Dual tasking interferes with dynamic balance in young and old healthy adults

BACKGROUND: Functional mobility requires an ability to adapt to environmental factors together with an ability to execute a secondary task simultaneously while walking. A complex dual-tasking gait test may provide an indication of functional ability and falls risk among community-dwelling older adults. PURPOSE: The aim of this cross-sectional study is to investigate age-related differences in dual-tasking ability and to evaluate whether dual-tasking ability is related to executive function. METHODS: Forty-one community-dwelling healthy older and forty-one younger adults completed a dual-tasking assessment in which concurrent tasks were incorporated into the Functional Gait Assessment (FGA). The manual dual-task involved carrying a glass of water (FGA-M) while the cognitive dual-tasks involved numeracy (FGA-N) and literacy (FGA-L) related tasks. FGA scores under single (FGA-S) and dual-task conditions together with associated dual-task costs and response accuracy were determined. Executive function was assessed using The Behavioural Assessment of the Dysexecutive Syndrome (BADS). RESULTS: FGA-N and FGA-L scores were adversely affected in both groups compared to FGA-S (p≤0.001). However, score reductions and dual-task costs were significantly greater for older adults compared to younger adults on FGA-N (p≤0.05) and FGA-L (p≤0.001), with older adult performance on FGA-N associated with falls risk (p≤0.05). Executive function did not appear to be related to dual-tasking ability. CONCLUSION: Findings suggest that cognitively demanding tasks while walking, have a deleterious effect on dynamic balance and could place older adults at a greater risk of falls

Achieving adherence in home-based rehabilitation with novel human machine interactions that stimulate community-dwelling older adults

Balance disorders are expressed with main symptoms of vertigo, dizziness instability and disorientation. Most of them are caused by inner ear pathologies, but neurological, medical and psychological factors are also responsible. Balance disorders overwhelmingly affect daily activities and cause psychological and emotional hardship. They are also the main cause of falls which are a global epidemic. Home based balance rehabilitation is an effective approach for alleviating symptoms and for improving balance and self-confidence. However, the adherence in such programs is usually low with lack of motivation and disease related issues being the most influential factors. Holobalance adopts the Capability, Opportunity and Motivation (COM) and Behaviour (B) model to identify the sources of the behaviour that should be targeted for intervention and proposes specific Information Technology components that provide the identified interventions to the users in order to achieve the target behavioural change, which in this case is adherence to home base rehabilitation

Comprehension of acoustically degraded speech in Alzheimer's disease and primary progressive aphasia

Successful communication in daily life depends on accurate decoding of speech signals that are acoustically degraded by challenging listening conditions. This process presents the brain with a demanding computational task that is vulnerable to neurodegenerative pathologies. However, despite recent intense interest in the link between hearing impairment and dementia, comprehension of acoustically degraded speech in these diseases has been little studied. Here we addressed this issue in a cohort of 19 patients with typical Alzheimer's disease and 30 patients representing the three canonical syndromes of primary progressive aphasia (nonfluent/agrammatic variant primary progressive aphasia; semantic variant primary progressive aphasia; logopenic variant primary progressive aphasia), compared to 25 healthy age-matched controls. As a paradigm for the acoustically degraded speech signals of daily life, we used noise-vocoding: synthetic division of the speech signal into frequency channels constituted from amplitude-modulated white noise, such that fewer channels convey less spectrotemporal detail thereby reducing intelligibility. We investigated the impact of noise-vocoding on recognition of spoken three-digit numbers and used psychometric modelling to ascertain the threshold number of noise-vocoding channels required for 50% intelligibility by each participant. Associations of noise-vocoded speech intelligibility threshold with general demographic, clinical and neuropsychological characteristics and regional grey matter volume (defined by voxel-based morphometry of patients' brain images) were also assessed. Mean noise-vocoded speech intelligibility threshold was significantly higher in all patient groups than healthy controls, and significantly higher in Alzheimer's disease and logopenic variant primary progressive aphasia than semantic variant primary progressive aphasia (all p < 0.05). In a receiver-operating-characteristic analysis, vocoded intelligibility threshold discriminated Alzheimer's disease, non-fluent variant and logopenic variant primary progressive aphasia patients very well from healthy controls. Further, this central hearing measure correlated with overall disease severity but not with peripheral hearing or clear speech perception. Neuroanatomically, after correcting for multiple voxel-wise comparisons in pre-defined regions of interest, impaired noise-vocoded speech comprehension across syndromes was significantly associated (p < 0.05) with atrophy of left planum temporale, angular gyrus and anterior cingulate gyrus: a cortical network that has previously been widely implicated in processing degraded speech signals. Our findings suggest that the comprehension of acoustically altered speech captures an auditory brain process relevant to daily hearing and communication in major dementia syndromes, with novel diagnostic and therapeutic implications

