Spastic Hypertonia and Movement Disorders: Pathophysiology, Clinical Presentation, and Quantification
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.
To access this article, please choose from the options below
Editor’s note: This Special Section on Spasticity is a series of 5 clinical focused review articles that was developed from the “Advanced Assessment and Management Skills for Spasticity, Dystonia, and Related Motor Disorders” Pre-course at the 2008 AAPM&R Annual Assembly in San Diego, CA. These articles are not an exact representation of that course nor are they designed to represent comprehensive coverage of the field. However, these reviews do provide clinically pertinent and practical information that the clinician will hopefully be able to incorporate into his or her practice. The authors of these articles are expert practitioners who served on the faculty for this course. For further details, the course content can be accessed at http://me.e-aapmr.org/
Disclosure Key can be found on the Table of Contents and at www.pmrjournal.org
PII: S1934-1482(09)00763-1
doi:10.1016/j.pmrj.2009.08.002
© 2009 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.
