Decline In Motor Function Research Articles

Deterioration in Motor Function Over Time in Older Adults With Type 2 Diabetes is Associated with Accelerated Cognitive Decline

Type 2 diabetes (T2D) is associated with motor impairments and a higher dementia risk. The relationships of motor decline with cognitive decline in T2D older adults has rarely been studied. Using data from the Israel Diabetes and Cognitive Decline study (N = 892), we examined associations of decline in motor function with cognitive decline over a 54-month period. Motor function measures were strength (handgrip) and gait speed (time to walk 3 m). Participants completed a neuropsychologic battery of 13 tests transformed into z-scores, summarized into 4 cognitive domains: episodic memory, attention/working memory, executive functions, and language/semantic categorization. The average of the 4 domains' z-scores defined global cognition. Motor and cognitive functions were assessed in 18-months intervals. A random coefficients model delineated longitudinal relationships of cognitive decline with baseline and change from baseline in motor function, adjusting for sociodemographic, cardiovascular, and T2D-related covariates. Slower baseline gait speed levels were significantly associated with more rapid decline in global cognition (P = .004), language/semantic categorization (P = .006) and episodic memory (P = .029). Greater decline over time in gait speed was associated with an accelerated rate of decline in global cognition (P = .050), attention/working memory (P = .047) and language/semantic categorization (P<.001). Baseline strength levels were not associated with cognitive decline but the rate of declining strength was associated with an accelerated decline in executive functions (P = .025) and language/semantic categorization (P = .006). In T2D older adults, the rate of decline in motor function, beyond baseline levels, was associated with accelerated cognitive decline, suggesting that cognitive and motor decline share common neuropathologic mechanisms in T2D.

Cardiac sympathetic dysfunction associated with dopaminergic depletion in striatal subregions in de novo Parkinson's disease

Objective: It has been documented that low cardiac uptake of 123I-metaiodobenzylguanidine (MIBG) at early stage of illness is associated fast decline in motor and cognitive function in patients with Parkinson's disease (PD). The aim of this study is to investigate the association between cardiac sympathetic dysfunction and striatal subregional dopaminergic depletion in patients with PD.

Cognition and motor function: The gait and cognition pooled index.

There is a need for outcome measures with improved responsiveness to changes in pre-dementia populations. Both cognitive and motor function play important roles in neurodegeneration; motor function decline is detectable at early stages of cognitive decline. This proof of principle study used a Pooled Index approach to evaluate improved responsiveness of the predominant outcome measure (ADAS-Cog: Alzheimer's Disease Assessment Scale-Cognitive Subscale) when assessment of motor function is added. Candidate Pooled Index variables were selected based on theoretical importance and pairwise correlation coefficients. Kruskal-Wallis and Mann-Whitney U tests assessed baseline discrimination. Standardized response means assessed responsiveness to longitudinal change. Final selected variables for the Pooled Index include gait velocity, dual-task cost of gait velocity, and an ADAS-Cog-Proxy (statistical approximation of the ADAS-Cog using similar cognitive tests). The Pooled Index and ADAS-Cog-Proxy scores had similar ability to discriminate between pre-dementia syndromes. The Pooled Index demonstrated trends of similar or greater responsiveness to longitudinal decline than ADAS-Cog-Proxy scores. Adding motor function assessments to the ADAS-Cog may improve responsiveness in pre-dementia populations.

Brain pathologies are associated with both the rate and variability of declining motor function in older adults.

Brain pathologies are associated with both the rate and variability of declining motor function in older adults.

Motor outcome measures in patients with FKRP mutations: A longitudinal follow-up.

