Intrathecal Baclofen Therapy for the Control of Spasticity

Introduction

Intrathecal baclofen therapy (IBT) has been used for 3 decades in the management of spastic hypertonia associated with the upper motor neuron syndrome ( ). This chapter will describe patient selection, initial trialing, management of the newly implanted patient, chronic maintenance therapy, and management of intrathecal (IT) baclofen overdose and withdrawal. As of 2016 only one manufacturer (Medtronic) has United States Food and Drug Administration (FDA) approval for chronic IT baclofen infusion. Recognizing this, the chapter focuses on management of the Medtronic system while acknowledging that the principles of management would likely be similar with other systems with relatively minor differences in technical application ( ).

Patient Selection

IBT is formally indicated for the management of severe spasticity of spinal and cerebral origins. Prior to delving into the details of patient selection, it is a worthwhile exercise to define formally spasticity and severe spasticity. Despite its ubiquity, spasticity is a challenging entity to delineate with an evolving definition. Perhaps the best description that captures the depth and breath of this phenomenon is “a disordered sensorimotor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles” ( ). This definition shifts the focus away from measurement of stiffness to the measurement of the abnormal muscle activity. Thus terms such as clonus, cocontraction, associated reaction, dystonia, and spasms are included in this spasticity definition but are potentially omitted with other attempts at explanations. This description attempts to exclude the negative sign of muscle weakness associated with the upper motor neuron syndromes, as well as the changes in the rheologic properties of soft tissue ( ). The disease processes classically associated with this phenomenon are clearly divergent. Ultimately the word spasticity likely represents an umbrella term for a multiplicity of movement disorders. Clinicians must recognize the limitations of the term spasticity when considering intrathecal baclofen or any other spasticity-modulating therapy.

The next level of medical decision-making for spasticity management is to determine the gravity of the condition. It is reasonable to consider what the term “severe” implies, despite the vagaries of the spasticity definition described above. Colloquial definitions of severe include terminology such as “causing discomfort or hardship” as well as “very painful or harmful.” It is certainly reasonable to consider spasticity as severe when it is problematic, interfering with comfort, function, or caregiving. Spasticity intensity should include both the clinician’s impression and the patient’s perception. Clinicians should consider how problematic the spasticity is to the patient/caregiver, rather than solely relying on a numerical rating of a particular spasticity assessment measure. For example, modest resistance to passive motion, which could be evaluated as mild to the physician, may have a significant functional impact for the patient, who could describe the same phenomenon as severe. Even mild degrees of spasticity can lead to an inability to perform basic activities of daily living, including hygiene, dressing, and toileting. In addition, involuntary movement and spasms can cause pain, interrupt sleep, negatively impact mood, and impair mobility. These considerations are paramount when contemplating spasticity-reduction techniques ( ).

Spasticity can be both beneficial and deleterious. Advantageous effects of spasticity potentially include assistance with mobility, maintenance of posture, improvement of vascular circulation, preservation of muscle mass and bone mineral density, prevention of venous thrombosis, and assistance in reflexive bowel and bladder function. Conversely, spasticity can interfere with positioning, mobility, comfort, and hygiene. Spasticity has also been linked to increased metabolic demands, which can be problematic in the nutritionally compromised patient. Spontaneous spasms can interfere with sleep or duration of wheelchair use ( ). Spasms can also lead to skin breakdown because of shearing effects or impaired healing of surgical wounds due to tension along suture lines. Clinicians must consider all aspects of a patient’s spasticity before embarking on a treatment plan. The goal may not be complete elimination of spasticity, but rather titration to maximize the risk/benefit ratio.

Hypertonia, a condition marked by an abnormal increase in muscle tension and a reduced ability of a muscle to stretch, can be evaluated clinically using a number of well-established rating scales ( ). The most commonly utilized scales include the Ashworth ( ), Modified Ashworth ( ), and Tardieu ( ), summarized in Table 72.1 . The interrater and intrarater reliability of these scales is generally considered fair to good, with occasional reports of suboptimal consistency ( ). One potential criticism of the Ashworth and Modified Ashworth scales is their inability to distinguish between the rheologic properties of the soft tissues and the neural contributions to hypertonia. In this setting, rheology is defined as the study of deformation of materials. The Tardieu scale attempts to address the difficulty by measuring two angles: the angle (R1) at which resistance is first encountered with a quick muscle stretch, and the final angle (R2) which reflects the maximum range of movement with a slow muscle stretch. The difference between the two is claimed to represent the true amount of spasticity or spasticity angle. More sophisticated measures of hypertonia include neurophysiologic testing that attempts to quantify the muscle response to stretch (surface electromyographic activity, H-reflex response, the H-reflex standardized to the M-wave max, or the F-wave response) or instrumented measurements of stiffness and torque with accelerometers ( ). Some subjective measures include patient assessment of spasm intensity and/or logs of spasm frequency. There is an inconsistent correlation between subjective report and objective measures of spasticity ( ).

Given the diversity of spasticity presentations and the variety of diseases that create spasticity, it is not unexpected that there are a multiplicity of treatment options. These therapeutic modalities can be divided into nonpharmacologic, oral agents, chemodenervation techniques, IT therapy, orthopedic surgical techniques, and neurosurgical interventions ( ). A detailed review of each of these modalities is beyond the scope of this chapter, but Table 72.2 summarizes the nature of each intervention with their associated advantages and disadvantages. How each of these techniques is applied to each patient population is an evolving art and science. The role of IBT within the armamentarium of spasticity modification continues to evolve and define itself.

An important differentiation to be recognized by managing clinicians is severe spasticity, which is a dynamic process amenable to IBT, and contracture, which is a static occurrence that is unresponsive to IBT. Contracture is primarily managed by orthopedic interventions ( ). Distinguishing between these two entities may be impossible on routine clinical examination. An IBT trial may be a useful technique in determining to what degree each phenomenon is present. For patients who demonstrate both contracture and spasticity, there is a suggestion that treatment of spasticity should be undertaken first, followed by orthopedic lengthening or release ( ).