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Falls and Gait Impairment
Published in K. Rao Poduri, Geriatric Rehabilitation, 2017
Kristen Thornton, Thomas V. Caprio
Impaired peripheral motor function may occur due to lower motor neuron lesions, myopathic weakness, pain, or musculoskeletal deformities. A lower motor neuron patterned gait may involve weakened quadriceps, toe, and foot plantar flexion. The hip flexors often remain strong in a lower motor neuron patterned gait and may result in high steppage and foot drop. Myopathic weakness in the limb girdle may present with a waddling gait and abnormal pelvic tilt. An antalgic gait often results from attempting to limit weight bearing on a painful area or surrounding a painful joint. A parkinsonian gait may result from idiopathic Parkinson’s disease, or parkinsonism from other neurodegenerative conditions, such as supranuclear palsy, multiple system atrophy, or corticobasal degeneration. Parkinsonism may also be a manifestation of cerebrovascular disease, subcortical dementia, or even dementia with Lewy bodies. Persons with a parkinsonian gait demonstrate a festinating, shuffling, short stride strength, absent or reduced arm swing, and turning “en bloc.” In patients with Parkinson’s disease, gait impairment may improve with a trial of levodopa therapy. Failure to respond to levodopa therapy may suggest an atypical parkinsonism.
Dementia and lower urinary tract dysfunction
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Among these factors, many studies have shown that the severity of immobility and that of dementia are positively correlated with functional incontinence.36 The parkinsonian gait in these diseases is characterized as slow and short stepped, with festination and postural instability. A wide-based ataxic gait often overlaps the short-stepped gait, particularly in cases of multiple cerebral infarctions. The sites responsible for the gait disorder seem to be in the basal ganglia and medial frontal lobe, particularly the supplementary motor area or its pathways,37 which partially overlaps the frontal micturition center. In addition, lesions in the basal ganglia cause both motor and micturition disorders, as seen in Parkinson’s disease. In contrast, cognitive and motivation disorders are thought to reflect broad cortical dysfunction, as seen in Alzheimer’s disease. Gait disorder and DO may be early and prominent features of multiple cerebral infarction and DLB, and may lead to functional incontinence and frequent falls, whereas they are very uncommon in the early stage of Alzheimer’s disease. Taken together, these findings show that neurogenic urinary dysfunction (particularly DO) and gait disorder often appear together, as both reflect rather focal brain dysfunction (the basal ganglia and the medial frontal cortex). In contrast, functional incontinence appears secondarily from gait disorder and/or cognitive/motivation disorders, the latter reflecting more widespread brain dysfunction.
Parkinson disease
Published in John M. Saxton, Exercise and Chronic Disease, 2011
Among all the effects of exercise on function in PD, the benefits to gait are arguably the most well-substantiated by the literature (Figure 13.1). Parkinsonian gait is characterized by short, shuffling steps and reduced gait velocity, both of which can be improved with exercise. Summary effect sizes for stride length and gait velocity as assessed by de Goede et al. (2001) were 0.46 and 0.49, respectively. Effect sizes for gait velocity may actually be even larger, with an average value of greater than 0.6 (Figure 13.1). Improvements in stride length and velocity have been noted following aerobic training, treadmill exercise training, physical therapy, multiple-task training, dance and Tai Chi. Some studies have suggested that treadmill exercise training may be superior to conventional approaches for improving gait in PD (Miyai et al., 2000, 2002). Gains noted with treadmill exercise training could be attributed to several different mechanisms including cardiopulmonary adaptations, walking pace retraining (with the treadmill serving as an external pacemaker), enhancements in corticomotor excitability (Fisher et al., 2008) and motor learning. For a more thorough discussion please see Herman et al. (2009).
Posterior cortical atrophy: clinical, neuroimaging, and neuropathological features
Published in Expert Review of Neurotherapeutics, 2023
John Best, Marianne Chapleau, Gil D. Rabinovici
The neurologic exam in individuals with PCA frequently demonstrates dyspraxia or apraxia. Upon initial observation, patients may have trouble orienting themselves properly in the exam room, sometimes bumping into objects. They may have difficulty seeing the examiner and maintaining adequate eye contact due to loss of visual fixation. The examiner should assess a patient’s ability to perform movements under visual guidance, locate objects in the room, copy hand positions, draw and copy geometric figures, and read and write. A careful exam can uncover subtle visual field deficits or extinction to simultaneous bilateral visual stimuli. Gait is hesitant in the context of poor vision. There may be evidence of Balint’s syndrome, specifically oculomotor apraxia (inability to intentionally move eyes toward an object) or optic ataxia (difficulty reaching for an object they are looking at). The motor exam is variable and can sometimes show evidence of parkinsonism, myoclonus, or tremor. Sensory exam shows normal primary sensory function but can show evidence of impaired cortical sensory function, such as inability to identify an object by touch (astereognosis) or inability to perceive written numbers or letters on their skin (agraphesthesia). The gait exam is typically normal; however, evidence of a parkinsonian gait could suggest co-morbid or primary Lewy body pathology.
A novel instrumented walker for individualized visual cue setting for gait training in patients with Parkinson’s disease
Published in Assistive Technology, 2020
Hsiao-Kuan Wu, Huang-Ren Chen, Wei-Ying Chen, Chia-Feng Lu, Mei-Wun Tsai, Chung-Huang Yu
Patients with Parkinson’s disease exhibit cardinal motor symptoms, such as resting tremor, rigidity, bradykinesia, hypokinesia and posture instability (Olanow & Tatton, 1999). The progression of this disorder leads to gait disturbances, such as shuffling, festination, freezing of gait (FOG), and turning “en bloc” (Hausdorff, 2009; Jankovic, 2008). From a biomechanical standpoint, the Parkinsonian gait includes a short stride length, fast cadence, slow walking speed, prolonged double-stance phase, and decreased arm swing (Knutsson & Martensson, 1971; Morris, Iansek, Matyas, & Summers, 1994; Morris, McGinley, Huxham, Collier, & Iansek, 1999). As the disorder progresses, ambulation becomes very difficult or too dangerous, and patients may be confined to a wheelchair or bed (Chapuis, Ouchchane, Metz, Gerbaud, & Durif, 2005; Moore, Peretz, & Giladi, 2007).
Effects of a ballet intervention on trunk coordination and range of motion during gait in people with Parkinson’s
Published in Cogent Medicine, 2019
Ashley McGill, Sara Houston, Raymond Y. W. Lee
Recent studies have evidenced the effect of instability and dysfunctional gait patterns on fall risk for people living with Parkinson’s (Hausdorff, 2009). Characteristic features of Parkinsonian gait include a smaller step and stride length, increased double support time, increased cadence, decreased walking velocity, and instability with greater step and stride variability. Individuals tend to walk with a flexed posture and demonstrate a reduced or absent arm swing with rigidity in trunk movements (Hackney, Kantorovich, & Earhart, 2007; Morris, Iansek, Matyas, & Summers, 1994; Pedersen, Oberg, Larsson, & Lindval, 1997; Van Emmerick, Wagenaar, Winogrodzka, & Wolters, 1999). This along with the fact that people with Parkinson’s often find they have decreased clearance of the swinging leg from the floor can put them at risk of falling during dynamic situations (Hackney et al., 2007; Hausdorff, 2009).