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I have been reading about radiologically isolated syndrome. My understanding is that people having an MRI for a non-MS related condition (such as a headache or trauma) may have white matter lesions identified. These patients have “radiologically isolated syndrome” and according to the literature are at high risk for developing MS.

From what I have read, in autopsy studies between 0.08% and 0.2% of people may have evidence of MS. I have also read that up to 2% of people may have white matter lesions, although not sure if that number is not accurate. Finally, I have read that 1/3 to 1/2 of people with radiologically isolated syndrome advance to MS over 5 years.

I was wondering what people here feel about this topic? Is it easy for a physician to misdiagnose a person as having radiologically isolated syndrome or a positive MRI? My friend was told her MRI looks like someone with advanced MS (despite only have one lesion) and despite not having any symptoms for about 1.5 years, she has been quite concerned. I am concerned that she is assuming any symptom is MS because of what her doctors told her. (She clearly needs to meet with additional doctors, but up until now, had limited access due to her geographic location.)


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Two references used for the numbers above are listed below:

Neurology Bulletin, 5:22-26 (2013)
Multiple Sclerosis Journal 19(3) 271-280 (2012)

There are several diseases which can cause white matter lesions. One of these is a vitamin B12 deficiency which can cause periventricular lesions similar to those in MS. As such, I think that anybody that is given a diagnosis of radiologically isolated syndrome should be tested for B12 deficiency.


Plasma vitamin B12 status and cerebral white-matter lesions.
J Neurol Neurosurg Psychiatry. 2009 Feb;80(2):149-57.

• BACKGROUND AND OBJECTIVE: Elevated homocysteine has been associated with a higher prevalence of cerebral white-matter lesions and infarcts, and worse cognitive performance. This raises the question whether factors involved in homocysteine metabolism, such as vitamin B(12), are also related to these outcomes. This study examined the association of several markers of vitamin B(12) status with cerebral white-matter lesions, infarcts and cognition.
  
  METHODS: The study evaluated the association of plasma concentrations of vitamin B(12), methylmalonic acid, holotranscobalamin and transcobalamin saturation with cerebral white-matter lesions and infarcts at baseline and cognition at baseline and during follow-up among 1019 non-demented elderly participants of the population-based Rotterdam Scan Study. Analyses were adjusted for several potential confounders, including homocysteine and folate concentration.
  
  RESULTS: Poorer vitamin B(12) status was significantly associated with greater severity of white-matter lesions, in particular periventricular white-matter lesions, in a concentration-related manner. Adjustment for common vascular risk factors (including blood pressure, smoking, diabetes and intima media thickness) did not alter the associations. Adjustment for homocysteine and folate modestly weakened the associations. No association was observed for any of the studied markers of vitamin B(12) status with presence of brain infarcts and baseline cognition or cognitive decline during follow-up.
  
  CONCLUSIONS: These results indicate that vitamin B(12) status in the normal range is associated with severity of white-matter lesions, especially periventricular lesions. Given the absence of an association with cerebral infarcts, it is hypothesised that this association is explained by effects on myelin integrity in the brain rather than through vascular mechanisms.

Magnetic resonance imaging (MRI), cranial computerized tomography (CCT), evoked potentials and cerebrospinal fluid (CSF) analysis in five patients with funicular myelosis.
Neurosurg Rev. 1987;10(3):209-11.

• Five Patients with vitamin B12 deficiency were examined by means of MRI, CCT, VEP, BAEP, EEG, and CSF. In 3 patients medianus-SEP and EMG/ENG were recorded as well. Partly, findings of MRI, CCT, VEP, BAEP, SEP, and CSF were similar to those in multiple sclerosis. This is not very surprising considering that the central nervous system lesions in vitamin B12 deficiency consist of disseminated demyelination. Because of this all these investigative techniques must be considered non-specific. Appraisal of findings is only possible in connection with the case history, clinical findings, and supplementary diagnostic measurements.