Wednesday, April 25, 2018

Restless Leg Syndrome: Non-pharmacologic Strategies

I get lots of emails about tricks and tips to treat Restless Leg Syndrome other than medication. I discuss this a lot in office visits, and patients tell me about things they have stumbled upon which seem to work. Broadly speaking, I think it is always a good idea to consider non-pharmacologic options for any problem when reasonable and safe. First, many things can cause or unnecessarily aggravate RLS symptoms that should be treated as an underlying issue otherwise. For instance, iron deficiency, neuropathy, gastric bypass, kidney disease, sedentary lifestyle, lumbar stenosis, etc. can all cause RLS or worsen it and should be treated first to reduce unnecessary poly-pharmacy. Second, for many people, RLS is genetic, passed down to you no different than your eye color, but more of a bother. I think this is important to keep in mind, because sometimes it is just something that ends up really needing medication to treat, depending on its severity, and you can’t wish it away or think of it as some existential external thing that has come upon you. Sometimes, medications really are your friend. Third, although sometimes medications are just plain necessary, non-pharmacologic strategies always have a place in complementing prescription medications, to reduce the overall dose burden or frequency of baseline medication use and/or frequency/dose of breakthrough medication need.
So these tips/tricks are a compilation of things I know, or things patients have told me work for them. If you have RLS and are reading this, I would print it out and pragmatically work through the list on a trial basis a few weeks at time to see which element(s) work best for you. 

Exercise: Well, a sudden uptick in exercise, like weekend warrior exercise or a spontaneous fun run, or Fall-related leaf raking marathon or Spring-related garden planting for many people will aggravate their RLS symptoms. HOWEVER, regular walking in the evening/weight training or some such similar consistent—that is the key-- consistent amount can actually help reduce the RLS presence. There are many theories about why this may help. I have a theory that the endorphins released work on RLS symptoms indirectly through the pain pathway (dorsal horn of the spinal cord). The problem with this theory is that I am not sure why more exercise/sudden exercise is often counterproductive… perhaps through some lactic acid buildup mechanism and a reduction in pH. I am open to the literature on this question still. 

Soap under the bed: I have thought a lot about this. There is actually NO WAY for soap under your bed to physiologically directly reduce RLS symptoms. It is just not possible. BUT, I have patients who swear by it, so this is my theory. It is a valid use of the placebo effect. We know stress can bring out or exacerbate RLS symptoms, and if you believe soap will work, I believe the belief itself is a treatment, by reducing stress, and indirectly therefore truly helping. Unfortunately, if you just read this and believe me, then I ruined it for you. Sorry. 

Stress: Stress worsens symptoms, so I often recommend a strong pre-sleep calming ritual, deep breaths, a “worry journal” to help relieve immediate concerns until the next morning, etc.

Soak: Many patients swear by a pre-bedtime ritual of soaking the feet in cool water. I would think hot water for some reason (which I have also heard from patients), but more seem to report cool water benefits. Ice water = bad, though, as it can cause nerve injury. I have a patient who swears by Epson salts, cool water, and a short story (her “timer”) from a book of short stories every night as part of her ritual, to reduce the dosage of Mirapex used for her RLS. 

Heating pad: Ok, so not as many people like warm or hot water, but many people DO like heating pad use, wrapped around their feet WHILE IN BED. 

Iron: Iron deficiency is an obvious target, but many people don’t understand this point, so let me partially clarify. There have been many articles dedicated to this, but I just want you to understand my particular view on this. RLS is likely a heterogeneous group of “diseases” which are slightly different (which is why very different strategies work for different people). For some, it is utilization of dopamine in the right place at the right time in the brain (localized “storage centers” of iron and “production centers” of dopamine). For many people there is some poorly understood connection to the benzodiazepine receptor. For some it is possibly a slight general decrease in dopamine production, not enough to cause Parkinson’s but enough to cause RLS. And I believe that for others there is a problem making dopamine efficiently, specifically, converting its precursor, Tyrosine, into –L-dopa(mine). Numerous cofactors are needed to make this conversion, iron being a big one (along with indirect factors such as magnesium, zinc, Vit C & D & B3 & B6). Ferritin is protein that helps you store protein when available to be stored, a more sensitive test than testing for iron amount directly. A “normal” level of ferritin is 20 ng/mL, but for RLS individuals, it should be 50 ng/mL or more (more like 70 to 80 ng/mL). By the way, only about a third (or less, depending on the study) of patients with a low ferritin have a low serum iron level, the general iron level being what is usually checked by doctors. 

Folate: Try 5 to 30mg daily for a month. Some people, even with normal levels (10-12ng/mL) noted a subjective benefit.

Magnesium: Try magnesium oxide supplements 400-600mg about an hour before symptoms usually starts. I recommend trying 200mg or less increments, 2 weeks at a time while seeing what works and giving your stomach/intestines a chance to get used to the dose before trying higher doses. This seems to help for some people earlier in the diagnosis than in more progressed forms.

Review meds: These are the most common culprits I see: SSRIs, TCAs (Tricyclic antidepressants), Prochloperazine, Metoclopramide, Diphenhydramine.

Caffeine (including in chocolate), Alcohol, and Nicotine: These can all be associated with worsening RLS symptoms, sometimes hours after taking in a manner that is unexpected by the patient. 

Eating too late can worsen symptoms for a variety of reasons.  I will say that many patients have noted trends in what type of food can cause this, such as high fat, or salty food, but often, high carbohydrate food seems to be a common trend I hear. I suspect it has something to do with a change of blood flow to the GI system slightly away from the brain that somehow causes this.