To test the hypothesis that we will be able to detect change in motor outcome measures over time in a cohort with mutations in FKRP. Individuals with documented FKRP mutations were evaluated annually with a battery of established motor outcome measures including limited quantitative myometry and timed function measures. Results were analyzed using random coefficient regression to determine annual change in each measure. Due to the nonlinear progression through the lifespan of the study participants, pediatric (<19 years) and adult (≥19 years) cohorts were analyzed separately. Effect of genotype was evaluated in each cohort. Sixty-nine participants (30 pediatric, 44 adult) with at least 2 evaluations were included. There was a small but statistically significant decline in timed motor function measures in both pediatric and adult cohorts. Genotype significantly affected rate of decline in the pediatric but not the adult cohort. Some pediatric patients who are homozygous for the c.826C>A mutation showed improving motor performance in adolescence. Performance on the 10-meter walk/run was highly correlated with other timed function tests. There is a slow annual decline in motor function in adults with FKRP mutations that can be detected with standard motor outcome measures, while the results in the pediatric population were more variable and affected by genotype. Overall, these analyses provide a framework for development of future clinical trials. The dystroglycanopathies natural history study (Clinical Trial Readiness for the Dystroglycanopathies) may be found on clinicaltrials.gov (NCT00313677).

Muscle strength and motor function in adolescents and adults with spinal muscular atrophy.

To assess longitudinal patterns of muscle strength, motor function, and maximal compound muscle action potential amplitudes (CMAPMAX) in older patients with spinal muscular atrophy (SMA), hypothesizing a continued decline of motor function parameters throughout life. We measured muscle strength (Medical Research Council), motor function (Hammersmith Functional Motor Scale Expanded [HFMSE] and Motor Function Measure), and CMAPMAX in treatment-naive patients. We used both longitudinal and cross-sectional data in mixed models to analyze natural history patterns. We included 250 patients with SMA types 1c through 4. Median patient age at assessment was 26.8 years, the number of assessments per patient ranged from 1 to 6. Baseline muscle strength and motor function scores differed significantly between SMA types, but annual rates of decline were largely similar and mostly linear. HFMSE floor effects were present for all patients with SMA type 1c, and adolescents and adults with types 2 and 3a. CMAPMAX differed significantly between SMA types but did not decline significantly with increasing age. Muscle strength correlated very strongly with motor function (τ ≥ 0.8) but only moderately with CMAPMAX (τ ≈ 0.5-0.6). Muscle strength and motor function decline in older patients with SMA are constant without periods of slower progression or a plateau phase. The floor effects of the HFMSE preclude its use for long-term follow-up of adult patients with SMA types 1c through 3a. Muscle strength sum scores represent an alternative, feasible outcome measure for adolescent and adult patients with SMA.

Safety of intrathecal delivery of recombinant human arylsulfatase A in children with metachromatic leukodystrophy: Results from a phase 1/2 clinical trial

BackgroundMetachromatic leukodystrophy (MLD) is an autosomal recessive disorder caused by deficient arylsulfatase A (ASA) activity and characterized by neurological involvement that results in severe disability and premature death. We examined the safety and tolerability of intrathecally delivered recombinant human ASA (rhASA; SHP611, now TAK-611) in children with MLD (NCT01510028). Secondary endpoints included change in cerebrospinal fluid (CSF) sulfatide and lysosulfatide levels, and motor function (assessed by Gross Motor Function Measure-88 total score). MethodsTwenty-four children with MLD who experienced symptom onset aged ≤ 30 months were enrolled. Patients received rhASA every other week (EOW) for 38 weeks at 10, 30, or 100 mg (cohorts 1–3; n = 6 per cohort), or 100 mg manufactured using a revised process (cohort 4; n = 6). ResultsNo rhASA-related serious adverse events (SAEs) were observed; 25% of patients experienced an SAE related to the intrathecal device or drug delivery method. Mean CSF sulfatide and lysosulfatide levels fell to within normal ranges in both 100 mg cohorts following treatment. Although there was a general decline in motor function over time, there was a tendency towards a less pronounced decline in patients receiving 100 mg. ConclusionIntrathecal rhASA was generally well tolerated at doses up to 100 mg EOW. These preliminary data support further development of rhASA as a therapy for patients with MLD.

