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Pain in multiple sclerosis may be neuropathic, related to spasticity, musculoskeletal, associated with abnormal gait, trigeminal neuralgia, migraine, optic neuritis, or caused by a condition that is not related to MS at all.
Effective treatment therefore begins not with choosing another painkiller, but with identifying the pain mechanism. More than one mechanism may coexist in the same patient.
Two patients may both rate their pain as 7 out of 10 and still require completely different treatment. The mechanism of pain is more important than the intensity score alone.
Damage to central sensory pathways may cause dysesthesia, allodynia, burning pain and abnormal painful responses to touch or temperature.
Short, very severe, electric-shock-like attacks affecting one or more divisions of the trigeminal nerve.
A brief electrical sensation running down the neck or spine, sometimes into the limbs, often triggered by neck flexion.
Increased tone, spasms, clonus and abnormal limb positions may themselves become painful.
Weakness, altered walking, prolonged sitting, use of walking aids and abnormal biomechanics can produce secondary musculoskeletal pain.
Central, peripheral, musculoskeletal and pain-processing mechanisms may coexist in long-standing pain.
Lesions affecting sensory pathways in the brain or spinal cord can alter the processing of sensory information. A normally non-painful signal may then be perceived as unpleasant or painful.
Pain may be triggered by a stimulus that is normally not painful, such as clothing, light touch or temperature change.
The words “burning” or “numbness” do not automatically prove that pain is central. A similar phenotype can occur with peripheral neuropathy and small fiber neuropathy.
Trigeminal neuralgia in MS typically causes short, extremely severe attacks of facial pain triggered by touch, chewing, speaking, washing the face or brushing the teeth.
Carbamazepine and oxcarbazepine remain the principal first-line medications.
Other medications or combinations may be considered when response is insufficient or adverse effects limit treatment.
For refractory trigeminal neuralgia, interventional or neurosurgical approaches may be considered, including percutaneous procedures, stereotactic radiosurgery and in selected cases microvascular decompression.
Treatment selection in MS requires individual assessment.
Lhermitte sign is a brief, electric-shock-like sensation running down the neck or spine, sometimes radiating into the arms or legs. It is commonly triggered by neck flexion.
If episodes are infrequent and brief, understanding the symptom and avoiding obvious triggers may be sufficient.
For frequent or painful episodes, medications that reduce neuronal hyperexcitability may be considered. The choice depends on symptom severity, other MS symptoms and concomitant medication.
Spasticity can cause persistent tightness, painful night-time spasms, pain during stretching and secondary joint overload.
For generalized spasticity, baclofen, tizanidine and other medications may be used.
For a focal painful pattern, botulinum toxin can target the specific muscles responsible for pain or abnormal limb posture.
Positioning, stretching, orthotic management and correction of abnormal movement patterns may be as important as medication.
Not all pain in MS results from demyelination. Abnormal gait, asymmetric loading, weakness, contractures and prolonged use of mobility aids can produce conventional musculoskeletal pain.
Limping, foot drop and compensatory movements alter loading of the pelvis, knees, ankles and lumbar spine.
A person with MS can develop exactly the same causes of back pain as anyone else: degenerative disease, muscular overload or radiculopathy.
Walking aids, transfers and compensation for leg weakness may substantially increase loading of the shoulders and arms.
Migraine is common among people with MS, but migraine itself does not indicate MS activity.
Migraine is treated according to modern migraine principles: appropriate acute therapy and, when attacks are frequent or disabling, preventive treatment.
A major change in headache pattern, new neurological symptoms, fever, altered consciousness or other warning features require separate evaluation.
Typical optic neuritis often causes pain around or behind the eye, frequently worsened by eye movement, together with reduced vision or altered colour perception.
Burning feet, allodynia, abnormal temperature sensation or painful distal paresthesia should not automatically be attributed to brain or spinal cord lesions. Sometimes a peripheral pain mechanism needs to be investigated.
Small fiber neuropathy affects thinly myelinated Aδ fibers and unmyelinated C fibers involved in pain, temperature sensation and autonomic function.
Standard nerve conduction studies primarily assess large nerve fibers. Therefore, results can remain normal in isolated small fiber neuropathy.
Depending on the clinical phenotype, testing may include skin biopsy with intraepidermal nerve fiber density, quantitative sensory testing and autonomic investigations.
There is no single “MS pain medication.” Treatment depends on the dominant pain mechanism.
| Type of pain | Possible approaches | Important considerations |
|---|---|---|
| Central neuropathic pain | Gabapentin, pregabalin, duloxetine, amitriptyline or other neuropathic pain treatments depending on the individual situation. | Sedation, dizziness, cognitive symptoms, fall risk and drug interactions must be considered. |
| Trigeminal neuralgia | Carbamazepine or oxcarbazepine; other medications or interventional treatments for refractory cases. | Conventional analgesics are often ineffective for typical short paroxysmal attacks. |
| Spasticity-related pain | Spasticity management, baclofen, tizanidine, botulinum toxin and physiotherapy. | Reducing tone excessively may worsen function if spasticity partly compensates for weakness. |
| Musculoskeletal pain | Physiotherapy, load correction, strengthening, gait management, orthoses and treatment of the specific musculoskeletal cause. | Neuropathic pain medications are not universal treatment for mechanical pain. |
| Focal peripheral neuropathic pain | Selected topical treatments, TENS, interventional pain procedures or PNS in appropriate cases. | A peripheral mechanism and anatomical pain generator should be identified first. |
| Migraine | Acute migraine treatment, CGRP-targeted treatment, botulinum toxin and other preventive therapies when indicated. | Migraine is treated as a separate neurological disorder, not as evidence of MS activity. |
Medical cannabis is a particularly relevant topic for patients in Israel. However, it is important to distinguish between the evidence for cannabinoids in MS-related spasticity and the evidence for chronic neuropathic pain. They are not the same.
