People with disability are insufficiently physically active for health. This study identified the volume, quality, and findings of research that exposes environmental and personal barriers of physical activity participation for people with neurological conditions. CINAHL, Sport Discus, EMBASE, Medline, and AMED were systematically searched between 1999 and week one 2010 for peer reviewed studies that fit the aim of the review. Identified barriers to physical activity participation were categorized into the World Health Organization’s ICF framework of domains. Of the 2,061 studies uncovered in the search, 29 met inclusion criteria and 28 met quality appraisal. Findings showed that barriers to physical activity participation arise from personal factors that, coupled with lack of motivational support from the environment, challenge perceptions of safety and confidence to exercise.
Hilda F. Mulligan, Leigh A. Hale, Lisa Whitehead and G. David Baxter
Mohsen Shafizadeh, Nicola Theis and Keith Davids
An estimated 6% of people in the United Kingdom have some form of neurological motor disorder ( MacDonald, Cockerell, Sander, & Shorvon, 2000 ) that affects participation in health-related activities and poses a challenge for society to promote the health and well-being of all its members ( Coates
Byron Lai, Katie Cederberg, Kerri A. Vanderbom, C. Scott Bickel, James H. Rimmer and Robert W. Motl
People with neurologic disabilities, including multiple sclerosis (MS), spinal cord injury (SCI), and traumatic brain injury (TBI), remain largely inactive, despite a substantial growth in evidence from clinical trials demonstrating beneficial outcomes following exercise training. For example, a
Gregory G. Billy and Sayers J. Miller
An avid weightlifter presented with complaints of right arm and hand numbness. His workup was consistent with neurologic thoracic outlet syndrome with severe conduction block at the level of the supraclavicular fossa. He chose conservative treatment, which focused on correction of thoracic and cervical segmental dysfunction, upper crossed syndrome muscle imbalances, and upper trunk and anterior forward head postural concerns. Upon completion of the therapy program and continuation of a home exercise program, his conduction block and symptoms resolved. Conservative treatment may be an effective alternative to surgery for neurologic thoracic outlet syndrome.
Kay Tetzlaff, Holger Schöppenthau and Jochen D. Schipke
It has been widely believed that tissue nitrogen uptake from the lungs during breath-hold diving would be insufficient to cause decompression stress in humans. With competitive free diving, however, diving depths have been ever increasing over the past decades.
A case is presented of a competitive free-diving athlete who suffered stroke-like symptoms after surfacing from his last dive of a series of 3 deep breath-hold dives. A literature and Web search was performed to screen for similar cases of subjects with serious neurological symptoms after deep breath-hold dives.
A previously healthy 31-y-old athlete experienced right-sided motor weakness and difficulty speaking immediately after surfacing from a breathhold dive to a depth of 100 m. He had performed 2 preceding breath-hold dives to that depth with surface intervals of only 15 min. The presentation of symptoms and neuroimaging findings supported a clinical diagnosis of stroke. Three more cases of neurological insults were retrieved by literature and Web search; in all cases the athletes presented with stroke-like symptoms after single breath-hold dives of depths exceeding 100 m. Two of these cases only had a short delay to recompression treatment and completely recovered from the insult.
This report highlights the possibility of neurological insult, eg, stroke, due to cerebral arterial gas embolism as a consequence of decompression stress after deep breath-hold dives. Thus, stroke as a clinical presentation of cerebral arterial gas embolism should be considered another risk of extreme breath-hold diving.
Brandon R. Rigby, Ronald W. Davis, Marco A. Avalos, Nicholas A. Levine, Kevin A. Becker and David L. Nichols
Parkinson’s disease (PD) is a chronic, progressive, neurological disorder caused by the destruction of dopamine-producing neurons in the substantia nigra of the brain ( Jacobs, Svoboda, & Lepeley, 2018 ). It is the most common neurodegenerative disease that affects movement and is prevalent in 1
Bentley Andrew Krause
Column-editor : Catherine Stemmans
Leah S. Goudy, Brandon Rhett Rigby, Lisa Silliman-French and Kevin A. Becker
.1177/145749690709600115 10.1177/145749690709600115 Chaudhuri , K.R. , Healy , D.G. , & Schapira , A.H. ( 2006 ). Non-motor symptoms of Parkinson’s disease: Diagnosis and management . The Lancet Neurology, 5 , 235 – 245 . PubMed ID: 16488379 doi:10.1016/S1474-4422(06)70373-8 10.1016/S1474-4422(06)70373-8 Ciolac
Michelle M. Porter, Miriam E. Nelson, Maria A. Fiatarone Singh, Jennifer E. Layne, Christine M. Morganti, Isaiah Trice, Christina D. Economos, Ronenn Roubenoff and William J. Evans
Resistance training (RT) increases strength in older adults, but there have been few studies of long-term RT or detraining in older adults. Postmenopausal participants (51–71 years of age) were randomized to RT or a control group for Year 1. For Year 2, participants chose whether to resistance train or not. Three groups emerged: train/train (n = 8: 60 ± 4 years), train/no train (n = 11: 62 ± 3 years), or controls (n = 17; 58 ± 6 years). Both training groups increased strength (p < .05) in Year 1. In Year 2, train/train maintained strength, whereas train/no train lost strength for knee extension (p < .001) but not for arm pulldown. Controls did not change. Reported physical activity levels were significantly increased in trainers in Year 1 and remained high regardless of RT in Year 2 (p < .05). Therefore, sustained changes in strength and physical activity behavior might be possible even if RT is discontinued.