REM sleep behavior disorder in 703 sleep-disorder patients: The importance of eliciting a comprehensive sleep history

ObjectivesThe aim of our study was to evaluate the frequency of REM sleep behavior disorder (RBD) in a mixed sleep laboratory population and to assess potential associations. Moreover, we investigated referral diagnoses of patients subsequently diagnosed with RBD and assessed the frequency of incidental RBD.MethodsCharts and polysomnographic reports of 703 consecutive patients comprising the full spectrum of ICSD-2 sleep disorders [501 males, 202 females; mean age, 51.0 ± 14.1 years (range: 10–82 years)] were carefully reviewed. The vast majority of patients were adults (98.7%). Patients were categorized into those with and without RBD. For associations, all concomitant sleep and neurological diagnoses and medications were evaluated.ResultsThirty-four patients (4.8%) were diagnosed with RBD (27 men; 7 women, mean age, 57.7 ± 12.3 years). RBD was idiopathic in 11 patients (1.6%; 9 men) and symptomatic in 23 patients (3.3%; 18 men) secondary to Parkinsonian syndromes (n = 11), use of antidepressants (n = 7), narcolepsy with cataplexy (n = 4), and pontine infarction (n = 1). Six out of 34 patients were referred for suspected RBD, 20 reported RBD symptoms only on specific questioning, and 8 patients had no history of RBD but showed typical RBD behavioral manifestations in the video-polysomnography. Logistic regression analysis revealed significant associations between RBD and the presence of Parkinsonian syndromes (odds ratio [OR] 16.8, 95%CI: 6.4–44.1; P < 0.001), narcolepsy with cataplexy (OR 10.7, 95%CI: 2.9–40.2; P < 0.001), SSRI use (OR 3.9, 95%CI: 1.6–9.8; P = 0.003), and age (OR 1.5/10-year increase, 95%CI: 1.0–2.0; P = 0.039).ConclusionIn this population of 703 consecutive sleep-disorder patients, RBD was uncommon. Its etiology was predominantly symptomatic. The majority of RBD patients reported RBD symptoms on specific questioning only, underlining the importance of eliciting a comprehensive sleep history for the diagnosis of RBD.     

The effects of repetitive neck-muscle vibration on postural disturbances after a chronic stroke

ObjectiveWe aimed to test a repeated program of vibration sessions of the neck muscles (rNMV) on postural disturbances and spatial perception in patients with right (RBD) versus left (LBD) vascular brain damage.MethodsThirty-two chronic stroke patients (mean age 60.9 ± 10 yrs and mean time since stroke 4.9 ± 4 yrs), 16 RBD and 16 LBD, underwent a program of 10 sessions of NMV over two weeks. Posturography parameters (weight-bearing asymmetry (WBA), Xm, Ym, and surface), balance rating (Berg Balance Scale (BBS), Timed Up and Go (TUG)), space representation (subjective straight ahead (SSA), longitudinal body axis (LBA), subjective visual vertical (SVV)), and post-stroke deficiencies (motricity index, sensitivity, and spasticity) were tested and the data analyzed by ANOVA or a linear rank-based model, depending on whether the data were normally distributed, with lesion side and time factor (D-15, D0, D15, D21, D45).ResultsThe ANOVA revealed a significant interaction between lesion side and time for WBA (P < 0.0001) with a significant shift towards the paretic lower limb in the RBD patients only (P = 0.0001), whereas there was no effect in the LBD patients (P = 0.98). Neither group showed a significant modification of spatial representation. Nonetheless, there was a significant improvement in motricity (P = 0.02), TUG (P = 0.0005), and BBS (P < 0.0001) in both groups at the end of treatment and afterwards.ConclusionsrNMV appeared to correct WBA in RBD patients only. This suggests that rNMV could be effective in treating sustainable imbalance due to spatial cognition disorders.     

