IMPORTANCE Little is known of glutamic acid decarboxylase antibodies (GAD-abs) in the paraneoplastic context. Clinical recognition of such cases will lead to prompt tumor diagnosis and appropriate treatment.OBJECTIVE To report the clinical and immunological features of patients with paraneoplastic neurological syndromes (PNS) and GAD-abs. DESIGN, SETTING, AND PARTICIPANTSRetrospective case series study and immunological investigations conducted in February 2014 in a center for autoimmune neurological disorders. Fifteen cases with GAD65-abs evaluated between 1995 and 2013 who fulfilled criteria of definite or possible PNS without concomitant onconeural antibodies were included in this study. MAIN OUTCOMES AND MEASURESAnalysis of the clinical records of 15 patients and review of 19 previously reported cases. Indirect immunofluorescence with rat hippocampal neuronal cultures and cell-based assays with known neuronal cell-surface antigens were used. One hundred six patients with GAD65-abs and no cancer served as control individuals.RESULTS Eight of the 15 patients with cancer presented as classic paraneoplastic syndromes (5 limbic encephalitis, 1 paraneoplastic encephalomyelitis, 1 paraneoplastic cerebellar degeneration, and 1 opsoclonus-myoclonus syndrome). When compared with the 106 non-PNS cases, those with PNS were older (median age, 60 years vs 48 years; P = .03), more frequently male (60% vs 13%; P < .001), and had more often coexisting neuronal cell-surface antibodies, mainly against γ-aminobutyric acid receptors (53% vs 11%; P < .001). The tumors more frequently involved were lung (n = 6) and thymic neoplasms (n = 4). The risk for an underlying tumor was higher if the presentation was a classic PNS, if it was different from stiff-person syndrome or cerebellar ataxia (odds ratio, 10.5; 95% CI, 3.2-34.5), or if the patient had coexisting neuronal cell-surface antibodies (odds ratio, 6.8; 95% CI, 1.1-40.5). Compared with the current series, the 19 previously reported cases had more frequent stiff-person syndrome (74% vs 13%; P = .001) and better responses to treatment (79% vs 27%; P = .005). Predictors of improvement in the 34 patients (current and previously reported) included presentation with stiff-person syndrome and the presence of a thymic tumor. CONCLUSIONS AND RELEVANCEPatients with GAD-abs must be screened for an underlying cancer if they have clinical presentations different from those typically associated with this autoimmunity or develop classic PNS. The risk for cancer increases with age, male sex, and the presence of coexisting neuronal cell-surface antibodies.
Patients, predominantly male, with NMOSD and AQP4-IgG should be investigated for an underlying cancer if they present with nausea and vomiting, or LETM after 45 years of age.
Electroencephalographic neurofeedback (EEG-NFB) represents a broadly used method that involves a real-time EEG signal measurement, immediate data processing with the extraction of the parameter(s) of interest, and feedback to the individual in a real-time. Using such a feedback loop, the individual may gain better control over the neurophysiological parameters, by inducing changes in brain functioning and, consequently, behavior. It is used as a complementary treatment for a variety of neuropsychological disorders and improvement of cognitive capabilities, creativity or relaxation in healthy subjects. In this review, various types of EEG-NFB training are described, including training of slow cortical potentials (SCPs) and frequency and coherence training, with their main results and potential limitations. Furthermore, some general concerns about EEG-NFB methodology are presented, which still need to be addressed by the NFB community. Due to the heterogeneity of research designs in EEG-NFB protocols, clear conclusions on the effectiveness of this method are difficult to draw. Despite that, there seems to be a well-defined path for the EEG-NFB research in the future, opening up possibilities for improvement.
Acute exposure to both hypoxia and bedrest (HBR) results in greater sleep fragmentation due to more awakenings attributed to bedrest, and lighter sleep as a result of reduced slow wave sleep caused by the hypoxic environment.
AimTo examine the effect of acute sleep deprivation under light conditions on the expression of two key clock genes, hPer2 and hBmal1, in peripheral blood mononuclear cells (PBMC) and on plasma melatonin and cortisol levels.MethodsBlood samples were drawn from 6 healthy individuals at 4-hour intervals for three consecutive nights, including a night of total sleep deprivation (second night). The study was conducted in April-June 2006 at the University Medical Centre Ljubljana.ResultsWe found a significant diurnal variation in hPer2 and hBmal1 expression levels under baseline (P < 0.001, F = 19.7, df = 30 for hPer2 and P < 0.001, F = 17.6, df = 30 for hBmal1) and sleep-deprived conditions (P < 0.001, F = 9.2, df = 30 for hPer2 and P < 0.001, F = 13.2, df = 30 for hBmal1). Statistical analysis with the single cosinor method revealed circadian variation of hPer2 under baseline and of hBmal1 under baseline and sleep-deprived conditions. The peak expression of hPer2 was at 13:55 ± 1:15 hours under baseline conditions and of hBmal1 at 16:08 ± 1:18 hours under baseline and at 17:13 ± 1:35 hours under sleep-deprived conditions. Individual cosinor analysis of hPer2 revealed a loss of circadian rhythm in 3 participants and a phase shift in 2 participants under sleep-deprived conditions. The plasma melatonin and cortisol rhythms confirmed a conventional alignment of the central circadian pacemaker to the habitual sleep/wake schedule.ConclusionOur results suggest that 40-hour acute sleep deprivation under light conditions may affect the expression of hPer2 in PBMCs.
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