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Psychiatry AND Tardive dyskinesia [keywords]
- Difficult morning awakening from rapid eye movement sleep and impaired cognitive function in delayed sleep phase disorder patients. [JOURNAL ARTICLE]
- Sleep Med 2014 Jul 3.
Difficult awakening is a key symptom of delayed sleep phase disorder (DSPD), but no studies have quantified awakening thresholds in a sleep laboratory. This study assessed whether cognitive function was impaired after awakening and whether difficult awakening was associated with specific polysomnographic features such as slow wave sleep stage N3.Nine patients with DSPD and nine sex- and age-matched healthy controls were included. Polysomnography was performed at our university hospital from midnight. An alarm clock was activated at 07:00 with sound intensity increasing from 72 to 104 dB. Participants performed a continuous performance test (CPT) the previous afternoon and immediately upon awakening.Three DSPD patients and zero controls did not wake up to the maximum 104 dB alarm sound; all three patients were in rapid eye movement (REM) sleep when the alarm clock went off (difference in proportions, P = 0.047). In patients, CPT reaction time was prolonged in the morning compared to the afternoon [analysis of variance (ANOVA) interaction, P = 0.01]. DSPD patients made more omission errors than controls regardless of time of the day (ANOVA main effect, P = 0.046).Difficult awakening from slow wave sleep was not observed. A subgroup of DSPD patients may have a severe problem waking up from REM sleep. DSPD patients may also have a state-like impairment in cognitive function in the morning and a trait-like impairment not depending on time of day, compared to normal sleepers.
- Association of altered CuZn superoxide dismutase and cognitive impairment in schizophrenia patients with tardive dyskinesia. [JOURNAL ARTICLE]
- J Psychiatr Res 2014 Aug 8.
Free radical-mediated abnormalities may contribute to the development of tardive dyskinesia (TD) and specific aspects of schizophrenia symptomatology such as cognitive deficits. Superoxide dismutase (SOD), a critical enzyme in the detoxification of superoxide radicals, was found to be abnormal in TD. While most of previous studies focused on the manganese isoform located in mitochondria, this study investigated the activities of isoform CuZnSOD present in the plasma. We recruited 113 male chronic patients with TD (n = 43) and without TD (n = 70) meeting DSM-IV criteria for schizophrenia, and 84 male control subjects. We examined the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), CuZnSOD activity for both the patient and control groups along with total antioxidant status (TAS) and malondialdehyde (MDA) levels in a subset of the cohort. Positive and Negative Symptom Scale (PANSS) and the Abnormal Involuntary Movement Scale (AIMS) were assessed in the patient group. Our results showed lower CuZnSOD activity and TAS levels, but higher MDA levels in patients with TD than those without TD (all p < 0.05). Patients with TD had lower RBANS subscales of Visuospatial/Constructional (p < 0.05) and attention (p < 0.01) than those without TD. Multiple regression analysis showed that in either TD or non-TD group, CuZnSOD was an independent contributor to the attention index of RBANS (both p < 0.05). These results implicated that TD patients suffered greater oxidative stress and cognitive dysfunction than non-TD patients. Oxidative stress could contribute to both TD development and cognitive impairment.
- Genetics of Obsessive-Compulsive Disorder and Related Disorders. [REVIEW]
- Psychiatr Clin North Am 2014 Sep; 37(3):319-335.
Twin and family studies support a significant genetic contribution to obsessive-compulsive disorder (OCD) and related disorders, such as chronic tic disorders, trichotillomania, skin-picking disorder, body dysmorphic disorder, and hoarding disorder. Recently, population-based studies and novel laboratory-based methods have confirmed substantial heritability in OCD. Genome-wide association studies and candidate gene association studies have provided information on specific gene variations that may be involved in the pathobiology of OCD, though a substantial portion of the genetic risk architecture remains unknown.
- Neurological abnormalities in recent-onset schizophrenia and asperger-syndrome. [Journal Article]
- Front Psychiatry 2014.:91.
Neurological abnormalities including a variety of subtle deficits such as discrete impairments in sensory integration, motor coordination (MOCO), and sequencing of complex motor acts are frequently found in patients with schizophrenia (SZ) and commonly referred to as neurological soft signs (NSS). Asperger-syndrome (AS) is characterized by sensory-motor difficulties as well. However, the question whether the two disorders share a common or a disease-specific pattern of NSS remains unresolved.A total of 78 age- and education-matched participants [26 patients with recent-onset SZ, 26 individuals with AS, and 26 healthy controls (HC)] were recruited for the study. Analyses of covariance (ANCOVAs), with age, years of education, and medication included as covariates, were used to examine group differences on total NSS and the five subscale scores. Discriminant analyses were employed to identify the NSS subscales that maximally discriminate between the three groups.Significant differences among the three groups were found in NSS total score and on the five NSS subscales. The clinical groups differed significantly in the NSS subscale MOCO. The correct discriminant rate between patients with SZ and individuals with AS was 61.5%. The correct discriminant rate was 92.3% between individuals with AS and HC, and 80.8% between SZ patients and HC, respectively.Our findings provide new evidence for the presence of NSS in AS and lend further support to previously reported difficulties in movement control in this disorder. According to the present results, SZ and AS seem to be characterized by both quantitative and qualitative NSS expression.
