I got my results. They weren’t anything unexpected — for the most part. This was my fifth (I think … I’ve lost count) overnight sleep study, and the results of each have been pretty much the same. And the solution has been as well. I did this sleep study in the raw, that is, without using my audiovisual entrainment device to help me fall asleep so that they could measure my sleep in its natural state.
The good news is that I don’t have sleep apnea or any respiratory problems during sleep apparently. The so-so news is that this sleep study caught something others didn’t, something I knew I had — restless legs. The irony: they are not such a problem for me as they used to be, in fact, it’s a problem I rarely think about. I can’t believe it’s finally being noticed when I’m no longer bothered by it!
Now for the report.
They diagnose mild PLMS. I had to look that up. It stands for Periodic Limb Movement Disorder. It’s when one’s limbs move involuntarily during sleep. Apparently Restless Leg Syndrome (RLS), which is what I thought I had, includes limb movements when awake. Well, that’s what used to happen with me, way back when. RLS also includes “a voluntary response to an uncomfortable feeling in the legs” — something I used to do every night, it seemed like. But though I may have that uncomfortable feeling when I’m rather more tired than usual, and at any time during the day, I no longer have the voluntary response or the urge to move or jerk my legs. In other words, I’m better. And now the sleep study reveals it. The doctor who gave me my results offered me meds, specifically clonazepam. They’d titrate me up to when morning grogginess kicked in. Oh goody, like I’m not weary enough when I awaken. No thank you.
The other sleep problems included increased sleep onset latency (I took longer than normal to fall asleep); 5.9 hours of sleep (almost 6 hours, not bad); 37 minutes of being awake after initially falling asleep; decreased sleep efficiency, though if we don’t include how long it took me to fall asleep, sleep efficiency was normal; increased wakefulness; increased alpha-wave EEG or alpha wave intrusions; increased stage 1 sleep; decreased stage 2 sleep; increased stage 3 sleep; and increased stage 4 sleep with increased total slow wave sleep in total sleep time; decreased REM sleep; 143 arousals. of which 116 spontaneous, 17 leg movement, 10 RERAs (hey, I thought the report said no respiratory events — is it cause this Respiratory Effort Related Arousal is an EEG thing with barely perceptible respiratory changes pre-arousal that it’s not considered an actual event? Still my oxygen saturation was 100% in the 90-100% range); 17 leg movement arousals with 2 short arousals from slow wave sleep but without abnormal behaviour noted. In other words, I didn’t sleep talk or walk. And I don’t snore! But otherwise I’m pretty screwed, eh? Especially as I was — again — given no firm solution after hearing that litany of goodness.
In any case, although the increased alpha wave EEG during sleep is something I’ve had for years, long before my brain injury, the increased slow wave sleep and decreased REM I did not. I spent years after my brain injury not dreaming at all. I couldn’t tell if I was just forgetting all my dreams, something totally new to me, or truly not dreaming. However, in the last couple of years or so, the dreaming returned. And I had thought it was normal again … but then it had been so long since I had had a rich dream life, what would I know what is normal?
I could not find much information on why I am exhibiting these changes and when I was told my test results, the doc didn’t say much about the why. But perhaps that’s because this is just another area medicine knows extremely little about. One 2012 study noted this deficiency in research and noted that:
“Objective sleep studies show reduced sleep efficiency, increased sleep onset latency, and increased time awake after sleep onset. Depression and pain exacerbate but cannot entirely account for these problems. There is increased slow-wave sleep. Individuals with TBI show lower levels of evening melatonin production, associated with less rapid-eye movement sleep.“
I do not know what my melatonin production is, but to test it would cost me $600, so that ain’t happening. Anyway my hypothalamus fix pretty much allows me to fall asleep at a decent time and quickly.
So what’s the upshot of all this? I was sent back to my referring doctor with the instructions to try Lyrica (a pregabalin, a GABA analogue). It may help with my sleep. It may not. It may also calm those restless legs too. One would think you go to a specialist, you get a definitive answer, a solution that works. When it comes to the brain, not friggin likely. But I have other plans. More on that in a later post.