Treatment outcomes in REM sleep behavior disorder

ObjectiveREM sleep behavior disorder (RBD) is usually characterized by potentially injurious dream enactment behaviors (DEB). RBD treatment aims to reduce DEBs and prevent injury, but outcomes require further elucidation. We surveyed RBD patients to describe longitudinal treatment outcomes with melatonin and clonazepam.MethodsWe surveyed and reviewed records of consecutive RBD patients seen at Mayo Clinic between 2008–2010 to describe RBD-related injury frequency–severity as well as RBD visual analog scale (VAS) ratings, medication dosage, and side effects. Statistical analyses were performed with appropriate non-parametric matched pairs tests before and after treatment, and with comparative group analyses for continuous and categorical variables between treatment groups. The primary outcome variables were RBD VAS ratings and injury frequency.ResultsForty-five (84.9%) of 53 respondent surveys were analyzed. Mean age was 65.8 years and 35 (77.8%) patients were men. Neurodegenerative disorders were seen in 24 (53%) patients and 25 (56%) received antidepressants. Twenty-five patients received melatonin, 18 received clonazepam, and two received both as initial treatment. Before treatment, 27 patients (60%) reported an RBD associated injury. Median dosages were melatonin 6 mg and clonazepam 0.5 mg. RBD VAS ratings were significantly improved following both treatments (p_m = 0.0001, p_c = 0.0005). Melatonin-treated patients reported significantly reduced injuries (p_m = 0.001, p_c = 0.06) and fewer adverse effects (p = 0.07). Mean durations of treatment were no different between groups (for clonazepam 53.9 ± 29.5 months, and for melatonin 27.4 ± 24 months, p = 0.13) and there were no differences in treatment retention, with 28% of melatonin and 22% of clonazepam-treated patients discontinuing treatment (p = 0.43).ConclusionsMelatonin and clonazepam were each reported to reduce RBD behaviors and injuries and appeared comparably effective in our naturalistic practice experience. Melatonin-treated patients reported less frequent adverse effects than those treated with clonazepam. More effective treatments that would eliminate injury potential and evidence-based treatment outcomes from prospective clinical trials for RBD are needed.     

Delayed emergence of a parkinsonian disorder or dementia in 81% of older men initially diagnosed with idiopathic rapid eye movement sleep behavior disorder: a 16-year update on a previously reported series

ObjectiveTo provide a 16-year update from the authors’ 1996 report documenting a 38% conversion from idiopathic rapid eye movement sleep behavior disorder (iRBD) to a parkinsonian disorder at a mean interval of nearly 13 years after the onset of iRBD in a series of 29 males ⩾50 years old.MethodsThe methods of evaluation, diagnosis and follow-up were previously described in the 1996 report. All patients had video-polysomnography (vPSG) confirmed RBD.Results80.8% (21/26) of patients who were initially diagnosed with iRBD eventually developed parkinsonism/dementia (three of the original 29 patients were lost to follow-up). The distribution of diagnoses was as follows: n = 13, Parkinson’s disease (PD); n = 3, dementia with Lewy bodies (DLB); n = 1, dementia (unspecified; profound); n = 2, multiple system atrophy (MSA); n = 2, clinically diagnosed Alzheimer’s Disease (AD) with autopsy-confirmed combined AD plus Lewy body disease pathology. Among the 21 iRBD “converters,” the mean age (±SD) of iRBD onset was 57.7 ± 7.7 years; mean age (±SD) of parkinsonism/dementia onset was 71.9 ± 6.6 years; and mean interval (±SD) from iRBD onset to parkinsonism/dementia onset was 14.2 ± 6.2 years (range: 5–29 years).ConclusionThe vast majority of men ⩾50 years old initially diagnosed with iRBD in this study eventually developed a parkinsonian disorder/dementia, often after a prolonged interval from onset of iRBD, with the mean interval being 14 years while the range extended to 29 years. Also, the specificity of iRBD converting to parkinsonism/dementia is striking. These findings carry important clinical and research implications in the convergent fields of sleep medicine, neurology, and neuroscience, and identify an optimal clinical group for conducting prospective research studies utilizing putative neuroprotective agents to delay the emergence of, or halt the progression to, parkinsonism and/or cognitive impairment as manifestations of either PD, DLB or MSA.     

