Efectos de la terapia con videojuegos comerciales sobre el equilibrio postural en pacientes con esclerosis múltiple: revisión sistemática y metaanálisis de ensayos clínicos controlados aleatorizados

IntroductionCommercial video games are considered an effective tool to improve postural balance in different populations. However, the effectiveness of these video games for patients with multiple sclerosis (MS) is unclear.ObjectivesTo analyse existing evidence on the effects of commercial video games on postural balance in patients with MS.Material and methodWe conducted a systematic literature search on 11 databases (Academic-Search Complete, AMED, CENTRAL, CINAHL, WoS, IBECS, LILACS, Pubmed/Medline, Scielo, SPORTDiscus, and Science Direct) using the following terms: “multiple sclerosis”, videogames, “video games”, exergam*, “postural balance”, posturography, “postural control”, balance. Risk of bias was analysed by 2 independent reviewers. We conducted 3 fixed effect meta-analyses and calculated the difference of means (DM) and the 95% confidence interval (95% CI) for the Four Step Square Test, Timed 25-Foot Walk, and Berg Balance Scale.ResultsFive randomized controlled trials were included in the qualitative systematic review and 4 in the meta-analysis. We found no significant differences between the video game therapy group and the control group in Four Step Square Test (DM: –.74; 95% CI, –2.79-1.32; P = .48; I² = 0%) and Timed 25-Foot Walk scores (DM: .15; 95% CI, –1.06-.76; P = .75; I² = 0%). We did observe intergroup differences in BBS scores in favour of video game therapy (DM: 5.30; 95% CI, 3.39-7.21; P < .001; I² = 0%), but these were not greater than the minimum detectable change reported in the literature.ConclusionsThe effectiveness of commercial video game therapy for improving postural balance in patients with MS is limited.     

Association of high body lead store with severe intracranial carotid atherosclerosis

ObjectiveLead is involved in the pathogenesis of atherosclerosis and hypertensive disease and may be related to cerebrovascular disease. We studied the association of body lead level with stroke subtypes and severity of cerebral atherosclerosis in order to identify the significance of lead exposure to cerebrovascular disease.MethodsFrom April, 2002 to March, 2005, we studied the lead level in all patients receiving digital subtraction angiography. Diameter stenosis at extracranial carotid, intracranial carotid and vertebrobasilar system was calculated according to the NASCET criteria. A blood sample and a mobilization test of 72-h urine sample were collected for lead measurement.ResultsIn a total of 213 subjects, 19 were free of stroke (blood lead level = 4.62 ± 2.41 μg/dL, body lead store = 39.04 ± 20.91 μg) and 194 were stroke patients (4.89 ± 2.75 μg/dL, 45.13 ± 29.8 μg; all stroke vs. non-stroke, P > 0.05). In the 153 subjects with atherosclerotic origin, body lead store but not blood lead level in the intracranial carotid system was significantly higher in ≥50% group than <50% group (blood lead: 5.61 ± 3.02 μg/dL vs. 4.80 ± 2.50 μg/dL, Student's t-test, P = 0.129; body lead store: 51.7 ± 27.0 μg vs. 41.9 ± 23.5 μg, Student's t-test, P = 0.038, multivariate logistic regression, odds ratio = 1.02, 95% CI: 1.00–1.03, P = 0.043). However, there was no significant association between lead level and stenotic severity in extracranial and vertebrobasilar systems (P > 0.05).ConclusionOur study demonstrated that long-term lead exposure as measured by body lead store might carry a potential risk of intracranial carotid atherosclerosis.     

