A 47-year-old woman with Parkinson disease (PD) complicated by severe motor fluctuations had been treated with deep brain stimulation (DBS) for 11 years and intestinal carbidopa/levodopa infusion for 5 years. Three months after her most recent clinic visit, at which both the DBS and infusion pump systems were confirmed to be functioning appropriately, she presented to the emergency department with abnormal movements. On examination, she had continuous, generalized, involuntary hyperkinetic movements with an erratic, dance-like quality, consistent with levodopa-associated dyskinesia. Evaluation revealed rhabdomyolysis, subcutaneous emphysema, and pneumomediastinum. She required admission to the intensive care unit for sedation and airway protection. After a key surgical intervention, she rapidly returned to her previous neurologic status and was discharged home. This case highlights the approach to acute dyskinesia and underscores the challenges of managing severe motor fluctuations in patients with PD.

Striatal Dopamine Transporter and Rest Tremor in Parkinson Disease: A Clinical Validation.

Physical frailty has been longitudinally linked to multiple neurologic disorders but has not yet been extrapolated to epilepsy. The study aimed to investigate the prospective association between physical frailty and incident epilepsy and to explore potential biological processes associated with this relationship. This prospective cohort study included 421,383 UK Biobank participants free of epilepsy, Parkinson disease, dementia, stroke, or migraine at baseline. Physical frailty status was assessed using a modified Fried frailty phenotype model based on 5 components (weight loss, exhaustion, low physical activity, slow gait speed, and low grip strength) that categorized participants as nonfrail, prefrail, or frail. Incident epilepsy was ascertained through linked health records. Cox proportional hazard models were conducted to calculate hazard ratios (HRs) and 95% CIs for the association between physical frailty and incident epilepsy. Hypothesis-driven mediation analyses were used to investigate potential biological pathways associated with the frailty-epilepsy association. During a mean follow-up of 13.2 years, 2,752 incident epilepsy cases were identified. Compared with nonfrail individuals, the multivariable-adjusted HRs (95% CIs) for incident epilepsy among those with prefrailty and frailty were 1.29 (1.19-1.40) and 1.81 (1.54-2.13), respectively. Among the 5 frailty components, slow gait speed (HR 1.46; 95% CI 1.29-1.65), low grip strength (HR 1.19; 95% CI 1.08-1.32), exhaustion (HR 1.18; 95% CI 1.06-1.32), and weight loss (HR 1.17; 95% CI 1.06-1.29) were associated with higher hazards of incident epilepsy. Biomarker analyses observed that blood biomarkers reflecting liver and kidney function, immune-inflammatory response, endocrine activity, and hematologic profiles were associated with both frailty and incident epilepsy and may collectively explain approximately 18.57% (95% CI 13.18%-26.83%) of the frailty-epilepsy association. In addition, several metabolically related biomarkers, involving lipoprotein particle size, amino acids, ketone bodies, total lipids, and triglycerides, were identified as potential contributors. Physical frailty was associated with a higher incidence of epilepsy in this prospective cohort. Biomarker analyses provided preliminary insights into biological domains potentially related to this association, including organ function, inflammation, endocrine regulation, hematologic status, and metabolic homeostasis.

Quantitative ultrasound radiofrequency analysis for monitoring Parkinson's disease.

In vivo classification of neuropathological disease stages in Parkinson's disease by diffusion tensor imaging.

Molecular neuroimaging of Parkinson's disease: association of motor and non-motor symptoms with synaptic density, dopaminergic and serotonergic systems.

Causal relationships between plasma lipidomics, trace elements, cerebrospinal fluid metabolites, and Parkinson's disease using Mendelian randomization.

Salivary dysfunction, including xerostomia and drooling, is common in Parkinson's disease and further impairs oral health and quality of life, which are already compromised in this population. Their effective management demands deeper insight into the complexity of salivary dysfunction. To examine the occurrence and associations of xerostomia and drooling complaints in individuals with Parkinson's disease. 111 individuals with Parkinson's disease (69.9 ± 7.7 years; 46.8% female) participated in an online survey. The questionnaire used validated scales (e.g., Xerostomia Inventory) and original questions. After descriptive analyses, multiple linear regression analyses identified factors (e.g., severity of motor impairment) associated with severity of xerostomia and drooling. Xerostomia (64.9%) and drooling (27.0%) were common, with 18.0% of the individuals experiencing both concurrently. Xerostomia was associated with the presence of jaw symptoms (B = 4.63; 95% CI 1.86-7.40), chewing gum usage (B = 1.27; 95% CI 0.52-2.02), swallowing difficulties (B = 0.41; 95% CI 0.04-0.78) and taste alterations (B = 0.15; 95% CI 0.00-0.30). Drooling was associated with the severity of motor impairment (B = 0.40; 95% CI 0.18-0.60) and with swallowing difficulties (B = 0.64; 95% CI 0.14-1.15). Xerostomia and drooling complaints frequently co-occur in individuals with Parkinson's disease. To prevent further deterioration of the oral health-related quality of life, a comprehensive evaluation of the underlying aetiology of salivary issues in people with Parkinson's disease is crucial to assist in determining suitable treatment.

