Symptoms of MS flare

Treating Multiple Sclerosis Relapses

Relapses, also referred to as exacerbations, attacks, flare-ups, episodes, or bouts, are initially experienced by most people diagnosed with multiple sclerosis (MS). Relapses occur with relapsing-remitting, progressive-relapsing, and sometimes secondary-progressive forms of MS. Relapses do not occur with primary-progressive MS, although patients may experience day-to-day fluctuations in how they feel.

During a relapse, patients will have a temporary worsening or recurrence of existing symptoms and/or the appearance of new symptoms. This typically lasts for a few days to a few months, followed by a complete or partial recovery (remission). Acute physical symptoms and neurological signs must be present for at least 24 to 48 hours, without any signs of infection or fever, before the treating physician may consider this type of flare-up to be a true relapse.

With relapses, inflammation is occurring along the nerves and the myelin. Myelin is the protective covering that insulates the nerves of the central nervous system (CNS) – a system that consists of the brain, spinal cord, and optic nerves. Please visit the MS Overview section of MSAA’s website for more information about the MS process and what happens during an MS relapse.

Less-severe relapses are usually not treated with steroids, so their use may be reserved for more severe flare-ups. When treatment is required, relapses are usually treated with a high-dose course of powerful corticosteroids (a type of steroid) over a period of three to five days. These are given by intravenous (IV) infusion, providing the drug directly into the bloodstream for a quicker response. Administration may be performed in a hospital, infusion center, or sometimes at home. Corticosteroids work by reducing inflammation in the CNS. While they usually lessen the severity and duration of a relapse, they do not appear to affect the long-term progression of the disease.

As approved by the United States Food and Drug Administration (FDA), patients are often given methylprednisolone (Solu-Medrol®) to treat an MS relapse. In practice, doctors may sometimes prescribe the corticosteroid dexamethasone (Decadron®), in place of methylprednisolone. An oral steroid (prednisone) may be prescribed after the high-dose treatment to ease the patient off the treatment, tapered over one to two weeks.

Acthar® Gel is also approved by the FDA to treat MS relapses and has been used as an alternative to corticosteroids for more than 30 years. This may be helpful for individuals who are not able to tolerate the side effects of steroids, who have found that previous treatments were not effective, or who may have difficulty getting timely medical support for IV infusions. Studies suggest that the effectiveness of Acthar Gel is similar to corticosteroids.

Acthar contains a highly purified form of the adrenocorticotropin (ACTH) in gelatin. It is given once daily for two to three weeks and is injected either into the muscle or under the skin. This is then absorbed slowly into the bloodstream. Acthar works differently than corticosteroids by helping the body to produce its own natural steroid hormones that reduce inflammation and aid in recovery.

Other therapies include plasmapheresis (plasma exchange or “PE”) and intravenous immunoglobulin (IVIG). Neither of these is approved by the FDA specifically for MS relapses, but either may sometimes used for individuals who are experiencing a severe relapse and are not responding to other treatments. With PE, blood is taken from the patient, cleansed of potentially toxic elements, and returned to the patient. IVIG therapy uses human immunoglobulin, an antibody derived from the blood of healthy donors. With both of these therapies, more studies are needed to determine their individual effectiveness.

To follow is a list of drugs and therapies that may be used in the treatment of an MS relapse. Not all of these treatments are approved by the United States Food & Drug Administration (FDA) specifically for the treatment of MS.

  • Solu-Medrol® (IV methylprednisolone)
  • Prednisone
  • Decadron® (dexamethasone)
  • Acthar® Gel
  • Plasmapheresis (plasma exchange or PE)*
  • Intravenous immunoglobulin (IVIG) therapy*

*Please note that with these latter two therapies, clinical trial results have been mixed. Studies continue to determine the effectiveness of these treatments with MS.

For more information, including details on the effectiveness and side effects of the different treatments for relapses, please visit MSAA’s online MS Relapse Resource Center. Individuals may also view MSAA’s brochure, Understanding and Treating MS Relapses, as well as MSAA’s MS Relapse Toolkit.

Please note that MSAA does not endorse or recommend any specific drug or treatment. Individuals are advised to consult with a physician about the potential benefits and risks of the different treatment therapies.