For chronic pain in general, predominantly neuropathic pain, standardized THC-containing products or products with comparable THC:CBD exposure produce on average a small reduction in pain intensity.
At the same time, dizziness, drowsiness, nausea and other adverse effects become more common.
For chronic neuropathic pain specifically in people with MS, the evidence is substantially less certain than the evidence for improvement in patient-reported spasticity.
The most interpretable evidence comes from standardized products where the dose and active cannabinoid content are known.
The popularity of CBD is greater than the strength of evidence for analgesia. Current reviews do not show convincing clinically meaningful pain relief from CBD alone.
Evidence is harder to interpret when cannabis strains, oils and other preparations have widely different THC/CBD concentrations and bioavailability.
Cannabinoids are symptomatic therapy. They do not prevent relapses, replace disease-modifying therapy or suppress new MRI activity.
Cannabinoid-based treatment may be discussed in carefully selected patients with chronic pain, particularly when standard approaches have provided insufficient benefit or are limited by adverse effects.
A treatment goal should ideally be defined before starting: not only a lower pain score, but also better sleep, improved mobility, better daily function or reduced need for other medication.
In Israel, medical cannabis may be considered under several neurological and pain-related pathways. Multiple sclerosis is specifically relevant in the setting of spasticity.
For neuropathic pain with a documented organic source, a separate pain-related pathway exists under the current Ministry of Health framework and may include previous standard treatment and specialist follow-up through an appropriate pain clinic.
For patients with MS, this distinction is important: medical cannabis may be considered because of disabling spasticity, because of a qualifying neuropathic pain syndrome, or occasionally because both are present. The clinical rationale should be clearly defined.
Regulatory criteria may change. Current Ministry of Health requirements should therefore be checked before treatment authorization is pursued.
Chronic pain is often managed more successfully when movement, sleep, biomechanics and daily function are addressed alongside medication.
Particularly important for musculoskeletal pain, abnormal gait, weakness, restricted movement and secondary overload.
Complete avoidance of movement may lead to deconditioning and worsen chronic pain. Activity should be adjusted to the individual's neurological function.
Pain disrupts sleep, while poor sleep increases pain sensitivity. Both components often need treatment.
CBT and other chronic pain strategies do not imply that pain is “psychological.” They help reduce the impact of pain on function and quality of life.
Orthoses, FES, walking aids, appropriate footwear and gait training may reduce abnormal mechanical loading.
Complex chronic pain may require collaboration between a neurologist, pain physician, rehabilitation specialist, physiotherapist and other professionals.
Neuromodulation includes very different technologies. Some are non-invasive and may supplement conventional treatment. Others require implanted electrodes and are used only in carefully selected patients with refractory chronic pain.
Transcutaneous electrical nerve stimulation is a relatively simple, non-invasive approach.
Small studies have evaluated TENS for pain in MS, but responses vary and the evidence remains limited.
Transcranial stimulation aims to alter activity within central pain-processing networks.
Studies in MS, particularly with tDCS, suggest possible pain reduction, but sample sizes are small and these approaches are not universal standard therapy.
An electrode is positioned near a specific peripheral nerve. Modern pain practice uses PNS for selected chronic peripheral neuropathic pain conditions.
PNS is not an MS-specific therapy. In a patient with MS, there should be a corresponding peripheral pain generator.
Electrodes are placed in the epidural space to modify transmission and processing of pain signals.
SCS is an established option for selected forms of refractory chronic neuropathic pain.
Positive reports also exist in patients with MS, but the MS-specific evidence is much weaker than for the main established indications for spinal cord stimulation.
Dorsal root ganglion stimulation provides a more targeted form of neuromodulation for certain localized neuropathic pain syndromes. It is used in interventional pain medicine, but there is currently no robust evidence supporting it specifically for pain caused by MS.
When several appropriately chosen treatments have failed, the first step may be to reconsider the pain mechanism rather than simply add more medication.
Radiculopathy, localized neuropathic pain or injury to a specific nerve may justify discussion of blocks, PNS or other interventional techniques.
Before implantation, the diagnosis, previous treatments, functional goals, MRI requirements and expected benefit should be reviewed carefully.
When central, peripheral and musculoskeletal pain coexist, multidisciplinary management is often more useful than escalating medication alone.
Particularly when accompanied by pain with eye movement or impaired colour vision.
New persistent weakness, sensory loss, coordination problems or other neurological symptoms require assessment of the cause.
Especially with new weakness, bladder dysfunction, saddle sensory loss, fever or recent trauma.
Infection may both worsen existing MS symptoms and represent an independent cause of pain.
A new symptom should first be diagnosed rather than automatically attributed to known multiple sclerosis.
Rapidly worsening pain, systemic symptoms or unexplained deterioration require separate evaluation.
When chronic pain does not respond to treatment, the first question is often not “which additional painkiller should be tried?” but whether the source and mechanism have been correctly identified.
For example, central burning pain, painful spasticity and mechanical low-back pain may require three different treatment strategies.
Assessment can help determine whether the symptom fits a central MS lesion or whether a peripheral cause should be investigated.
Sedation, dizziness and worsening imbalance may limit standard pharmacological treatment.
In a complex chronic pain syndrome, the diagnosis, pain mechanism and sequence of treatments can be reviewed.