Search

Background: Walking impairment represents a relevant symptom in patients with neurological diseases often compromising social participation. Currently, mixed methods studies on robot-assisted gait training (RAGT) in patients with rare neurological diseases are lacking. This study aimed to explore the feasibility, acceptability, goal attainment and preliminary effects of RAGT in patients with common and rare neurological diseases and understand the intervention context and process., Methods: A mixed-methods feasibility study was conducted at an Austrian rehabilitation centre. Twenty-eight inpatients after stroke in the subacute and chronic phases, with multiple sclerosis, Parkinson's disease, spinal cord injury, spinocerebellar ataxia, acute/chronic inflammatory demyelinating polyneuropathy and motor neuron disease were included. Patients received RAGT for 45 minutes, 4x/week, for 4 weeks. Baseline and post-intervention assessments included gait parameters, walking and balance, and questionnaires. Semi-structured observations were conducted twice during the intervention period and analysed using thematic analysis. Descriptive statistics within the respective disease groups and calculation of effect sizes for the total sample were performed. Triangulation was employed to develop a deeper understanding of the research topic., Results: Data from 26 patients (mean age 61.6 years [standard deviation 13.2]) were analysed. RAGT was highly accepted by patients and feasible, indicated by recruitment, retention, and adherence rates of 84.8% (95% confidence interval, CI 0.7-0.9), 92.2% (95% CI 0.7-1.0) and 94.0% (95% CI 91.4-96.2), respectively. Goal attainment was high, and only mild adverse events occurred. Improvements in walking speed (10-Metre Walk Test, effect size r = 0.876), walking distance (6-Minute Walk Test, r = 0.877), functional mobility (Timed Up and Go, r = 0.875), gait distance (r = 0.829) and number of steps (r = 0.834) were observed. Four themes were identified: familiarising with RAGT; enjoyment and acceptance through a trusting therapeutic relationship; actively interacting; and minimising dissatisfaction., Discussion: Sufficiently powered randomised controlled trials are needed to validate our results., Trial Registration: German Clinical Trials Register, DRKS00027887., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Hotz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Objectives: To describe changes in balance, walking speed, functional mobility, and eye movements following an activity-oriented physiotherapy (AOPT) or its combination with eye movement training (AOPT-E) in patients with Parkinson's disease (PD). To explore the feasibility of a full-scale randomised controlled trial (RCT)., Methods: Using an assessor-blinded pilot RCT, 25 patients with PD were allocated to either AOPT or AOPT-E. Supervised interventions were performed 30 minutes, 4x/weekly, for 4 weeks, alongside inpatient rehabilitation. Outcomes were assessed at baseline and post-intervention, including dynamic balance, walking speed, functional and dual-task mobility, ability to safely balance, health-related quality of life (HRQoL), depression, and eye movements (number/duration of fixations) using a mobile eye tracker. Freezing of gait (FOG), and falls-related self-efficacy were assessed at baseline, post-intervention, and 4-week follow-up. Effect sizes of 0.10 were considered weak, 0.30 moderate, and ≥0.50 strong. Feasibility was assessed using predefined criteria: recruitment, retention and adherence rates, adverse events, falls, and post-intervention acceptability using qualitative interviews., Results: Improvements were observed in dynamic balance (effect size r = 0.216-0.427), walking speed (r = 0.165), functional and dual-task mobility (r = 0.306-0.413), ability to safely balance (r = 0.247), HRQoL (r = 0.024-0.650), and depression (r = 0.403). Falls-related self-efficacy (r = 0.621) and FOG (r = 0.248) showed varied improvements, partly sustained at follow-up. Eye movement improvements were observed after AOPT-E only. Feasibility analysis revealed that recruitment was below target, with less than two patients recruited per month due to COVID-19 restrictions. Feasibility targets were met, with a retention rate of 96% (95% confidence interval [CI]: 77.68-99.79) and a 98.18% (95% CI: 96.12-99.20) adherence rate, exceeding the targets of 80% and 75%, respectively. One adverse event unrelated to the study intervention confirmed intervention safety, and interview data indicated high intervention acceptability., Conclusions: AOPT-E and AOPT appeared to be effective in patients with PD. Feasibility of a larger RCT was confirmed and is needed to validate results., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Mildner et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Purpose: Radial nerve compression caused by crossing branches of the recurrent radial artery - so called hypertrophic "leash(es) of Henry" (LoH) - is rare. Nevertheless it is important to diagnose the type of compression neuropathy in the forearm., Materials and Methods: We report 2 subjects with unclear neuropathy of the deep branch of the radial nerve (DBRN) who showed compression by an LoH on high resolution ultrasound (HRUS) assessment. The shape and echotexture of the radial nerve were assessed with respect to the typical outer and inner texture of peripheral nerves in HRUS. Using color and/or power Doppler, an exact analysis of the surrounding soft tissues follows to search for possible atypical vessels compressing the nerve., Results: In both patients a hypertrophic leash of Henry was identified with color/power Doppler ultrasound and the direct vascular compression of the DBRN was readily demonstrated. The involved nerve segment was enlarged with a mean transverse diameter of 2.7 mm and 1.9 mm, with a hypoechoic change and partial masking of the inner fascicular texture of the nerve at the level of the LoH., Conclusion: In summary, both presented patients showed a unique topographic concordance of a textural change of the deep radial nerve (i. e., swelling and inner hypoechoic fascicular change) and the causative hypertrophic crossing artery. The use of power Doppler ultrasound in addition to caliber and texture changes shown on grayscale ultrasound and the functional visualization of pulsating vessels should be included in every sonographic examination of patients with chronic forearm pain symptoms., (© Georg Thieme Verlag KG Stuttgart · New York.)