Clinical manifestations of Parkinson disease and the onset of rapid eye movement sleep behavior disorder

ObjectiveTo identify whether the presence and/or timing of rapid eye movement (REM) sleep behavior disorder (RBD) onset were associated with differences in clinical features and sleep parameters of Parkinson disease (PD).MethodsIn all, 112 PD patients were enrolled and all underwent extensive clinical evaluations and video-polysomnography (PSG). Clinical features and PSG parameters were compared in PD patients with (PD + RBD) or without (PD − RBD) RBD, RBD preceding (RBD > PD), or not (PD ⩾ RBD) PD onset.ResultsSixty-three of the 112 PD patients were affected by RBD. Adjusted for age, gender, education, body mass index (BMI), levodopa equivalent daily dose (LED) and PD duration, PD + RBD patients had higher Hoehn & Yahr stage, higher scores for UPDRS parts I, II and III, more dyskinesia, higher ratio of axial/limb manifestations, and more hallucinations. Their cognitive and quality-of-life status was significantly lower (all P < 0.05). For PSG, PD + RBD patients exhibited higher percentages of phasic and tonic EMG activities, lower apnea hypopnea (AHI) and oxygen desaturation index (ODI), and less time in arterial oxygen saturation (SaO₂) <90% during REM sleep (all P < 0.05). PD ⩾ RBD (n = 22) patients did not significantly differ from RBD > PD (n = 41) patients in clinical manifestations, whereas the PD ⩾ RBD subgroup had significantly higher UPDRS part I score, lower PDQ score and lower AHI during REM than the PD − RBD group (all P < 0.05), but not RBD > PD subgroup. Correlation analysis showed that worse cognition was associated with shorter interval of RBD preceding PD onset (r = 0.297, P = 0.018), but not RBD duration (P = 0.202).ConclusionsClinical manifestations of PD may vary depending on the presence and timing of RBD onset. These findings are compatible with the hypothesis that RBD may be a marker of complex subtypes of PD.     

Effects of long-term use of clonazepam on nonrapid eye movement sleep patterns in rapid eye movement sleep behavior disorder

ObjectiveWe aim to analyze in detail the characteristics of nonrapid eye movement (NREM) sleep in drug-free patients with idiopathic rapid eye movement sleep behavior disorder (iRBD). We compare drug-free iRBD patients to both normal controls and drug-free patients with narcolepsy/RBD and evaluate the changes following the long-term use of bedtime clonazepam.Participants and methodsForty-six participants were recruited: 15 with iRBD (13 men, 2 women; mean age, 65.8 ± 4.39 years), 13 with narcolepsy/RBD (10 men, 3 women; mean age, 63.0 ± 6.73 years), and 18 normal controls (10 men, 8 women; mean age 69.4 ± 7.72 years). Sleep was video polysomnographically recorded and the RBD severity scale (RBDSS) was obtained. Chin electromyography (EMG) amplitude was quantitatively assessed and the atonia index was computed. Additionally, NREM sleep instability was evaluated using an automatic quantitative analysis. Participants with iRBD were re-evaluated after 2.75 ± 1.62 years of regular therapy with 0.5 to 1-mg clonazepam at bedtime.ResultsSlow transient electroencephalography (EEG) events were increased in iRBD and decreased in narcolepsy/RBD, while fast transient events decreased in iRBD and increased in narcolepsy/RBD. During rapid eye movement (REM) sleep the atonia index was reduced in both iRBD and narcolepsy/RBD groups and during NREM sleep atonia index was increased in iRBD participants, remaining low in narcolepsy/RBD participants. After long-term therapy with clonazepam, wakefulness after sleep onset was decreased together with an increase in both slow-wave sleep (SWS) and sleep stage 2, in which the latter reached statistical significance; sleep stages 1 and 2 instability significantly decreased and the duration of EEG transients also slightly but significantly decreased. Finally, chin tone was not modified by clonazepam.ConclusionsOur study confirms that clonazepam modifies some aspects of NREM sleep in iRBD participants with a decrease in its instability. Moreover, we also show that a complex modification of sleep chin atonia exists in these participants, which also involves NREM sleep; for iRBD more complex neuropathologic models encompassing REM sleep and NREM sleep mechanisms are needed.     