The Brain Basis for Misophonia.

Misophonia is an affective sound-processing disorder characterized by the experience of strong negative emotions (anger and anxiety) in response to everyday sounds, such as those generated by other people eating, drinking, chewing, and breathing [1-8]. The commonplace nature of these sounds (often referred to as "trigger sounds") makes misophonia a devastating disorder for sufferers and their families, and yet nothing is known about the underlying mechanism. Using functional and structural MRI coupled with physiological measurements, we demonstrate that misophonic subjects show specific trigger-sound-related responses in brain and body. Specifically, fMRI showed that in misophonic subjects, trigger sounds elicit greatly exaggerated blood-oxygen-level-dependent (BOLD) responses in the anterior insular cortex (AIC), a core hub of the "salience network" that is critical for perception of interoceptive signals and emotion processing. Trigger sounds in misophonics were associated with abnormal functional connectivity between AIC and a network of regions responsible for the processing and regulation of emotions, including ventromedial prefrontal cortex (vmPFC), posteromedial cortex (PMC), hippocampus, and amygdala. Trigger sounds elicited heightened heart rate (HR) and galvanic skin response (GSR) in misophonic subjects, which were mediated by AIC activity. Questionnaire analysis showed that misophonic subjects perceived their bodies differently: they scored higher on interoceptive sensibility than controls, consistent with abnormal functioning of AIC. Finally, brain structural measurements implied greater myelination within vmPFC in misophonic individuals. Overall, our results show that misophonia is a disorder in which abnormal salience is attributed to particular sounds based on the abnormal activation and functional connectivity of AIC

Peripheral hearing loss at age 70 predicts brain atrophy and associated cognitive change

BACKGROUND: Hearing loss has been proposed as a modifiable risk factor for dementia. However, the relationship between hearing, neurodegeneration, and cognitive change, and the extent to which pathological processes such as Alzheimer's disease and cerebrovascular disease influence these relationships, is unclear. METHODS: Data from 287 adults born in the same week of 1946 who underwent baseline pure tone audiometry (mean age=70.6 years) and two time point cognitive assessment/multimodal brain imaging (mean interval 2.4 years) were analysed. Hearing impairment at baseline was defined as a pure tone average of greater than 25 decibels in the best hearing ear. Rates of change for whole brain, hippocampal and ventricle volume were estimated from structural MRI using the Boundary Shift Integral. Cognition was assessed using the Pre-clinical Alzheimer's Cognitive Composite. Regression models were performed to evaluate how baseline hearing impairment associated with subsequent brain atrophy and cognitive decline after adjustment for a range of confounders including baseline β-amyloid deposition and white matter hyperintensity volume. RESULTS: 111 out of 287 participants had hearing impairment. Compared with those with preserved hearing, hearing impaired individuals had faster rates of whole brain atrophy, and worse hearing (higher pure tone average) predicted faster rates of hippocampal atrophy. In participants with hearing impairment, faster rates of whole brain atrophy predicted greater cognitive change. All observed relationships were independent of β-amyloid deposition and white matter hyperintensity volume. CONCLUSIONS: Hearing loss may influence dementia risk via pathways distinct from those typically implicated in Alzheimer's and cerebrovascular disease in cognitively unimpaired older adults