ACTH gel in the treatment of multiple sclerosis exacerbation: a case study


Multiple sclerosis (MS) is a chronic demyelinating and degenerative autoimmune disease of the central nervous system (CNS) resulting from genetic and environmental risk factors. Proposed etiologies include autoimmunity against the CNS, an infectious agent, and a primary degenerative process targeting oligodendrocytes.1 Relapsing-remitting MS (RRMS), the most common subtype, involves episodes of clinical symptom exacerbation separated by periods of full or partial recovery. A relapse is defined as a sustained new or worsening neurologic symptom, in the absence of fever or infection, lasting greater than 24 hours and potentially lasting for days to weeks or even months at a time.2,3 Effective relapse treatment remains a challenge, yet is critical as patients’ level of disability may continue to increase rather than return to baseline following each relapse.4 It is believed that by limiting the severity and frequency of relapses over time, one may also prevent severe disability and disease progression over time.3

To treat the acute disability seen in RRMS as well as hasten recovery from a relapse, MS practitioners have long used corticosteroid therapy. The most common treatment is a 3- to 5-day course of corticosteroids, primarily intravenous (IV) methylprednisolone (MP) or dexamethasone, with or without an oral steroid taper over 1 to 2 weeks.5 High-dose oral prednisone also is sometimes used. These medications can cause deleterious side effects that may limit their use, including stomach irritation, elevation of blood sugar, water retention, restlessness, insomnia, and mood swings, and long-term use is not recommended due to the potential for serious side effects, including stomach ulcers, weight gain, acne, cataracts, osteoporosis, and diabetes. Additionally, at times the patient’s relapse recovery response may not be adequate following treatment with steroids. Treatment with adrenocorticotropic hormone (ACTH) gel, Food and Drug Administration (FDA)-approved to treat MS relapse, is an option for patients who are unable to tolerate the side effects of high-dose IVMP or oral prednisone, do not adequately respond to corticosteroid treatment, do not have access to IV therapy, or who have difficulty accessing veins and receiving IV medication.

ACTH gel (HP Acthar® Gel, repository corticotropin injection; Questcor Pharmaceuticals, Inc., Hayward, CA, USA) is a long-acting formulation of the full sequence ACTH(1–39) that includes other proopiomelanocortin peptides.6,7 In 2010, the FDA reviewed and modernized the entire ACTH gel label alongside granting a new indication for infantile spasms, and following reexamination of the study data submitted in 1978, the MS exacerbation indication was reapproved for treatment of acute exacerbations in adults.7 ACTH gel has been used for several decades to treat acute exacerbations in MS8–12 and has an established safety profile. Randomized, controlled clinical trials examining ACTH gel treatment in acute exacerbations of MS (total of 298 subjects) include two placebo-controlled, double-blind studies and one double-blind comparator trial versus IVMP.8–10 Early placebo-controlled studies of ACTH gel treatment of MS exacerbation demonstrated faster recovery from rapidly worsening MS compared with placebo, and the comparator study with IVMP showed equivalent, marked improvement outcomes.8–10

Interestingly, the use of corticosteroids as the common therapy to treat MS relapse is derived from these early randomized, placebo-controlled studies of ACTH treatment showing rapid improvement of relapse.8,9 The belief that the mechanisms of action and treatment effects of ACTH and high-dose corticosteroids are relatively equivalent in treating MS acute exacerbations is longstanding, with the assumption that the efficacy of ACTH is due to its corticosteroid effects on immune function and inflammation.10,11,13 However, evidence suggests ACTH may have actions independent of steroidogenesis, such as in the treatment of infantile spasms, in which ACTH has been shown effective and corticosteroid treatment has had limited effectiveness.14–17 ACTH is one of several melanocortin peptides, and the emerging characterization of the melanocortin system and receptor functions beyond steroidogenesis indicates the need to reconsider ACTH in the treatment of acute MS exacerbations.7,18

The clinical case presented below describes a patient who, following nonresponse to a trial of IVMP for new-onset MS exacerbation, was effectively stabilized with ACTH gel treatment. Stabilization of the disease exacerbation then allowed the initiation of long-term disease-modifying therapy with monthly IV natalizumab.