Estimating motor unit discharge patterns from high-density surface electromyogram

ObjectiveWe systematically tested the capability of the Convolution Kernel Compensation (CKC) method to identify motor unit (MU) discharge patterns from the simulated and experimental surface electromyogram (sEMG) during low-force contractions.MethodssEMG was detected with a grid of 13 × 5 electrodes. In simulated signals with 20 dB signal-to-noise ratio, 11 ± 3 out of 63 concurrently active MUs were identified with sensitivity >95% in the estimation of their discharge times. In experimental signals recorded at 0–10% of the maximal force, the discharge patterns of (range) 11–19 MUs (abductor pollicis; n = 8 subjects), 9–17 MUs (biceps brachii; n = 2), 7–11 MUs (upper trapezius; n = 2), and 6–10 MUs (vastus lateralis; n = 2) were identified. In the abductor digiti minimi muscle of one subject, the decomposition results from concurrently recorded sEMG and intramuscular EMG (iEMG) were compared; the two approaches agreed on 98 ± 1% of MU discharges.ConclusionIt is possible to identify the discharge patterns of several MUs during low-force contractions from high-density sEMG.SignificancesEMG can be used for the analysis of individual MUs when the application of needles is not desirable or in combination with iEMG to increase the number of sampled MUs.     

Depression and anxiety among high-risk obstetric inpatients

ObjectiveTo assess the following among women hospitalized antenatally due to high-risk pregnancies: (1) rates of depression symptoms and anxiety symptoms, (2) changes in depression symptoms and anxiety symptoms and, (3) rates of mental health treatment.MethodsSixty-two participants hospitalized for high-risk obstetrical complications completed the Edinburgh Postnatal Depression Scale (EPDS), Generalized Anxiety Disorder 7-item scale (GAD-7) and Short-Form 12 weekly until delivery or discharge, and once postpartum.ResultsAverage length of total hospital stay was 8.3±7.6days for women who completed an initial admission survey (n= 62) and 16.3±8.9 (n= 34), 25.4±10.2 (n= 17) and 35±10.9 days (n= 9) for those who completed 2, 3 and 4 surveys, respectively. EPDS was ≥ 10 in 27% (n= 17) and GAD-7 was ≥ 10 in 13% (n= 8) of participants at initial survey. Mean anxiety (4.2±6.5 vs. 5.2±5.1, p= .011) and depression (4.4±5.6 vs. 6.9±4.8, p= .011) scores were lower postpartum compared to initial survey. Past mental health diagnosis predicted depression symptoms [odds ratio (OR)=4.54; 95% confidence interval (CI) 1.91–7.17] and anxiety symptoms (OR=5.95; 95% CI 3.04–8.86) at initial survey; however, 21% (n= 10) with no diagnostic history had EPDS ≥ 10. Five percent (n= 3) received mental health treatment during pregnancy.ConclusionHospitalized high-risk obstetrical patients may commonly experience depression symptoms and/or anxiety symptoms and not receive treatment. A history of mental health treatment or diagnosis was associated with depression symptoms or anxiety symptoms in pregnancy. Of women with an EPDS ≥ 10, > 50% did not report a past mental health diagnosis.     

Mazindol in narcolepsy and idiopathic and symptomatic hypersomnia refractory to stimulants: A long-term chart review

ObjectiveMazindol is a tricyclic, anorectic, non-amphetamine stimulant used in narcolepsy and obesity since 1970. This study aimed to evaluate the long-term benefit/risk ratio in drug-resistant hypersomniacs and cataplexy sufferers.MethodsBy retrospective analysis of the patients’ files in the hospitals of Paris-Salpêtrière (n = 91), Montpellier (n = 40) and Lyon (n = 8), the benefit (Epworth Sleepiness Score (ESS), cataplexy frequency, authorization renewal) and tolerance (side-effects, vital signs, electrocardiogram and cardiac echography) of mazindol were assessed.ResultsThe 139 patients (45% men) aged 36 ± 15 years (range: 9–74) suffered narcolepsy (n = 94, 66% with cataplexy), idiopathic (n = 37) and symptomatic hypersomnia (n = 8) refractory to modafinil, methylphenidate and sodium oxybate. Under mazindol (3.4 ± 1.3 mg/day, 1–6 mg) for an average of 30 months, the ESS decreased from 17.7 ± 3.5 to 12.8 ± 5.1, with an average fall of −4.6 ± 4.7 (p < 0.0001) and the frequency of cataplexy fell from 4.6 ± 3.1 to 2 ± 2.8 episodes per week. The cataplexy was eliminated in 14.5% of patients, improved in 27.5%, and unchanged in 29% (missing data in 29%). The treatment was maintained long term in 83 (60%) patients, and stopped because of a lack of efficacy (22%) and/or secondary effects (9%). There was no pulmonary hypertension in the 45 patients who underwent a cardiac echography. The most common adverse effects were dry mouth (13%), palpitations (10%, including one with ventricular hyperexcitability), anorexia (6%), nervousness (6%) and headaches (6%).ConclusionMazindol has a long-term, favorable benefit/risk ratio in 60% of drug-resistant hypersomniacs, including a clear benefit on cataplexy.     