Influence of pilates method training on the balance of the elderly: a systematic review

Introduction: Getting older is a process characterized by physical changes, which include, among other, the loss of reproductive function and the decline of motor function and it is sometimes associated with chronic diseases. The aging process induces a natural functional decline, and considering this phenomenon, it is primordial research studies that indicate interventions that promote improvements in the health status of the elderly. Objective: To analyse, through a sistemic review, the effects of the pilates method on the static and dinamic balance in the elderly. Method: This systematic review followed the recommendations of the Preferred Reporting Itens for Systematic Reviews and Meta-Analyses (PRISMA) and the searches were carried out in database: IBECS, PubMed, LILACS, EMBASE, SCIELO e PEDro from descriptors “pilates, exercício físico e idosos”, and their names in english and spanish. Results: There were analysed 11 original articles about the theme and most of them showed positive results of the pilates method on the static and dinamic balance in the elderly. Conclusion: The pilates method showed significant results on the static and dinamic balance in the elderly, but there should be better quality studies to guarantee its effectiveness.

H63D variant of the homeostatic iron regulator (HFE) gene alters α-synuclein expression, aggregation, and toxicity.

Pathological features of Parkinson's disease include the formation of Lewy bodies containing α-synuclein and the accumulation of iron in the substantia nigra. Previous studies have suggested that iron accumulation contributes to the Parkinson's disease pathology through reactive oxygen species production and accelerated α-synuclein aggregation. This study examines the effects of commonly occurring H63D variant of the homeostatic iron regulatory (HFE) gene on α-synuclein pathology in cell culture and animal models. H63D HFE expression in SH-SY5Y cells lowered endogenous α-synuclein levels and significantly decreased pre-formed fibril-induced α-synuclein aggregation. H63D HFE cells were also protected from pre-formed fibril-induced apoptosis. Autophagic flux, a major pathway for α-synuclein clearance, was increased in H63D HFE cells. Expression of REDD1 was elevated and rapamycin treatment was unable to further induce autophagy, indicating mTORC1 inhibition as the main mechanism of autophagy induction. Moreover, siRNA knockdown of REDD1 in H63D HFE cells decreased autophagic flux and increased the sensitivity to PFF-mediated toxicity. While iron chelator (deferiprone) treatment rescued WT HFE cells from pre-formed fibril toxicity, it exacerbated or was unable to rescue H63D HFE cells. In the in vivo pre-formed fibril intracranial injection model, H67D Hfe (mouse homolog of the human H63D HFE variant) C57BL/6J×129 mice showed less α-synuclein aggregation and less decline in motor function compared to WT Hfe. Collectively, this study suggests that H63D HFE variant modifies α-synuclein pathology through the induction of autophagy and has the potential to impact the pathogenesis and treatment response in Parkinson's disease.

Motor neuroplasticity: A MEG-fMRI study of motor imagery and execution in healthy ageing

Age-related decline in motor function is associated with over-activation of the sensorimotor circuitry. Using a multimodal MEG-fMRI paradigm, we investigated whether this neural over-recruitment in old age would be related to changes in movement-related beta desynchronization (MRBD), a correlate of the inhibitory neurotransmitter γ-aminobutyric acid (GABA), and whether it would characterize compensatory recruitment or a reduction in neural specialization (dedifferentiation). We used MEG to assess age-related changes in beta band oscillations in primary motor cortices, fMRI to localize age-related changes in brain activity, and the Finger Configuration Task to measure task performance during overt and covert motor processing: motor execution (ME) and motor imagery (MI). The results are threefold: first, showing age-related neuroplasticity during ME of older adults, compared to young adults, as evidenced by increased MRBD in motor cortices and over-recruitment of sensorimotor areas; second, showing similar age-related neuroplastic changes during MI; and finally, showing signs of dedifferentiation during ME in older adults whose performance negatively correlated with connectivity to bilateral primary motor cortex. Together, these findings demonstrate that elevated MRBD levels, reflecting greater GABAergic inhibitory activity, and over-activation of the sensorimotor network during ME may not be compensatory, but rather might reflect an age-related decline of the quality of the underlying neural signal.