Reference voluntary jitter values using disposable monopolar needle electrodes in the extensor digitorum communis muscle

ObjectiveTo measure normal variability in neuromuscular transmission in the extensor digitorum communis (EDC) muscle voluntarily activated using a disposable monopolar needle electrode (MNPE).MethodsWe examined the EDC muscle using MNPE in 50 healthy volunteers (12 male and 38 female, mean age: 41.5 ± 12.9 years, age range: 18–74 years). The high-pass filter setting was 3 kHz.ResultsJitter values are expressed as the mean consecutive difference (MCD) of 20 potential pairs. Mean MCD (n = 50) was 21.3 ± 3 μs (upper 95% confidence limit (CL): 27.3 μs). Mean MCD in all potential pairs (n = 1000) was 21.3 ± 6.6 μs (upper 95% CL: 34 μs). Mean MCD for the 18th highest value was 28 ± 4.7 μs (upper 95% CL: 37.5 μs).ConclusionThe suggested practical upper limit for mean MCD was set to 28 μs; for outliers it was 38 μs.SignificanceThe present study defines the normative value for jitter recorded with disposable MNPE, which is a low-cost alternative for the evaluation of neuromuscular transmission, although certain precautions must be taken.     

Increased blood phenylalanine to tyrosine ratio in HIV-1 infection and correction following effective antiretroviral therapy

ObjectiveHigher blood levels of the essential amino acid phenylalanine (phe) have been documented in patients with HIV-1 infection. They may relate to a diminished conversion of phe to tyrosine (tyr) by the enzyme phenylalanine-hydroxylase (PAH). PAH is rate-limiting in the biosynthesis of dopamine, and impaired PAH activity is reflected by an increased phe to tyr ratio (phe/tyr).MethodsPlasma phe/tyr was measured in 107 patients with HIV-1 infection before and after 12 months of effective antiretroviral therapy (ART). Results were compared with CD4⁺ cell counts, HIV-1 RNA levels and concentrations of immune activation marker neopterin.ResultsBefore ART, phe/tyr was mean ± S.D.: 0.99 ± 0.57 μmol/μmol. Phe/tyr correlated significantly with plasma and urine neopterin concentrations (rs = 0.434, and rs = 0.392; both p < 0.001) and less strongly with HIV-RNA levels (rs = 0.173) and CD4⁺ counts (rs = ?0.182, both p < 0.05). After ART, phe/tyr dropped to 0.72 ± 0.16 (=?27%; U = 5.21, p = 0.01) which was due to an average decline of ?14% of phe concentrations from 73.1 ± 34.0 μmol/L at baseline to 62.9 ± 17.8 μmol/L after ART (U = 2.51, p = 0.01) and a concomitant increase of tyr concentrations (+13%, U = 2.46, p = 0.01). In parallel, significant reductions of plasma and urine neopterin concentrations were observed during ART.ConclusionsIncreased phe/tyr is frequent in patients with HIV-1 infection and is related to immune activation. ART was found to decrease phe/tyr and this change could indicate and influence on PAH activity. Future studies might be able to show whether the decline of phe/tyr under ART may concur with the often improved neuropsychiatric status in treated patients.     

Walking-induced muscle fatigue impairs postural control in adolescents with unilateral spastic cerebral palsy

BackgroundFatigue is likely to be an important limiting factor in adolescents with spastic cerebral palsy (CP).AimsTo determine the effects of walking-induced fatigue on postural control adjustments in adolescents with unilateral CP and their typically developing (TD) peers.MethodsTen adolescents with CP (14.2 ± 1.7 yr) and 10 age-, weight- and height-matched TD adolescents (14.1 ± 1.9 yr) walked for 15 min on a treadmill at their preferred walking speed. Before and after this task, voluntary strength capacity of knee extensors (MVC) and postural control were evaluated in 3 conditions: eyes open (EO), eyes closed (EC) and with dual cognitive task (EODT).ResultsAfter walking, MVC decreased significantly in CP (−11%, P < 0.05) but not in TD. The CoP area was only significantly increased in CP (90%, 34% and 60% for EO, EC and EODT conditions, respectively). The CoP length was significantly increased in the EO condition in CP and TD (20% and 21%) and was significantly increased in the EODT condition by 18% in CP only.ConclusionsUnlike TD adolescents, treadmill walking for 15 min at their preferred speed lead to significant knee extensor strength losses and impairments in postural control in adolescents with unilateral spastic CP.     