Validation de la batterie rapide de dénomination (BARD) chez 382 témoins et 1004 patients d’une consultation mémoire

IntroductionThe Rapid BAttery of Denomination (BARD) is a short 10-item naming test derived from the 60-item Boston Naming Test. It is easily performed in less than 15 seconds by normal controls independently of age, gender and education (Croisile, 2005, Croisile, 2007, Croisile, 2008). Our aim was to evaluate the BARD in various conditions seen in a memory clinic.Patients and methodsThe BARD was used in 382 normal subjects (165 men and 217 women, aged from 20 to 97 years) and 1004 patients attending a memory clinic. Three groups of 505 patients with Alzheimer's disease (AD) were compared: mild patients (n = 402), moderate patients (n = 84) and moderately severe patients (n = 19). The BARD was also used in 499 patients with a Mini Mental Status (MMSE) ≥ 20: 173 patients with amnestic Mild Cognitive Impairment (aMCI), 56 patients with frontotemporal dementia (FTD), 41 patients with Lewy Body dementia (LBD), 36 patients with nonfluent primary progressive aphasia (NFPPA), 27 patients with semantic dementia (SD), 16 patients with posterior cortical atrophy (PCA), 150 patients with anxiety or depression (ADD).ResultsThe performance of the patients was not affected by age, gender or education. aMCI had a score of 9.97 ± 0.18, ADD a score of 9.97 ± 0.2. A mild anomia was observed in three groups: mild AD (9.78 ± 0.5), FTD (9.79 ± 0.65) et LBD (9.98 ± 0.16). A more pronounced anomia was present in moderate AD (9.10 ± 1.06), moderately severe AD (8.05 ± 1.27), PCA (8.12 ± 3.28) and NFPPA (8.44 ± 1.61). The anomia was severe in SD (5.85 ± 2.46). The 10 items were perfectly named by 98 % of ADD, 96.53 % of aMCI, 82.09 % of mild AD, 87.5 % of FTD patients, 97.56 % of LBD patients, 68.75 % of PCA patients, but only 45.24 % moderate AD, 5.26 % of moderately severe AD, 27.78 % of NFPPA, and 3.7 % of SD. In the patients with MMS ≥ 20, Anova showed that the BARD scores of the ADD, aMCI, mild AD, FTD and LBD groups were significantly greater than the BARD scores of NFPPA, SD and PCA. PCA and NFPPA groups did not differ for BARD scores whereas they were significantly better than SD. A ROC curve comparing the 822 mild anomic patients (AD, FTD, LBD, aMCI, ADD) with the 79 more anomic patients (NFPPA, SD, PCA) showed that for a BARD score of 10, sensitivity was 72.2 %, specificity was 89.2 %, and 87.7 % of the patients were correctly classified.ConclusionThe BARD is a quick and useful tool for identifying naming disorders in a memory clinic. In patients with MMSE ≥ 20, making one error at the BARD is highly abnormal and significantly characteristic of cognitive disorders: the more frequent the errors are, the more probable is the presence of a visual agnosia (PCA), an aphasia (NFPPA), or a semantic disorder (SD).     

