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Clinical management of spasticity
  1. A J Thompson2,
  2. L Jarrett1,
  3. L Lockley1,
  4. J Marsden2,
  5. V L Stevenson1
  1. 1National Hospital for Neurology and Neurosurgery, Queen Square, London WC1, UK
  2. 2Institute of Neurology, Queen Square
  1. Correspondence to:
 Professor Alan J Thompson
 Institute of Neurology, Queen Square, London WC1N 3BG, UK; a.thompsonion.ucl.ac.uk

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Physical and pharmacological treatments can reduce pain and discomfort without compromising function

Spasticity is a common symptom seen in many neurological conditions, notably head injury, spinal cord injury, stroke, cerebral palsy, and multiple sclerosis. It is also the dominant feature in several rarer conditions such as tropical and hereditary spastic paraparesis. The fact that it is relevant to many chronic neurological conditions and that the absence of multidisciplinary input can result in progressive disability makes it an ideal model to reflect service provision In the future more long term care for such patients will be done in primary care and the community. It is therefore essential that a multidisciplinary approach is used with successful liaison between secondary, primary, and social care.

Optimum management of spasticity is dependent on an understanding of its underlying physiology, an awareness of its natural history, an appreciation of the impact on the patient, and a comprehensive approach to minimising that impact which is both multidisciplinary and consistent over time. Regrettably, these essential requirements are rarely met; consequently, inadequately managed spasticity results in a range of painful and disabling sequelae which, with the right approach, are for the most part preventable.

PATHOPHYSIOLOGY OF SPASTICITY AND SPASMS

Stretch reflexes in healthy subjects are complex. At rest the reflex response is mediated through IA afferents that connect monosynaptically with the parent motor neurone. However, with the muscle activated other reflex components may also be elicited through group II spindle afferents and transcortical pathways. Stretch reflexes are normally modulated by task and during the different phases of walking. Such modulation reflects changes in motoneuronal and spinal cord inhibitory interneuronal activity. This inhibitory influence is in turn controlled by descending and peripheral inputs. In spasticity an enhanced and prolonged response to muscle stretch is seen at rest. Here both group IA and group II afferents …

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Footnotes

  • Competing interests: none declared