Risk Assessment by Presurgical Tractography Using Navigated TMS Maps in Patients with Highly Motor- or Language-Eloquent Brain Tumors.

Patients with functionally eloquent brain lesions are at risk of functional decline in the course of resection. Given tumor-related plastic reshaping and reallocation of function, individual data are needed for patient counseling and risk assessment prior to surgery. This study evaluates the utility of mapping by navigated transcranial magnetic stimulation (nTMS) and nTMS-based diffusion tensor imaging fiber tracking (DTI FT) for individual risk evaluation of surgery-related decline of motor or language function in the clinical setting. In total, 250 preoperative nTMS mappings (100 language and 150 motor mappings) derived from 216 patients (mean age: 57.0 ± 15.5 years, 58.8% males; glioma World Health Organization (WHO) grade I & II: 4.2%, glioma WHO grade III & IV: 83.4%, arteriovenous malformations: 1.9%, cavernoma: 2.3%, metastasis: 8.2%) were included. Deterministic tractography based on nTMS motor or language maps as seed regions was performed with 25%, 50%, and 75% of the individual fractional anisotropy threshold (FAT). Lesion-to-tract distances (LTDs) were measured between the tumor mass and the corticospinal tract (CST), arcuate fascicle (AF), or other closest language-related tracts. LTDs were compared between patients and correlated to the functional status (no/transient/permanent surgery-related paresis or aphasia). Significant differences were found between patients with no or transient surgery-related deficits and patients with permanent surgery-related deficits regarding LTDs in relation to the CST (p < 0.0001), AF (p ≤ 0.0491), or other closest language-related tracts (p ≤ 0.0435). The cut-off values for surgery-related paresis or aphasia were ≤12 mm (LTD—CST) and ≤16 mm (LTD—AF) or ≤25 mm (LTD—other closest language-related tract), respectively. Moreover, there were significant associations between the status of surgery-related deficits and the LTD when considering the CST (range r: −0.3994 to −0.3910, p < 0.0001) or AF (range r: −0.2918 to −0.2592, p = 0.0135 and p = 0.0473 for 25% and 50% FAT). In conclusion, this is the largest study evaluating the application of both preoperative functional mapping and function-based tractography for motor and language function for risk stratification in patients with functionally eloquent tumors. The LTD may qualify as a viable marker that can be seamlessly assessed in the clinical neurooncological setup.

In vivo stress granule misprocessing evidenced in a FUS knock-in ALS mouse model.

Many RNA-binding proteins, including TDP-43, FUS, and TIA1, are stress granule components, dysfunction of which causes amyotrophic lateral sclerosis (ALS). However, whether a mutant RNA-binding protein disrupts stress granule processing in vivo in pathogenesis is unknown. Here we establish a FUS ALS mutation, p.R521C, knock-in mouse model that carries impaired motor ability and late-onset motor neuron loss. In disease-susceptible neurons, stress induces mislocalization of mutant FUS into stress granules and upregulation of ubiquitin, two hallmarks of disease pathology. Additionally, stress aggravates motor performance decline in the mutant mouse. By using two-photon imaging in TIA1-EGFP transduced animals, we document more intensely TIA1-EGFP-positive granules formed hours but cleared weeks after stress challenge in neurons in the mutant cortex. Moreover, neurons with severe granule misprocessing die days after stress challenge. Therefore, we argue that stress granule misprocessing is pathogenic in ALS, and the model we provide here is sound for further disease mechanistic study.

