Multiple sclerosis (MS) is an inflammatory and demyelinating disease characterized by multiple lesions (or plaques) in the white matter of the central nervous system (CNS), destruction of the myelin sheaths of nerve fibers (demyelination), perivascular infiltration of inflammatory cells, and gliosis (scarring). Approximately 350,000 Americans have MS, making it the most common cause of neurologic dysfunction of young adults between 20 and 40 years of age. Women are affected twice as often as men, and whites are affected twice as often as African Americans. It is almost unknown in black native Africans and rare in native Japanese, but not uncommon in African-Americans and Japanese-Americans.

The etiology of MS is unknown; it is thought to begin with an infectious agent (virus) in childhood that primes the immune system for an autoimmune attack against myelin components in early adulthood. Prevalence data support the suggested role of environmental exposure, as epidemics of MS have been described. A genetic predisposition is suggested by family clusters: first-degree relatives of an index case have a 2% to 5% increased risk of developing MS, and the concordance rate is 25% to 30% for monozygotic twins and 2% to 5% for diazygotic twins.

• First-degree relatives with MS
• Age between 20 and 40
• Living in the northern latitudes for the first 15 years of life
• Northern European, Northern American, or Scandinavian ancestry
• Possession of immune response genes (e.g., HLA-DR2)

• Blurred vision from optic neuritis or diplopia (double vision) due to internuclear ophthalmoplegia
• Motor weakness presenting as fatigue, gait disturbances, loss of dexterity, or hyperreflexia
• Sensory disturbances such as paresthesia (tingling) or hypesthesia (numbness)
• Loss of proprioception and muscle coordination (ataxia)
• Pain due to trigeminal neuralgia, Lhermitte's sign (painful, lightning-like sensations down the back elicited by flexion of the neck), dysesthesia (pain from normal stimuli such as touch), or tonic seizures
• Vertigo (dizziness) that appears suddenly and is severe
• Intention tremor and spasticity
• Heat sensitivity (Uhthoff's phenomena), in which symptoms worsen after exposure to heat
• Urinary bladder dysfunction (e.g., frequency, urgency, incontinence, retention)
• Cognitive impairment (e.g., memory loss, problem-solving difficulties)
• Depression or inappropriate jocularity

• Cerebrovascular disease (e.g., subdural hematoma, embolism, cavernous angioma)
• Brain abscess
• CNS vasculitides (e.g., Sjogren's syndrome, Behcet's disease, Binswanger's disease)
• Metastatic tumors
• Primary CNS tumors
• Lyme disease
• Metabolic disturbances (e.g., hypoglycemia)
• Psychogenic disorder

There is no definitive diagnostic test for MS; the diagnosis depends on a history of intermittent clinical manifestations which leave the patient more impaired, physical examination findings of neurological deficits, and laboratory tests which support the suspected diagnosis.

• Cerebrospinal fluid (CSF) examination—for elevated protein, high immunoglobulin G (IgG) levels, and CSF IgG/CSF albumin ratio over 1.7, which are characteristic of MS
• Agar gel electrophoresis—to determine presence of oligoclonal IgG bands, which are found in 90% of MS patients

• Magnetic resonance imaging (MRI)—to detect small, bright foci in the periventricular area and on spinal cord
• Computed tomography (CT) scan—to detect areas of decreased attenuation or contrast
• Gadolinium-enhanced MRI—to detect a breach in the blood-brain barrier
• Myelogram—to examine lesions with low resolution on MRI
• Radioimmunoassay—to detect high concentrations of myelin basic protein (MBP) during relapses

Determination of visual-, auditory-, somatosenory-, and motor-evoked potential responses—to detect subclinical areas of demyelination

Currently only immunosuppressive and anti-inflammatory drugs appear to reduce the severity of initial attacks and exacerbations; no drugs have any effect on the progression of the disease.

Rehabilitative measures such as braces, wheelchairs, ramps, lifts, and cars with manual controls should be pursued to delay the bedridden stage of MS. Physical and occupational therapy should begin early to ensure optimal physical functioning for as long as possible. Physical therapy and passive muscle stretching are necessary for optimum management of spasticity of the lower extremities.

• Methylprednisolone (500 mg daily for three to five days) followed by high dose oral prednisone—to shorten an acute exacerbation of optic neuritis (Caution: Oral prednisone without methylprednisolone has been reported to increase the risk of subsequent episodes of optic neuritis.)
• Immunosuppressive drugs (e.g., methotrexate (7.5 mg once a week for two years), azathioprine (2 to 3 mg/kg daily), cyclophosphamide, cyclosporin A)—to improve the clinical course of some patients; however, severe toxicity is a problem.
• Interferon-beta 1a (6 MIU intramuscularly once a week), and interferon-beta 1b (8.0 MIU subcutaneously every other day)—to decrease white matter lesions and the frequency and severity of attacks
• Copolymer I, a polymer of MBP—to improve the clinical course of relapsing-remitting MS
• Amantadine (100 mg bid) or pemoline (37.5 mg bid)—to treat fatigue
• Isoniazid (300 to 1200 mg/day) with pyridoxine (100 mg/day)—to treat postural tremor
• Oxybutynin (5 mg bid) and propantheline (7.5 to 15 mg qid)—to treat bladder disturbances
• Baclofen (15 to 80 mg/day), clonazepam (0.5 to 1.0 mg bid or tid), primidone (125 to 250 mg bid or tid), or ondansetron (4 to 8 mg bid or tid)—to treat spasticity and increased muscle tone of lower extremities
• Carbamazepine (100 to 1200 mg/day), phenytoin (300 mg/day), or amitriptyline (50 to 200 mg/day)—to treat trigeminal neuralgia and painful dysesthesias

• Ventrolateral thalamotomy—to treat severe and disabling tremor
• Rhizotomy or myelotomy—to reduce severe spasticity

Nutritional therapies are helpful in reducing inflammation and slowing the progression of MS. Mind/body techniques such as meditation, yoga, and tai chi may be beneficial in reducing the effects of stress. Some patients with MS have a high level of Candida in their stool culture and respond well to treatment with anti-fungals.