ACTH gel patient case

Demographics and medical history

The patient was a 49-year-old right-handed female who worked as a dental hygienist. She presented with a 1-day history of blurry vision, off-balance feeling, and slurred speech. She started having double vision when looking toward the left, stated that “everything seemed fuzzy,” and said she felt as if she needed to hold onto something in order to keep her balance. The patient had no past medical or surgical history and no family history for MS. Diagnosis of new-onset MS exacerbation followed a neurological exam and finding of cerebral spinal fluid positive for six oligoclonal bands, comprehensive metabolic and blood panels to rule out alternative diagnoses, and magnetic resonance imaging (MRI) at baseline and post-IVMP treatment consistent with McDonald 2010 criteria of dissemination of lesions in space (T2 callosal and spinal cord lesions on initial MRI) and time (new T2 dorsal pontine lesion at second MRI).2

Physical and neurological exam

The exam of cranial nerves II-XII showed possible left-sided, mild internuclear ophthalmoplegia (INO). Her gait showed slight ataxia when walking, with some difficulties with heel-toe walking after three steps. MRI testing of the patient’s brain without enhancement showed findings typical for primary demyelinating disease, with several callosal plaques, right greater than left (Figure 1). No changes were seen in the brainstem or at the cervical level. MRI testing at the thoracic level showed possible demyelinating plaque at T3–T4.

Figure 1 Pretreatment MRI.
Notes: (A–D, Top) Findings in brain images (images A, B FLAIR axial sequences and images C, D FLAIR sagittal sequences) are typical for primary demyelinating disease with several callosal plaques. (A–B, Bottom) Thoracic images (image A, T2 sagittal and image B, T2 axial), suggest possible demyelinating plaque at T3-4.
Abbreviations: MRI, magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery.


The patient was admitted to the hospital for 5 days of IVMP at 1,000 mg/day. After 3 days, she still had persistent left INO with nystagmus; however, her gait was slightly improved. The patient requested an additional 2 days of treatment as an outpatient, and she was discharged with physical therapy and neurology follow-up within 7 days.

Follow-up neurological exam

The patient was seen within 7 days of discharge, and despite 5 days of IVMP, she presented to the outpatient neurology MS center with new-onset right facial weakness. The patient also complained of drooling and gait instability. Neurologic exam at this time showed mild bilateral INO and mild-to-moderate right facial weakness affecting the forehead, with slight Bell’s phenomenon. Coordination testing showed mild finger-to-nose ataxia bilaterally, and gait testing showed mild gait instability with difficulty in tandem, and equivocal toes. Herpes simplex virus evaluation was negative. The patient received an urgent MRI scan and spinal fluid analysis. The MRI revealed a new dorsal pontine white matter lesion located slightly eccentric to the right that was consistent with the clinical hypothesis of a demyelinating lesion affecting cranial nerve VII (Figure 2). The lesion did not show abnormal enhancement, but the radiologist commented that the lesion possibly showed restricted diffusion. The remainder of the brain was unchanged.

Figure 2 MRI following treatment with IVMP for 5 days.
Notes: T2 sagittal (image A) and axial (images B, C) images and T1 with gadolinium (image D) show new dorsal pontine white matter lesion as depicted by the arrows in image A and image B, located slightly eccentric to the right. Images do not show abnormal enhancement. No other changes were seen compared with pretreatment.
Abbreviations: IVMP, intravenous methylprednisolone; MRI, magnetic resonance imaging.

At a follow-up visit 4 days later, the patient complained of worsening symptoms of right-sided facial weakness, gait instability, and drooling. She now required assistance at times, to walk. The diagnosis given was MS exacerbation. Treatment considerations included the severity of the exacerbation, the brainstem location, and the patient’s acute worsening despite high-dose IVMP. The treatment plan options included natalizumab injection, pulse IV cyclophosphamide, plasma exchange, and ACTH gel. The treatment recommendation was to treat the patient with ACTH gel 80 U subcutaneous injection for 5 consecutive days with the goal to rapidly stabilize disease.

At the follow-up visit 7 days later, the patient had completed her course of ACTH gel and reported improvement in her vision and gait. She reported feeling more steady on her feet but said she still required some walking assistance at times. The patient’s facial weakness was no longer a complete Bell’s-like phenomenon and was significantly improved. The neurologic exam at this time showed mild residual bilateral INO, improved right facial weakness with improved forehead and frontalis musculature strength, and improved asymmetry. The patient had mild finger-to-nose ataxia and some slight gait instability with some difficulty in tandem. The patient showed stabilization of disease exacerbation in response to ACTH gel, despite being an IVMP nonresponder. The patient was in the most severe form of an MS exacerbation, with worsening brainstem presentation. Treatment with ACTH gel stabilized the continued worsening of the patient’s persistent disease progression and actually improved some of the patient’s brainstem symptoms, such as facial weakness and eye movement weakness. The patient was subsequently started on monthly IV natalizumab, approximately 1 to 2 weeks following cessation of ACTH gel, for long-term immune-modulating MS treatment.

