My Adventure with Insomnia Continues...

As we said in Beating the Dementia Monster, the most powerful weapon against Alzheimer's disease is physical exercise - especially sustained aerobic exercise.  However, some experts I've spoken with will tell you that #2 is getting adequate sleep.  And in Beating the Dementia Monster, we discussed why that is.  So I've put a lot of emphasis in my own battle on sleeping well, at least seven hours a night.

But I haven't slept well since early 2020.  And I've tried everything.  Last year, we wrote glowingly about the prescription medication suvorexant, sold under the brand name Belsomra.  How did that go?  In my experience, it simply stopped working after a short period of time.  And then when I stopped taking it, I couldn't sleep at all.  I also tried ramelteon with similar results.  Except ramelteon seemed to make me depressed.

So am I out of possibilities?

I don't have any trouble getting to sleep, and I'll have been quite tired when I first lay down.  But I'll be suddenly very awake an hour and a half or 90 minutes later.  (These times correspond with the ends of the 90-minute sleep cycle we discussed in Beating the Dementia Monster.)  Often, I could go back to bed after an hour and a half or two hours, but getting to sleep was very difficult.  If I went back to bed at around 7 or 8 in the morning, I could often get another hour or so, but I have a lot of morning commitments that make this hard.  

One way I fought it was by going to bed earlier and earlier.  For a while my bedtime was 9 and 9:30, and then 8:30.  So I would end up taking 10 hours to get six hours of sleep.  Or often five hours.

I guess the YouTube algorithm began to feel sorry for me, and it started sending me links to various videos on insomnia.  (It must have seen what I was Googling in the middle of the night.)  One of the videos described something I'd never heard of before, called "bed restriction therapy."  The video was by two Australian therapists, but after I watched it, the algorithm sent me a whole bunch more by other therapists.  While I'd never heard of bed restriction therapy before, I guess it's pretty commonly recommended.

The concept is straightforward and is based on the idea that our sleep patterns are a consequence of habit.  So you create a new habit by strongly limiting the time you're in bed.  You want to force all of your sleep time into a single segment.  In my case, I've developed a habit of waking up for long periods during the night.  I've also apparently trained my brain to believe that lying awake in bed during the night for long periods of time is just part of life.

So to do this therapy, we start out with two things:  How long do you actually sleep during the night, and when will you get up.  The sleep time, of course, excludes the hours when you're awake.  According the my FitBit, I've been sleeping a total of about five hours a night, although often a little less.  I'd like to get up at six a.m., but for a long time I haven't been able to sleep beyond 5:00.  So you take the time you will get up and roll the clock back the total number of hours you sleep.  That's your new (temporary) bed time.  So if I will be getting up at five, and I sleep five hours, I go to bed at midnight.  Which is a big switch from 8:30.  

And then no naps during the day ... at all.

Of course, that five hours of sleep is normally distributed over about an 8 to 10-hour period.  So I will not be getting those five hours of sleep.  In fact, when I started doing it, I was lucky to get three hours.  And you do that for a full week.

One of the therapists said that her patients really, really hate her for that week.  And I can see why.  I have just finished that first week, and it was horrible.  Most days, I realized I shouldn't have been driving, but I had so much to do.

They said it would be discouraging, but just stick it out for one week.  They say you really need a sleep coach to do it right, someone to encourage you and help stick it out.  On night six, I almost threw in the towel.  But on the seventh night, I finally slept the whole five hours without waking up (except for a couple of trips to the bathroom).

The plan now is to adjust bed time in one hour increments, taking one week with each adjustment.  So I'll be going to bed at 11 each night for one more week and hopefully getting up at five a.m.  The following week I will go to bed at 10, which is my goal.  I want to go to bed at 10 and wake up at 5 a.m.  Hopefully, I'll be doing that in another week.

I sure feel great today, but was last night a fluke?  They said after a week, the therapy will begin to work, and you'll begin to feel a lot better.  And I feel a lot better today.  We'll see how it goes.

Lecanemab Graduates

We wrote in January that lecanemab (marketed as Leqembi) had been approved by the FDA to treat Alzheimer's disease.  This was the consequence of a fast-track approval based on the phase 2 trial, so it was a kind of provisional approval.  Normally, approval is based on the phase 3 trial, and that wasn't complete yet.  And after the phase 3 trial is done, an advisory panel normally reviews the trial data and recommends approval.  In this case, that's the Peripheral and Central Nervous System Drugs Advisory Committee (PCNS).  

You will recall that when aducanumab (now Aduhelm) hit this stage, several members of the advisory panel disagreed that the treatment should be approved.  When the FDA approved it anyway, several members of the panel resigned. 

Things are calmer for lecanemab.  The PCNS has just voted unanimously to recommend approval of the treatment.  I understand the naysayers from the aducanumab days are no longer on the panel, but we also know more about how these monoclonal antibody treatments work for Alzheimer's disease.  Although lecanemab was provisionally approved in January based on the phase 2 trial data, what this vote does is make the approval more conventional ... and more convincing.  No shortcuts.  The phase 3 trial is done, and the PCNS has now reviewed all of the data.  They are unanimously comfortable in recommending that the FDA approve the treatment for use.

