ObjectiveFunctional processes in the brain are segregated in both the spatial and spectral domain. Motivated by findings reported at the cortical level in healthy participants we test the hypothesis in the basal ganglia of Parkinson’s disease patients that lower frequency beta band activity relates to motor circuits associated with the upper limb and higher beta frequencies with lower limb movements.MethodsWe recorded local field potentials (LFPs) from the subthalamic nucleus using segmented “directional” DBS leads, during which patients performed repetitive upper and lower limb movements. Movement-related spectral changes in the beta and gamma frequency-ranges and their spatial distributions were compared between limbs.ResultsWe found that the beta desynchronization during leg movements is characterised by a strikingly greater involvement of higher beta frequencies (24–31 Hz), regardless of whether this was contralateral or ipsilateral to the limb moved. The spatial distribution of limb-specific movement-related changes was evident at higher gamma frequencies.ConclusionLimb processing in the basal ganglia is differentially organised in the spectral and spatial domain and can be captured by directional DBS leads.SignificanceThese findings may help to refine the use of the subthalamic LFPs as a control signal for adaptive DBS and neuroprosthetic devices. 相似文献
ObjectiveWe aimed to establish an objective neurophysiological test protocol that can be used to assess the somatosensory nervous system.MethodsIn order to assess most fiber subtypes of the somatosensory nervous system, repetitive stimuli of seven different modalities (touch, vibration, pinprick, cold, contact heat, laser, and warmth) were synchronized with the electroencephalogram (EEG) and applied on the cheek and dorsum of the hand and dorsum of the foot in 21 healthy subjects and three polyneuropathy (PNP) patients. Latencies and amplitudes of the modalities were assessed and compared. Patients received quantitative sensory testing (QST) as reference.ResultsWe found reproducible evoked potentials recordings for touch, vibration, pinprick, contact-heat, and laser stimuli. The recording of warm-evoked potentials was challenging in young healthy subjects and not applicable in patients. Latencies were shortest within Aβ-fiber-mediated signals and longest within C-fibers. The test protocol detected function loss within the Aβ-fiber and Aδ-fiber-range in PNP patients. This function loss corresponded with QST findings.ConclusionIn this pilot study, we developed a neurophysiological test protocol that can specifically assess most of the somatosensory modalities. Despite technical challenges, initial patient data appear promising regarding a possible future clinical application.SignificanceEstablished and custom-made stimulators were combined to assess different fiber subtypes of the somatosensory nervous system using modality-specific evoked potentials. 相似文献
Objective: To assess the relationship between the Screen for Cognitive Impairment in Psychiatry (SCIP) score and illness severity, subjective cognition and functioning in a cohort of major depressive disorder (MDD) patients.
Methods: Patients (n?=?40) diagnosed with MDD (DSM-IV-TR) completed the SCIP, a brief neuropsychological test, and a battery of self-administered questionnaires evaluating functioning (GAF, SDS, WHODAS 2.0, EDEC, PDQ-D5). Disease severity was evaluated with the Hamilton Depression Rating Scale (HDRS) and the Clinical Global Impression (CGI).
Results: Age and sex were associated with performance in the SCIP. The SCIP-Global index score was associated with disease severity (r?=??0.316, p?<?.05), the SDS, a patient self-assessment of daily functioning (r?=??0.368, p?<?.05), and the EDEC subscales of patient-reported cognitive deficits (r?=??0.388, p?<?.05) and their functional impacts (r?=??0.335, p?<?.05). Multivariate analysis adjusted for age and sex confirmed these tests are independent predictors of performance in the SCIP (CGI-S, F[3,34]?=?4.478, p?=?.009; SDS, F[3,34]?=?3.365, p?=?.030; EDEC-perceived cognitive deficits, F[3,34]?=?5.216, p?=?.005; EDEC-perceived impacts of functional impairment, F[3,34]?=?5.154, p?=?.005).
