Chapter 56: Spasticity and Contractures

INTRODUCTION

This chapter focuses on the clinical diagnosis, pathophysiology, and physiatric management of spasticity and contractures.

• Spasticity is an involuntary velocity-dependent increase in muscle tone, a component of upper motor neuron syndrome.

• Contractures are a loss of full active and passive range of motion in a limb that can be due to limitations imposed by the joint, muscle, or soft tissue.

• Spasticity and contractures are significant contributors to disability.

• Clinical measurement of spasticity includes the Modified Ashworth and Tardieu scales.

• Spasticity can be treated systemically with oral medications such as baclofen and tizanidine and with an intrathecal baclofen pump. Botulinum toxin and other neurolytic injections are used for localized treatment.

• Prevention is critical for contracture management. Once they occur, contractures can be managed with rehabilitation modalities, including stretching, proper positioning, and splinting.

• Once a contracture has developed, surgical release may be required.

DEFINING THE CLINICAL ENTITIES

Spasticity

Lance et al defined spasticity as a “motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerk, resulting from hyper-excitability of the stretch reflex.”¹ While valuable, this definition omits common clinical manifestations of spasticity. For example, clonus and flexor withdrawal spasms seen with spasticity arising from spinal cord injury are not encompassed by the Lance definition. Although a number of alternative definitions have been proposed, no universally accepted definition has yet been established.²

Spasticity is a common finding in central nervous system (CNS) injury as a feature of the upper motor neuron (UMN) syndrome. This syndrome, addressed in more detail in other chapters, is defined as injury to the motor neurons in the brain or their connecting pathways leading to the (lower) motor neurons in the anterior horn of the spinal cord. Damage to any portion of this pathway results in a characteristic set of clinical signs and symptoms.³ These signs include clonus, flexor spasms, and hyperactive tendon reflexes from excessive or inappropriate muscle activity (Fig. 56–1). Spasticity has become a term that encompasses all these features.⁴ The majority of positive UMN symptoms arise from reflexes that result from abnormal processing of the sensory feedback from the periphery such as pain, cutaneous stimulation, and muscle stretch.⁴ Stretch reflexes refer to proprioceptive reflexes that are either tonic, from a sustained stretch, as in the case of clonus, or phasic, from a short stretch, as in the case of deep tendon reflexes.⁴ Examples of the nociceptive reflexes are flexor and extensor spasms and the Babinski sign, a familiar cutaneous reflex.⁴