Dysfunctional schema modes as determinants of psychiatric comorbidities: a study in a cohort of people with epilepsy.

INTRODUCTION AND AIMS: Symptomatology of epilepsy and its' associated alteration in brain processes, stigma of experiencing seizures, and adverse sequelae of anti-epileptics have been demonstrated to impact behaviour and exacerbate psychopathology. This study examines the role of dysfunctional schema modes in People with Epilepsy (PWE) and their association with psychiatric symptoms. METHODS: Semi-structured interviews were conducted with 108 PWE treated with anti-epileptics for at least one year and with no history or mental disorder or psycho-active substance use. Clinical symptoms were measured utilising the Symptom Checklist-90 (SCL-90) with schema modes measured utilising the Schema Mode Inventory (SMI). RESULTS: Maladaptive coping and child schema modes were significantly higher in individuals from lower socio-economic status group (p < 0.01), with several maladaptive schema modes more prevalent in males. Hostility symptoms were increased in individuals from lower socio-economic classes and were more prevalent early in disease course. Several psychological symptoms including somatisation, interpersonal, obsession, depression, paranoia, hostility, phobia, anxiety, and psychoticism, were predicted by various maladaptive schema modes (p < 0.001). CONCLUSION: This study highlights the impact of maladaptive schemas, suggesting that PWE might benefit from the introduction of appropriate psychotherapeutic interventions such as schema-focused therapy, particularly if from lower socio-economic classes or in the early stages of theirdisease course.

Suppression of nuclear factor kappa B ameliorates astrogliosis but not amyloid burden in APPswe/PS1dE9 mice.

Neuroinflammation has been linked to the pathologies of Alzheimer's disease (AD), however, its effects on beta-amyloid (Abeta) burden are unclear. This study investigated the role of nuclear factor kappa B (NF-kappaB) in regulating neuroinflammation and Abeta deposition in a transgenic mouse model of AD. The APPswe/PS1dE9 mice and their wild-type controls received either the NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC, i.p. 50 mg/kg daily) or saline starting at 7 months of age for 5 months. Expression of cyclooxygenase-2 (COX-2), tissue necrosis factor alpha (TNFalpha) precursor protein and microtubule-associated protein 2 was determined, and astrogliosis was assessed. Hippocampal and cortical levels of Abeta(1-40) and Abeta(1-42) were measured using ELISA. PDTC treatment effectively suppressed NF-kappaB signaling in APPswe/PS1dE9 mice as evidenced by the abolishment of COX-2 and TNFalpha induction. Inhibition of NF-kappaB further attenuated astrogliosis in the transgenic AD mice, yet markedly increased cerebral Abeta(1-42) burden. Our findings suggest that NF-kappaB can mediate induction of COX-2, TNFalpha and astrogliosis in APPswe/PS1dE9 mice. Additionally, these results support the idea that neuroinflammation contributes to the clearance of Abeta.

A multidimensional scaling analysis of vowel discrimination in humans and monkeys.

Multidimensional scaling (MDS) was used to compare perceptual maps for 10 synthetic English vowels in humans and Old World monkeys (Macaca fuscata and Cercopithecus albogularis). Subjects discriminated among the vowels using a repeating background procedure, and reaction times were submitted to an MDS analysis to derive measures of perceive similarity. The dimensions that emerged related to the frequencies of the first (F1), second (F2), and third (F3) formants. Human data indicated a good match to previous MDS studies using rating procedures or confusion matrices: The dominant dimension mapped onto vowel F2, the phonetically most important formant, and the second and third dimensions mapped onto F1 and F3, respectively. For monkeys, equal weightings occurred for F1 and F2, and F3 was not clearly represented. Monkey sensitivity to the formants appeared to relate to formant amplitudes. If monkeys are giving an accurate representation of the psychoacoustic relations among the formants, then our human results suggest that species-specific mechanisms, reflecting the salience of the phonetic feature of advancement, may contribute to vowel coding in humans.