Feasibility study of a 10-week community-based program using the WalkWithMe application on physical activity, walking, fatigue and cognition in persons with Multiple Sclerosis

BackgroundPeople with Multiple Sclerosis (pwMS) show diverse symptoms, such as fatigue and decline in motor and cognitive function. Physical activity shows to have a positive impact on many of these symptoms. However, many pwMS lead sedentary lives. Objectives of this study were to evaluate the feasibility of prolonged use of the WalkWithMe, a personalized mobile application that supports pwMS in walking at home, and its effect on physical activity, walking, fatigue and cognition in persons with MS. MethodsNineteen pwMS were enrolled in a 10-week home-based intervention with the WalkWithMe application after setting personal goals based on baseline testing values, where twelve patients completed the program. Before and after the intervention, motor (6MWT, T25FW, 5-STS, NHPT) and cognitive function (PASAT and SDMT) were evaluated, together with the patient reported impact on walking, physical activity, quality of life and fatigue by MSWS-12, IPAQ, SF-36, MSIS-29, MFIS and FSS, respectively. ResultsSignificant improvement was seen for some parts of self-reported physical activity and quality of life (IPAQ: walking, p = 0.04, leisure, p = 0.02; SF-36: physical functioning, p = 0.02), cognition (SDMT, p = 0.01), cognitive fatigability (PASAT, p = 0.05), lower limb strength (5-STS, p = 0.05) and dominant hand function (NHPT, p = 0.002). ConclusionThis feasibility study was successful at improving categories of self-reported physical activity, lower limb functional strength, hand function and cognition, but results need to be interpreted with caution, given the small and not always clinically relevant changes. Larger sample sizes in a controlled experimental design are needed to confirm these results.

Lysosomal PPT1‐insufficiency is a common pathogenic link between INCL and JNCL

Neuronal Ceroid Lipofuscinoses (NCLs), also known as Batten disease, constitute a group of the most common inherited childhood neurodegenerative lysosomal storage disorders (LSDs). Even though mutations in &gt;13 different genes cause various NCLs, at the cellular level, all the NCLs characteristically accumulate autofluorescent material (ceroid) in lysosomes and clinically, develop seizures, visual failure and a progressive decline in cognitive and motor functions. These findings suggest shared pathogenic mechanism(s) in these diseases. While inactivating mutations in the CLN1 gene, encoding lysosomal PPT1, cause infantile NCL (INCL), mutations in the CLN3 gene encoding a lysosomal membrane protein of unknown function underlie juvenile NCL (JNCL). PPT1 catalyzes depalmitoylation of S‐acylated proteins, required for their degradation by lysosomal hydrolases. Thus, PPT1‐deficiency causes lysosomal accumulation of S‐acylated proteins (ceroid) leading to INCL. The Cln1−/− and Cln3−/− mice are reliable animal models of INCL and JNCL, respectively. Here we report for the first time that Cln3‐protein requires S‐palmitoylation for its endosomal transport to the lysosomal membrane. Moreover, we found that in the brain of Cln3−/− mice, lysosomal PPT1‐protein as well as Ppt1‐enzymatic activity are significantly lower compared with lysosomes derived from their age‐ and sex‐matched WT counterparts. Unexpectedly, we found that the lysosomes from Cln3−/− mice accumulate significantly higher levels of S‐palmitoylated proteins, characteristically found in those from Cln1−/− mice. Previously, it has been reported that CLN3 mutations suppress the exit of cation‐independent mannose 6‐phosphate receptor (CI‐M6PR) from trans‐Golgi network (TGN), essential for its endosomal trafficking to the late endosome/lysosome. Since CI‐M6PR transports soluble proteins including Ppt1 to the lysosome, we hypothesized that Cln3 mutations may adversely affect the transport of PPT1 to the lysosome causing Ppt1‐insufficiency. Biochemical and confocal microscopic analyses of brain tissues from Cln3−/− mice revealed significantly higher levels of Ppt1 and CI‐M6PR in the Golgi compared to those of their WT counterparts. Collectively, our results demonstrate that lysosomal Ppt1‐insufficiency is a common pathogenic link between INCL and JNCL and suggest that a recently identified Ppt1‐mimetic, neuroprotective small molecule, NtBuHA, may have therapeutic implications for both INCL and JNCL.Support or Funding InformationIntramural Research Program of the Eunice Kennedy Shriver NICHD, NIH

Apoptosis inhibition mitigates aging effects in Drosophila melanogaster.