Role of serum levels of neurotensin in children with autism spectrum disorder

AimNeuroinflammation may play a role in the pathogenesis of autism in some patients. The aim of this study was to measure serum levels of neurotensin (NTS) in relation to the degree of the severity of autism.MethodsSerum NTS was measured in autistic children (n = 38; mean age 7.02 ± 2.03 years) and healthy, unrelated sex matched controls (n = 39); mean age 7.25 ± 1.64 years). The severity of autism symptoms was assessed using Childhood Autism Rating Scale (CARS) scores.ResultsThe serum level of NTS was significantly (P < 0.001) lower in autistic children (mean ± S.D. = 54.71 ± 12.4 pg/ml) than control group (mean ± S.D. = 77.58 ± 10.29 pg/ml). Children with severe autism had significantly lower serum NTS levels than patients with mild to moderate autism (P < 0.002). There was significant negative correlation between serum levels of NTS and CARS SCORES (r² = 0.79, P = 0.001).ConclusionsSerum NTS levels were elevated in some autistic children and they were significantly correlated with the severity of autism. However, this is an initial report that warrants further research to determine the pathogenic role of NTS and its possible link to neuroinflammation in autism.     

Olfactory dysfunction in narcolepsy with and without cataplexy

BackgroundNot only patients in whom REM behavior disorder (RBD) is associated with narcolepsy, but also those with narcolepsy alone are reported to have olfactory dysfunction. We investigated if hyposmia is specific to narcolepsy with cataplexy (N–C) or if narcolepsy without cataplexy (NwC) is also associated with olfactory dysfunction.MethodsWe studied olfactory function in two groups of patients: N–C group (n = 66, 26 men and 40 women; mean age 41 ± 18 years), and NwC group (n = 17, 7 men and 10 women; mean age 46 ± 20 years). As a control group we used published normative data for particular smell tests.ResultsBoth patients with N–C and patients suffering from NwC had a significantly higher olfactory threshold (N–C group, p < 0.0001; NwC group, p < 0.0001) and impaired odor identification (N–C group, p < 0.0001; NwC group, p < 0.0001). Our results show for the first time that narcolepsy without cataplexy, where the majority of cases have normal CSF hypocretin levels, is associated with olfactory dysfunction.ConclusionsIt appears that also a partial loss of hypothalamic hypocretin neurons without a clear CSF level decrease can affect smell projection.     

Cardiovascular and metabolic risk in outpatients with schizoaffective disorder treated with antipsychotics: Results from the CLAMORS study

AimTo assess the coronary heart disease (CHD) risk and prevalence of the metabolic syndrome (MS) in patients with schizoaffective disorder (SD) receiving antipsychotics.MethodsPatients meeting DSM-IV criteria for SD and receiving antipsychotic treatment were recruited in a retrospective, cross-sectional, multicenter study (the CLAMORS study). MS was defined as at least three of the following components: waist circumference greater than 102 cm (men)/greater than 88 cm (women); serum triglycerides greater or equal to 150 mg/dl; HDL cholesterol less than 40 mg/dl (men)/less than 50 mg/dl (women); blood pressure greater or equal to 130/85 mmHg; fasting blood glucose greater or equal to 110 mg/dl. The 10-year CHD risk was assessed by the Systematic coronary risk evaluation (SCORE) (cardiovascular mortality) and Framingham (any cardiovascular event) functions. Clinical severity was assessed using the PANSS and CGI-S scales.ResultsA total of 268 valuable patients with SD (127 men, 48.1%), 41.9 ± 12.3 years (mean ± S.D.), were analyzed. The 10-year overall cardiovascular mortality and CV-event risk were 0.8 ± 1.6 (SCORE) and 6.5 ± 6.8 (Framingham), respectively. A high/very high risk of any CV event (Framingham ≥ 10%) was associated with severity [CGI-S = 3–4; OR: 4.32 (1.15–16.26), P = 0.03)]. MS was present in 26.5% (95%CI: 21.2–31.8) of subjects, without gender differences, but significantly associated with patient's impression of severity: CGI = 3–4; OR = 1.90 (0.83–4.36), and CGI = 5–7; OR = 3.13 (1.06–9.24), P = 0 < 0.001, and age [OR = 1.91 (1.09–3.34), P < 0.024)].ConclusionsCHD risk and MS prevalence were high among patients with SD, being MS prevalence associated with age and severity of disease.     