- Suppression of antipsychotic-induced tardive dyskinesia with aripiprazole in an elderly patient with bipolar I disorder. [Journal Article]
- Acta Neuropsychiatr 2014 Feb; 26(1):61-4.
Introduction Aripiprazole has a low risk for causing extrapyramidal syndrome and can remit neuroleptic-induced tardive dyskinesia (TD). Here, we presented a case in which TD was suppressed, but not cured, by long-term aripiprazole treatment. Case This 74-year-old male patient had bipolar I disorder and had developed TD many times after several antipsychotic treatments. The lowest chlorpromazine dose equivalent among the previous antipsychotic treatments was 25 mg/day of quetiapine. His TD always improved immediately after the dosage was shifted to aripiprazole. However, his insomnia or other psychiatric symptoms worsened the first three times when the treatment was shifted to aripiprazole, making the transition a failure. Before the fourth attempt of aripiprazole transition, the patient was in a euthymic state but again developed TD under olanzapine 10 mg/day treatment. During the fourth attempt of aripiprazole transition, his TD had remained in complete remission for more than 1 year after the dosage shifted to 10 mg/day of aripiprazole. He developed TD again when we tapered the aripiprazole dose to 5 mg/day, but his TD remitted when we restored his aripiprazole dose to 10 mg/day.Aripiprazole could be an effective drug in elderly bipolar patients with antipsychotic-induced TD while the patients are in a euthymic state. However, aripiprazole may only suppress TD rather than cure it.
- The cognitive neuropsychological phenotype of carriers of the FMR1 premutation. [Journal Article, Review]
- J Neurodev Disord 2014; 6(1):28.
The fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder affecting a subset of carriers of the FMR1 (fragile X mental retardation 1) premutation. Penetrance and expression appear to be significantly higher in males than females. Although the most obvious aspect of the phenotype is the movement disorder that gives FXTAS its name, the disorder is also accompanied by progressive cognitive impairment. In this review, we address the cognitive neuropsychological and neurophysiological phenotype for males and females with FXTAS, and for male and female unaffected carriers. Despite differences in penetrance and expression, the cognitive features of the disorder appear similar for both genders, with impairment of executive functioning, working memory, and information processing the most prominent. Deficits in these functional systems may be largely responsible for impairment on other measures, including tests of general intelligence and declarative learning. FXTAS is to a large extent a white matter disease, and the cognitive phenotypes observed are consistent with what some have described as white matter dementia, in contrast to the impaired cortical functioning more characteristic of Alzheimer's disease and related disorders. Although some degree of impaired executive functioning appears to be ubiquitous among persons with FXTAS, the data suggest that only a subset of unaffected carriers of the premutation - both female and male - demonstrate such deficits, which typically are mild. The best-studied phenotype is that of males with FXTAS. The manifestations of cognitive impairment among asymptomatic male carriers, and among women with and without FXTAS, are less well understood, but have come under increased scrutiny.
- Electronic monitoring of psychomotor activity as a supplementary objective measure of depression severity. [JOURNAL ARTICLE]
- Nord J Psychiatry 2014 Aug 18.:1-8.
Background: Rating scales used to assess the severity of depression e.g. the Hamilton Depression Rating Scale 17-item (HDRS-17) partly rely on the patient's subjective experience and reporting. Such subjective measures tend to have low reliability and adding objective measures to complement the assessment of depression severity would be a major step forward. Aims: To investigate correlations between electronic monitoring of psychomotor activity and severity of depression according to HDRS-17. Methods: A total of 36 patients with unipolar disorder (n = 18) or bipolar disorder (n = 18) and 31 healthy control persons aged 18-60 years were included. Psychomotor activity was measured using a combined heart rate and movement sensor device (Actiheart) for 3 consecutive days, 24 h a day. Results: We found that sleeping heart rate (beats/min) correlated with HDRS-17 in both patients with unipolar disorder and bipolar disorder (unadjusted model: B = 0.46, 95% CI 0.037-0.89, P = 0.034). In contrast, correlations between activity energy expenditure (kJ/kg/day), cardio-respiratory fitness (mlO2/min/kg) and HDRS-17 were non-significant. Conclusions: These results suggest that measuring sleeping heart rate in non-experimental daily life could be an objective supplementary method to measure the severity of depression and perhaps indicate presence of insomnia.
