1. Canada has one of the world’s highest burdens of MS, at 133 cases per 100,000 (the MS Society estimates up to 240 per 100,000). The WHO ranks Canada 5th in the world, behind the U.S., Germany, Norway and Hungary.
2. Women with MS outnumber men by more than 2-to-1 in Canada. But in the 1930s, there were 1.9 female diagnoses for each male one. By the 1980s, that ratio had risen to 3.2-to-1. Some blame the oral contraceptive pill. Yet most research shows that taking the Pill reduces MS risk and alleviates its symptoms. So does pregnancy, another high-estrogen state. But the 6 months after pregnancy, when estrogen is low, see new MS cases arise at 3 times the normal rate. Multiparity reduces lifetime risk. There are trials underway of female sex hormones as MS treatments.
3. Canadians born in May are significantly more likely than average (about 10%) to get MS. Those born in November are significantly less likely. Is a winter virus somehow involved? And higher latitudes mean more MS — but not for First Nations, who are almost untouched by MS.
4. The question of sunlight and vitamin D is at least nearing resolution. The Ausimmune study is looking at MS across the natural laboratory of Australia, where genes are fairly homogenous but sunlight varies sharply. Preliminary results suggest that yes, healthy controls do have more lifetime sun exposure and higher vitamin D levels than patients with a first demyelinating event (FDE). Ausimmune will also look for two viruses: Herpes 6 and EBV.
5. Of course, a new cause has recently been postulated for MS: chronic cerebrospinal venous insufficiency (CCSVI). Seven Canadian and American trials are looking for this association, and all are due to report this summer. In any case, CCSVI can’t be the whole story. Leukocytes may be trapped in the CNS by poor drainage, but they shouldn’t be there in the first place unless the blood-brain barrier is compromised.
6. Relapsing-remitting MS (RRMS) is by far the commonest form, seen in about 85% of new cases, while 15% present initially with hard-to-treat primary progressive MS. Most RRMS cases eventually move on to secondary progressive MS, with or without symptoms and progressive disability. The course is benign in about 15% of these.
7. MS specialists have a saying: “early is late.” When symptoms bring demyelination to notice, the disease process is already advanced. Swift intervention is tied to better long-term outcome. This is why the McDonald criteria replaced the Poser criteria — instead of waiting for a second event, and thus delaying treatment, we can use MRI and CSF to look for other CNS lesions, separated in time and space, essential to MS diagnosis.
8. It’s now known that while symptoms may be episodic, the underlying process is fairly constant, with extensive axonal damage that may be key to long-term disability progression. But imaging doesn’t correlate well with symptoms, making repeat MRIs a poor tool for tracking patient progress. Clinical status is what counts.
9. Optic neuritis is the commonest first clinically isolated syndrome (CIS) suggestive of MS, but the 2010 international meeting that updated McDonald criteria warns of a distinct relapsing demyelinating syndrome, neuromyelitis optica (NMO), which can mimic optic neuritis of MS. It has a different prognosis and underlying pathology and doesn’t respond to most MS disease-modifying drugs. It can be recognized by the presence of serum aquaporin-4 (AQP4) autoantibodies. Look for it when there’s bilateral involvement, recent nausea or severe hiccough, swollen optic nerve, or very long lesions of the central spinal cord with normal brain MRI.
10. In a first neurological exam, don’t bother with Hoffmann’s reflex. Contrary to popular wisdom, it’s not a Babinski’s sign for the arms. The true Babinski reflex (big toe points up when sole is stroked) always points to CNS damage in anyone over 24 months old.