Aging is a natural biological process that results in progressive loss of cell, tissue, and organ function. One of the causing factors of the aging process is the decrease in muscle mass, which has not been fully verified in Drosophila. Apoptotic cell death may result in aberrant cell loss and can eventually diminish tissue function and muscle atrophy. If so, inhibition of apoptosis may prolong longevity and reduce motor function and muscle mass decline with age in Drosophila flies. Here, we used Drosophila melanogaster as study material, and induced the overexpression of Drosophila inhibitor of apoptosis protein 1 gene to inhibit apoptosis, and investigated theeffect of apoptosis inhibition on the longevity and age-related declines in flight and climbing ability and muscle mass. As a result, the inhibition of apoptosis tended to mitigate the aging effects and prolonged longevity and reduced climbing ability decline with age. The current study suggests that apoptosis inhibition could mitigate the aging effects in D. melanogaster. Although such effects have already been known in mammals, the current results suggest that the apoptosis may play a similar role in insects as well.

Drug-Resistant Epilepsy in Children with Juvenile Huntington's Disease: A Challenging Case and Brief Review.

Huntington's Disease (HD) is an autosomal dominant neurodegenerative disorder with a progressive decline in cognitive, motor, and psychological function. Chorea tends to be the most common associated movement disorder, although other variants of several abnormal movements are also seen. Adult-onset HD is the most common subtype. Juvenile Huntington's disease (JHD) accounts for 5%–10% of all HD cases and presents as a rapidly progressive disorder with a multitude of characteristics. We report on a 9-year-old male with JHD who presented with refractory epilepsy. His EEG findings, seizure type, and antiepileptic drug usage are discussed with a brief review of the currently available relevant literature. The currently reported case sheds light on antiepileptic drugs that proved effective in our patient and the importance of screening for JHD when a child presents with seizures that are difficult to control.

Changing Times for CLN2 Disease: The Era of Enzyme Replacement Therapy.

Neuronal ceroid lipofuscinosis type 2 (CLN2 disease) is a progressive neurodegenerative disease that results in early-onset, severe, progressive, neurological disabilities, leading to death in late childhood or early adolescence. Management has relied on symptomatic care, and supportive and palliative strategies, but the approval of the enzyme replacement therapy cerliponase alfa in the USA and Europe in 2017 brought different treatment opportunities. We describe the natural history of CLN2 disease, its diagnosis and management, and the preclinical and clinical development of cerliponase alfa. A PubMed search was undertaken for cerliponase alfa and rhTPP1 to identify preclinical and clinical studies. The hallmark-presenting symptoms of CLN2 disease are unprovoked seizures and a history of language delay, and progression involves motor dysfunction, and cognitive and visual decline. Cerliponase alfa has shown efficacy and tolerability in mouse and canine models of CLN2 disease when delivered intracerebroventricularly. Administration of cerliponase alfa in patients with CLN2 disease has led to significant reductions in the rate of decline of motor and language functions in comparison with a natural history population. The approval of cerliponase alfa has brought a new era for CLN2 disease, highlighting the need to understand different patterns of disease progression and clinical needs in treated patients.

Survival analysis and quality of life of pediatric low grade glioma treated by postoperative radiotherapy

Objective To analyze the clinical characteristics of children with low grade glioma (LGG) and evaluate their survival status and quality of life in LGG pediatric patients after postoperative radiotherapy. Methods Clinical data of 27 LGG children aged≤14 years admitted to Department of Radiation Oncology of our hospital from January 2011 to December 2017 were retrospectively analyzed. The 5-year overall survival (OS) and progression-free survival (PFS) were estimated with the Kaplan-Meier method.The quality of life was evaluated by body mass index (BMI), WeeFIM and enrollment situation. Results The 5-year OS and PFS of 27 pediatric patients were 92% and 87%. BMI was measured in 25 children who were still alive and the results showed that 1 child was slightly emaciated, 3 were overweight and 21 were normal. The total score of WeeFIM was> 108 in 21 cases and< 90 in 4 cases. In terms of social role-playing assessment, 5 cases delayed enrollment for≥ 2 years, 2 cases had good adaptation except the difficulties due to lameness, 7 of them had poor study performance, but had no communication barrier. Conclusions Children with LGG can obtain relatively excellent OS and PFS after postoperative radiotherapy. Part of the children with long-term survival may experience a declined quality of life, which is mainly manifested with a decline in motor and cognitive functions. Key words: Pediatric low grade glioma/radiotherapy; Survival; Quality of life