- The neural correlates of tic inhibition in Gilles de la Tourette syndrome. [JOURNAL ARTICLE]
- Neuropsychologia 2014 Aug 13.
Tics in Gilles de la Tourette syndrome (GTS) resemble fragments of normal motor behaviour but appear in an intrusive, repetitive and context-inappropriate manner. Although tics can be voluntarily inhibited on demand, the neural correlates of this process remain unclear.14 GTS adults without relevant comorbidities participated in this study. First, tic severity and voluntary tic inhibitory capacity were evaluated outside the scanner. Second, patients were examined with resting state functional magnetic resonance imaging (RS-fMRI) in two states, free ticcing and voluntary tic inhibition. Local synchronization of spontaneous fMRI-signal was analyzed with regional homogeneity (ReHo) and differences between both states (free ticcing<tic inhibition) were contrasted. Clinical correlations of the resulting differential ReHo parameters between both states and clinical measures of tic frequency, voluntary tic inhibition and premonitory urges were also performed.ReHo of the left inferior frontal gyrus (IFG) was increased during voluntary tic inhibition compared to free ticcing. ReHo increases were positively correlated with participants' ability to inhibit their tics during scanning sessions but also outside the scanner. There was no correlation with ratings of premonitory urges.Voluntary tic inhibition is associated with increased ReHo of the left IFG. Premonitory urges are unrelated to this process.
- Associations of sleep disturbance with ADHD: implications for treatment. [JOURNAL ARTICLE]
- Atten Defic Hyperact Disord 2014 Aug 17.
Attention-deficit/hyperactivity disorder (ADHD) is commonly associated with disordered or disturbed sleep. The relationships of ADHD with sleep problems, psychiatric comorbidities and medications are complex and multidirectional. Evidence from published studies comparing sleep in individuals with ADHD with typically developing controls is most concordant for associations of ADHD with: hypopnea/apnea and peripheral limb movements in sleep or nocturnal motricity in polysomnographic studies; increased sleep onset latency and shorter sleep time in actigraphic studies; and bedtime resistance, difficulty with morning awakenings, sleep onset difficulties, sleep-disordered breathing, night awakenings and daytime sleepiness in subjective studies. ADHD is also frequently coincident with sleep disorders (obstructive sleep apnea, peripheral limb movement disorder, restless legs syndrome and circadian-rhythm sleep disorders). Psychostimulant medications are associated with disrupted or disturbed sleep, but also 'paradoxically' calm some patients with ADHD for sleep by alleviating their symptoms. Long-acting formulations may have insufficient duration of action, leading to symptom rebound at bedtime. Current guidelines recommend assessment of sleep disturbance during evaluation of ADHD, and before initiation of pharmacotherapy, with healthy sleep practices the first-line option for addressing sleep problems. This review aims to provide a comprehensive overview of the relationships between ADHD and sleep, and presents a conceptual model of the modes of interaction: ADHD may cause sleep problems as an intrinsic feature of the disorder; sleep problems may cause or mimic ADHD; ADHD and sleep problems may interact, with reciprocal causation and possible involvement of comorbidity; and ADHD and sleep problems may share a common underlying neurological etiology.
- A diagnostic flow chart for POLG-related diseases based on signs sensitivity and specificity. [JOURNAL ARTICLE]
- J Neurol Neurosurg Psychiatry 2014 Aug 11.
Diseases due to mutations of POLG gene, encoding the mitochondrial DNA polymerase, are reputed to have very diverse clinical presentations and have been proposed to cause up to 25% adult mitochondrial diseases. Our objective was the evaluation of the specificity and sensitivity of the signs encountered with POLG mutations.Forty-four patients out of 154 with sequenced POLG gene had mutations affecting either one (POLG(+/-) group) or two POLG alleles (POLG(+/+) group). Phenotyping included clinical signs, electroneuromyography and brain imaging while mitochondrial investigations encompassed muscle histochemistry, respiratory chain assays and search for multiple mitochondrial deletions. The specificity and sensitivity of the signs associated with POLG mutations were analysed by comparison between POLG(+/+) and patients without POLG mutation.High sensitivity but low specificity was observed with single signs such as axonal sensory neuropathy, cerebellar syndrome, movement disorders and weakness involving ocular, pharyngeal, axial and/or limb muscles. Specificity was increased with combination of previous signs plus psychiatric symptoms, cognitive impairment and epilepsy. High specificity and sensitivity was only obtained with sensory neuronopathy associated with one of the following signs: weakness of ocular, pharyngeal, axial and/or limb muscles. Mitochondrial investigations did not suffice for diagnosis. The widespread neuromuscular signs were often present since disease onset and were the rule above 50 years of age leading to a very low probability of POLG mutations in patients with less than three signs and absent sensory neuropathy.Phenotypes associated with POLG mutations follow a reproducible pattern, which allows establishing a diagnostic flow chart.