There is no known cause for multiple sclerosis. Viruses are often implicated as the primary cause, but in no case has this been substantiated. There is no apparent risk of transmitting multiple sclerosis to spouses or medical personnel.
Symptoms and exacerbations frequently follow virus infections (Sibley et al 1985; Panitch et al 1991; Edwards et al 1998), bacterial and bladder infections (Rapp et al 1995), prostatitis, and decayed or missing teeth (Craelius 1978). Exacerbations during systemic infections are twice as likely to lead to sustained clinical deficits, though there is no difference on MRI (Buljevac et al 2002). It is wise to prevent immune activation with good bladder and dental hygiene and by minimizing exposure to people with upper respiratory infections.
There is a 1.6 relative risk of multiple sclerosis in smokers (Hernan et al 2001). Smokers are more likely to develop a progressive course (Durfee et al 2008), possibly from an effect on the blood-brain barrier or an influence of chronic bronchitis.
Vaccinations and immunizations usually do not cause exacerbations of multiple sclerosis (Sibley et al 1985; Ascherio et al 2001). Measles, mumps, rubella, and human papilloma virus vaccines are considered safe. Tetanus and diphtheria vaccinations are associated with a reduced chance of developing multiple sclerosis (0.67) (Hernan et al 2006). Influenza vaccination should be encouraged in order to obviate the risk of exacerbation following virus infections. There is debate about exacerbations from recombinant hepatitis B vaccine (Hernan et al 2004). Live virus vaccines, however, are likely to induce a cytokine storm and should be administered with caution. Yellow fever vaccinations, for instance, increase the risk of exacerbations 9-fold in relapsing-remitting multiple sclerosis.
Diet and environment appear to affect the development and course of multiple sclerosis. In Norway, cod liver oil and fish intake (omega-3 fatty acids) reduces risk of developing multiple sclerosis (Kampman and Steffensen 2010). High risk groups such as unaffected relatives of multiple sclerosis patients could benefit from a dirty environment, a diet rich in polyunsaturated fats (evening primrose and flaxseed oil), sunlight, and vitamin D (Bielby personal communication 2005; Ponsonby et al 2005).
Theoretical reasons exist to avoid several drugs, but therapeutic need may outweigh theory. Cimetidine, a histamine H2 blocker (Anlar 1993), and melatonin (Constantinescu 1995) enhance immune function, and may oppose the ability of H1 agonists to reduce blood-brain barrier permeability. Beta-adrenergic blockers inhibit suppressor cell function (Karaszewski et al 1991). Occasional patients worsen with fluoroquinolone antibiotics (eg, ciprofloxacin), which induce inflammatory cytokines in addition to their antibacterial effects (Riesbeck 2002). Some patients are extremely sensitive to low doses of carbamazepine; weakness is probably caused by blockade of Na+ channels in demyelinated axons.
Stress does not provoke attacks of multiple sclerosis in controlled trials, despite widespread anecdotes of stress worsening multiple sclerosis.
Exercise, physical therapy, social contacts, better diet, and drug treatment of symptoms can improve quality of life. All of these interventions allow patients to realize that they can control some of the symptoms of multiple sclerosis.