Impact of COPD and anemia on motor and cognitive performance in the general older population: results from the English longitudinal study of ageing

BackgroundCognitive and motor-performance decline with age and the process is accelerated by decline in general health. In this study, we aimed to estimate the effects of COPD and HB levels on cognitive and motor performance in the general older population and assess potential interaction.MethodsThe English Longitudinal Study of Aging is a population-based cohort study including measurements of lung-function and HB levels together with cognitive and motor performance testing. Data were collected from 5709 participants including three measurement time over eight years. COPD was defined using lung-function-parameters and clinical symptoms. HB was assessed continuously and low HB was defined using clinical anemia cutoffs. Linear mixed-effects regression models were used to quantify the associations of COPD and HB with outcome measures, both individually and in combination.ResultsParticipants with both low HB and COPD demonstrated worse motor performance compared to individuals with only one exposure, resulting in up to 1 s (95%CI, 0.04–1.8) longer time needed to complete the five times sit to stand task than what would be expected based on purely additive effects. Additionally in individuals with COPD, the time to complete the motor-performance task per unit decrease in continuous HB levels was longer than in participants without COPD after full adjustment for confounding (up to 1.38 s/unit HB level, 95% CI: 0.65–2.11).ConclusionIn persons with COPD low HB levels may contribute to low motor-performance in a supra additive fashion. Further studies should re-evaluate whether earlier treatment of lower HB in these individuals might be beneficial.

A usability study of a multicomponent video game-based training for older adults

BackgroundAging is often accompanied by a decline in sensory, motor and cognitive functions. These age- and lifestyle-related impairments may lead to reduced daily life functioning including gait disturbances, falling and injuries. Most daily life activities, e.g. walking, are tasks which require the concurrent interplay of physical and cognitive functions. Promising options for combined physical-cognitive training are video game-based physical exercises, so-called exergames. This study aimed to [i] determine the usability of a newly developed multicomponent exergame and [ii] explore its effects on physical functions, cognition and cortical activity.MethodsTwenty-one healthy and independently living older adults were included (10 female, 71.4 ± 5.8 years, range: 65–91) and performed 21 training sessions (each 40 min) over seven weeks. The multicomponent exergame included strength and balance training with Tai Chi-inspired and dance exercises. Participants rated the usability of the exergame (System Usability Scale) and reported on their emotional experience (Game Experience Questionnaire). Attendance and attrition rates were calculated to determine training compliance. Before and after the intervention, physical and cognitive functions as well as resting state electroencephalography (EEG) were assessed.ResultsResults showed a high training attendance rate (87.1%, 18/21 training sessions on average) and a low attrition rate (9.5%, 2 drop-outs). System usability was rated high with a mean score of 75/100. Affective game experience was rated favorable. Gait speed under dual-task condition, lower extremity muscle strength and reaction times in a cognitive task (divided attention) showed significant improvements (p < .05). No significant pre-post differences were found for resting state EEG.ConclusionsThe newly developed exergame seems usable for healthy older adults. Nevertheless, some aspects of the exergame prototype can and should be improved. The training showed to positively influence physical and cognitive functions in a small convenience sample. Future trials are warranted which evaluate the feasibility and usability of the exergame training in a more “real-life” in-home setting and assess the behavioral and neuroplastic changes in a larger population after a longer training period with comparison to a control group.