Most older pedestrians are unable to cross the road in time: a cross-sectional study

Objectives: to compare walking speed in the UK older population with the speed required to utilise pedestrian crossings (≥1.2?m/s), and determine health and socio-demographic associations with walking impairment. Design: cross-sectional study using Health Survey for England 2005 data. Setting: private households in England. Participants: random population sample of 3,145 adults (1,444 men) aged ≥65 years. Main outcome measures: walking speed was assessed by timing a walk of 8 feet at normal pace. Walking impairment was defined as walking speed <1.2?m/s or non-participation in the test due to being unsafe or unable. Results: the mean walking speed was 0.9?m/s in men and 0.8?m/s in women; 84% of men and 93% of women ≥65 years had walking impairment. Female gender, increasing age, lower socio-economic status, poorer health and lower grip strength were predictors of walking impairment. Conclusion: most older adults either cannot walk 8 feet safely or cannot walk fast enough to use a pedestrian crossing in the UK. The health impacts on older adults include limited independence and reduced opportunities for physical activity and social interaction. An assumed normal walking speed for pedestrian crossings of 1.2?m/s is inappropriate for older adults and revision of these timings should be considered.     

RNA quality control and protein aggregates in amyotrophic lateral sclerosis: A review

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in adults. The biologic basis of ALS remains unknown. However, ALS research has taken a dramatic turn over the past 4 years. Ground breaking discoveries of mutations of genes that encode RNA processing proteins, and demonstration that abnormal aggregates of these and other proteins precede motor neuron loss in familial and sporadic ALS, have initiated a paradigm shift in understanding the pathogenic mechanisms of ALS. Curiously, some of these RNA binding proteins have prion‐like domains, with a propensity to self‐aggregation. The emerging hypothesis that a focal cascade of toxic protein aggregates, and their consequent non–cell‐autonomous spread to neighborhood groups of neurons, fits the classical temporo‐spatial progression of ALS. This article reviews the current research efforts toward understanding the role of RNA‐processing regulation and protein aggregates in ALS. Muscle Nerve 47:330‐338, 2013     

Associative memory impairment in acute stress disorder: Characteristics and time course

Stress and episodic memory impairment have previously been associated. Acute stress disorder (ASD) is a maladaptive stress response, which develops in some individuals following traumatic life events. Recently, the authors demonstrated a specific deficit in associative memory for emotionally neutral stimuli in ASD and posttraumatic stress disorder (PTSD). This study further tested the relationship between this memory impairment and the course of ASD. We assessed new learning and memory for item and associative information in patients diagnosed with ASD (n=14) and matched trauma naïve controls (n=14). Memory performance and posttraumatic symptoms were examined for approximately 1 and 10 week periods following the traumatic experience. In the two experiments, participants studied a list of stimuli pairs (verbal or visual) and were then tested for their memory of the items (item recognition test), or for the association between items in each pair (associative recognition test). In both experiments, ASD patients showed a marked associative memory deficit compared to the control group. After 10 weeks, ASD symptoms were resolved in most patients. Interestingly, their performance on associative recognition for verbal stimuli improved, while the associative deficit for visual stimuli remained unchanged. Potential mechanisms underlying such an associative memory deficit in post-trauma patients are discussed.     

The history of parkinsonism: Descriptions in ancient Indian medical literature

The clinical syndrome of parkinsonism was identified in ancient India even before the period of Christ and was treated methodically. The earliest reference to bradykinesia dates to 600 bc . Evidences prove that as early as 300 bc , Charaka proposed a coherent picture of parkinsonism by describing tremor, rigidity, bradykinesia, and gait disturbances as its components. The scenario was further developed by Madhava, Vagbhata, and Dalhana all through history. The 15th‐century classic “Bhasava rajyam” introduced the term kampavata, which may be regarded as an ayurvedic analogue of parkinsonism. The pathogenesis of kampavata centered on the concept of imbalance in the vata factor, which controls psychomotor activities. The essential element in therapy was the administration of powdered seed of Mucuna pruriens, or atmagupta, which as per reports, contains 4%?6% of levodopa. In addition to proving the existence and identification of parkinsonism in ancient India, the study points to the significance of ancient Indian Sanskrit works in medical history. © 2013 Movement Disorder Society