Lecanemab does not cure Alzheimer's disease, it just slows its progress.  This appears to be because it is treating symptoms, not the disease itself.  It appears that amyloid plaques are interfering with how the brain functions and may be killing brain cells.  Clearly, getting rid of them helps with memory and cognition, at least for some people.  But why are the plaques forming in the first place, and how do you stop that?  Do the plaques actually form for a good reason, perhaps to protect the brain from bacteria and viruses?  The more we learn, the more questions we find ourselves asking.

A new twist

We did go to Walla Walla yesterday and met with the neurosurgeon.  I gave him a writeup describing my experience to date along with a copy of Beating the Dementia Monster.  He was intrigued by my story, and concluded that I have multiple issues with my brain, not just normal pressure hydrocephalus (NPH), and not just Alzheimer's disease.  

His only role was to help me decide if a shunt would be appropriate for me, not evaluate my disease(s).  Nevertheless, he shared some thoughts with me.  He was cautious in his statements, and I hope I didn't misunderstand him.  

The first outcome of our meeting was that he did not think a shunt would help me much.  The results of the "large volume lumbar puncture" that I got last December were not positive enough to compel him to go in the direction of a shunt.  The next level of testing in situations like mine would be a test involving placement of a drain in my brain with a three-day stay in the hospital.  During the three days they would frequently check my balance and cognition.  He said this is the real gold standard test for NPH.  But insurance companies don't like paying for it, and he thought there was a high probability I would be disappointed in the results.  So maybe NPH is not the main driver for my gait and balance problem.

Consistent with what the NPH expert in Seattle told me back in February of last year, my most significant problem at this point may be ataxia due to cerebelar dysfunction.  This is a syndrome, and there are multiple possible causes.  The most common is "RFC1 associated ataxia."  Aside from speech and gait & balance problems, people with this syndrome often display a chronic cough.  Guess what?  I've had an annoying chronic cough now for more than five years.

So what does this mean?  He said that it does not mean that I don't have Alzheimer''s disease.  My issues with memory and cognition appear to be separable from the gait and balance issues.  I told him that the premise of our book is that I have Alzheimer's disease, and I wondered if I needed to backtrack on that in a new edition of the book ... or a whole new book.  He didn't seem to think so.

But ataxia is a whole new challenge, and I've been studying up on it.  There can be many causes of ataxia, but in my case it appears to be an irreversible, progressive neurodegenerative disease.  It seems right now that I just need to keep doing what I'm doing to help my memory and cognition but recognize that my speech, balance, and gait will continue to deteriorate.  We discussed problems I have with speech in Beating the Dementia Monster.  These problems have continued to come and go, but it's the gait and balance that seems to steadily worsen over time.

When I have questions about physical therapy, I like to go to the YouTube channel of Bob and Brad.   Maybe you've seen them, since they're pretty popular. Well, about a year ago, they published this episode about Bob's diagnosis of ataxia.  At the time, I felt sorry for Bob, but didn't think there would be a connection with my own situation.  Then I saw that they published this update of Bob's condition just last Sunday.  I saw that and then listened to my neurosurgeon ... and I realized that Bob and I are likely dealing with the same thing.  Based on deterioration of his speech, I'd say he's a little ahead of me, but not much.

So how do I feel about this?  I got up this morning and the sun was shining.  I didn't hear any birds chirping, but they're out there somewhere.  I had my morning devotional time and then went to the gym.  Life goes on.

A big day tomorrow...

As we wrote earlier, it's suddenly unclear if my neurological issue is Alzheimer's disease or normal pressure hydrocephalus (NPH) - or both.  NPH is often misdiagnosed as Alzheimer's disease, but also, the two disease often occur together.  Thirty percent of NPH patients also have Alzheimer's disease.

Tomorrow morning, I have an appointment for a consult with a neurosurgeon in Walla Walla.  Walla Walla is about an hour's drive from here. The purpose of the visit is to lean on his experience with cognitive and balance-impaired patients to see if it's appropriate for me to receive a shunt.  The high volume spinal tap I had in December suggests that it would be, but my neurologist cautions that there are many potential surprises here.  She wanted me to see an experienced neurosurgeon to find out what his experience says about my scenario.

One thing I want to discuss with him is the changes in my computed hippocampus volumes.  The evidence is that the normalized values for men my age went down from 2015 to 2017, stayed steady to 2018, but then improved remarkably into 2021.  My ventricle volumes remained unnaturally enlarged throughout this time.  NPH would explain my ventricle volumes, but not the changes in hippocampus volumes.  Alzheimer's disease could be responsible for hippocampus changes from 2015 to 2017, and lifestyle changes could explain the hippocampus changes from 2017 to 2021.  Or that's how it looks to my uneducated eye. 

I'll know more tomorrow.  I hope.