reconsidered.

Tetrahydrobiopterin metabolism in mental disorders

Changes in DHPR activity in those aged 12 and under with a variety of mental disorders were investigated using dried blood spots on Guthrie cards. DHPR activity was found to be lowered in autism and Rett's syndrome. DHPR activity was unaffected in non specific mental retardation suggesting that the deficit seen in autism and Rett's syndrome does not arise secondary to the mental dysfunction. In Down's syndrome blood biopterin levels correlated with blood spot DHPR activity. Human brain BH4 synthetic activity was investigated in aging and senile dementia of the Alzheimer type (SDAT). BH4 synthetic activity and DHPR activity decline with age in non-demented controls. In SDAT, decreases in BH4 synthetic activity were seen in temporal and visual cortices and locus coeruleus. The site of the defect is probably at 6-pyruvoyl-tetrahydropterin synthase. Aluminium inhibits human brain BH4 synthesis in vitro and produces an `Alzheimeresque' pattern of abnormalities in rats chronically exposed to the acetate salt in drinking water. Aluminium appears to chiefly affect enzymes requiring a metal ion cofactor. Aluminium induced inhibition of BH4 synthesis can be reversed by treatment with transferrin, an aluminium chelator. Transferrin treatment improves BH4 synthetic activity in SDAT brains whilst having no effect on controls, further implicating aluminium as the key neurotoxin in SDAT. Lithium inhibits human brain BH4 synthesis in vitro and lowers rat brain total biopterins and inhibits rat brain BH4 synthesis on chronic exposure to the carbonate salt in drinking water. A possible mechanism for the anti-manic actions of lithium is suggested. Monoamine oxidase inhibitors decrease human brain BH4 synthetic activity in vitro. 5-methyl-tetrahydrofolate had no effect on human brain BH4 synthesis in vitro but methionine increased BH4 synthesis in vitro. Oxotremorine is a potent inhibitor of BH4 synthesis in man and the rat. This may prove useful as a tool for modelling BH4 deficiency.

Automated assessment of visual fields and their inter-relation to evoked potentials in visual disorders

The Octopus Automated Perimeter was validated in a comparative study and found to offer many advantages in the assessment of the visual field. The visual evoked potential was investigated in an extensive study using a variety of stimulus parameters to simulate hemianopia and central visual field defects. The scalp topography was recorded topographically and a technique to compute the source derivation of the scalp potential was developed. This enabled clarification of the expected scalp distribution to half field stimulation using different electrode montages. The visual evoked potential following full field stimulation was found to be asymmetrical around the midline with a bias over the left occiput particularly when the foveal polar projections of the occipital cortex were preferentially stimulated. The half field response reflected the distribution asymmetry. Masking of the central 3° resulted in a response which was approximately symmetrical around the midline but there was no evidence of the PNP-complex. A method for visual field quantification was developed based on the neural representation of visual space (Drasdo and Peaston 1982) in an attempt to relate visual field depravation with the resultant visual evoked potentials. There was no form of simple, diffuse summation between the scalp potential and the cortical generators. It was, however, possible to quantify the degree of scalp potential attenuation for M-scaled full field stimuli. The results obtained from patients exhibiting pre-chiasmal lesions suggested that the PNP-complex is not scotomatous in nature but confirmed that it is most likely to be related to specific diseases (Harding and Crews 1982). There was a strong correlation between the percentage information loss of the visual field and the diagnostic value of the visual evoked potential in patients exhibiting chiasmal lesions.

Different molecular pathologies result in similar spatial patterns of cellular inclusions in neurodegenerative disease:a comparative study of eight disorders

Recent research suggests cell-to-cell transfer of pathogenic proteins such as tau and α-synuclein may play a role in neurodegeneration. Pathogenic spread along neural pathways may give rise to specific spatial patterns of the neuronal cytoplasmic inclusions (NCI) characteristic of these disorders. Hence, the spatial patterns of NCI were compared in four tauopathies, viz., Alzheimer's disease, Pick's disease, corticobasal degeneration, and progressive supranuclear palsy, two synucleinopathies, viz., dementia with Lewy bodies and multiple system atrophy, the 'fused in sarcoma' (FUS)-immunoreactive inclusions in neuronal intermediate filament inclusion disease, and the transactive response DNA-binding protein (TDP-43)-immunoreactive inclusions in frontotemporal lobar degeneration, a TDP-43 proteinopathy (FTLD-TDP). Regardless of molecular group or morphology, NCI were most frequently aggregated into clusters, the clusters being regularly distributed parallel to the pia mater. In a significant proportion of regions, the regularly distributed clusters were in the size range 400-800 μm, approximating to the dimension of cell columns associated with the cortico-cortical pathways. The data suggest that cortical NCI in different disorders exhibit a similar spatial pattern in the cortex consistent with pathogenic spread along anatomical pathways. Hence, treatments designed to protect the cortex from neurodegeneration may be applicable across several different disorders. © 2012 Springer-Verlag.

The influence of emotional intensity on facial emotion recognition in disordered eating

Significant facial emotion recognition (FER) deficits have been observed in participants exhibiting high levels of eating psychopathology. The current study aimed to determine if the pattern of FER deficits is influenced by intensity of facial emotion and to establish if eating psychopathology is associated with a specific pattern of emotion recognition errors that is independent of other psychopathological or personality factors. Eighty females, 40 high and 40 low scorers on the Eating Disorders Inventory (EDI) were presented with a series of faces, each featuring one of five emotional expressions at one of four intensities, and were asked to identify the emotion portrayed. Results revealed that, in comparison to Low EDI scorers, high scorers correctly recognised significantly fewer expressions, particularly of fear and anger. There was also a trend for this deficit to be more evident for subtle displays of emotion (50% intensity). Deficits in anger recognition were related specifically to scores on the body dissatisfaction subscale of the EDI. Error analyses revealed that, in comparison to Low EDI scorers, high scorers made significantly more and fear-as-anger errors. Also, a tendency to label anger expressions as sadness was related to body dissatisfaction. Current findings confirm FER deficits in subclinical eating psychopathology and extend these findings to subtle expressions of emotion. Furthermore, this is the first study to establish that these deficits are related to a specific pattern of recognition errors. Impaired FER could disrupt normal social functioning and might represent a risk factor for the development of more severe psychopathology.

