By Jodie Copley
- A entire advisor to dealing with spastic hypertonia after mind harm and the 1st complete evaluation of this area
- The perfect reference for healing interventions that optimise arm and hand functionality to help aim achievement
- An large scientific handbook for neurological perform, a key reference for college students and certified practitioners, and a beneficial source for all occupational therapists and physiotherapists operating with brain-injured clients
Read Online or Download Neurorehabilitation of the Upper Limb Across the Lifespan: Managing Hypertonicity for Optimal Function PDF
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Extra resources for Neurorehabilitation of the Upper Limb Across the Lifespan: Managing Hypertonicity for Optimal Function
3. 5). The main reasons for the emergence of negative features following brain injury are the reduction in descending, supraspinal influences on motor units and consequent changes in motor unit functions [19,42]. Negative features include muscle weakness (insufficient muscle activation or paresis), poorly differentiated muscle control [40,60,64] and learned non-use. 1 including stretch reflexes, are depressed, leading to an extreme form of muscle weakness. Flaccidity is usually an immediate and transient response to brain injury, however, when it persists, it is correlated with poorer functional outcome .
1). Therefore, disruption anywhere along the pathway (cortex, internal capsule, brainstem or spinal cord proximal to the anterior horn cell) leads to presentation of the UMNS. UMN injury interferes with the balance of supraspinal regulation on the alpha motor neurons at the spinal level. Simultaneously, feedback from the somatosensory system (including the muscle spindles, golgi tendon organs, superficial and deep cutaneous receptors) sends excitatory signals to the same spinal level neurons, leading to hyperactive spinal cord reflexes.
Wrist and grip strength are described as indicators of upper limb function for children with hemiplegia . Further, overall upper limb strength is reported to directly influence activity measures and, therefore indirectly, to influence functional or participatory outcomes for children with cerebral palsy . 1). 6). 6 Contributors to agonist muscle weakness after brain injury [19,65,74,76,78–81]. Contributor Effect Central Nervous System: Reduced descending activation of the spinal-level motor neuron pool • Loss of large (high threshold) motor units • Reduced motor unit ﬁring rates • Compressed recruitment threshold (more motor units recruited more quickly) • Changed motor unit innervation ratios due to collateral sprouting (more muscle ﬁbres per motor unit) • Disrupted motor unit recruitment order Somatosensory system • Reduced proprioceptive feedback • Inappropriate central processing of sensory input Skeletal muscles: Reduced innervation of muscle ﬁbres due to degeneration of motor neuron axons • Changes in the contractile properties of muscle ﬁbres due to shortening • Reduced ability of muscles to contract effectively at shortened lengths • Changes in mechanical properties (increased stiffness) • Variation in muscle ﬁbre size and density • Prolonged contraction time • Impaired insulin–glucose metabolism (reduced fuel stores) Muscle weakness Muscle weakness can vary following brain injury, from partial or mild loss of strength (paresis) to severe (plegia) or complete (paralysis or flaccidity) loss of strength .