Mobile EEG assessment of inhibitory control during dual-task walking in Parkinson's disease.

A liver-mitochondria-immune axis in Parkinson's disease: emerging perspectives on a hepatic origin for mitochondrial autoimmunity as a driver of Parkinson's disease.

Risk of somatoform and sleep-related disorders in Parkinson's disease: A nationwide matched cohort study.

Association of choroid plexus volume with MRI indices of DTI-derived parameters and perivascular spaces in patients with neurodegenerative diseases.

Association between auditory event-related potential latencies and apathy severity in Parkinson's disease: a cross-sectional study.

An update on the monogenic causes of Parkinson's disease: Impact on patient stratification and personalised medicine.

Research progress on employing medicinal plants and their active compounds to target autophagic pathways for Parkinson's disease therapy.

New evidence on the clinical, genetic, and biochemical bases of GBA1-Parkinson's disease: prospects for treatment.

Motor memory consolidation is a process by which newly acquired skills become stable over time in the absence of practice. Sleep facilitates consolidation, yet it remains unknown whether sleep-dependent consolidation is intact in people with Parkinson's disease. Here, we investigated whether a post-learning nap-as compared to wakefulness-improves motor memory consolidation in Parkinson. Thirty-two people with Parkinson's disease and 32 healthy older adults learnt a finger-tapping sequence task before a nap or wake intervention (pseudo-randomised assignment). Consolidation was measured as the change in performance between pre- and post-intervention and at 24-h retention. Automaticity was measured with dual-task cost, assessed at post-intervention and at post-night. Sleep architecture and electrophysiological markers of plasticity were extracted from the post-learning nap, to assess their association with performance change. The behavioural results suggest similar consolidation effects after sleep and wakefulness in both populations. Moreover, there was no effect of napping automaticity. Results also suggest positive associations between performance improvement and slow wave amplitude and slope in people with Parkinson's disease, and inconclusive associations between cross-frequency coupling and performance change in both populations. To conclude, napping did not have a beneficial effect on the consolidation of a finger-tapping task as compared to wakefulness in either people with Parkinson's disease or healthy older adults. Finally, in patients, sleep markers of plasticity were associated with performance improvements, implying that equivalent memory consolidation may be differently associated to sleep-related processes in Parkinson's and healthy ageing. Trial Registration: NCT04144283.

Fixational microsaccades (FM) encompass the involuntary, small-scale movements of the eye that occur as we attempt to fixate on a single point. These movements are crucial for maintaining a steady visual perception despite our gaze's constant, subtle changes. FM is significant because it can serve as an indicator of central nervous system disorders; for example, altered FM correlated with multiple sclerosis disability levels and disease progression. This study aims to characterize FM in patients with Parkinson disease (PD). Fourteen older adults (age 71.0 ± 7.2 years, 6 females) with PD and 17 controls (age 73.4 ± 4.4 years, 15 females) were recruited. Retinal motion traces were recorded using a tracking scanning laser ophthalmoscope (TSLO, RetiTrack, C. Light Technologies, Cambridge, MA). The number of FM, saccade amplitude, velocity, peak velocity, and frequency were measured. All FM measurements were significantly different between PD and controls (P values < 0.05): the number of saccades (19.45 ± 7.40 vs 10.19 ± 6.69, P = 0.001), average amplitude (0.44 ± 0.15 vs 0.33 ± 0.10°, P = 0.027), average velocity (7.45 ± 1.44 vs 6.46 ± 0.96°/s, P = 0.037), average peak velocity (10.48 ± 2.99 vs 8.49 ± 2.03°/s, P = 0.044), and saccade frequency (1.95 ± 0.74 vs 1.07 ± 0.69 Hz, P = 0.002). Furthermore, the average amplitude strongly correlated with the Movement Disorders Society-sponsored Unified Parkinson Disease Rating Scale part III (MDS UPDRS III) motor subscale (r = 0.62, P = 0.02) and the Unified Parkinson Disease Rating Scale Hoehn and Yahr Stage (UPDRS HY Stage) (r = 0.62, P = 0.02). Similarly, average velocity and average peak velocity significantly correlated with both UPDRS III (r = 0.56, P = 0.04) and UPDRS HY Stage (r = 0.59, P = 0.03-0.04). These results indicated that PD patients had larger, more frequent, and quicker microsaccades, which were associated with disease severity. To our knowledge, this is the first study to characterize FM using TSLO in patients with PD. The tracking scanning laser ophthalmoscope appears to have high precision and sensitivity, offering detailed, real-time retinal imaging with minimal motion artifact. The results indicate that impaired fixational microsaccades in PD correlate with disease severity, suggesting that altered FM could serve as a biomarker for progression and treatment response.

Comparative analysis of static and dynamic postural balance control in multiple system atrophy and Parkinson's disease using an intermittent control model.

Up-regulation of tRNA-derived miR-1274b in tears of Parkinson's disease patients.