Parkinson’s disease and REM sleep behavior disorder result in increased non-motor symptoms

ObjectiveRapid eye movement (REM)-sleep behavior disorder (RBD) is often comorbid with Parkinson’s disease (PD). The current study aimed to provide a detailed understanding of the impact of having RBD on multiple non-motor symptoms (NMS) in patients with PD.MethodsA total of 86 participants were evaluated for RBD and assessed for multiple NMS of PD. Principal component analysis was utilized to model multiple measures of NMS in PD, and a multivariate analysis of variance was used to assess the relationship between RBD and the multiple NMS measures. Seven NMS measures were assessed: cognition, quality of life, fatigue, sleepiness, overall sleep, mood, and overall NMS of PD.ResultsAmong the PD patients, 36 were classified as having RBD (objective polysomnography and subjective findings), 26 as not having RBD (neither objective nor subjective findings), and 24 as probably having RBD (either subjective or objective findings). RBD was a significant predictor of increased NMS in PD while controlling for dopaminergic therapy and age (p = 0.01). The RBD group reported more NMS of depression (p = 0.012), fatigue (p = 0.036), overall sleep (p = 0.018), and overall NMS (p = 0.002).ConclusionIn PD, RBD is associated with more NMS, particularly increased depressive symptoms, sleep disturbances, and fatigue. More research is needed to assess whether PD patients with RBD represent a subtype of PD with different disease progression and phenomenological presentation.     

Coprolalia and copropraxia in patients with Gilles de la Tourette syndrome

Background and purposeInvoluntary expression of socially unacceptable words (coprolalia) or gestures (copropraxia) is the best-known symptom of Gilles de Tourette syndrome (GTS) that contributes to the social impairment. The aim of the study was to assess the prevalence, age at onset and co-occurring symptoms of coprophenomena.Materials and methodsOne hundred and sixty-eight consecutive subjects with GTS including 94 adults and 74 children and aged between 4 and 54 years (mean: 18.0 ± 8.3) were studied. Demographic and clinical data were obtained from medical history and neurological examination.ResultsCoprolalia or copropraxia appeared in 44 patients. Both coprophenomena were present in 9 patients. Coprolalia occurred in 25.0% (n = 42) and copropraxia in 6.5% (n = 11) of patients. Mean age at onset was 12.2 ± 5.7 years (range: 4–33) for coprolalia and 12.4 ± 4.9 years (range: 7–24) for copropraxia. Coprolalia started 4.4 ± 3.7 years (range: 0–16) after the onset of disease; copropraxia started 6.1 ± 4.0 years (range: 1–12) after the onset of the disease. Coprolalia began in adulthood in six patients only, and copropraxia in one person. In six patients, coprolalia appeared in the first year of the disease. Copropraxia was never seen in the first year of the disease. Coprophenomena were more frequent in patients with comorbid mental disorders, behavioral problems and severe tics. Three quarters of patients reported significant influence of coprophenomena on daily living.ConclusionsCoprophenomena affect one quarter of GTS patients, appear in the time when tics are most severe, and are positively associated with comorbidity and more severe form of disease. Coprophenomena may reflect more widespread dysfunction of brain in GTS.     

Olfactory dysfunction in idiopathic REM sleep behavior disorder

BackgroundOlfactory dysfunction is frequently observed in patients with idiopathic REM sleep behavior disorder (iRBD) such as Parkinson’s disease or dementia with Lewy bodies.MethodsOlfactory function tests using Sniffin’ Sticks and Odor Stick Identification Test for Japanese (OSIT-J) were performed in 73 consecutive middle-aged (range, 50–69 years) patients with iRBD, 33 consecutive older-aged (71–82 years) patients with iRBD, and 28 control subjects (55–70 years).ResultsOdor identification was more frequently impaired than odor threshold or discrimination among the iRBD group and allowed better discrimination between the middle-aged iRBD group and age-adjusted control subjects. The area under the curve for threshold, discrimination, identification, TDI score and OSIT-J score determined from receiver operating characteristic curves were 0.831 (0.753–0.909), 0.761 (0.666–0.855), 0.938 (0.894–0.982), 0.939 (0.897–0.981), and 0.965 (0.931–0.999), respectively. Discrimination and identification scores were significantly lower in the older-aged iRBD group than in the middle-aged iRBD group. A significant correlation was observed between the identification score on Sniffin’ Sticks and OSIT-J score (r = 0.5910, P < 0.0001, n = 106, Spearman’s rank).ConclusionAnosmia/hyposmia may be a feature of iRBD. Olfactory dysfunction in iRBD is a consistent, widespread central nervous abnormality of different olfactory modalities with different cognitive complexity.     