Auditory event-related potentials at preschool age in children born very preterm

ObjectiveTo assess auditory event-related potentials at preschool age in children born very preterm (VP, 27.4 ± 1.9 gestational weeks, n = 70) with a high risk of cognitive dysfunction.MethodsWe used an oddball paradigm consisting of a standard tone randomly replaced by one of three infrequent deviants (differing in frequency, sound direction or duration).ResultsThe P1 and N2 latencies were inversely correlated to age (50–63 months) both in VP (r = −0.451, p < 0.001, and r = −0.305, p = 0.01, respectively) and term born controls (TC; n = 15). VP children had smaller P1 than near-term (n = 12) or TC (1.70 ± 0.17 μV vs 2.68 ± 0.41 and 2.92 ± 0.43, respectively; p < 0.05). Mismatch negativity response did not differ between groups.ConclusionsOur data suggest a fast maturation of P1 and N2 responses with fast decrease in P1 and N2 latencies around the age of 5 years. Mismatch negativity response does not seem to be a robust measure for defining abnormalities in VP children.SignificanceIn ERP studies in preschool children, even small, non-significant group differences in age at recording should be corrected for. Very preterm born children at preschool age have aERP patterns as earlier described in full-term born children with cognitive deficits.     

Cross sectional area reference values for sonography of peripheral nerves and brachial plexus

ObjectiveUltrasound measurements of the cross sectional area (CSA) variability have been recently introduced to quantify pathological changes in peripheral nerves (PN).MethodsReference values from 75 healthy subjects and their correlation to age, height, weight and sex are reported.ResultsThe mean values in PN were: (1) intranerve CSA-variability: median 1.05 (SD ± 0.13), ulnar 1.53 (SD ± 0.51), fibular 1.33 (SD ± 0.37), tibial 1.39 (SD ± 0.39), (2) internerve CSA-variability 1.76 (SD ± 0.37), (3) intraplexus CSA-variability 1.52 (SD ± 0.37), (4) side-to-side difference ratio of the CSA-variability: median 1.21 (SD ± 0.04), ulnar 1.2 (SD ± 0.25), fibular 1.19 (SD ± 0.23), tibial 1.28 (SD ± 0.24) and brachial plexus 1.19 (SD ± 0.23). CSA did not correlate with height in PN, but correlated with weight in the ulnar nerve [Guyon’s canal, r = 0.411, p = 0.0237, elbow r = 0.409, p = 0.0248]. Significant changes between sex were found only in the ulnar (Guyon’s canal, p = 0.0265), fibular (popliteal fossa, p = 0.0336) and sural nerve (p = 0.048). CSA decreased with age in the median (axilla, p = 0.0236), and radial nerve (spiral groove, p = 0.0037) and increased in the tibial nerve (ankle, p < 0.0001).ConclusionsThe CSA reference values reported seem to correlate at certain sites with age, weight and sex but not with height.SignificanceThe new CSA variability measures may be helpful in investigating pathologies of the PN.     

Ocular vestibular evoked myogenic potentials to head tap and cervical vestibular evoked myogenic potentials to air-conducted sounds in isolated internuclear ophthalmoplegia

ObjectiveThe central pathways responsible for ocular vestibular evoked myogenic potentials (VEMPs) to forehead tapping remain to be determined. This study aimed to determine whether the medial longitudinal fasciculus (MLF) carries the signals for ocular VEMPs (oVEMPs) in response to this mode of stimulation.MethodsTwelve patients with isolated unilateral internuclear ophthalmoplegia (INO) due to brainstem infarction underwent evaluation of the ocular tilt reaction (ocular torsion and skew deviation), tilt of the subjective visual vertical (SVV), cervical VEMPs (cVEMPs) in response to tone burst sound, and oVEMPs induced by tapping the forehead.ResultsEight (67%) patients showed abnormal oVEMPs that included no wave formation (n = 4) and decreased amplitude (n = 3) in the lesion side, and bilaterally absent responses in the remaining patient. Furthermore, the patients showed diminished oVEMPs responses in the lesion side compared with normal side (6.0 ± 5.6 vs. 11.7 ± 5.5 μV, paired t-test, p = 0.001) and increased IAD_amp(%) of the oVEMPs compared with normal controls (43.6 ± 41.2 vs. 9.1 ± 6.2, t-test, p = 0.018). In contrast, cVEMPs were abnormal in only three (25%) patients, decreased (n = 2) or no response in the lesion side. Eleven (92%) patients showed contraversive ocular tilt reaction or SVV tilt.ConclusionPatients with INO frequently show impaired formation of ipsilesional oVEMPs in response to forehead tapping. The occasional abnormality and decreased amplitude of ipsilesional cVEMPs also suggest a modulatory pathway for the inhibitory sacculocollic reflex descending in the MLF.SignificanceThis study suggests that the MLF contains the fibers for the otolith-ocular reflex from the contralateral ear.     

