Oral medications
A number of medications have been used to treat generalised spasticity. Although there is variability in response to and tolerability of different medications, most practitioners will suggest baclofen as a first line agent. It works at the level of the spinal cord to help the body inhibit muscle movement. A number of studies have shown that baclofen is effective in reducing pain, improving gait and overall function, as well as decreasing spasm frequency.

However, baclofen can cause fatigue, dry mouth, dizziness and nausea and many people start on baclofen and say it doesn’t work for them. However, if assessed carefully and consideration is given to dose and timing, the results may be more positive. A written regime, with slowly increasing doses that help a person with MS assess how baclofen affects them over a period of time, and regular review can make the use of baclofen much more successful. Even so, some people with MS still find they cannot tolerate the dose of baclofen required for efficacy because of the side effects.

Another medication clinicians frequently prescribe is tizanidine. Again starting at a low dose, tizanidine appears to be particularly effective for painful spasms at night. Like baclofen, it can cause sleepiness, dry mouth, dizziness and fatigue.

Diazepam is also effective in treating spasticity in some people. It appears to have a greater risk of causing sleepiness and muscle weakness, and it has the potential for dependence and addiction which can affect adherence.

Dantrolene can be used for spasticity and it works at the level of the muscles to limit contractions.

Besides sharing most of the side-effects of diazepam, baclofen and tizanidine, dantrolene also requires frequent laboratory monitoring to ensure the medication does not damage the liver. As a result, dantrolene is not prescribed as frequently as the other medications.

Other medications that may be prescribed include clonazepam and gabapentin, although again, side effects can be problematic.

A combination of therapies may also be helpful for some people, and this approach has become increasingly utilised by clinicians.

Local treatments for spasticity
For those with spasticity affecting a small area (focal spasticity), or who do not get relief from oral medications, local injections of botulinum toxin or phenol into the muscles can improve quality of life. You probably know that “Botox” is now a well known and frequently used poison which paralyses the muscles and is used in non-surgical cosmetic treatment of moderate to severe frown lines.
A typical example of spasticity treatable with botulinum toxin would be the overactivity of muscles that flex the wrist, reducing the ability to reach and grasp objects. Making those muscles weaker can improve both function and pain.

There are two types of botulinum toxin, type A, known as Botox® in the United States and Dysport® in Europe; and type B, Myoblock®. A local injection of botulinim toxin can last 3–6 months and make functional activities easier to undertake.

Phenol or alcohol blocks are done less frequently, and involve identifying a point where nerve and muscle meet. Phenol is injected to destroy the nerve endings in that area only.

With both phenol and botulinum toxin, the effects are temporary and may require frequent injections. Also, individuals can build up antibodies to the botulinum toxin over time, making it ineffective. Some people are able to switch from the type A toxin to type B to prolong the therapeutic effect. The most appropriate treatment plan usually includes work with a physical and/or occupational therapist after the injection to improve functional movement of the affected area.

Surgery for spasticity
Orthopaedic surgeons and neurosurgeons might get involved in the management of spasticity in two ways. If a person experiences spasticity that has caused permanent deformity, a surgeon can lengthen tendons or fuse joints or otherwise address malformations. Surgical correction of deformity coupled with proper rehabilitation interventions can prolong sitting times in a chair, prevent skin breakdown or its recurrence, and reduce pain.

Cannabinoids and spasticity

Experimental pharmacological studies support the hypothesis that cannabinoid chemicals within cannabis, such as delta-9-tetrahydrocannabinol (delta-9-THC) and cannabidiol (CBD), exert muscle relaxant effects. While delta-9-THC does this via a specific cannabinoid receptor (the CB1 receptor) which was discovered in the central nervous system in the late 1980’s, CBD appears to have more complicated actions and may affect cytokines (proteins that are released by cells of the immune system and play a role in the generation of an immune response).

Initial clinical trial data did not support the efficacy of delta-9-THC in reducing spasticity. The first report from the “Cannabinoids in Multiple Sclerosis” (CAMS) trial, a blind and placebo-controlled trial in the UK, suggested that delta-9-THC had no statistically significant effect on spasticity when evaluated by the objective Ashworth scale.

However, in a 12-month follow-up study involving 630 patients, delta-9-THC was shown to have a small but significant effect. Nonetheless, in both studies the patients reported a subjective improvement in spasticity. It is a matter of some controversy whether the initial lack of effect using the Ashworth scale reflects the lack of sensitivity of that scale for quantifying spasticity.