Lifetime presence of psychotic symptoms in bipolar disorder is associated with less favorable socio-demographic and certain clinical features

BackgroundThe presence of psychotic symptoms in bipolar disorder (BD) is considered a feature of higher severity of illness and, in particular, of manic episodes in bipolar I disorder (BD I). However, the possibility to apply the “with psychotic features” specifier to major depressive episodes in either bipolar II disorder (BD II) or BD I highlights the need for additional research in this area.MethodsThe present study assessed the lifetime presence of psychotic symptoms and related socio-demographic and clinical features in a large sample of BD patients (N = 360), with (BDPs, N = 207) and without a lifetime history of psychosis (BDNPs, N = 153).ResultsAn overall less favorable socio-demographic profile was observed in BDPs vs BDNPs. In terms of clinical variables, BDPs vs BDNPs had: earlier age at onset (27.7 ± 10.5 vs 30.1 ± 12.3 years; p = 0.02), higher rates of BD I diagnosis (95.7% vs 45.8%; p < 0.001), more elevated (manic/hypomanic/mixed) polarity of first (55.2% vs 24.4%; p < 0.001) and most recent episode (69.8% vs 35.6%; p < 0.001), more comorbid alcohol/substance use disorder (38.1% vs 21.9%; p = 0.002), more lifetime hospitalizations (3.8 ± 6.1 vs 2 ± 3; p = 0.002) and involuntary commitments (1 ± 1.9 vs 0.1 ± 0.4; p < 0.001), more history of psychosocial rehabilitation (17.9% vs 5.7%; p = 0.001), more current antipsychotic use (90.1% vs 70.9%; p < 0.001), and lower GAF (62.3 ± 14.2 vs 69.3 ± 12.5; p < 0.001), but shorter duration of most recent episode (34.1 ± 45.4 vs 50.3 ± 65.7 days; p = 0.04), lower rates of comorbid anxiety disorders (23.9% vs 38.2%; p = 0.005), and antidepressant use (19.4% vs 56.6%; p < 0.001).ConclusionsThe present findings indicate an overall worse profile of socio-demographic and certain clinical characteristics associated with the lifetime presence of psychotic symptoms in bipolar patients.     

A shared low-frequency oscillatory rhythm abnormality in resting and sensory gating in schizophrenia

ObjectivesWe hypothesized that an oscillatory abnormality that is consistently observed across various testing paradigms may index an elementary neuronal abnormality marking schizophrenia risk.MethodsCompared neural oscillations in resting EEG and sensory gating conditions in schizophrenia patients (n = 128), their first-degree relatives (n = 80), and controls (n = 110) and calculated phenotypic and/or genetic correlation of the abnormal measure across these conditions.ResultsUsing a uniform, single trial analytical approach, we identified two prominent oscillatory characteristics in schizophrenia: (1) augmented neural oscillatory power was pervasive in medicated schizophrenia patients in most frequencies, most prominent in the theta–alpha range (4–11 Hz) across the two paradigms (all p < 0.007); and (2) their first-degree relatives shared significantly augmented oscillatory energy in theta–alpha frequency in resting (p = 0.002) and insufficient suppression of theta–alpha in sensory gating (p = 0.01) compared with normal controls. Heritability estimates for theta–alpha related measures for resting and gating conditions ranged from 0.44 to 0.49 (p < 0.03). The theta–alpha measures were correlated genetically with each other (RhoG = 0.82 ± 0.43; p < 0.05).ConclusionsAugmented theta–alpha rhythm may be an elementary neurophysiological problem associated with genetic liability of schizophrenia.SignificanceThis finding helps to refine key electrophysiologic biomarkers for genetic and clinical studies of schizophrenia.