At 5 months follow-up, the patient had returned to baseline function and had been working for 3 months. The patient was doing very well except for some mild loss of energy, and the neurologic exam was normal. MRI testing of the brain revealed findings compatible with the patient’s known history of demyelinating disease; however, the previously described lesion in the dorsal pons was less prominent (Figure 3).

Figure 3 MRI 5 months following treatment with ACTH gel for 5 days, followed by monthly IV natalizumab.
Notes: Images are compatible with the patient’s known history of demyelinating disease. The lesion in the dorsal pons, shown by the arrows in image A (FLAIR sagittal) and image B (FLAIR axial), is less prominent than was seen prior to treatment with ACTH gel and IV natalizumab.
Abbreviations: ACTH, adrenocorticotropic hormone; IV, intravenous; MRI, magnetic resonance imaging; FLAIR, fluid-attenuated inversion recovery.


Effects of melanocortin signaling on immune function and inflammation provide a basis for understanding the clinical experience with ACTH gel in the treatment of patients with MS relapse.7,18,19 Emerging understanding of the melanocortin system and interaction of ACTH with widespread melanocortin receptors strongly suggests that the mechanisms of action of ACTH gel in MS are not limited to steroidogenesis effects.20,21 Although no studies are currently available examining ACTH gel efficacy in patients with MS exacerbation who are refractory to steroids and other therapies, this has been shown in other disorders, including infantile spasms.14–17 Consistent with the emerging understanding of ACTH gel mechanisms of action, ACTH gel has been proposed within a relapse management treatment algorithm for MS, as a second-line treatment for patients who do not improve or are unable to tolerate steroid treatment.22 In the clinical case that was presented, the patient experienced severe progression of new-onset MS exacerbation with brainstem presentation. Despite 5 days of high-dose IVMP, the patient’s symptoms actually worsened. ACTH gel stabilized the progressive course of the MS exacerbation, was associated with some improvement in vision and gait, and provided valuable time needed to initiate long-term disease-modifying therapy with natalizumab. Patients with RRMS who show nonresponse to conventional IV steroid formulations, or who are unable to tolerate associated side effects, are an important subgroup of patients for consideration of treatment with ACTH gel. Thus, the awareness of a treatment alternative such as ACTH gel, with demonstrated efficacy and suggested mechanisms of action beyond steroidogenesis, is important.


The author thanks Lynanne McGuire, PhD, of MedVal Scientific Information Services, LLC, for providing medical writing and editorial assistance. This manuscript was prepared according to the International Society for Medical Publication Professionals’ “Good Publication Practice for Communicating Company-Sponsored Medical Research: The GPP2 Guidelines.”

Funding to support preparation of this manuscript was provided by Questcor Pharmaceuticals.


SN has had speaking and consultancy relationships with the following entities: Questcor Pharmaceuticals, Teva Neuroscience, Biogen, Pfizer, Accorda, Serono, and Novartis. The author reports no other conflicts of interest.

Boppana S, Huang H, Ito K, Dhib-Jalbut S. Immunologic aspects of multiple sclerosis. Mt Sinai J Med. 2011;78(2):207–220.

Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 2011;69(2):292–302.

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Lublin FD, Baier M, Cutter G. Effect of relapses on development of residual deficit in multiple sclerosis. Neurology. 2003;61(11):1528–1532.

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HP Acthar® Gel (repository corticotropin) injection . Hayward, CA: Questcor Pharmaceuticals, Inc.; 2012.

Arnason BG, Berkovich R, Catania A, Lisak RP, Zaidi M. Mechanisms of action of adrenocorticotropic hormone and other melanocortins relevant to the clinical management of patients with multiple sclerosis. Mult Scler. 2013;19(2):130–136.

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Rose AS, Kuzma JW, Kurtzke JF, Namerow NS, Sibley WA, Tourtellotte WW. Cooperative study in the evaluation of therapy in multiple sclerosis. ACTH vs placebo – final report. Neurology. 1970; 20(5):1–59.

Thompson AJ, Kennard C, Swash M, et al. Relative efficacy of intravenous methylprednisolone and ACTH in the treatment of acute relapse in MS. Neurology. 1989;39(7):969–971.

Filippini G, Brusaferri F, Sibley WA, et al. Corticosteroids or ACTH for acute exacerbations in multiple sclerosis. Cochrane Database Syst Rev. 2000:CD001331.

