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At least 847 records · Page 47Linked to original sources
PubMed1996

Benefits of aerobic exercise after stroke.

The debilitating loss of function after a stroke has both primary and secondary effects on sensorimotor function. Primary effects include paresis, paralysis, spasticity, and sensory-perceptual dysfunction due to upper motor neuron damage. Secondary effects, contractures and disuse muscle atrophy, are also debilitating. This paper presents theoretical and empirical benefits of aerobic exercise after stroke, issues relevant to measuring peak capacity, exercise training protocols, and the clinical use of aerobic exercise in this patient population. A stroke, and resulting hemiparesis, produces physiological changes in muscle fibres and muscle metabolism during exercise. These changes, along with comorbid cardiovascular disease, must be considered when exercising stroke patients. While few studies have measured peak exercise capacity in hemiparetic populations, it has been consistently observed in these studies that stroke patients have a lower functional capacity than healthy populations. Hemiparetic patients have low peak exercise responses probably due to a reduced number of motor units available for recruitment during dynamic exercise, the reduced oxidative capacity of paretic muscle, and decreased overall endurance. Consequently, traditional methods to predict aerobic capacity are not appropriate for use with stroke patients. Endurance exercise training is increasingly recognised as an important component in rehabilitation. An average improvement in maximal oxygen consumption (VO2max) of 13.3% in stroke patients who participated in a 10-week aerobic exercise training programme has been reported compared with controls. This study underscored the potential benefits of aerobic exercise training in stroke patients. In this paper, advantages and disadvantages of exercise modalities are discussed in relation to stroke patients. Recommendations are presented to maximise physical performance and minimise potential cardiac risks during exercise.

Cerebrovascular Disorders↗
PubMed1991

Effects of a single session of prolonged plantarflexor stretch on muscle activations during gait in spastic cerebral palsy.

Activations of the triceps surae (TS) and tibialis anterior (TA) muscles during gait were studied in children with spastic cerebral palsy (CP) immediately before and after 30 min of standing on a tilt-table with the ankle dorsiflexed to stretch the TS in the experimental group (n = 8) or after a rest period in the control group (n = 11). The EMG activity from the TS and TA was recorded concomitantly with electronic footswitch signals by a computer. Video records were made of the sagittal gait movements. Effects of PMS were determined by comparing change scores for selected spatiotemporal and muscle activation parameters between the groups. The change scores defined for the muscle activations were: a post-test/pre-test ratio of the EMG activity in specific segments of the gait cycle and a locomotor spasticity index. PMS did not significantly (p greater than 0.05) affect any of the spatiotemporal parameters nor did it alter any of the TS and most of the TA activation parameters or the SI indexes for the TS and TA. Only the TA post/pre activation ratio for the 0-16% segment of the gait cycle was smaller (p less than 0.01), indicating a decrease in TA activation post-PMS.

Adolescent↗
PubMed1996

Reflex hyperexcitability and muscle contracture in relation to spastic hypertonia.

Mechanisms of spasticity and possible therapeutic interventions continue to dominate research into motor disorders following cerebral lesions. However, the accumulated evidence suggests that this focus on spasticity may be out of step with its effects. In contrast, hypertonia remains an important problem. Further investigation into its link with muscle contracture is required and it needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.

Brain Damage, Chronic↗
PubMed1977

Spasticity: its physiology and management. Part III. Identifying and assessing the mechanisms underlying spasticity.

Patients with spasticity may have similar motor signs and yet have completely different underlying neural mechanisms. This paper reviews some experimental tests which have been developed to detect and analyze excitatory excesses and inhibitory deficits giving rise to the abnormal motor signs of spasticity. Although at the present time these tests may not lend themselves to routine clinical application, their results are creating a body of knowledge which will become the foundation for diagnosis and treatment of spasticity in the future.

Brain↗
PubMed1999

The use of gait analysis for surgical recommendations in traumatic brain injury.

Traumatic brain injury causes unpredictable errors in the patient's gait by introducing varying mixtures of spasticity, contractures, primitive flexion and extension synergies, and impaired selective control. Surgical release or transfer of the offending muscles can improve the patient's ability to walk if functional errors have been accurately identified. While clinical testing is inadequate, instrumented motion analysis and dynamic electromyography can supply an accurate definition of the abnormalities in muscle action and provide guidelines for distinguishing local from referred motion errors. Examples of the diagnostic differences related to the equinovarus foot and the common types of knee dysfunction are presented.

Brain Injuries↗
PubMed2001

Spasticity in kids. An intrathecal option.

The painful muscle rigidity and severe spasms suffered by patients with brain and spinal injury can be managed even more successfully than in the past with intrathecal baclofen. For many, it's provided effective relief and improved levels of function.

Baclofen↗