Upper Motor Neurone Syndrome and Spasticity: Clinical by Michael P. Barnes, Garth R. Johnson

By Michael P. Barnes, Garth R. Johnson

Spasticity is a disabling challenge for lots of adults and kids with various neurological issues akin to a number of sclerosis, stroke, cerebral palsy and annoying mind harm. a realistic advisor for clinicians occupied with the administration of spasticity, this booklet covers all facets of higher motor neurone syndrome from simple neurophysiology and size strategies to useful remedy and using orthoses. Surgical thoughts also are lined, in addition to the actual difficulties of administration of spasticity in youth. within the moment version of this key textual content, all chapters were completely up to date, with extra insurance of recent thoughts and new medications and cures, when carrying on with the layout that has made the 1st version the middle textual content in its box. This advisor can be helpful to physicians, physiotherapists, surgeons, orthotists, scientific engineers and future health execs.

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Extra resources for Upper Motor Neurone Syndrome and Spasticity: Clinical Management and Neurophysiology

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14) during a nonisometric contraction. Finally, there are examples where the antagonist co-contraction overwhelms the agonist, producing the movement opposite of that intended (Fig. 15). A common clinical scenario is the patient with spastic finger flexors and weak extensors whose fingers flex more when he or she is trying to extend them. Despite this, there is some indication that hyperactive stretch reflexes in an antagonist could interfere with movement. This is discussed further on, under ‘The spastic movement disorder’.

G. tendon tap, passive stretch) are complex, involving interneurones that are under strong supraspinal control, is it possible that either the gain of these circuits is increased or the threshold lowered? The latter is the prevailing view, although it is difficult to investigate the possibility of hyperexcitable alpha motoneurones without using spinal reflexes, as discussed further on (see p. 47, ‘Alpha motoneurone excitability’). Thus, the basis of stretch reflex hyperexcitability, which underlies the clinical signs of enhanced tendon reflexes and reflex irradiation, clonus and spasticity, is abnormal processing of proprioceptive information within the spinal cord.

Patients may, after several months, settle into a state of predominant extensor spasms (Hagbarth, 1960; Kugelberg, 1962), but paraplegia in flexion is also common. Perhaps the dominant posture is a matter of the net effect of the many afferent (exteroceptive and proprioceptive) inputs at the time. A bed sore on the heel or a urinary infection could transform paraplegia in extension into paraplegia in flexion. For reasons outlined earlier, partial spinal cord lesions tend to have fewer flexor spasms and take on a more dominant extensor tone (Barolat & Maiman, 1987).

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