Multiple sclerosis (MS) is an inflammatory demyelinating disease with a high prevalence of pain.¹ Although one may not typically think of pain itself as a symptom of MS, many MS patients will develop pain syndromes throughout their disease state.¹,² The reported range of prevalence of pain in MS patients ranges widely from near 50% up to 86%.¹,²,³,⁴ The pain can be classified into four main categories as listed in Table 28.1.

Some types of pain such as muscle spasms and low-back pain may fit into more than one category depending on their cause. O’Connor et al further proposed a separate classification for MS-related pain: neuropathic pain, musculoskeletal, and nociceptive (i.e., pain secondary to tonic spasms, spasticity, and headaches).² There are not many research studies on the assessment and treatment of MS-related pain, and most therapies recommended today are based on studies conducted in patients with similar symptoms from other disorders. Risk factors for pain in MS patients are included in Table 28.2.

Furthermore, individuals with neuropathic or chronic pain are more likely to experience sleep disturbances, anxiety disorders, and depression, therefore making it even more critical that pain is appropriately evaluated and managed.³ Pain management is essential in improving
the functionality and quality of life for MS patients. In this chapter, we will discuss some of the most common pain syndromes that MS patients may experience.

Spasticity and painful muscle spasms affect many individuals with MS including interfering with ambulation, performing activities of daily living, decreased functionality, and increased pain and suffering.⁵ Spasticity can affect 60% to 80% of individuals with MS.⁶ Treatment for spasticity aims to decrease muscle tone and spasms with the goal to improve function and decrease pain, without compromising all muscle tone. Although there are no conclusive studies on MS patients at this time, it is generally accepted that physiotherapy, with a focus on both active and passive treatment, can be helpful at all stages of management.⁴,⁷,⁸,⁹ Physiotherapy can include training for appropriate posture and positioning, while avoiding triggers
which worsen spasticity.⁴ First-line oral therapy for spasticity includes the use of baclofen (10-120 mg/d oral) and tizanidine (2-24 mg/d oral), while diazepam and gabapentin are generally secondary agents.⁴,⁵,⁷,⁸,⁹ Baclofen, diazepam, and gabapentin work via activating the inhibitory γ-amino butyric acid (GABA) receptors.⁷ Tizanidine, on the other hand, functions on the presynaptic alpha 2 receptors to decrease excitatory output from these neurons.⁷ Overall, there is limited evidence for the efficacy for these oral therapies at this time, particularly when it comes to functionality; however, they are commonly used for spasticity in clinical practice.⁵,⁷ Additionally, there are side effects from these medications, particularly dry mouth, drowsiness, and weakness, which may not be well tolerated by patients.⁴,⁷ When patients cannot tolerate oral medications or require higher doses of medications, an intrathecal baclofen delivery system is a good alternative. This system is an implanted intrathecal pump, which is more invasive and expensive, and as such, it is generally used as a last resort. The pump itself is positioned subcutaneously in the abdomen attached to a catheter, which is placed into the lumbar intrathecal space allowing for medication to be delivered into the spinal fluid. As there are high levels of GABA receptors in the lumbar spinal cord, much smaller doses of baclofen are needed for treatment.⁷,⁸ There is good evidence for intrathecal baclofen therapy to reduce muscle tone and spasm frequency; however, this therapy comes with its own set of side effects including pump infections, catheter dislocations, muscle weakness, drowsiness, and headaches.⁸

Botulinum toxin muscle injections are an alternative treatment, particularly for focal spasticity.⁴,⁷,⁸ Injections are especially helpful when initiated with physiotherapy.⁴,⁸ Botulinum toxin is a neurotoxin which causes prolonged muscle relaxation by inhibiting the release of acetylcholine (ACH) at the neuromuscular junction, therefore blocking nerve conduction.⁷,¹⁰,¹¹ The effects of the injections are seen after 10 to 14 days and last a few months, after which the injections will need to be repeated.⁷ In this case, the involved muscle groups need to be identified and the injections should be made into those specific muscles. Studies have shown that botulinum toxin injections can reduce muscle tone and improve passive function such as ease of dressing.⁷

Recently, there has been greater interest in cannabinoids for the management of spasticity. Studies looking at tetrahydrocannabinol (THC) or cannabis extract did not find a significant decrease in spasticity, although they may still have a role in pain management given that they did have an effect on the patient’s overall mobility and subjective reduction of pain. Based on the available evidence and potential side effects; however, it is generally not recommended as a treatment for spasticity in MS patients except in specific refractory cases.⁴,⁹

As this is a new patient to the clinic, a thorough assessment of the level and location of spasticity is warranted. The Ashworth Scale and Modified Ashworth Scale are common tools used in the assessment of spasticity (Table 28.3). These scales are determined during passive tissue stretching. The Ashworth Scale was particularly developed for spasticity in MS patients, and the Modified Ashworth Scale added a sixth point to the scale to differentiate between the lower levels of spasticity.¹²

In the case of our patient, based on history and physical examination, it appears as though the patient has back, lower extremity, and upper extremity spasticity and muscle spasms. Initial therapy for him should begin with physiotherapy, possible hydrotherapy, followed by initiation of oral antispasticity medications. Particularly given that his spasticity is global, the patient would benefit from systemic oral medications. Medications such as baclofen or tizanidine may be started at a low dose. As there is no one focal area of spasticity, botulinum injections would be less appropriate given there are many muscle groups involved, although a combination of oral therapy and specific muscle group botulinum injections would not be unreasonable. The patient’s oral medication dose may be escalated until an appropriate dosage is reached where the patient has enough muscle relaxation, without excessive weakness or loss of muscle tone. Alternatively, the patient may be switched to second-line spasticity oral medications such as gabapentin or diazepam if the initially started
medication is not effective or poses undesired side effects. However, if the patient does well on baclofen, but cannot tolerate its side effects, and no other treatment options appear to be helpful, an intrathecal baclofen pump can be an excellent option as a last resort to provide long-term, low-concentration intrathecal baclofen with less chance for side effects.