This Is MS Multiple Sclerosis Knowledge & Support Community

Hi everyone, I think I posted on here back in 2016, but had to create a new account so maybe it was on a different page. Long story, well, long, I had an episode of double vision back in 2011, it was preceded with massive pain over left eye for about a week, then it went away, and the next day I woke up with a lazy eye and double vision that slowly went back to normal over a couple of months. Went to ER, got MRI of brain no contrast, found some small lesions, I think 5, they told me to follow up with neuro. I didn't have insurance but found one that saw me for 50 bucks. He said that it was probably a migraine that strained eye muscle. I was relieved because my sister has ms, and had double vision that made eye lazy, so I was obviously worried. Fast forward to September 2016, same thing, pain over eye, double vision started, no lazy eye this time and it subsided rather quickly, but did have some other symptoms, extremely fatigued, left side of face went numb for a day or two, some pain in my jaw. Just overall I felt unwell and it lingered for weeks, slowly got better. I did see a new neuro and he ran labs, MRI of brain and c-spine with and without contrast. Labs were pretty good except a low positive ANA with titer of 1:80. Brain MRI showed no change from the 2011 one so that was good. He sent me for visual evoked potentials, it was after vision was better, but overall passed with flying colors. He did have me do a sleep study and said I have sleep apnea, but only when I sleep on my back. I had decided not to get cpap machine and found ways to sleep on my side. He felt though my MRI determined MS not excluded, but felt maybe it was due to sleep apnea causing migraines. I don't get migraines besides I guess these two incidents, but I was feeling better and again relieved that VEP was normal. February of this year I was doing dishes, started shaking out of nowhere, then noticed my toes felt numb, the shaking subsided for the most part but my lower legs and feet had a burning/tingling sensation going on and even though I was no longer visibly shaking, kind of felt like I was shaking inside, if that makes sense. I did wake up pretty ill the next day with what I thought was the flu but turned out just being viral, for the next couple weeks it was like my body went nuts. In addition to being sick I had shooting pains that were very fast in my right leg and hip, once in face, strange vibrations in my neck, vision kinda shaky, which has happened intermittently over past year, but passes quickly. Had lots of muscle spasms while I was sick, but could just be due to virus. Some other random things that I'm sure I'm forgetting about, arms and hands weaker than they used to be and some numbness on and off. Even as it all started to slowly subside, I still have the internal shaky feeling and get the occasional wiggle vision, as I call it. I get some pain over eyes that comes and goes but nothing to the intensity that it was in the past that preceded the double vision. So I go back to neuro, but by the time I got in I was feeling much better, just lingering trembling and definitely still tingling at night especially. He ran labs, all good except ANA was positive again, even lower titer 1;40. He basically just wants me to get cpap machine and said to come back in may. Should I push for repeating MRI's and have him do spine too? I'm just not feeling as convinced that MS is off the table anymore as I was before. I do have degeneration in neck and probably back too, so maybe just inflammation from virus caused some issues there but an MRI would show that anyway. I don't want to second guess the guy, but I don't see how sleep apnea would affect me in an episodic fashion, and seems out of the 3 episodes, more random symptoms pop up. And he did say that maybe something autoimmune was going on, it does seem to run in my family (my 3 year old was diagnosed with JDM in late 2016, sister MS) but didn't seem like he wanted to explore anything other than me trying a cpap. My husband doesn't really get the sleep apnea thing either as I don't snore at all, but nevertheless I'm willing to try it. I don't know, I just don't want to seem pushy, but don't want to ignore something that could potentially affect me in the future, or compromise my ability to take care of my little ones. Sooo sorry for how long this is. Any thoughts? Should I suck it up and go see an ms specialist to rule it out or in?

I should also add that after VEP last year he said we could do a lumbar puncture to rule out MS, but I wasn't exactly jumping at that as it seemed invasive and expensive, so I declined. Maybe I should have?

greengirl35 wrote:My husband doesn't really get the sleep apnea thing either as I don't snore at all, but nevertheless I'm willing to try it.

There is obstructive sleep apnea and central sleep apnea. Obstructive sleep apnea is due to a partially blocked airway and may be more commonly associated with snoring. However, central sleep apnea is more of a problem with the central nervous system. It occurs when the brain fails to tell the body to breathe. In either case, it's best to get treatment for your sleep apnea as untreated sleep apnea is strongly correlated with dementia.


Can sleep apnea cause Alzheimer's disease?
Neurosci Biobehav Rev. 2014 Nov;47:656-69.

• Both obstructive sleep apnea (OSA) and Alzheimer's disease (AD) are increasing health concerns. The objective of this study is to review systematically the effects of OSA on the development of AD. The search was conducted in PubMed and Cochrane CENTRAL, and followed by a manual search of references of published studies. Cross-sectional, cohorts, and randomized clinical trials were reviewed. Besides clinical studies, we also discuss neuroimaging data, experimental animal evidence, and molecular mechanisms. Although a causal relationship between OSA and AD is not yet established, OSA induces neurodegenerative changes as a result of two major contributing processes: sleep fragmentation and intermittent hypoxia. As such, inflammation and cellular stress are sufficient to impair cell-cell interactions, synaptic function, and neural circuitry, leading to a decline of cognitive behavior. Sustained OSA could promote cognitive dysfunction, overlapping with that in AD and other neurodegenerative diseases. Early treatment by positive airway pressure and other current standards of care should have a positive impact to alleviate structural and functional deterioration. With better understanding of the cellular and neurophysiological mechanisms by which OSA contributes to AD, we may identify novel molecular targets for intervention.

Obstructive Sleep Apnea is Associated With Early but Possibly Modifiable Alzheimer's Disease Biomarkers Changes.
Sleep. 2017 May 1;40(5).

• Study Objectives: Obstructive sleep apnea (OSA) is a common sleep disorder. The, literature lacks studies examining sleep, cognition, and Alzheimer's Disease (AD) cerebrospinal fluid (CSF) biomarkers in OSA patients. Therefore, we first studied cognitive performances, polysomnographic sleep, and CSF β-amyloid42, tau proteins, and lactate levels in patients affected by subjective cognitive impairment (SCI) divided in three groups: OSA patients (showing an Apnea-Hypopnea Index [AHI] ≥15/hr), controls (showing an AHI < 15/hr), and patients with OSA treated by continuous positive airway pressure (CPAP).
  
  Methods: We compared results among 25 OSA, 10 OSA-CPAP, and 15 controls who underwent a protocol counting neuropsychological testing in the morning, 48-hr polysomnography followed by CSF analysis.
  
  Results: OSA patients showed lower CSF Aβ42 concentrations, higher CSF lactate levels, and higher t-tau/Aβ42 ratio compared to controls and OSA-CPAP patients. OSA patients also showed reduced sleep quality and continuity and lower performances at memory, intelligence, and executive tests than controls and OSA-CPAP patients. We found significant relationships among higher CSF tau proteins levels, sleep impairment, and increased CSF lactate levels in the OSA group. Moreover, lower CSF Aβ42 levels correlate with memory impairment and nocturnal oxygen saturation parameters in OSA patients.
  
  Conclusions: We hypothesize that OSA reducing sleep quality and producing intermittent hypoxia lowers CSF Aβ42 levels, increases CSF lactate levels, and alters cognitive performances in SCI patients, thus inducing early AD clinical and neuropathological biomarkers changes. Notably, controls as well as OSA-CPAP SCI patients did not show clinical and biochemical AD markers. Therefore, OSA may induce early but possibly CPAP-modifiable AD biomarkers changes.

All great info, thanks! Yes, he said I have OSA, so I am going to give cpap a try for sure.