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.     

Association between depressive symptoms and fibrosis markers: The Cardiovascular Health Study

ObjectiveFibrosis plays an important role in heart failure (HF) and other diseases that occur more frequently with increasing age. Depression is associated with an increased risk of heart failure and other age-related diseases. This study examined the association between depressive symptoms and fibrosis markers in adults aged 65 years and above.MethodsFibrosis markers and depressive symptoms were assessed in 870 participants (age = 80.9 ± 5.9 yrs, 49% women) using a case-control design based on heart failure status (307 HF patients and 563 age- and sex-matched controls, of whom 284 with CVD risk factors (hypertension, diabetes mellitus, or hypercholesterolemia) and 279 controls without these CVD risk factors). Fibrosis markers were procollagen type I (PIP), type I collagen (CITP), and procollagen type III (PIIINP). Inflammation markers included C-reactive protein, white blood cell counts and fibrinogen. Depression was assessed using the Center for Epidemiological Studies-Depression (CES-D) scale using a previously validated cut-off point for depression (CES-D ? 8). Covariates included demographic and clinical variables.ResultsDepression was associated with higher levels of PIP (median = 411.0, inter-quartile range (IQR) = 324.4–472.7 ng/mL vs. 387.6, IQR = 342.0–512.5 ng/mL, p = 0.006) and CITP (4.99, IQR = 3.53–6.85 vs. 4.53, IQR = 3.26–6.22 μg/L, p = 0.024), but not PIIIINP (4.07, IQR = 2.75–5.54 μg/L vs. 3.58, IQR = 2.71–5.01 μg/L, p = 0.29) compared to individuals without depression. Inflammation markers were also elevated in depressed participants (CRP, p = 0.014; WBC, p = 0.075; fibrinogen, p = 0.074), but these inflammation markers did not account for the relationship between depression and fibrosis markers.ConclusionsDepression is associated with elevated fibrosis markers and may therefore adversely affect heart failure and other age-related diseases in which extra-cellular matrix formation plays a pathophysiological role.     

Chronic intermittent hypoxia causes endothelial dysfunction in a mouse model of diet-induced obesity

BackgroundObstructive sleep apnea (OSA) is a common disorder characterized by chronic intermittent hypoxia (CIH). OSA is prevalent in obese subjects and is associated with endothelial dysfunction and cardiovascular disorders. We tested the hypothesis that the deleterious effects of IH could be further modulated by diet-induced obesity.DesignThirty adult (8–10 weeks) male C57BL/6J mice were divided into four groups. Mice were subjected to CIH or intermittent air (IA) for 12 h a day and fed either a high fat (HF) or a low fat control diet (CD) for 6 weeks. We analyzed endothelial function using a wire myograph, and measured markers of oxidative stress (plasma malondialdehyde (MDA) and total antioxidant capacity (TAC)) using colorimetrical assays. We also measured C-reactive protein (CRP) using ELISA and endothelial nitric oxide (eNOS) gene expression using real time PCR.ResultsStimulated endothelial dependent dilation was significantly impaired only in the group fed high fat diet and subjected to CIH (E_max: HFIH 78 ± 2%, p < 0.0001) when compared to the other groups (E_max: HFIA 95 ± 0.7%, CDIH 94 ± 2%, CDIA 97 ± 1%). Also basal endothelial dependant dilation was attenuated in the HFIH group compared to the HFIA group (E_max: HFIH: 179 ± 10% vs. HFIA: 149 ± 11% in the presence of L-NAME). Levels of MDA were elevated in the CDIH group when compared to CDIA (0.68 ± 0.04 vs. 0.41 ± 0.03 μM, p < 0.05) but were greatest in the HFIH group (0.83 ± 0.08 μM, p < 0.05). However, there was no significant increase in MDA levels in the HFIA group (0.45 ± 0.03 μM, p = NS) when compared to all other groups. Similar effects were observed with CRP levels; CRP levels were significantly higher in the CDIH group compared with intermittent air (10.39 ± 0.38 vs. 8.70 ± 0.21 μg/ml, p < 0.05) but the HFIH had the greatest levels of CRP (11.87 ± 0.31 μg/ml, p < 0.05). In the HFIA group, CRP levels were not elevated (9.96 ± 0.37 μg/ml, p = NS). Nevertheless, total antioxidant capacity and eNOS gene expression were not significantly different in the groups.ConclusionCIH caused endothelial dysfunction in mice fed an obesogenic diet. Inflammation and oxidative stress were increased in CIH and an obesogenic diet exacerbated these effects.     