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Stafstrom CE, Arnason BG, Baram TZ, et al. Treatment of infantile spasms: emerging insights from clinical and basic science perspectives. J Child Neurol. 2011;26(11):1411–1421.

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Am I having an MS relapse?

I saw that question asked the other day on one of the social sites I follow. At first, I thought, “Gee, doesn’t everyone with MS know when they’re having a relapse?” Then I realized that for several years after I was diagnosed, I was never sure if what was happening to me was technically a relapse and worth a call to the doctor. I’d wind up in the hospital being treated for a relapse, but only after my wife would spot a symptom getting worse and tell me that I needed to see my neurologist. It rarely dawned on me that what was happening was what we used to call an “exacerbation.” But I always walked better after getting treated with a course of steroids.

MSAA’s “MS Relapse Toolkit” (Courtesy of MSAA)

There’s a guide that can help

So, how can you know that you’re having a relapse? There’s now a really useful booklet that can help. It’s called, appropriately, the “MS Relapse Toolkit,” and it’s just been published by the Multiple Sclerosis Association of America. The booklet can be read online, downloaded as a PDF file, or ordered as a hard copy at the MSAA website. Here’s a thumbnail of what’s in it:

What’s a relapse?

  • Existing symptoms have worsened temporarily or recurred, or …
  • New symptoms have appeared
  • The symptoms have lasted for at least one or two days with no sign of a fever or infection (e.g. a UTI)
  • Tests show your myelin or nerves have been damaged or inflamed

When to call your neurologist?

The MSAA booklet, written by Aaron Boster, MD, and Jacqueline A. Nicholas, MD, MPH, suggests you call your doctor if:

  • The new or recurring symptom(s) has been present for at least 24 to 48 hours, or …
  • It’s been less than 24 hours, but your symptoms are severe and could affect your health or safety

As long as…

  • You don’t have a fever or any other signs of infection
  • Your body isn’t overheated, which might have resulted from the temperature around you, exercise, etc.
  • You didn’t overexert yourself
  • You aren’t having an unusually stressful day

The idea seems to be that the trigger for your problem should be medical and not the result of some external stimulus.

What else is in the Relapse Toolkit?

The booklet has another half-dozen chapters that include a list of questions to ask your neurologist about relapses, some handy, fill-in-the-blank forms for contact information and the drugs that you use, what to tell your doctor when you call, details of various treatment options, and some really useful ideas about planning, at home and at work, for a possible relapse. It even includes a crossword puzzle that uses relapse-related words.

The price is right

Did I mention that the “MS Relapse Toolkit” is free? As we used to say when I was growing up in New York City: “Such a deal!”

You’re invited to follow my personal blog at:


Note: Multiple Sclerosis News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Multiple Sclerosis News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to multiple sclerosis.

  • Author Details

Ed Tobias is a retired broadcast journalist. Most of his 40+ year career was spent as a manager with the Associated Press in Washington, DC. Tobias was diagnosed with Multiple Sclerosis in 1980 but he continued to work, full-time, meeting interesting people and traveling to interesting places, until retiring at the end of 2012. × Ed Tobias is a retired broadcast journalist. Most of his 40+ year career was spent as a manager with the Associated Press in Washington, DC. Tobias was diagnosed with Multiple Sclerosis in 1980 but he continued to work, full-time, meeting interesting people and traveling to interesting places, until retiring at the end of 2012. Latest Posts

Identifying and Managing MS Relapse

Multiple sclerosis (MS) is a chronic, autoimmune-mediated ­disorder of the central nervous system that affects more than 40,000 people in the United States. About 85% of cases are categorized as relapsing remitting multiple sclerosis (RRMS), based on the clinical and radiographic pattern of focal demyelination in different regions of the brain and spinal cord over time. Though not fully understood, the pathophysiology of RRMS involves axonal degeneration and inflammatory demyelination; the latter is considered a relapse in patients with an established MS diagnosis.


MS relapse can have a significant impact on patients’ short- and long-term function, quality of life, and finances. Relapse may be identified via

  • New neurologic symptoms reported by the patient
  • New neurologic findings on physical examination
  • New radiographic findings on contrast-enhanced MRI of the central nervous system, or
  • Abnormal results of cerebrospinal fluid analysis.

Patient-reported symptoms and abnormal signs identified on physical exam should correspond with the area of the central nervous system affected. In some cases, patients may have radiographic evidence of relapse without symptoms or signs.

