Tags

Type your tag names separated by a space and hit enter

Spastic hypertonia and movement disorders: pathophysiology, clinical presentation, and quantification.
PM R 2009; 1(9):827-33PM R

Abstract

A delayed consequence of a lesion affecting the upper motor neuron pathways is the appearance of some forms of motor overactivity, including spasticity. Many of these are caused by hyperexcitability of spinal reflexes, such as stretch reflexes (spasticity, tendon hyperreflexia) or flexor withdrawal reflexes (flexor spasms), and are elicited at rest by sensory stimulation. Spastic co-contraction is probably attributable to failure of reciprocal inhibition; it occurs only during active voluntary movement and constrains such movement. The basic underlying mechanism of these changes is not clear, although a change in the balance between the inhibitory and excitatory supraspinal upper motor neuron pathways toward net excitation most likely contributes. Increased intrinsic excitability of the alpha motor neurons is another possible factor. Spastic dystonia is most often seen as the presence of tonic muscle contraction in the absence of voluntary movement or spinal reflex activation, and the underlying mechanisms are obscure. Prolonged shortening of tissues, either because of weakness or muscle contraction, leads to stiffness of the soft tissues, which contributes to hypertonia and is thus self-perpetuating, and ultimately to contracture with fixed shortening. Some of these forms of motor overactivity produce involuntary movements (hyperkinetic), eg, flexor spasms, whereas others impair movement (hypokinetic), either voluntary movement, eg, spastic co-contraction, or passive movement, eg, spasticity. Quantification has mostly focused on hypertonia, that is, increased resistance at rest to passive movement. In the upper motor neuron syndrome, hypertonia could be caused by a combination of spasticity, spastic dystonia, and soft tissue stiffness (rheologic changes). Some measures, such as the Ashworth or Modified Ashworth Scales, quantify hypertonia but are very poor at distinguishing between spasticity and soft tissue stiffness. Another, the Tardieu Scale, is better at making this distinction, but quantification of the spasticity portion of hypertonia remains difficult, at least in a clinical setting.

Authors+Show Affiliations

University of California San Diego, San Diego, CA 92103, USA. gsheean@ucsd.eduNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19769916

Citation

Sheean, Geoffrey, and John R. McGuire. "Spastic Hypertonia and Movement Disorders: Pathophysiology, Clinical Presentation, and Quantification." PM & R : the Journal of Injury, Function, and Rehabilitation, vol. 1, no. 9, 2009, pp. 827-33.
Sheean G, McGuire JR. Spastic hypertonia and movement disorders: pathophysiology, clinical presentation, and quantification. PM R. 2009;1(9):827-33.
Sheean, G., & McGuire, J. R. (2009). Spastic hypertonia and movement disorders: pathophysiology, clinical presentation, and quantification. PM & R : the Journal of Injury, Function, and Rehabilitation, 1(9), pp. 827-33. doi:10.1016/j.pmrj.2009.08.002.
Sheean G, McGuire JR. Spastic Hypertonia and Movement Disorders: Pathophysiology, Clinical Presentation, and Quantification. PM R. 2009;1(9):827-33. PubMed PMID: 19769916.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Spastic hypertonia and movement disorders: pathophysiology, clinical presentation, and quantification. AU - Sheean,Geoffrey, AU - McGuire,John R, PY - 2009/07/16/received PY - 2009/08/06/accepted PY - 2009/9/23/entrez PY - 2009/9/23/pubmed PY - 2009/12/16/medline SP - 827 EP - 33 JF - PM & R : the journal of injury, function, and rehabilitation JO - PM R VL - 1 IS - 9 N2 - A delayed consequence of a lesion affecting the upper motor neuron pathways is the appearance of some forms of motor overactivity, including spasticity. Many of these are caused by hyperexcitability of spinal reflexes, such as stretch reflexes (spasticity, tendon hyperreflexia) or flexor withdrawal reflexes (flexor spasms), and are elicited at rest by sensory stimulation. Spastic co-contraction is probably attributable to failure of reciprocal inhibition; it occurs only during active voluntary movement and constrains such movement. The basic underlying mechanism of these changes is not clear, although a change in the balance between the inhibitory and excitatory supraspinal upper motor neuron pathways toward net excitation most likely contributes. Increased intrinsic excitability of the alpha motor neurons is another possible factor. Spastic dystonia is most often seen as the presence of tonic muscle contraction in the absence of voluntary movement or spinal reflex activation, and the underlying mechanisms are obscure. Prolonged shortening of tissues, either because of weakness or muscle contraction, leads to stiffness of the soft tissues, which contributes to hypertonia and is thus self-perpetuating, and ultimately to contracture with fixed shortening. Some of these forms of motor overactivity produce involuntary movements (hyperkinetic), eg, flexor spasms, whereas others impair movement (hypokinetic), either voluntary movement, eg, spastic co-contraction, or passive movement, eg, spasticity. Quantification has mostly focused on hypertonia, that is, increased resistance at rest to passive movement. In the upper motor neuron syndrome, hypertonia could be caused by a combination of spasticity, spastic dystonia, and soft tissue stiffness (rheologic changes). Some measures, such as the Ashworth or Modified Ashworth Scales, quantify hypertonia but are very poor at distinguishing between spasticity and soft tissue stiffness. Another, the Tardieu Scale, is better at making this distinction, but quantification of the spasticity portion of hypertonia remains difficult, at least in a clinical setting. SN - 1934-1482 UR - https://www.unboundmedicine.com/medline/citation/19769916/Spastic_hypertonia_and_movement_disorders:_pathophysiology_clinical_presentation_and_quantification_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1934-1482(09)00763-1 DB - PRIME DP - Unbound Medicine ER -