Book contents
- Frontmatter
- Contents
- Preface
- Acknowledgements
- List of abbreviations
- 1 General methodology
- 2 Monosynaptic Ia excitation and post-activation depression
- 3 Muscle spindles and fusimotor drive: microneurography and other techniques
- 4 Recurrent inhibition
- 5 Reciprocal Ia inhibition
- 6 Ib pathways
- 7 Group II pathways
- 8 Presynaptic inhibition of Ia terminals
- 9 Cutaneomuscular, withdrawal and flexor reflex afferent responses
- 10 Propriospinal relay for descending motor commands
- 11 Involvement of spinal pathways in different motor tasks
- 12 The pathophysiology of spasticity and parkinsonian rigidity
- Index
- References
12 - The pathophysiology of spasticity and parkinsonian rigidity
Published online by Cambridge University Press: 08 August 2009
- Frontmatter
- Contents
- Preface
- Acknowledgements
- List of abbreviations
- 1 General methodology
- 2 Monosynaptic Ia excitation and post-activation depression
- 3 Muscle spindles and fusimotor drive: microneurography and other techniques
- 4 Recurrent inhibition
- 5 Reciprocal Ia inhibition
- 6 Ib pathways
- 7 Group II pathways
- 8 Presynaptic inhibition of Ia terminals
- 9 Cutaneomuscular, withdrawal and flexor reflex afferent responses
- 10 Propriospinal relay for descending motor commands
- 11 Involvement of spinal pathways in different motor tasks
- 12 The pathophysiology of spasticity and parkinsonian rigidity
- Index
- References
Summary
As discussed in Chapters 3–10, transmission in spinal pathways is controlled from descending tracts. This descending control is exerted on all interneurones, whether they mediate presynaptic inhibition of primary afferent terminals or postsynaptic effects. Transmission in multiple spinal pathways may be altered after a lesion of the central nervous system. These alterations contribute to the pathophysiological mechanisms underlying movement disorders following upper motor neurone lesions and basal ganglia diseases. A tonic imbalance between descending excitatory and inhibitory inputs on various spinal pathways accounts for the changes in muscle tone of spasticity and parkinsonian rigidity at rest. On the other hand, the loss of the normal descending modulation of these pathways during motor tasks, together with the abnormal descending command to motoneurones, contributes to the motor impairment of the patients. Methods used in clinical neurophysiology help determine the extent to which spinal pathways malfunction after a lesion of the central nervous system. Only spasticity following upper motor neurone lesions and Parkinson's disease are considered in the overview given in this chapter. The involvement of spinal pathways in the pathophysiology of other motor disorders, such as dystonia, has been discussed in previous chapters.
Spasticity
Spasticity is one of the components of the upper motor neurone syndrome, and occurs in a variety of diseases and disorders of the central nervous system, such as spinal cord injuries and diseases, multiple sclerosis, brain injuries, stroke and cerebral palsy.
- Type
- Chapter
- Information
- The Circuitry of the Human Spinal CordIts Role in Motor Control and Movement Disorders, pp. 556 - 600Publisher: Cambridge University PressPrint publication year: 2005
References
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