It is essential for health care providers to identify relapse, as it is an important marker of disease activity that may warrant treatment—particularly if symptoms are impacting function or if there is optic neuritis. MS relapse is also an indicator of suboptimal response to disease-modifying therapies.

Treatment of relapse is one component of RRMS management, which also includes symptom management and use of disease-modifying therapy to reduce risk for disease activity and decline in function.


Because risk for MS relapse cannot be predicted, both patients and providers need to have a high index of suspicion in the setting of new neurologic symptoms or decline in function. Relapse should be considered when these symptoms last longer than 24 hours in the absence of fever or infection. The clinical features of relapse should have corresponding radiographic evidence of active demyelination on contrast-enhanced MRI.

A pseudo-relapse is characterized by new or worsening neurologic symptoms lasting longer than 24 hours with concurrent fever, infection, or other metabolic derangement. Pseudo-relapse does not show radiographic evidence of active demyelination on contrast-enhanced MRI.

Continue to: Aggravation of longstanding neurologic symptoms…

Multiple Sclerosis and Pain

Does pain occur in multiple sclerosis (MS)?

In the past, pain was not thought of as a symptom of multiple sclerosis (MS). While neurologists accepted numbness, tingling, itching, and other sensory symptoms as occurring in the MS patient, they often did not recognize pain as part of the spectrum of symptoms of MS.

Over the past few years physicians have come to realize that pain is not only possible as a symptom of MS, but that in some patients, pain is a key symptom. It can be a major cause of reduced function, decreased sense of well-being, and an important target for treatment. In some studies, up to one in four people with MS have ongoing pain which in some way affects their function.

Psychosocial variables have long been shown to have a significant impact on pain perception, and in turn disability due to pain.

Specifically, the intensity of the pain, the degree to which it interferes with activities, the extent to which it disrupts mood, and predict chronicity of pain. Identification of the presence of such possible co-morbid problems can guide appropriate early intervention.

Today we know that the pathophysiology of pain is complex, with messages being sent from the periphery to the brain, from the brain down and strongly influenced by emotions. Context, catastrophizing, acceptance, central sensitization, opioid-induced hyperalgesia, emotions, expectations for future pain, prior experience, repeated exposure to painful stimuli, past exposure to trauma all have an effect on the perception of pain. The emotional component of pain or the suffering endured by patients is equally important as the somatosensory component.

What kind of pain can occur with multiple sclerosis?

There are a variety of pain types that may occur with MS, including:

  • Trigeminal neuralgia: There is a facial pain syndrome known as trigeminal neuralgia which is more common in people with MS than in the general population. It is a sharp, electrical jabbing pain on one side of the face, usually in the cheek. It can be very severe, and lasts a few seconds. It may occur many times a day. It may be triggered by touching the face, feeling a breeze on the face, or even chewing.

Treatment of trigeminal neuralgia includes medications that alter nerve function such as carbamazepine, phenytoin, lamotrigine, Neurontin®, Lyrica®, and so on. Sometimes, surgical procedures may be useful (for example, using a balloon catheter to put pressure on the nerve to numb it, or heating the nerve up electrically). Some patients may benefit from a focused radiation beam directed at the nerve.

  • Burning limb pain: A second type of pain is a burning pain that often involves the legs but may occur anywhere in the body. This may be worse at night and is often constant. There may be sensitivity to the touch, and sometimes the affected limb feels cold. This is likely due to altered sensory signals to the spinal cord and brain due to demyelination.

Medications that are used to treat burning limb pain include some antidepressants such as nortryptiline which are effective in nerve pain, and some anti-seizure medications such as carbamazepine, gabapentin, and others. Duloxetine hydrochloride has been approved for peripheral nerve pain and may also be used for the pain related to MS. Tramadol may be useful for such pain. Sometimes long-acting pain medications may have to be used. Physical measures such as exercise and stretching may be useful. Lidocaine patches may provide relief at more severely affected locations.

  • Neck and back pain: Some people with MS can experience neck and back pain. This may be due to immobility, or to the same type of wear and tear that many people without MS experience. This type of pain is often an aching, stiff sensation that can be moderately severe. At times, imaging to rule out other causes of pain such as lumbar disc disease may be important. Trials of anti-inflammatory medications may be beneficial. Therapy, stretching, aquasize, and other physical measures may be useful.
  • Other sources of pain: Finally, there are occasional patients who have hip or shoulder disease related to prior steroid therapy. On occasion, repeated steroid use causes an alteration of blood supply to the hip or shoulder joint, and this may cause injury to the joint. Imaging with X-ray or MRI scanning may show damage if this is the case. If the damage is severe enough, the patient may require joint replacement surgery. Since many other disorders can cause pain, it’s important to consider other sources of pain and not just ‘pin it on MS’.