Non-verbal sound processing in the primary progressive aphasias

Little is known about the processing of non-verbal sounds in the primary progressive aphasias. Here, we investigated the processing of complex non-verbal sounds in detail, in a consecutive series of 20 patients with primary progressive aphasia [12 with progressive non-fluent aphasia; eight with semantic dementia]. We designed a novel experimental neuropsychological battery to probe complex sound processing at early perceptual, apperceptive and semantic levels, using within-modality response procedures that minimized other cognitive demands and matching tests in the visual modality. Patients with primary progressive aphasia had deficits of non-verbal sound analysis compared with healthy age-matched individuals. Deficits of auditory early perceptual analysis were more common in progressive non-fluent aphasia, deficits of apperceptive processing occurred in both progressive non-fluent aphasia and semantic dementia, and deficits of semantic processing also occurred in both syndromes, but were relatively modality specific in progressive non-fluent aphasia and part of a more severe generic semantic deficit in semantic dementia. Patients with progressive non-fluent aphasia were more likely to show severe auditory than visual deficits as compared to patients with semantic dementia. These findings argue for the existence of core disorders of complex non-verbal sound perception and recognition in primary progressive aphasia and specific disorders at perceptual and semantic levels of cortical auditory processing in progressive non-fluent aphasia and semantic dementia, respectively

Pure tone audiometry and cerebral pathology in healthy older adults.

BACKGROUND: Hearing impairment may be a modifiable risk factor for dementia. However, it is unclear how hearing associates with pathologies relevant to dementia in preclinical populations. METHODS: Data from 368 cognitively healthy individuals born during 1 week in 1946 (age range 69.2-71.9 years), who underwent structural MRI, 18F-florbetapir positron emission tomography, pure tone audiometry and cognitive testing as part of a neuroscience substudy the MRC National Survey of Health and Development were analysed. The aim of the analysis was to investigate whether pure tone audiometry performance predicted a range of cognitive and imaging outcomes relevant to dementia in older adults. RESULTS: There was some evidence that poorer pure tone audiometry performance was associated with lower primary auditory cortex thickness, but no evidence that it predicted in vivo β-amyloid deposition, white matter hyperintensity volume, hippocampal volume or Alzheimer's disease-pattern cortical thickness. A negative association between pure tone audiometry and mini-mental state examination score was observed, but this was no longer evident after excluding a test item assessing repetition of a single phrase. CONCLUSION: Pure tone audiometry performance did not predict concurrent β-amyloid deposition, small vessel disease or Alzheimer's disease-pattern neurodegeneration, and had limited impact on cognitive function, in healthy adults aged approximately 70 years

Hearing and dementia

Hearing deficits associated with cognitive impairment have attracted much recent interest, motivated by emerging evidence that impaired hearing is a risk factor for cognitive decline. However, dementia and hearing impairment present immense challenges in their own right, and their intersection in the auditory brain remains poorly understood and difficult to assess. Here, we outline a clinically oriented, symptom-based approach to the assessment of hearing in dementias, informed by recent progress in the clinical auditory neuroscience of these diseases. We consider the significance and interpretation of hearing loss and symptoms that point to a disorder of auditory cognition in patients with dementia. We identify key auditory characteristics of some important dementias and conclude with a bedside approach to assessing and managing auditory dysfunction in dementia

Retained capacity for perceptual learning of degraded speech in primary progressive aphasia and Alzheimer's disease

This work was supported by the Alzheimer’s Society (AS-PG-16-007), the National Institute for Health Research University College London Hospitals Biomedical Research Centre, the UCL Leonard Wolfson Experimental Neurology Centre (PR/ylr/18575) and the Economic and Social Research Council (ES/K006711/1). Individual authors were supported by the Medical Research Council (PhD Studentship to CJDH and RLB; MRC Clinician Scientist Fellowship to JDR), the Wolfson Foundation (Clinical Research Fellowship to CRM), Alzheimer’s Research UK (ART-SRF2010-3 to SJC) and the Wellcome Trust (091673/Z/10/Z to JDW)