Rapid processing of haptic cues for postural control in blind subjects

ObjectivesVision and touch rapidly lead to postural stabilization in sighted subjects. Is touch-induced stabilization more rapid in blind than in sighted subjects, owing to cross-modal reorganization of function in the blind?MethodsWe estimated the time-period elapsing from onset of availability of haptic support to onset of lateral stabilization in a group of early- and late-onset blinds. Eleven blind (age 39.4 years ± 11.7 SD) and eleven sighted subjects (age 30.0 years ± 10.0 SD), standing eyes closed with feet in tandem position, touched a pad with their index finger and withdrew the finger from the pad in sequence. EMG of postural muscles and displacement of centre of foot pressure were recorded. The task was repeated fifty times, to allow statistical evaluation of the latency of EMG and sway changes following the haptic shift.ResultsSteady-state sway (with or without contact with pad, no haptic shift) did not differ between blind and sighted. On adding the haptic stimulus, EMG and sway diminished in both groups, but at an earlier latency (by about 0.5 s) in the blinds (p <0.01). Latencies were still shorter in the early-than late-blinds. When the haptic stimulus was withdrawn, both groups increased EMG and sway at equally short delays.ConclusionsBlinds are rapid in implementing adaptive postural modifications when granted an external haptic reference. Fast processing of the stabilizing haptic spatial-orientation cues may be favoured by cortical plasticity in blinds.SignificanceThese findings add new information to the field of sensory-guided dynamic control of equilibrium in man.     

Disturbed dreaming during the third trimester of pregnancy

ObjectiveThe majority of women develop sleep impairments during pregnancy, but alterations in dream experiences remain poorly understood. This study aimed to assess prospectively and comparatively the recall of dreaming and of disturbed dreaming in late pregnancy.MethodsFifty-seven nulliparous, third-trimester pregnant women (mean age ± SD, 28.7 ± 4.06 years) and 59 non-pregnant controls (mean age ± SD, 26.8 ± 4.21 years) completed demographics and psychological questionnaires. A 14-day prospective home log assessed sleep and dream characteristics and the Sleep Disorders Questionnaire measured retrospective dream and disturbed dream recall.ResultsEven though pregnant and non-pregnant women showed similar prospective dream recall (P = 0.47), pregnant women reported prospectively more bad dreams (P = 0.004). More pregnant women (21%) than non-pregnant women (7%) reported a nightmare incidence exceeding moderately severe pathology (>1/week) (P = 0.03). Pregnant women also reported overall lower sleep quality (P = 0.007) and more night awakenings (P = 0.003). Higher prospective recall of bad dreams (r = −0.40, P = 0.002) and nightmares (r = −0.32, P = 0.001) both correlated with lower sleep quality in pregnant women.ConclusionsLate pregnancy is a period of markedly increased dysphoric dream imagery that may be a major contributor to impaired sleep at this time. Further polysomnographic assessments of pregnant women are needed to clarify relationships between sleep and disturbed dream production in this population.     

