Biomedical subjects

C Mehler-Wex

Publications and source records attributed to C Mehler-Wex.

7 recordsLinked to original sources

PubMed2006

Weight gain associated with clozapine, olanzapine and risperidone in children and adolescents.

The study was aimed at the evaluation of weight gain associated with atypical antipsychotics and its clinical risk factors in children and adolescents. Weight and body mass index (BMI) of initially hospitalised patients treated with clozapine (n = 15), olanzapine (n = 15), and risperidone (n = 15) were prospectively monitored on a weekly basis for the first 6 weeks. Different clinical risk factors were tested for their association with weight gain in the three groups. All three groups experienced significant weight gain between baseline and endpoint (p < 0.0001). For all weight measures, planned comparisons were all significant between olanzapine vs. clozapine and risperidone, respectively. Average weight gain was significantly higher for the olanzapine group (mean = 4.6 kg, SD = 1.9) than for the risperidone (mean = 2.8 kg, SD = 1.3) and clozapine (mean = 2.5 kg, SD = 2.9) groups. Olanzapine and risperidone, but not clozapine, caused a disproportionately higher weight gain in children and adolescents in comparison to adults.

Adolescent↗

PubMed2006

[Dysmorphophobia].

In the ICD-10 classification, the body dysmorphophobic (dysmorphic) disorder is subsumed under the code for somatoform or hypochondriacal disorders (F45.2). To the fore is an excessive preoccupation with an imagined, but not objectifiable, bodily defect, usually affecting a part of the body that is either exposed or considered to be of importance for the patient's attractiveness. In many cases, the patient insistently demands surgical correction. During the further course of the condition, depression, social phobia, obsessive-compulsive and self-destructive behavior may develop. The condition usually begins early in the patient's life, and the lifetime prevalence is estimated to be 5%. Since an involvement of the serotonergic system is assumed, selective serotonin reuptake inhibitors are considered to be the medication of first choice. Surgical interventions do not lead to remission but simply to a transference of symptoms. Referral to a psychiatric specialist with the aim of clarifying the diagnosis is indicated.

Adolescent↗

PubMed2006

Microarray analysis reveals distinct gene expression patterns in the mouse cortex following chronic neuroleptic and stimulant treatment: implications for body weight changes.

Atypical neuroleptics are associated with clinical significant weight gain, whereas stimulants are used as anorexiant drugs. The aim of this study was to examine gene expression changes in the mouse frontal cortex following chronic oral treatment with antipsychotics and a stimulant by microarray assessments. Twenty 10-12-week-old male C57BL6 mice received daily for 31 days either the typical neuroleptic haloperidol (1 mg/kg), the atypical neuroleptic clozapine (10 mg/kg) or the stimulant phenylpropanolamine (3 mg/kg). We identified a set of genes that was differently expressed between the neuroleptic-treated groups and the stimulant-treated group. Importantly, we found in the majority of gene alterations down-regulation in genes involved in ATP biosynthesis and lipid metabolism following the stimulant treatment, suggesting these genes as candidates that may regulate body weight. We also identified remarkable expression patterns of genes that encode signalling molecules (e.g. insulin, mitochondrial uncoupling protein 1) that are implicated in the control of food intake and are differently expressed in the neuroleptic groups.

Animals↗

PubMed2006

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: implications for the pathophysiology of Parkinson's disease, schizophrenia and attention deficit hyperactivity disorder.

