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You have already found the only published randomized trial of worms in MS (the JAMA neurology paper). If I were in your position, worms would not be the first option I would look into.
One meta-reason to be skeptical: one often sees worms touted as a solution for all autoimmune diseases. But therapies are not trivially transferable across autoimmune diseases. For example, anti-TNF therapies are effective in RA, but exacerbate MS; natalizumab is effective in MS, but exacerbates neuromyelitis optica. The latter case is especially shocking, as NMO is clinically nearly identical to MS, and was in fact considered a variant of MS for a long time. The biology is distinct across different autoimmune diseases. The concept of "autoimmune disease" has been of limited help in understanding the biology or treatment of MS.
(One further note: it's not even clear that MS is an autoimmune disease. It's definitely immune-mediated, but unlike in RA, nobody has been able to identify an antigen.)
In order of options that I would pursue in your situation:
1. Get an MRI. People with MS typically have radiological activity for years before their first clinical episode. Use a high-resolution MRI, which can spot lesions which are smaller or outside of white matter. 7T is the highest resolution, but (last I checked) is only available in research trials. You might be able to get into a trial related to familial MS. Otherwise get a 3T, which is widely available.
2. Get a test for serum neurofilament light levels. This measures the concentration of degraded proteins from the nervous system floating around in your blood. After MRI, this is the second-best validated biomarker of neuronal damage in MS, and likely can measure ongoing damage which is too diffuse to spot on MRI. Not in widespread clinical use in the US, but it is being used in the UK and Scandinavia, and likely to be widely available in the US soon.
3. Sunlight/vitamin D. Lots of evidence that low levels of sunlight exposure/vitamin D are associated with development of MS. The literature here is a mess, and there's less evidence that this is causal, but still some evidence. For example, people who move from high sunlight to low sunlight environments early in life have higher rates of MS than those who move later in life (https://jnnp.bmj.com/content/jnnp/63/5/565.full.pdf) and vice-versa. The causal evidence is largely confounded with the hygiene hypothesis, but there is much more associative evidence for Vitamin D (for example, people with MS typically have extremely low Vitamin D levels at diagnosis).
The reason to get more sunlight or supplement with vitamin D is that these are simple and safe in moderation.
There is another point here which is relevant to worms. The causal evidence points to MS risk being modifiable by early-life environment but not later life (post-teenage) environment. If the hygiene hypothesis is correct, I am not sure that exposure to worms will be useful to you now.
4. Minocycline. Probably going too far given the information you currently have, but it's widely used to treat acne, and has at least been shown to reduce the probability of MS onset in high-risk individuals (https://www.nejm.org/doi/full/10.1056/NEJMoa1608889).