Cerebrospinal fluid ferritin — Unspecific and unsuitable for disease monitoring

Background and purposeSubarachnoid hemorrhage is sometimes difficult to diagnose radiologically. Cerebrospinal fluid (CSF) ferritin has been proposed to be highly specific and sensitive to detect hemorrhagic central nervous system (CNS) disease. We analyzed here the specificity of CSF ferritin in a large series of various CNS diseases and the influence of serum ferritin.Materials and methodsCSF ferritin, lactate, protein and total cell count were analyzed in 141 samples: neoplastic meningitis (n = 62), subarachnoid hemorrhage (n = 20), pyogenic infection (n = 10), viral infection (n = 10), multiple sclerosis (n = 10), borreliosis (n = 5) and normal controls (n = 24). Cerebrospinal fluid ferritin was measured with a microparticle immunoassay. In addition, serum and CSF ferritin were compared in 18 samples of bacterial and neoplastic meningitis.ResultsIn CNS hemorrhage, median ferritin was 51.55 μg/L (sensitivity: 90%) after the second lumbar puncture. In neoplastic meningitis, the median CSF ferritin was 16.3 μg/L (sensitivity: 45%). Interestingly, ferritin was higher in solid tumors than that in hematological neoplasms. In 90% of pyogenic inflammation, ferritin was elevated with a median of 53.35 μg/L, while only 50% of patients with viral infection had elevated CSF ferritin. In ventricular CSF, median ferritin was 163 μg/L, but only 20.6 μg/L in lumbar CSF. Ferritin was normal in multiple sclerosis and borreliosis.ConclusionsFerritin was elevated not only in hemorrhagic disease, but also in neoplastic and infectious meningitis. Ferritin was not a reliable marker of the course of disease. The influence of serum ferritin on CSF ferritin is negligible. We conclude that elevated CSF ferritin reliably, but unspecifically indicates severe CNS disease.     

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.     

The effect of lamotrigine on learning in mice using the passive avoidance model

IntroductionLamotrigine (LTG) is an antiepileptic drug that inhibits the release of glutamate by blocking sodium channels. The present study was conducted to evaluate the effect of LTG in different stages of memory using a passive avoidance learning task in mice.MethodsMale albino mice in the weight range 20–25 g were used. They were divided into four groups (control group and three groups receiving various doses of LTG). LTG was given in three doses of 10, 25, and 50 mg/kg as intraperitoneal (IP) injections. The doses of LTG were used in three injection groups: before acquisition, after consolidation, and before retrieval at 24 h. The retention latency times in each group were recorded using a step-through passive avoidance task 24 h and one week after consolidation.ResultsRetention latency in the group receiving a high dose of LTG (25 mg/kg) after one week was significantly increased in comparison to the group receiving a low dose of LTG (10 mg/kg) (267 ± 49.96 vs. 198.87 ± 57.22, P = 0.015). With injection of LTG after consolidation, the retention latency times were increased in all doses after a one-week retrieval compared to the control (P = 0.023). Kaplan–Mayer surveillance analysis also showed significant differences in the latencies of the LTG-receiving group after 24 h and one week's retrieval (P = 0.041). Administration of LTG before retrieval at 24 h showed a significant difference in retention latency time, which was increased for two doses of LTG (10 and 50 mg/kg) after one week (203.5 ± 63.67 vs. 270.25 ± 19.78, P = 0.024).ConclusionLTG at higher doses may facilitate the learning process in mice and appears to improve memory function at different stages.     

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.     

Sleep and cardiometabolic function in obese adolescent girls with polycystic ovary syndrome