The basal ganglia form a forebrain system that collects signals from a large part of the neocortex, redistributes these cortical inputs both with respect to one another and with respect to inputs from the limbic system, and then focuses the inputs of this redistributed, integrated signals into particular regions of the frontal lobes and brainstem involved in aspects of motor planning and motor memory. Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorder (from which Parkinson's disease, PD, is the best-known-example) at one extreme to the hyperkinetic disorder (exemplified by Huntington's disease and hemiballism) at the other. In addition to disorders of movement, major mental disorders including schizophrenic-like states and attention deficit hyperactivity disorder (ADHD) have been linked to abnormalities in the basal ganglia and their allied nuclei. In this paper we discuss recent evidence indicating that a dopamine-induced dysbalance of basal ganglia neurocircuitries may be an important pathophysiological component in PD, schizophrenia and ADHD. According to our model, the deprivation of dopaminergic nigro-striatal input, as in PD, reduces the positive feedback via the direct system, and increases the negative feedback via the indirect system. The critical consequences are an overactivity of the basal ganglia output sites with the resulting inhibition of thalamo-cortical drive. In schizophrenia the serious cognitive deficits might be partly a result of a hyperactivity of the inhibitory dopamine D(2) transmission system. Through this dysinhibition, the thalamus exhibits hyperactivity that overstimulates the cortex resulting in dysfunctions of perception, attention, stimulus distinction, information processing and affective regulation (inducing hallucinations and delusions) and motor disabilities. Recent studies have strongly suggested that a disturbance of the dopaminergic system is also involved in the pathophysiology of ADHD. The most convincing evidence comes from the demonstration of the efficacy of psychostimulants such as the dopamine transporter (DAT) blocker methylphenidate in the symptomatic treatment of ADHD. Genetic studies have shown an association between ADHD and genes involved in dopaminergic neurotransmission (for example the dopamine receptor genes DRD4 and DRD5, and the DAT gene DAT1). DAT knockout mice display a phenotype with increased locomotor activity, which is normalized by psychostimulant treatment. Finally, imaging studies demonstrated an increased density of DAT in the striatum of ADHD patients. Which system is disturbed and whether this system is hyper- or hypoactive is not unambiguously known yet.

Antipsychotic Agents↗

PubMed2003

[Pharmacotherapy of compulsive disorders in childhood and adolescence].

OBJECTIVES: The review addresses the issue of the extent to which pharmacological treatment of obsessive-compulsive disorders (OCD) in childhood and adolescence is based on empirical studies. METHODS: Current literature is evaluated, including studies of adult cohorts if these contain approaches relevant for the pharmacological treatment of children and adolescents. RESULTS: The number of qualified empirical studies is few. These studies have shown clomipramine and serotonin-reuptake inhibitors to be very effective in the therapy of obsessive-compulsive disorders in childhood and adolescence. On the basis of the studies available, no specific recommendation can be made with regard to pharmacological dosage. For clomipramine the effective daily dose probably ranges somewhere between 75-150 mg, for fluoxetin between 20-60 mg, and for fluvoxamine between 100-250 mg. However, it must be kept in mind that in individual cases, improvement sometimes will not be noticeable until after 8 to 10 weeks of treatment have elapsed. CONCLUSION: Clomipramine and serotonin-reuptake inhibitors are effective in the treatment of obsessive-compulsive disorders in children and adolescents. There is an urgent need for therapy studies of obsessive-compulsive disorders in childhood and adolescence. Placebo-controlled studies of pharmacological treatment, controlled studies of psychotherapeutic treatment, and comparative studies of pharmacological and psychotherapeutic approaches are necessary.

Adolescent↗

PubMed2002

[Children in the drive for thinness. How early anorexia nervosa modifies development].

In adolescents and young women, the prevalence of anorexia nervosa is 0.5-1%. Approximately 5% of all anorectics are younger than 12 years of age. Frequent psychiatric concomitant conditions that develop during the long-term course are depression or dysthymia (in our own patient material approximately 14%) and anxiety (some 28%). In our own studies, healing success was achieved in 54% of the cases; 18% achieved partial remission with remnant symptoms of an unspecific eating disorder, and 28% continued to exhibit anorectic and/or bulimic symptoms. Of prognostic importance were eating disorders in the child's first year and the duration of the catamnesis. The prognosis of anorexia nervosa with onset in childhood does not appear to differ significantly from that of anorexia with onset in adolescence or adulthood.

Adolescent↗

PubMed2001

A study of cranial computer tomograms in very early and early onset schizophrenia.

The cranial computer-assisted tomograms of 19 patients suffering from schizophrenic psychoses with onset by age of 14 were examined. The emphasis was on the extent of the inner liquor spaces. Compared to healthy controls, at the beginning of illness a significant enlargement was revealed only in the patient group with very early onset schizophrenia (VEOS, onset prior to the age of 12), whereas children with early onset (EOS, 12 to 14 years of age) showed no significant brain pathology. As a second result, an increase in the extent of the inner liquor spaces seems to correlate with the duration of illness. It is therefore concluded that psychoses interfere with neurodevelopmental processes and cause more severe brain pathology in very young children, already detectable at the onset of the illness. EOS, on the other hand, induces progressive morphological abnormalities over the course of the illness.

Adolescent↗