Physiologic and clinical monitoring of spastic hypertonia.
Spasticity has been defined as "a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome." Increased motor neuron excitability and enhanced stretch-evoked synaptic excitation of motor neurons are potential neurophysiologic mechanisms to explain this phenomenon. The relative contribution of these two distinct mechanisms likely varies depending on the location of the lesion in the central nervous system. The patient history is an important component of the clinical evaluation focusing on potential nociceptive inputs that can worsen spasticity (e.g., urinary tract infections, skin breakdown). Assessment of the impact of the spasticity on function (positive and negative), position, care of the patient, and pain should be pursued. Clinical examination of spasticity is performed using methods to evoke and quantify spastic reflex responses to muscle stretch stimuli and to observe the patient performing functional tasks to note the impact of spasticity on their performance. Treatment is based on the negative impact of the spasticity on the patient, severity of the problems, and whether the hypertonicity is focal or diffuse in distribution (see article by Elovic elsewhere in this issue). First-line treatments include elimination of nociceptive stimuli, range of motion, seating and positioning, and other physical modalities. If additional intervention is necessary, oral medications are implemented for widespread spasticity, whereas focal problems are treated with prolonged stretching and splinting or casting to maintain muscle stretch and optimal positioning. In more severe cases, invasive procedures may be needed to supplement other treatments. Neurolytic procedures are pursued for focal tone problems. For generalized hypertonicity, intrathecal pump administration of medications or surgical interruption of reflex pathways has been helpful. Ultimately, the clinician must systematically approach the evaluation and treatment of spasticity. As decisions regarding moving from less to more invasive treatments are discussed, the potential risks and side effects of treatment options must be weighed versus the potential benefits that the patient might receive to maintain a rational approach to the management of spasticity.
Hinderer
S R
SR
Department of Physical Medicine and Rehabilitation, Wayne State University, Rehabilitation Institute of Michigan, Detroit, Michigan, USA. SHindere@dmc.org
Dixon
K
K
D018726:Anti-Dyskinesia Agents / Q000627:therapeutic use; D001418:Baclofen / Q000627:therapeutic use; D001905:Botulinum Toxins / Q000627:therapeutic use; D018755:GABA Agonists / Q000627:therapeutic use; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009128:Muscle Spasticity / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery / Q000628:therapy*; D010808:Physical Examination; D026741:Physical Therapy Modalities; D012026:Reflex, Stretch / Q000187:drug effects / Q000502:physiology
D018726:Anti-Dyskinesia Agents; D018755:GABA Agonists; D001905:Botulinum Toxins; D001418:Baclofen