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Multiple sclerosis is so weird. Sometimes I just put up with a strange sensation or painful problem because I do not know how to describe it to the doctor without sounding crazy.

I hope the problems will just go away, and sometimes they do. Maybe I am a little gun-shy from the year prior to my diagnosis, when each symptom I complained about just brought me a new antidepressant.

A couple of years ago, after suffering in silence for many months, I scheduled an appointment with a neurologist. Waiting in the exam room, symptom list in hand, I worried. My new sensation was causing problems, but I did not know how to describe it. The kind (and unusually personable, for a neurologist) doctor greeted me warmly. We covered the usual suspects — fatigue, paresthesia, foot drop. He asked if there was anything else.

“Well, sometimes I get a really weird sensation in my head,” I stammered. He asked questions: Was it painful? No, not really, just very uncomfortable. Where did I feel it? Sort of in my neck and the base of my skull. Could I describe it? The words finally tumbled out of me, in an awkward rush of pent-up stress.

“This will sound weird, but it feels like a giant hand is grabbing my head and squeezing the back of it. Or like I’m in a pressurized room, and my head is being squished. My neck gets really tight and I get kind of dizzy and sometimes it’s like the floor or the walls tilt. If I’m standing I sort of lose my balance, and if I’m sitting it feels like my head jerks to one side, but I don’t know if it really does.”

Thankfully, the kind doctor did not call for a priest to perform an exorcism. He asked about neck spasms and felt along my shoulders, neck and skull. He gently reminded me that I have lesions in my cervical spine and explained that this was likely a type of vertigo caused by neck spasms and my damaged nervous system. A prescription for Baclofen was sent to the pharmacy.

I have since sought additional ways to minimize this sensation, otherwise known as cervicogenic dizziness.

Good posture

  • Make sure any screen (computer, phone, TV) is at eye level
  • Get up and move around, don’t sit in one position too long
  • Shoulders down and back, sit up straight
  • Pilates lessons have helped with my posture and overall muscle spasms


  • Take this over-enthusiastic stretcher’s advice. G-E-N-T-L-E neck stretches. Less is more!
  • A heat pack can loosen neck muscles
  • Ask a pro for some stretching tips
  • Yoga, under the guidance of an instructor, is useful. I hurt myself if I try to do more than cow-cat at home; Or corpse pose, I am super good at that one!

Professional support

  • Massage therapy is my most effective treatment. However, it is not covered by my insurance for chronic conditions. So…
  • Chiropractic care can be useful. Word of warning: If my neck spasms are too severe, then chiropractic makes it worse. Pre-treatment with something like Baclofen may help.
  • Physical therapists can teach proper stretching techniques
  • Occupational therapists ensure that daily work and living activities do not aggravate neck problems
  • Check with your employer, local Division of Rehabilitation, or National MS Society to request an ergonomic assessment and modifications to your work environment.

Vitamins, Minerals and Supplements – Oh my!

  • Ask a naturopath or nutritionist for dietary and supplement recommendations
  • The National MS Society also has some information on supplements for MS
  • Calcium and magnesium (together!) relieve muscle spasms. I use a powder that dissolves in water for quick absorption.
  • Potassium also works well and is easy to get from bananas, coconut, dark leafy greens, avocadoes, sweet potatoes and other yummy foods.
  • Curcumin supplements seem to help my MS overall, including this dizziness

This is just one of many MS symptoms. When you throw in the other demands of life, it is to be expected that one cannot maintain “best practices” at all times. My recent 10 days of travel made MS management quite challenging. Multiple airplanes, buses, heavy luggage, uncomfortable conference chairs, awkwardly placed presentation screens, and stiff hotel pillows all conspired to invite my cervicogenic dizziness out to play. I took a little more Baclofen than usual. Thoughts of Botox bounced in my head as I lay in corpse pose on the hotel room floor. Elevators were favored over stairs, or — heaven forbid! — escalators. An unintentional sway or head-shift was just an opportunity to smile broadly at whoever I found myself looking at. Hopefully I passed as either super friendly or tipsy, or maybe both.