Conclusions: This study confirms that the SCIP can be used during routine clinical evaluation of MDD, and that cognitive deficits objectively assessed in the SCIP are associated with disease severity and self-reported cognitive dysfunction and impairment in daily life. 相似文献
ObjectiveHomonymous visual field deficits (HFVDs) are frequent following brain lesions. Current restoration treatments aim at activating areas of residual vision through numerous stimuli, but show limited effect. Recent findings suggest that spontaneous neural α-band coupling is more efficient for enabling visual perception in healthy humans than task-induced activations. Here, we evaluated whether it is also associated with the severity of HFVD.MethodsTen patients with HFVDs after brain damage in the subacute to chronic stage and ten matched healthy controls underwent visual stimulation with alternating checkerboards and electroencephalography recordings of stimulation-induced power changes and of spontaneous neural interactions during rest.ResultsVisual areas of the affected hemisphere showed reduced event-related power decrease in α and β frequency bands, but also reduced spontaneous α-band interactions during rest, as compared to contralesional areas and healthy controls. A multivariate stepwise regression retained the degree of disruption of spontaneous interactions, but not the reduced task-induced power changes as predictor for the severity of the visual deficit.ConclusionsSpontaneous α-band interactions of visual areas appear as a better marker for the severity of HFVDs than task-induced activations.SignificanceTreatment attempts of HFVDs should try to enhance spontaneous α-band coupling of structurally intact ipsilesional areas. 相似文献
BackgroundConcern about adverse events following immunization is frequently cited by both those who receive or decline vaccines. Neurological adverse events are especially concerning.ObjectivesOur aim was to detect associations between seasonal influenza vaccination and the occurrence of severe anesthesia/paresthesia or severe headaches.MethodsData were analyzed from the Canadian National Vaccine Safety network. Events occuring on days 0–7 were self-reported and prevented daily activity, led to school or work absenteeism, or required medical attention. Controls were the previous year’s vaccinees; events in controls were collected prior to the start of the influenza vaccination program of each year (2012/13 through 2016/17). Multivariable logistic regression was used to determine the association between seasonal influenza vaccination and the occurrence of anesthesia/paresthesia or severe headaches.ResultsThe total sample was 107,565 for investigating anesthesia/paresthesia and 97,420 for investigating severe headaches. Anesthesia/paresthesia was reported by 104/107,565 (0.10%) participants; 63/69,129 (0.09%) vaccinees and 41/38,436 (0.11%) controls (adjusted odds ratio (aOR) = 0.89; 95% CI = 0.60, 1.32). Severe headaches were reported by 1361/97,420 (1.40%) participants; 907/61,463 (1.48%) vaccinees and 454/35,957 (1.26%) controls (aOR = 1.21; 95% CI = 1.08, 1.36). No specific vaccine product was associated with severe headaches.ConclusionsOur study found no association between severe anesthesia/paresthesia and seasonal influenza vaccination. While there was an association with severe headaches as an adverse event following influenza vaccination, the rates of these events are similar to rates reported from clinical trials and are not a cause for additional concern. 相似文献
Background:The results of published articles on the relationship between the Val158Met polymorphism in the (Catechol-O-methyltransferase) COMT gene and the susceptibility of attention-deficit hyperactive disorder (ADHD) are controversial. We conducted an updated meta-analysis of case-control studies to assess the relationship between Val158Met polymorphism in COMT gene and ADHD susceptibility.Methods:A comprehensive literature search was conducted to identify all the case-control studies on the relationship between the COMT gene Val158Met polymorphism and ADHD susceptibility. According to the heterogeneity test results among studies evaluated with I2, the fixed effect model or random effect model was selected as the pooling method. Meta-regression as well as sensitive analysis were used to explore possible causes of between-study heterogeneity. The funnel plot and Harbord test were used to estimate publication bias.Results:Finally, seventeen studies that met the inclusion criteria were included. The Val158Met genotype distributions of COMT gene in controls were in Hardy–Weinberg equilibrium in all studies. In general, there was no significant association between the COMT gene Val158Met polymorphism and ADHD susceptibility in dominant, recessive, and codominant models. The recessive genetic model (I2 = 60.8%) showed strong heterogeneity among studies, and still no significant association was found after sensitivity analysis. Subgroup analysis stratified by ethnicity (Asian and Caucasian) also showed that there was no significant association in the above-mentioned three models.Conclusions:This updated meta-analysis indicated that the Val158Met polymorphism in the COMT gene may not be related to the risk of ADHD. Further researches are needed to confirm these results. 相似文献
Animal models of human diseases are crucial experimental tools to investigate the mechanisms involved in disease pathogenesis and to develop new therapies. In spite of the numerous animal models currently available that reproduce several neuropathological features of Parkinson disease (PD), it is challenging to have one that consistently recapitulates human PD conditions in both motor behaviors and biochemical pathological outcomes. Given that, we have implemented a new paradigm to expose rats to a chronic low dose of paraquat (PQ), using osmotic minipumps and characterized the developed pathologic features over time. The PQ exposure paradigm used lead to a rodent model of PD depicting progressive nigrostriatal dopaminergic neurodegeneration, characterized by a 41% significant loss of dopaminergic neuron in the substantia nigra pars compacta (SNpc), a significant decrease of 18% and 40% of dopamine levels in striatum at week 5 and 8, respectively, and a significant 1.5‐fold decrease in motor performance. We observed a significant increase of microglia activation state, sustained levels of α‐synucleinopathy and increased oxidative stress markers in the SNpc. In summary, this is an explorative study that allowed to characterize an improved PQ‐based rat model that recapitulates cardinal features of PD and may represent an attractive tool to investigate several mechanisms underlying the various aspects of PD pathogenesis as well as for the validation of the efficacy of new therapeutic approaches that targets different mechanisms involved in PD neurodegeneration. 相似文献