• Eliminate refined foods, alcohol, caffeine, saturated fats (e.g., animal products), and additives (especially monosodium glutamate and aspartame).
• Avoid food allergens and sensitivities. The most common allergens are wheat, dairy, eggs, soy, citrus, tomatoes, corn, chocolate, fish, and peanuts. An elimination/challenge trial may be helpful. Remove suspected allergens from the diet for two weeks. Reintroduce foods at the rate of one food every three days. Watch for reactions which may include gastrointestinal upset, mood changes, headaches, and exacerbation of symptoms. Do not perform a challenge with peanuts if there is a history of anaphylaxis. High percentage of MS patients are sensitive to all gluten-containing foods.
• Eat a diet high in protein and anti-inflammatory oils (nuts, seeds, and cold-water fish). Include orange, yellow, and dark green vegetables. Eat whole grains in small amounts.
• Omega-6 oils (borage, evening primrose, black currant oils) 1,500 mg bid to tid to reduce inflammation. Include zinc (30 mg/day) and selenium (200 mcg/day) to enhance fatty acid metabolism.
• B-complex vitamins, especially B₁₂ (1,000 mcg/day) and B₆ (100 mg/day), and minerals, such as calcium (1,000 mg/day) and magnesium (500 mg/day), optimize nerve function.
• Vitamin C (1,000 mg tid), vitamin E (400 IU/day), and coenzyme Q10 (100 mg bid) provide antioxidant protection.

Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes).

Herbs rich in bioflavonoids provide antioxidant protection and stabilize collagen tissues. Use one to two of the following: hawthorn (Crataegus monogyna) 200 mg bid to tid, ginkgo (Ginkgo biloba) 120 mg bid standardized extract, especially with cognitive impairment, quercetin (100 to 250 mg tid), especially with food sensitivities.

Combine the following herbs in equal parts to nourish the nervous system and help prevent constipation: oatstraw (Avena sativa), skullcap (Scutellaria laterifolia), lavender (Lavendula angustifolia), lemon balm (Melissa officinalis), passionflower (Passiflora incarnata), and horsetail (Equisetum arvense). Drink two to three cups tea daily or take 30 to 60 drops tincture bid.

An experienced homeopath would consider the individual's constitution. Combination remedies may be useful for adrenal fatigue, spasticity, and detoxification.

May be beneficial in alleviating symptomatic complaints.

Essential for maintaining flexibility and reducing spasticity, as well as improving the overall sense of well-being.

Patients need lifelong monitoring, especially during exacerbations. Drug toxicities must be monitored with frequent blood and liver studies. Health care practitioners must be sympathetic and supportive of patients with such a progressively incapacitating disease and its resultant psychological, social, and physical issues.

To qualify as an acute exacerbation, new symptoms or worsening of existing symptoms must last longer than 24 hours. These exacerbations may last days or weeks; some resolve completely, while others leave impairments. The interval between attacks is extremely variable, lasting several months to years.

Most patients (70%) follow a relapsing-remitting course after the initial attack; others (10% to 15%) follow a chronic progressive course from the beginning (usually patients with late onset MS). Many patients (50%) who begin with a relapsing-remitting course develop a secondarily chronic progressive course after about 10 years. Approximately 15% to 20% of MS patients follow a benign course and never develop permanent deficits. Poor outcome is associated with incomplete recovery from attacks, frequent attacks, and male gender. A small number of MS patients die within a few months or years of the diagnosis, but most patients live for 30 years or more, many still working and ambulatory.

There is a decreased incidence of relapse during pregnancy. Pregnancy is typically associated with clinical stability or improvement in symptoms. However, in the three months following parturition, there is an increased incidence of exacerbations. Pregnant women should be encouraged to minimize fatigue post-partum.

Adams RD, Victor M. Principles of Neurology. 6th ed. New York, NY: McGraw-Hill; 1997: 902–921.

Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace Publishers;1995:299-300.

Fauci AS, et al. Harrison's Principles of Internal Medicine. 14^th ed. New York, NY: McGraw-Hill; 1997: 2409–2419.

Kelley WN, et al. Textbook of Internal Medicine. 3^rd ed. Vol 2. Philadelphia, PA: Lippincott-Raven; 1997: 2385–2387.

Scalzo R. Naturopathic Handbook of Herbal Formulas. 2^nd ed. Durango, Colo: Kivaki Press; 1994: 63.

Taylor RB, et al. Family Medicine: Principles and Practice. 5th ed. Berlin, Germany: Springer; 1998: 589–591.

Rosen P, Barkin R, et al. Emergency Medicine: Concepts and Clinical Practice. Vol 3. St. Louis, MO: Mosby; 1998: 2219–2221.

Conn RB. Current Diagnosis. Philadelphia, PA: Saunders; 1991: 988–991.

Branch WT. Office Practice of Medicine. 3rd ed. Philadelphia, PA: Saunders;1994: 721, 766–767.