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Spasticity is one of the most common motor symptoms of multiple sclerosis. It may present as increased muscle tone, stiffness, painful spasms, difficulty walking and restriction of movement.
Treatment should not be based on muscle tone alone. It is important to understand which muscles are actually limiting function, whether weakness is also present, which factors are aggravating spasticity, and what specific treatment goal should be achieved.
In neurological terms, spasticity is a velocity-dependent increase in muscle tone caused by damage to central motor pathways.
A muscle shows excessive resistance during passive movement, particularly when it is stretched quickly.
Involuntary contractions may occur during the night, with movement, after touch or when body position changes.
Rhythmic repetitive contractions, often at the ankle, may interfere with standing and walking.
When previously stable spasticity suddenly becomes much worse, increasing the dose of a muscle relaxant is not always the first step. The cause may be outside the nervous system.
Urinary tract infection, respiratory infection and fever are common triggers.
Urinary retention, an overfilled bladder or other significant urinary symptoms may increase tone and spasms.
Constipation can markedly increase muscle tone and spasm frequency.
Pain from muscles, joints, skin or internal organs may aggravate spasticity.
Poor sitting position, an unsuitable orthosis or inappropriate footwear can provoke abnormal muscle activity.
Pressure injuries, wounds and other peripheral irritation may increase spasms.
In people with substantial leg weakness, increased extensor tone may help maintain standing, weight bearing or transfers.
Reducing this tone too aggressively can make the legs feel weaker and may worsen mobility.
Assessment includes muscle tone, strength, reflexes, clonus, range of motion, sensation and coordination.
Measures resistance during passive movement, but does not by itself show how much function is affected.
Takes movement velocity into account and may help distinguish dynamic spasticity from fixed limitation.
Frequency, pain, night-time spasms and effects on sleep should also be assessed.
Timed 25-Foot Walk, 6-Minute Walk Test and individual functional tasks may help quantify impairment.
A specific functional goal should ideally be defined before treatment is started.
| Medication | Typical role | Important considerations |
|---|---|---|
| Baclofen | One of the principal treatments for generalized MS-related spasticity. | Drowsiness, dizziness and increased weakness. It should not be stopped abruptly. |
| Gabapentin | May be useful, particularly when painful spasms or neuropathic pain coexist. | Drowsiness, dizziness and increased risk of imbalance. |
| Tizanidine | An alternative option for generalized or nocturnal spasms. | Drowsiness, dry mouth, hypotension and liver-related considerations. |
| Diazepam | Used selectively, more often for severe night-time spasms. | Sedation, impaired balance and dependence risk. |
| Dantrolene | Used much less frequently and in selected situations. | Muscle weakness and potential hepatotoxicity. |
Cannabinoids are among the most frequently discussed symptomatic treatments for MS-related spasticity. However, the term “cannabis” covers very different products, and the evidence for them is not equivalent.
The most consistent clinical evidence comes from standardized products containing both THC and CBD, particularly the oromucosal spray nabiximols (Sativex).
Recent systematic reviews suggest a modest average improvement in patient-reported spasticity for some people with MS, especially when conventional treatment has not provided sufficient relief. Effects on objective muscle-tone measurements are generally less consistent.
A standardized cannabis-based medicine containing THC and CBD in an approximately 1:1 ratio, administered as an oromucosal spray.
It is not equivalent to arbitrary cannabis flowers, oils or other non-standardized products.
Medical cannabis products may differ substantially in THC and CBD content, formulation and route of administration.
Results obtained with one standardized preparation cannot automatically be generalized to every cannabis product.
CBD is often perceived as a non-intoxicating alternative, but evidence for CBD alone in MS-related spasticity is considerably weaker than for standardized THC:CBD combinations.
Smoking cannabis or using non-standardized products is not equivalent to the treatment protocols studied in controlled clinical trials.
The dose, bioavailability, THC exposure and psychoactive effects may vary considerably.
The most evidence-based setting is moderate or severe spasticity that remains troublesome despite conventional medication, or when standard drug doses are limited by adverse effects.
A practical approach is to use a defined trial period and continue treatment only if there is a meaningful response. For example, NICE recommends a 4-week trial of THC:CBD spray after insufficient response to other pharmacological treatments, with continuation when patient-reported spasticity-related symptoms improve by at least about 20%.
Patient-reported spasticity is the outcome for which benefit has been demonstrated most consistently.
Responders may experience a reduction in the frequency or severity of muscle spasms.
For some patients, reduction of night-time spasms may improve sleep quality.
Cannabinoids are symptomatic treatments. They do not replace disease-modifying therapy for multiple sclerosis and are not used to prevent relapses, suppress new MRI lesions or slow the underlying disease itself.
Multiple sclerosis is among the neurological conditions for which medical cannabis may be considered in Israel under the applicable Ministry of Health framework. Eligibility, prescribing arrangements and product selection depend on the individual clinical situation and current regulations.
From a clinical perspective, the relevant question is not simply whether cannabis can be obtained, but whether a specific product achieves a predefined functional goal with acceptable adverse effects.
Botulinum toxin is particularly useful when spasticity is concentrated in specific muscles that interfere with function, cause pain or produce an abnormal limb position.
Treatment may be considered for equinus posture, foot inversion, hip adductor spasticity, knee flexor patterns and other focal abnormalities.
Goals may include improving hygiene, dressing, reducing pain, or improving the ability to use the arm.
The aim is not simply to inject the “tightest” muscles. The muscles selected should be those directly responsible for the specific functional problem.
For severe widespread spasticity that responds poorly to oral medication or requires doses that cause unacceptable side effects, intrathecal baclofen may be considered.
A programmable pump is implanted under the skin and delivers baclofen through a catheter directly into the cerebrospinal fluid.
This allows much smaller doses than oral treatment and can provide strong control of generalized spasticity.
A test dose is usually administered first to determine whether spasticity improves without an unacceptable loss of useful muscle tone.
Reducing muscle tone with medication rarely solves a functional problem by itself. Once excessive muscle activity is reduced, movement needs to be used in a functional way.
Help maintain joint mobility and reduce the risk of fixed contractures.
Weakness in MS should not automatically be attributed to spasticity. Targeted strengthening may be an important part of treatment.
Walking, turning, standing up, transfers and upper-limb function should be trained in meaningful tasks.
AFOs and other orthoses may improve foot position, stability and walking safety.
Functional electrical stimulation may be useful for selected patients with foot drop.
Water-based exercise may make movement training easier, although individual heat sensitivity should be considered in MS.
Walking impairment in multiple sclerosis usually has several contributors: weakness, spasticity, sensory loss, ataxia, foot drop and fatigue.
Adjustment of systemic therapy, botulinum toxin and rehabilitation of the abnormal movement pattern may be helpful.
Excessive reduction of muscle tone may make walking worse. Treatment should therefore focus on function, not simply on the Ashworth score.
It is important to determine whether it is caused mainly by weak dorsiflexors, spastic antagonists or a combination of both.
The contributions of spasticity, weakness and foot drop can be assessed separately.
It may be useful to consider whether systemic treatment should be adjusted or a more focal approach is appropriate.
The role of botulinum toxin and a specific functional treatment goal can be assessed.
Cannabinoids, combined treatment or specialist approaches may need to be considered.