An overview of psychological and neurobiological mechanisms by which early negative experiences increase risk of mood disorders

Objective: Early life experiences are associated with severe and long-lasting effects on behavioural and emotional functioning, which in turn are thought to increase the risk for unipolar depression and other disorders of affect regulation. The neurobiological and psychological mechanisms through which adverse early life experiences confer risk are poorly understood. Method: Alterations in brain structure and function in limbic and prefrontal cortical regions have been linked to early negative experiences and to mood disorders. Results: There are a number of psychological domains that may be dysfunctional in people with mood disorders, and which, if the dysfunction occurs prior to onset of mood symptoms, may signify a risk factor for depression. Cognitive dysfunction has been examined in patients with mood disorders, with some suggestion that changes in cognitive function may antedate the onset of mood symptoms, and may be exacerbated in those who experienced early negative trauma. Social cognition, including emotion comprehension, theory of mind and empathy, represent under-studied domains of psychological function that may be negatively influenced by early adverse experience. Temperament and personality factors may also leave people vulnerable to mood instability. Conclusion: This review summarizes the evidence for dysfunction in each of these domains for people with mood disorders.

Familial and disease specific abnormalities in the neural correlates of the Stroop Task in Bipolar Disorder

Patients with Bipolar Disorder (BD) perform poorly on tasks of selective attention and inhibitory control. Although similar behavioural deficits have been noted in their relatives, it is yet unclear whether they reflect dysfunction in the same neural circuits. We used functional magnetic resonance imaging and the Stroop Colour Word Task to compare task related neural activity between 39 euthymic BD patients, 39 of their first-degree relatives (25 with no Axis I disorders and 14 with Major Depressive Disorder) and 48 healthy controls. Compared to controls, all individuals with familial predisposition to BD, irrespective of diagnosis, showed similar reductions in neural responsiveness in regions involved in selective attention within the posterior and inferior parietal lobules. In contrast, hypoactivation within fronto-striatal regions, implicated in inhibitory control, was observed only in BD patients and MDD relatives. Although striatal deficits were comparable between BD patients and their MDD relatives, right ventrolateral prefrontal dysfunction was uniquely associated with BD. Our findings suggest that while reduced parietal engagement relates to genetic risk, fronto-striatal dysfunction reflects processes underpinning disease expression for mood disorders. © 2011 Elsevier Inc.

Increased prevalence of sex chromosome aneuploidies in specific language impairment and dyslexia

Aim: Sex chromosome aneuploidies increase the risk of spoken or written language disorders but individuals with specific language impairment (SLI) or dyslexia do not routinely undergo cytogenetic analysis. We assess the frequency of sex chromosome aneuploidies in individuals with language impairment or dyslexia. Method: Genome-wide single nucleotide polymorphism genotyping was performed in three sample sets: a clinical cohort of individuals with speech and language deficits (87 probands: 61 males, 26 females; age range 4 to 23 years), a replication cohort of individuals with SLI, from both clinical and epidemiological samples (209 probands: 139 males, 70 females; age range 4 to 17 years), and a set of individuals with dyslexia (314 probands: 224 males, 90 females; age range 7 to 18 years). Results: In the clinical language-impaired cohort, three abnormal karyotypic results were identified in probands (proband yield 3.4%). In the SLI replication cohort, six abnormalities were identified providing a consistent proband yield (2.9%). In the sample of individuals with dyslexia, two sex chromosome aneuploidies were found giving a lower proband yield of 0.6%. In total, two XYY, four XXY (Klinefelter syndrome), three XXX, one XO (Turner syndrome), and one unresolved karyotype were identified. Interpretation: The frequency of sex chromosome aneuploidies within each of the three cohorts was increased over the expected population frequency (approximately 0.25%) suggesting that genetic testing may prove worthwhile for individuals with language and literacy problems and normal non-verbal IQ. Early detection of these aneuploidies can provide information and direct the appropriate management for individuals. © 2013 The Authors. Developmental Medicine & Child Neurology published by John Wiley & Sons Ltd on behalf of Mac Keith Press.

Emotion recognition and alexithymia in females with non-clinical disordered eating

Objectives: The aims were to determine if emotion recognition deficits observed in eating disorders generalise to non-clinical disordered eating and to establish if other psychopathological and personality factors contributed to, or accounted for, these deficits. Design: Females with high (n=23) and low (n=22) scores on the Eating Disorder Inventory (EDI) were assessed on their ability to recognise emotion from videotaped social interactions. Participants also completed a face memory task, a Stroop task, and self-report measures of alexithymia, depression and anxiety. Results: Relative to the low EDI group, high EDI participants exhibited a general deficit in recognition of emotion, which was related to their scores on the alexithymia measure and the bulimia subscale of the EDI. They also exhibited a specific deficit in the recognition of anger, which was related to their scores on the body dissatisfaction subscale of the EDI. Conclusions: In line with clinical eating disorders, non-clinical disordered eating is associated with emotion recognition deficits. However, the nature of these deficits appears to be dependent upon the type of eating psychopathology and the degree of co-morbid alexithymia.