Traumatic brain injury (TBI) impacts the lives of 1.5 to 2 million new individuals each year; 75,000 to 100,000 of these are classified as severe, and will suffer enduring severe spasticity in addition to cognitive, vestibulomotor (balance), and other motor impairments. Following TBI, the onset of spasticity and associated orthopedic sequellae is rapid, beginning as early as one week following injury. The progressively developing spasticity and other disabilities often represent the most significant barriers for practical re-entry of TBI patients into the community. The lack of sufficient data regarding the neurobiology of TBI-induced spasticity and safety, feasibility and efficacy of early intervention therapy direct the current treatment guidelines to a conservative level. This chapter focuses on several quantitative physiological measures of spasticity, some recent findings regarding a neurobiological basis of spasticity, and finally, a section describing present treatments and the experimental treatments and rehabilitation of TBI-induced spasticity.
Clinically spasticity has been defined as an increased velocity-dependent lengthening resistance of skeletal muscles to passive movement. It is a secondary neurological condition induced by neurological hyperreflexia associated with TBI and spinal cord injury (SCI), stroke, multiple sclerosis (MS), cerebral palsy, amyotrophic lateral sclerosis (ALS), and few other disorders (e.g., anoxic brain damage; some metabolic disorders, such as adrenoleukodystrophy, phenylketonuria). Spasticity is often one of the most troublesome components of upper motor neuron injury (Katz and Rymer, 1989; Ordia et al., 1996) that greatly complicates daily living in individuals with these disorders. Its hallmark feature is altered skeletal muscle tone and spasm, and it is aptly named “spasticity.” The word spasm comes from the Greek word “σπασμµό” (spasmos), meaning “drawing, pulling.” Spasticity symptoms include increased muscle tone (hypertonicity), muscle spasms, increased deep tendon reflexes, clonus, scissoring, and fixed joints. The degree of spasticity varies from mild muscle stiffness to painful, severe uncontrollable muscle spasms. In addition to spasticity symptoms, muscles affected in this way have many other potential features of altered performance, including muscle weakness, decreased movement control, and decreased endurance.
Spasticity is associated with hyperreflexia of the muscle stretch reflexes (Ashby and Verrier, 1980; Bose et al., 2002b; Herman, 1968; Machta and Kuhn, 1948; Thilmann et al., 1991; Toft et al., 1993) that induce velocity-sensitive increased resistance of skeletal muscle lengthening. This dynamic stiffness differentiates spasticity from the changes in passive muscle properties, which are not velocity-sensitive and often seen in patients with spasticity. Although some insights have been made regarding the fundamental neurobiology of spasticity, many aspects of the specific pathophysiology still remain unclear. Therefore, experimental animal models of spasticity have been developed to increase scientific understanding of this clinically troublesome condition. The authors’ previous research works have provided evidence of neurophysiological changes in the tibial monosynaptic reflexes that use the neural pathways that subserve hindlimb muscle stretch reflexes (Thompson et al., 1992, 1993, 1998, 1999). These alterations included significant changes in rate-dependent processes that regulate sensory transmission to motoneurons (Thompson et al., 1992, 1998). More recent animal studies have shown that these physiological changes in the muscle stretch reflexes were accompanied by progressive and enduring spastic hypertonia (Bose et al., 2002b, 2012, 2013; Hou et al., 2014). These changes were severe in magnitude and highly relevant to features observed clinically in humans (Schindler-Ivens and Shields, 2000). Human studies have reported that neurophysiological changes in rate-dependent processes that regulate reflex excitability of the stretch reflex pathways also accompany spasticity (Boorman et al., 1992; Brown, 1994; Calancie et al., 1993; Lance, 1981; Nielsen et al., 1993; Schindler-Ivens and Shields, 2000; Thompson et al., 2001a, 2001b).
Rodent spasticity models for SCIs (Bose et al., 2002b, 2012; Hou et al., 2014), TBIs (Bose et al., 2013), experimental allergic encephalitis (EAE) Lewis rat model of MS (Bose et al., 2009), and a rodent white matter stroke model (Thompson et al., 2013) have been developed and studied in the authors’ laboratory to increase our scientific understanding about this condition and to find ways to prevent, treat, and diminish disabilities of this condition. There are some distinct differences in the pattern, time course of development, and severity of spasticity that is induced by these different injuries or disease processes. These different patterns of spasticity are presumed to be derived according to the manner in which the central nervous system (CNS) trauma or disease has induced alterations in supraspinal drive, their substrate systems (e.g., serotonergic and noradrenergic innervation of the motoneurons), and associated secondary changes at the cellular level in the spinal cord (e.g., both motor neuron and interneurons) below the lesion. Accordingly, an increased understanding of the mechanisms responsible for these injury/disease-induced neuroplastic changes at supraspinal and spinal levels may be of great importance in relation to the design of the most effective treatment and rehabilitation of spasticity.
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