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  3. Upper Motor Neurone Syndrome and Spasticity
  • Cited by 51
      • 2nd edition
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    • Publisher:
      Cambridge University Press
      Publication date:
      22 August 2009
      24 April 2008
      ISBN:
      9780511544866
      9780521689786
      DOI:
      https://doi.org/10.1017/CBO9780511544866
      Dimensions:
      Weight & Pages:
      Dimensions:
      (246 x 189 mm)
      Weight & Pages:
      0.57kg, 264 Pages
      • Subjects:
      Neurology and Clinical Neuroscience, Medicine
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    • Selected: Digital
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    Subjects:
    Neurology and Clinical Neuroscience, Medicine
    Information

    Book description

    Spasticity is a disabling problem for many adults and children with a variety of neurological disorders such as multiple sclerosis, stroke, cerebral palsy and traumatic brain injury. A practical guide for clinicians involved in the management of spasticity, this book covers all aspects of upper motor neurone syndrome from basic neurophysiology and measurement techniques to practical therapy and the use of orthoses. Surgical techniques are also covered, as well as the particular problems of management of spasticity in childhood. In the second edition of this key text, all chapters have been thoroughly updated, with additional coverage of new techniques and new drugs and therapies, whilst continuing the format that has made the first edition the core text in its field. This guide will be invaluable to physicians, physiotherapists, surgeons, orthotists, clinical engineers and health professionals.

    Reviews

    'In the second edition of this key and reference text, all chapters have been updated thoroughly, with new references and descriptions of new techniques and drugs, whilst continuing the format and practical conception that has made the first edition a core text in this field. All chapters are well written and understandable, with many informative subheadings, illustrations and tables, with introduction and summary or conclusion and extensive reference lists. An index allows rapid orientation within this complicated field of neurological rehabilitation. This guide is relevant to physicians, neurologists, surgeons, physiotherapists, orthotists and other health professionals.'

    Source: European Journal of Neurology

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    Contents

    Contents
    • 1 - An overview of the clinical management of spasticity
      pp 1-8
      • By Michael P. Barnes, Professor of Neurological Rehabilitation Walkergate Park International Centre for Neurorehabilitation and Neuropsychiatry, Newcastle upon Tyne, UK
    • View abstract

      Summary

      This introduction provides an overview of spasticity management. Spasticity can cause problems with activity and participation in people with a variety of neurological disorders. It is only one of the many different features of the upper motor neurone (UMN) syndrome. The clinical features of the UMN syndrome can be divided into two broad groups such as negative phenomena and positive phenomena. A characteristic feature of spasticity is that the hypertonia is dependent upon the velocity of the muscle stretch, in other words, greater resistance is felt with faster stretches. Thus, spasticity resists muscle stretch and lengthening. Severe muscle spasms are often found in UMN syndrome. These can be in either a flexor pattern or an extensor pattern. The description of the different patterns of the UMN syndrome makes it clear that there is a potentially wide range of functional problems.
    • 2 - Neurophysiology of spasticity
      pp 9-63
      • By Geoff Sheean, Professor Department of Neurosciences, University of California – San Diego Medical Centre San Diego, California, USA
    • View abstract

      Summary

      The pathophysiology of spasticity is a complex subject and one frequently avoided by clinicians. Spasticity and the other features, positive and negative, of the upper motor neurone (UMN) syndrome arise from disruption of certain descending pathways involved in motor control. Hyperexcitability of spinal reflexes forms the basis of most of the positive clinical signs of the UMN syndrome, which have in common excessive muscle activity. These spinal reflexes may be divided into two groups, proprioceptive reflexes and nociceptive/cutaneous reflexes. The clasp-knife phenomenon combines features of both groups, at least in the lower limbs. Contractures are a well known and feared complication of the UMN syndrome, reducing the range of motion of a joint. There has been a recent investigation of the relationship between the stretch reflex hyper excitability of spasticity and contractures. Spasticity does not appear to exist in contracting agonists and would not really interfere with movement.
    • 3 - The measurement of spasticity
      pp 64-78
      • By Garth R. Johnson, Professor of Rehabilitation Engineering Centre for Rehabilitation and Engineering Studies (CREST) School of Mechanical and Systems Engineering Newcastle University Newcastle upon Tyne, UK, Anand D. Pandyan, School of Health & Rehabilitation/Institute for Life Course Studies, Keele University, Staffordshire, UK
    • View abstract

      Summary

      Even today the measurement of spasticity at the level of impairment is probably in its infancy. Due to the lack of treatment or therapy to reduce spasticity, there has been limited development of methods for its measurement. There are four distinct levels of measurement that can be identified hierarchically as follows: nominal, ordinal, interval and ratio levels. Following the original research of Tardieu and colleagues in the early 1950s, a new scale for classifying spasticity based was developed. This scale has since been translated to English and undergone substantial modifications. The Tardieu method of assessment provides a composite measure of spasticity. The quality of the muscle reaction is a categorical level of measurement and therefore can primarily used for classification purposes only. There are two elements to be considered when exploring the reliability of the Tardieu scale.
    • 4 - Physiotherapy management of spasticity
      pp 79-98
      • By Roslyn N. Boyd, Associate Professor, Scientific Director Queensland Cerebral Palsy and Rehabilitation Research Centre, Department of Paediatrics and Child Health, University of Queensland, Brisbane, Australia, Louise Ada, Associate Professor Discipline of Physiotherapy University of Sydney Sydney, Australia
    • View abstract