Hypocretin (orexin) cerebrospinal fluid (CSF) levels have been previously found normal or decreased in Dementia with Lewy bodies and Parkinson disease, two synucleinopathies commonly associated with excessive daytime sleepiness (EDS). We evaluated CSF hypocretin-1 levels in 15 patients with moderately severe multiple system atrophy (MSA), another synucleinopathy where sleep disorders occur frequently and EDS has been reported, performing additional electrophysiological studies in 5 of them to assess the presence of EDS and sleep onset REM (SOREM) periods. Despite relatively low sleep efficiencies in nocturnal sleep, mean sleep latencies in the Multiple Sleep Latency Test were normal with no SOREM periods. All patients had CSF hypocretin-1 levels in the normal range (>200 pg/mL) suggesting that the hypocretin system is not altered in MSA, at least in patients with a moderately severe disease., ((c) 2007 Movement Disorder Society.)

We studied the response of the motor cortex to brief trains of suprathreshold repetitive transcranial magnetic stimulations (rTMS) in patients with the Parkinson-variant of multiple system atrophy (MSA-P) and compared it to patients with idiopathic Parkinson's disease (PD) and healthy controls. Eight subjects were studied in each group, and patients were matched for disease severity as assessed by Hoehn & Yahr stages. rTMS was delivered at rest and during low-level contractions in trains of 10 stimulations at 5 Hz, and stimulation intensity was set to result in an motor evoked potential (MEP) in the first dorsal interosseus muscle of 0.5 to 1.0 mV. In MSA-P, MEP amplitude at rest was already reduced after the second stimulus and remained so, while it did not change in PD and controls. During contraction, MEP size did not change during the train in any group. The silent period that followed the last stimulus was of similar duration as the first stimulus in MSA-P, but was increased in PD and controls. These findings indicate that abnormal inhibition occurs within the motor cortex in MSA-P, despite dopaminergic treatment and indicate differences in cortical dysfunction between MSA-P and PD. We suggest that these abnormalities reflect the motor cortex pathology found in MSA-P., ((c) 2006 Movement Disorder Society.)