ObjectiveTo compare the polysomnography findings and cardiometabolic function among adolescent girls with polycystic ovary syndrome (PCOS) and matched female and male controls.MethodRetrospective chart review of electronic medical records of 28 girls with PCOS (age: 16.8 ± 1.9 years, body mass index (BMI) Z-score 2.4 ± 0.4), 28 control females (age: 17.1 ± 1.8, BMI Z-score 2.4 ± 0.3) and 28 control males (age: 16.6 ± 1.6, BMI Z-score 2.5 ± 0.5) in a tertiary care centre.ResultsThe prevalence of obstructive sleep apnoea (OSA) was higher in girls with PCOS compared to control females (16/28 (57%) vs. 4/28(14.3%), p < 0.01); however, it was comparable to that of the control males (16/28(57%) vs. 21/28(75%), p = 0.4). Girls with PCOS had a significantly higher prevalence of insulin resistance compared to control females and control males (20/28 (71.4%) vs. 9/22 (41.0%) (p = 0.04) vs. 8/23 (34.8%) (p = 0.01). Among girls with PCOS, those with OSA had significantly higher proportions of metabolic syndrome (MetS) (9/16 (56.3%) vs. 1/12 (8.3%) p = 0.03), higher insulin resistance (14/16 (87.5%) vs. 6/12 (50%), p = 0.04), elevated daytime systolic blood pressure (128.4 ± 12.8 vs. 115.6 ± 11.4, p < 0.01), lower high-density lipoprotein (HDL) (38.6 ± 8.7 vs. 49 ± 10.9, p = 0.01) and elevated triglycerides (TG) (149.7 ± 87.7 vs. 93.3 ± 25.8, p = 0.03) compared to those without OSA.ConclusionsWe report a higher prevalence of OSA and metabolic dysfunction in a selected group of obese girls with PCOS referred with sleep-related complaints compared to BMI-matched control girls without PCOS. We also report higher prevalence of cardiometabolic dysfunction in girls with PCOS and OSA compared to girls with PCOS without OSA.     

Clinicopathologic correlations in 172 cases of rapid eye movement sleep behavior disorder with or without a coexisting neurologic disorder

ObjectiveTo determine the pathologic substrates in patients with rapid eye movement (REM) sleep behavior disorder (RBD) with or without a coexisting neurologic disorder.MethodsThe clinical and neuropathologic findings were analyzed on all autopsied cases from one of the collaborating sites in North America and Europe, were evaluated from January 1990 to March 2012, and were diagnosed with polysomnogram (PSG)-proven or probable RBD with or without a coexisting neurologic disorder. The clinical and neuropathologic diagnoses were based on published criteria.Results172 cases were identified, of whom 143 (83%) were men. The mean ± SD age of onset in years for the core features were as follows – RBD, 62 ± 14 (range, 20–93), cognitive impairment (n = 147); 69 ± 10 (range, 22–90), parkinsonism (n = 151); 68 ± 9 (range, 20–92), and autonomic dysfunction (n = 42); 62 ± 12 (range, 23–81). Death age was 75 ± 9 years (range, 24–96). Eighty-two (48%) had RBD confirmed by PSG, 64 (37%) had a classic history of recurrent dream enactment behavior, and 26 (15%) screened positive for RBD by questionnaire. RBD preceded the onset of cognitive impairment, parkinsonism, or autonomic dysfunction in 87 (51%) patients by 10 ± 12 (range, 1–61) years. The primary clinical diagnoses among those with a coexisting neurologic disorder were dementia with Lewy bodies (n = 97), Parkinson’s disease with or without mild cognitive impairment or dementia (n = 32), multiple system atrophy (MSA) (n = 19), Alzheimer’s disease (AD)(n = 9) and other various disorders including secondary narcolepsy (n = 2) and neurodegeneration with brain iron accumulation-type 1 (NBAI-1) (n = 1). The neuropathologic diagnoses were Lewy body disease (LBD)(n = 77, including 1 case with a duplication in the gene encoding α-synuclein), combined LBD and AD (n = 59), MSA (n = 19), AD (n = 6), progressive supranulear palsy (PSP) (n = 2), other mixed neurodegenerative pathologies (n = 6), NBIA-1/LBD/tauopathy (n = 1), and hypothalamic structural lesions (n = 2). Among the neurodegenerative disorders associated with RBD (n = 170), 160 (94%) were synucleinopathies. The RBD-synucleinopathy association was particularly high when RBD preceded the onset of other neurodegenerative syndrome features.ConclusionsIn this large series of PSG-confirmed and probable RBD cases that underwent autopsy, the strong association of RBD with the synucleinopathies was further substantiated and a wider spectrum of disorders which can underlie RBD now are more apparent.     

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.