      Summary

      Spasticity is one of the impairments affecting function following brain damage. If spasticity is only one of several impairments following brain damage, physiotherapists need to clarify how spasticity affects the ability to move. Historically, spasticity was seen as the major determinant of activity limitations. The difficulty in assessing the contribution of different impairments to activity limitations makes it possible for other impairments to be mislabeled as spasticity. The operational definitions and relative importance of spasticity are confounded by the issue of how spasticity affects growth and maturation in children with spastic-type cerebral palsy. An important component of the clinical management of brain damage is careful assessment of the contribution of various impairments to activity limitations. There are many pharmacological and surgical options available in the management of spasticity, which may be focal or general, reversible or permanent in action.
    • 5 - Seating and positioning
      pp 99-112
      • By Craig A. Kirkwood, Senior Rehabilitation Engineer Wheelchair & Seating Service Tayside Rehabilitation Engineering Services, Ninewells Hospital, Dundee, UK, Geoff I. Bardsley, Senior Rehabilitation Engineer, Wheelchair & Seating Service Tayside Rehabilitation Engineering Services, Ninewells Hospital, Dundee, UK
    • View abstract

      Summary

      Spasticity causes seating challenges for a variety of people with disabilities: from children with cerebral palsy, young adults with head injuries, middle aged people with multiple sclerosis (MS) and older persons who have suffered cerebrovascular accidents (CVAs) and use wheelchairs. Spasticity, in itself, is not necessarily a problem and may assist in maintaining a seated posture. This is in contrast to hypotonia, where providing seated support in a functional position is often very difficult. Detailed assessment is essential so that a full picture of patient's problems relating to spasticity is drawn up in order that clear, specific and realistic objectives can be agreed on by all those present and a detailed prescription produced to achieve the objectives. In any system that claims to reduce spasticity and thereby promote good seated posture, reduction in joint contractures and improvement in upper limb function, it is important that such claims are validated.
    • 6 - Orthoses, splints and casts
      pp 113-130
    • View abstract

      Summary

      Orthoses can be highly effective tools in the management of spasticity. By splinting in a position of maximum function with a rigid device even if the spasticity can not be inhibited then the abnormal movement caused by it may be prevented. A good understanding of biomechanics and materials is essential to appreciate fully the forces involved and their influence on the design of orthoses. There are several advantages of the use of casting versus providing a definitive orthoses, such as cost and availability. A system has been developed whereby orthoses are classified and named by reference to the parts of the body over which they pass. For example, an orthosis around the ankle is called an ankle-foot orthosis (AFO) and a full leg calliper is termed a knee-ankle-foot orthosis (KAFO). This classification is useful but does not describe the function, construction or aim of the orthosis.
    • 7 - Pharmacological management of spasticity
      pp 131-149
      • By Anthony B. Ward, Consultant in Rehabilitation Medicine North Staffordshire Rehabilitation Centre, University Hospital of North Staffordshire, Stoke-on-Trent, UK, Sajida Javaid, Specialist Registrar in Rehabilitation Medicine North Staffordshire Rehabilitation Centre, University Hospital of North Staffordshire, Stoke-on-Trent, UK
    • View abstract

      Summary

      The management of spasticity requires a multi-professional approach based on addressing the troublesome effects of the increased tone. This chapter discusses the oral agents and their place in overall management strategies. Oral antispastic agents are usually indicated in patients with diffuse or regional muscle spasticity rather than localized muscle spasticity. Despite the large number of drugs that have been reported to influence muscle tone, very few have been found useful in clinical practice. The commonly used antispastic drugs are baclofen, benzodiazepine, dantrolene sodium and tizanidine. The drugs can be used alone as monotherapy or in combination to reduce the spasticity effectively. Cannabis has been widely discussed, but there is no evidence that it has a sustained effect as an antispastic drug (CAMS Study), where as baclofen is a structural analogue of gamma amino butyric acid (GABA), which is one of the main inhibitory neurotransmitters in the central nervous system.
    • 8 - Chemical neurolysis in the management of muscle spasticity
      pp 150-164
      • By A. Magid O. Bakheit, Professor of Neurological Rehabilitation Department of Rehabilitation Medicine, Mount Gould Hospital, Plymouth, UK
    • View abstract