The natural cannabis extract in the pharmaceutical product marketed as Sativex® has been reported to alleviate spasticity in a number of clinical trials. Clearly , since cannabis is illegal a pharmaceutical product would be welcomed.

The most common adverse side effects reported have been oral pain, dizziness, diarrhoea and nausea. Of the other cannabinoids that have been investigated, the synthetic cannabinoid, nabilone, has been reported to reduce pain related to spasticity in one recent study.

There have now been more than 12 clinical trials published on the effects of cannabinoids on spasticity and pain in MS. Although not all of these studies demonstrate a significant improvement in symptoms with delta-9-THC or CBD, evidence is accumulating that cannabinoid drugs may be useful in at least a subset of patients, and at least as an adjuvant therapy.

Long-term studies suggest that cannabinoids are reasonably well tolerated by patients but there is still concern about potential long-term adverse effects, such as cognitive impairment, impaired foetal development and psychiatric side effects. However, it must be recognised that many conventional anti-spasticity drugs such as baclofen also have significant side effects. It should also be noted that in many countries cannabis is an illegal drug, which affects its accessibility.

Related posts

• No related posts.

Spasticity, ( feelings of muscle stiffness and involuntary muscle spasms), is a well defined consequence of MS.

It is recognised through various studies that spasticity occurs frequently in people with MS with Male gender, older age, and longer duration of the disease showing an increased severity of spasticity.

Quality of life can be affected with troublesome symptoms and functional limitations, and severe spasticity may even lead to medical complications such as skin breakdown or contractures, where a limb can become fixed in one position. So, as you can see, there is a  need to recognise and address spasticity and its consequences.

In many cases, initial interventions such as stretching, exercise and rehabilitation are helpful, but
they also enhance the efficacy of other interventions such as medication. Medications can  be useful and are usually safe, although the dosing and timing must be optimised to minimise potential side effects.

For some individuals a degree of spasticity serves as a functional crutch and helps them to walk or carry out other physical activities, so the biggest challenge with spasticity management is determining what the optimal level of muscle tone is for an individual.

What’s going on?

What is happening with the nervous system to cause spasticity? To explain this you must review the fact that there are two types of motor neurones.

The nerve pathway connecting the brain and spinal cord is made of upper motor neurones. The pathway between the spinal cord and muscles is made of lower motor neurones. Spasticity is a consequence of an “upper motor neuron (UMN) syndrome”. The interruption of signals caused by MS lesions means that the upper motor neurones can no longer regulate messages to the lower motor neurones. The lower motor neurones can then become overactive and hypersensitive, causing stiffness or spasms in the muscles.

Some of the detrimental consequences associated with spasticity are:

• interference with mobility, ability to exercise and the range of motion in joints
• negative impact on endurance and energy expenditure
• interference with the activities of daily living
• discomfort or pain
• sleep disturbance
• increased difficulty for caregivers (for example with transfers or hygiene).

Treating Spasticity .

Hot temperatures may cause a decrease in spasticity for people with MS while infections and exacerbations may cause a significant increase in spasticity. The cause of any change must first be identified. If it is due to an infection, it is crucial that the infection be treated first. Many people with MS recognise increased spasticity as a sign of a bladder or other infection, or of the increase in core body temperature that is associated with a fever or excessive exercise, or of a full bladder or colon.

When treating spasticity it is important to focus the aim on management and not necessarily on the elimination of the spasticity since some individuals use their spasticity to assist with functional movements. In addition, for individuals who have restricted movement, spasticity may help promote circulation by maintaining muscle contractions which can promote the return of blood to the heart.

The most important principle of treating spasticity is to develop reasonable and flexible goals that target specific manifestations of spasticity – pain, fatigue, stiffness or weakness – and, together with the person with MS, frequently reassess the effectiveness of treatments.

Spasticity can affect just a few parts of the body (focal spasticity), or it can manifest in multiple places (generalised spasticity). It can range from insignificant to incapacitating, with many levels in between. Spasticity can also increase and decrease.

Other causes of increased spasticity include:

• noxious stimuli such as a skin lesion
• a bladder or kidney stone
• fractures
• tight clothing
• menstruation
• psychological stress
• extreme environmental temperature
• hunger
• an MS exacerbation
• treatment with some disease modifying or antidepressant pharmaceutical agents.

In the next article I will be dealing with the treatments used in spasticity

Related posts

• No related posts.