Note: Multiple Sclerosis News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Multiple Sclerosis News Today, or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to multiple sclerosis.

Judy Lynn has been living with Multiple Sclerosis for 13 years. She remains amazed at the array of symptoms that this chronic degenerative disease of the nervous system may cause. The Greek philosopher, Heraclitus, is reported to have said, “The only thing constant is change.” Judy has found this to be particularly true living with MS. She will explore the varied MS symptoms and manifestations, and most importantly, the rainbow of creative adaptations, coping mechanisms, and remedies available for MS patients to try. × Judy Lynn has been living with Multiple Sclerosis for 13 years. She remains amazed at the array of symptoms that this chronic degenerative disease of the nervous system may cause. The Greek philosopher, Heraclitus, is reported to have said, “The only thing constant is change.” Judy has found this to be particularly true living with MS. She will explore the varied MS symptoms and manifestations, and most importantly, the rainbow of creative adaptations, coping mechanisms, and remedies available for MS patients to try.

Spasticity: A Literal Pain

Spasticity in MS is defined as a tightness or stiffness in the muscles that typically occurs in the legs, butt or groin. It is said to be caused by the demyelination along the nerves of the brain and spinal cord that control our movement. It can range from mild to severe. Involuntary muscle spasms also tend to happen with the tightness which amplifies the pain. The more severe the stiffness, the more painful. Spasticity has been an issue for me for a long time. For forever though, I didn’t realize that it was one of my symptoms.

Spasticity in the back is much less common

Spasticity in the back is much less common, but that is the most prominent spot that it occurs for me. My neck, back, and my hips are extremely tight, stiff, and uncomfortable. The stiffness in my upper back causes my back and neck muscles to compete. It has made my neck weak, and because of that, I’ve developed a head tremor. I tell my husband, I feel like a 27-year-old stuck in an old lady’s body. The heating pad and Salonpas pain relieving patches have become my best friends.

Tight, knotted ropes

The stiffness in my hips has been an ongoing issue. My hips have always been tight. But my hips are mild and thankfully do not cause me much pain or problems with walking. The spasticity in my neck and back, however, have worsened in the past 5 to 10 years. My back (my shoulders especially) feel like they are full of tight, knotted ropes. They are always tense, and it feels impossible to get them to relax. It is so painful. I notice my spasticity is worse when I’m unusually stressed or anxious. I also become more fatigued when I’m dealing with tightness in my back because it makes upper body movements seem more strenuous. It also doesn’t help to carry around a 30-pound toddler most of the day, but he’s worth it.

How I manage the pain

Pain caused by spasticity is influential over my mood and affects my ability to sleep. Pain is distracting, plain and simple. So what can we do to help that? There are several strategies I use to help ease discomfort from spasticity. The biggest thing that helps me is stretching. I enjoy Yoga and Pilates to help alleviate some of the stiffness. I love stretching the most, because it is so simple, yet so effective. Plus, it helps, so I’m all about that. I also benefit from the heating pad as I mentioned (I just have to make sure it’s not too hot) and Salonpas. I’ve used the prescription gel, Voltaren Gel as well. Another thing I’ve found to be effective is steroid shots in my upper back, to help calm down inflammation, but I have not used those in a couple of years.

Using a TENS unit

I also recently purchased a TENS Unit per recommendation of my doctor which is transcutaneous electric nerve stimulation (TENS). These types of units deliver short bursts of electricity to help safely stimulate the nerves. What this means is that it reduces the pain signals delivered from the pain sources to the central nervous system. And, that helps relax the muscles and provide pain relief. It also stimulates endorphin production which is our bodies natural pain relief hormones. You can find cheap TENS Units just about anywhere online, I happened to find mine on Amazon for a whole $30. If this is something you choose to also pursue (just like with any other form of pain treatment I’ve suggested), I highly recommend talking to your doctor first, and making sure to carefully follow the directions that come with your unit. They are not a quick fix, but will provide a bit of relief. I have also tried muscle relaxants in the past, Tizanidine to be exact. I love the temporary relief they provide, however, I don’t like that I can only take them at night because they knock me out. They also make me drowsy the next day, and at times seem to worsen the spasticity the following day as well.

Back spasticity?

Again, spasticity is relatively prevalent in the lower extremities, but not nearly as prevalent in the back. So my question to my readers is; Do any of you deal with back spasticity? And what have you found to help?



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