      Summary

      Destruction of peripheral nerves with chemical substances such as phenol and alcohol solutions was introduced as a novel therapeutic modality in the 1930s, but it became a popular method of treating severe, intractable pain associated with cancer in the mid 1950s. Severe chronic muscle spasticity often causes constant gnawing pain. Diagnostic nerve blocks with local anaesthetics are sometimes necessary to assess the risk/benefit ratio of chemical neurolysis. Phenol and ethyl alcohol are the drugs most commonly used for peripheral nerve and intrathecal blocks. Chemical neurolysis is most frequently used for blocks of the medial popliteal, the obturator, the sciatic and the musculocutaneous nerve of the arm. A number of factors contribute to the motor functional disability associated with long-standing upper motor neurone lesions. Administration of phenol or alcohol into the intrathecal subarachnoid space is generally reserved for severe symptomatic cases of lower limb spasticity refractory to other methods of treatment.
    • 9 - Spasticity and botulinum toxin
      pp 165-180
      • By Michael P. Barnes, Professor of Neurological Rehabilitation Walkergate Park International Centre for Neurorehabilitation and Neuropsychiatry, Newcastle upon Tyne, UK, Elizabeth C. Davis, Consultant in Rehabilitation Medicine Walkergate Park International Centre for Neurorehabilitation and Neuropsychiatry, Newcastle upon Tyne, UK
    • View abstract

      Summary

      Botulinum toxin (BoNT) is the most potent neurotoxin known, and its clinical effects have been recognized since the end of 19th century. There are seven immunologically distinct serotypes of botulinum toxin; there are two types in routine clinical use - BoNT type A (BoNT-A) and BoNT type B (BoNT-B). Most of the large-scale studies on botulinum toxin have been related to upper and lower limb spasticity. The usefulness of BoNT in the management of spasticity secondary to a variety of clinical conditions is increasing. It is now well accepted for the management of movement disorders, particularly dystonia. There is an increasing evidence base for the use as a management tool in spasticity. The products now have a licence for use in focal spasticity. Dysport is indicated for focal spasticity specifically including arm symptoms associated with focal spasticity in conjunction with physiotherapy.
    • 10 - Intrathecal baclofen for the control of spinal and supraspinal spasticity
      pp 181-192
      • By David N. Rushton, Consultant in Neurological Rehabilitation Frank Cooksey Rehabilitation Unit, Kings College Hospital, London, UK
    • View abstract

      Summary

      Penn and Kroin first described the benefits reporting the treatment of six patients with severe continuing spasticity and spasms resulting from spinal injury or multiple sclerosis. Baclofen is hydrophilic and crosses the blood-brain barrier poorly. Spinal intrathecal administration bypasses the blood-brain barrier, allowing effective treatment of spasticity with a dose range that is 100 to 1000 times smaller than that required for oral treatment. The plasma levels of baclofen in patients undergoing intrathecal infusion have been found to be vanishingly low. Intrathecal baclofen (ITB) reduces spasticity, as clinically assessed using the Ashworth scale. Flexion or extension spasms, more common in the lower limbs, may occur spontaneously or in response to cutaneous stimuli in association with spasticity. The threshold of the electrically induced flexion reflex in the lower limb has been found to be reduced in spinal spasticity and the response amplitude to be increased.
    • 11 - Surgical management of spasticity
      pp 193-213
      • By Patrick Mertens, Professor of Neurosurgery Hôpital Neurologique et Neuro-Chirurgical Pierre Wertheimer, Lyon, France, Marc Sindou, Professor of Neurosurgery Hôpital Neurologique et Neuro-Chirurgical Pierre Wertheimer, Lyon, France
    • View abstract

      Summary

      Spasticity is one of the commonest sequelae of neurological diseases. In most patients spasticity is useful in compensating for lost motor strength. Nevertheless, in a significant number of patients it may become excessive and harmful, leading to further functional losses. Stimulation of spinal cord was developed in the 1970s on the basis of the 'gate-control theory' of Melzach and Wall for the treatment of neurogenic pain. This method has been found to be partially effective in the treatment of spastic syndromes, such as those encountered in multiple sclerosis or spinal cord degenerative diseases, such as Strumpell-Lorrain syndrome. Orthopaedic procedures can reduce spasticity by means of muscle relaxation that results from tendon lengthening and may help in restoring articular function when deformities have become irreducible. Current techniques for correcting excessive shortness of the muscle tendon assembly are muscular desinsertion, myotomy, tenotomy and lengthening tenotomy.
    • 12 - Management of spasticity in children
      pp 214-240
      • By Rachael Hutchinson, Consultant Paediatric Orthopaedic Surgeon Norfolk and Norwich University Hospital NHS Trust, Norfolk, UK, H. Kerr Graham, Professor of Orthopaedic Surgery Royal Children's Hospital, Melbourne, Australia
    • View abstract

      Summary

      Spasticity in children continues to be a common and challenging problem for the foreseeable future. While reduction in the incidence of cerebral palsy would have the most impact in reducing the overall incidence of spasticity in children, prevention of traumatic brain injury and spinal cord injury is probably more realistic. Fixed musculoskeletal pathology in cerebral palsy is acquired during childhood. Children with cerebral palsy do not have contractures, dislocated hips or scoliosis at birth. These common deformities are acquired during childhood. There are few useful clinical measures of spasticity and none validated for use in children. The Ashworth and modified Ashworth scales are blunt and unresponsive tools in the assessment of the child with cerebral palsy. Botulinum toxin A (BoNT-A) is a reversible, focal agent which has been under evaluation since the early 1990s in the management of spasticity in children.
    References

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