Although multiple system atrophy (MSA) is a neurodegenerative disorder leading to progressive disability and decreased life expectancy, little is known about patients' own evaluation of their illness and factors associated with poor health-related quality of life (Hr-QoL). We, therefore, assessed Hr-QoL and its determinants in MSA. The following scales were applied to 115 patients in the European MSA-Study Group (EMSA-SG) Natural History Study: Medical Outcome Study Short Form (SF-36), EQ-5D, Beck Depression Inventory (BDI), Mini-Mental state examination (MMSE), Unified MSA Rating Scale (UMSARS), Hoehn & Yahr (H&Y) Parkinson's disease staging scale, Composite Autonomic Symptom Scale (COMPASS), and Parkinson's Disease Sleep Scale (PDSS). Forty-six percent of patients had moderate to severe depression (BDI > or = 17); Hr-QoL scores on the SF-36 and EQ-5D were significantly impaired. Pain, the only domain with similar scores in MSA and published PD patients, was reported more frequently in patients with MSA-P (predominantly parkinsonian motor subtype) than MSA-C (predominantly cerebellar motor subtype; 76% vs. 50%; P = 0.005). Hr-QoL scores correlated most strongly with UMSARS motor, COMPASS, and BDI scores but not with MMSE scores, age at onset, or disease duration. The COMPASS and UMSARS activities of daily living scores were moderate-to-strong predictors for the SF-36 physical summary score and the BDI and UMSARS motor scores for the SF-36 mental summary score. This report is the first study to show that Hr-QoL is significantly impaired in MSA. Although not all possible factors related to impaired Hr-QoL in MSA could be assessed, autonomic dysfunction, motor impairment, and depression were most closely associated with poor Hr-QoL, and therapeutic management, therefore, should concentrate upon these aspects of the disease.

A huge amount of evidence has implicated amyloid beta (A beta) peptides and other derivatives of the amyloid precursor protein (beta APP) as central to the pathogenesis of Alzheimer's disease (AD). It is also widely recognized that age is the most important risk factor for AD and that the innate immune system plays a role in the development of neurodegeneration. Little is known, however, about the molecular mechanisms that underlie age-related changes of innate immunity and how they affect brain pathology. Aging is characteristically accompanied by a shift within innate immunity towards a pro-inflammatory status. Pro-inflammatory mediators such as tumour necrosis factor-alpha or interleukin-1 beta can then in combination with interferon-gamma be toxic on neurons and affect the metabolism of beta APP such that increased concentrations of amyloidogenic peptides are produced by neuronal cells as well as by astrocytes. A disturbed balance between the production and the degradation of A beta can trigger chronic inflammatory processes in microglial cells and astrocytes and thus initiate a vicious circle. This leads to a perpetuation of the disease.

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that usually manifests in the early sixth decade of life and progresses relentlessly with a mean survival of 9 years. Clinically, MSA is dominated by autonomic/urogenital failure, which may be associated with either levodopa (L-dopa) -unresponsive parkinsonism in 80% of cases (MSA-P subtype) or with cerebellar ataxia in 20% of cases (MSA-C subtype). Pathologically, MSA is characterized by a neuronal multisystem degeneration and abnormal glial cytoplasmic inclusions containing alpha-synuclein aggregates. Pharmacological treatment of motor features is disappointing except for a transient L-dopa response in a minority of MSA-P patients. In contrast, autonomic and urogenital features of MSA should be identified early on, because they can be treated effectively in many instances. Neuroprotective strategies are presently unavailable, however, two multicentre European trials have been launched to evaluate the effects of riluzole and human recombinant growth hormone on disease progression in MSA. Clearly, further randomised, controlled trials are required to identify effective symptomatic or neuroprotective agents in MSA. Several in vivo models have become available to allow a careful preselection of candidate agents. Several research groups have been formed in Europe (EMSA-SG, NNIPPS) and United States (NAMSA-SG), providing a framework for coordinated trial activity in MSA., (Copyright 2003 Movement Disorder Society)