Aspirin before bed. If you take aspirin, try taking at night before bed instead of the morning. If you don’t take aspirin, I would try 81mg  (enteric coated) before bed for a few weeks, then 2 of them before bed for 2 weeks if 81mg didn’t work, just to see if you are one of these people it helps. I don’t know mechanistically HOW it would help which means either there is a gap in my knowledge or ability to logically make the connection; there is a gap in Medicine’s knowledge; it is placebo effect; or it is working through another mechanism. I DO know that patients with vascular claudication, poor circulation to the legs, seem to notice less leg cramping and less non-classic RLS-like leg pain when placed on Plavix to help with blood flow to their legs… so if you are older and aspirin helps, I think you should probably at least ponder whether this possibility is relevant for you. 

For some people “mechanical” strategies seem to help, either by themselves early in the diagnosis, or as adjunctive strategy later, to complement medications or supplements and help reduce the medication dose burden. Common strategies include tight cotton socks or actual compression hoses. Sometimes just massaging your legs with your hands or with a device just before bed can be enough. I have had patients use weighted blankets folded over at the base of the bed too, and even electric hospital-grade pneumatic compression devices typically used in the hospital to prevent DVTs. Some people notice that vibration helps and will try plug-in vibrating blankets. 

I hope these strategies help. There are others of course, many of which I am SURE are JUST placebo (like Himalayan salt lights or Manuka honey spreads…) but these are the big ones that I find myself discussing with patients.

Monday, June 26, 2017

Things Called TIA (transient ischemic attack) ...
but Are NOT

In my recent post, I addressed some terminology such as TIA versus “mini-stroke” versus small stroke. A TIA means that the CAUSE of your symptoms was a lack of blood flow to some part of your brain that returned BEFORE permanent damage was done (which would be called a stroke). I see patients all the time that were told they had a TIA but retrospectively did not.

They may have had transient neurologic symptoms.... but the "I" in TIA (ischemic--lack of blood flow) may not have been the problem.
A key word above is: RETROSPECTIVELY. At the time of symptoms, the clinician who evaluated the patient may not have had all the necessarily tools to be completely sure, so erred on the potential diagnosis that allowed for more generous, non-debated testing per your insurance company, or that allowed for the more generous level of cautious concern (both for your benefit) in case you really are having a TIA that could turn into a stroke… Or the presentation is confusing and we just can’t know for certain at the time what the cause was; you may have risk factors for a TIA or stroke but just be having an anxiety attack, for instance. Or your medical situation is complicated; maybe you have risk factors for TIA or stroke and a history of complex migraines that can appear stroke-like.

But when I hear about a patient having a TIA, I keep these other possibilities lingering in my mind, and you should know about these mimics too. That doesn’t mean you should avoid going immediately to the ER if you are having stroke-like symptoms, since up to a 3rd of strokes are preceded by a TIA, often that same day (Most strokes DON'T give you a warning at all).
But AFTER you get out of the hospital, if there was some question of whether you really experienced a TIA, these things should be considered as well, primarily because it may have longer-term implications regarding what medications you are on or should be on.

In order, these are the most common mimics of TIAs:

Complex migraines

Syncope (passing out)

BPPV/peripheral vestibular disturbance (inner ear problem that causes dizziness or vertigo, sometimes with additional complaints like nausea, falling, mildly blurred vision, perceived change in hearing)

Seizure (usually simple or complex partial seizures, not the more dramatic generalized shaking kind)

Anxiety or a psychological cause otherwise

Transient Global Amnesia

Bell’s Palsy (weakness of one side of the face due to a viral insult to the 7th cranial nerve)

Peripheral nerve disease from various causes

Postural hypotension (brief diminished blood supply to your brain as you stand due to a heart or vascular issue in your body)


Viral illness

Cardiac arrhythmia (kind of the same issue as postural hypotension)

Multiple Sclerosis

Drug/Medication related


Parkinson’s Disease symptom fluctuation

Retinal/Ocular pathology

Spinal pathology

Trigeminal neuralgia



Thursday, June 22, 2017

“Mini-stroke,” I Hate You

When I discuss strokes, stroke-like symptoms, “mini-strokes”, TIAs with patient, I realize that there is a lot of misinformation out there, not only from the internet, but also due to the patient’s lack of medical training (which makes sense of course) and, frankly, coming from us doctors.

All doctors have different ways of explaining things, some better than others, either because they misjudge what the patient is willing to understand or is capable of understanding overall or understanding just in the complicated moment, or because maybe they themselves are not completely confident in the cause of symptoms or proper neurologic terminology or actual proper pathophysiology.

I present an example that I particularly hear quite frequently:


I don’t know what this means.

I don’t know if the person had a SMALL stroke, or transient ischemic attack (TIA) that someone has called a mini-stroke or they are interpreting as a mini-stroke. Or I don’t if they didn’t have anything clot/stroke/TIA-related at all and maybe they just had some temporary symptoms that were related to, say, a urinary tract infection that got out of hand, too much cold medication, the wrong medication/medication side effect, an anxiety attack, etc.

I wish the term mini-stroke would go away.

Either you had a stroke (which is permanent and NOT temporary or transient).

Or you didn’t.
If you have a TIA, by definition it is transient (since the “T” always stands for transient) and therefore NOT permanent (I guess we would call that a PIA—PERMANENT ischemic attack—but we don’t use that terminology) and a TIA is therefore NOT a stroke, so a mini-stroke cannot be a TIA. That’s like saying it was a…. “small-permanent-non-permanent lack of blood flow to my brain”… which inherently makes no sense.

I admit I am biased by profession. But am I splitting hairs? Does it matter if I understand what happened as a TIA or mini-stroke or small stroke? Of course it does. Why would we worry about funny moles on our skin or our fat or wrinkles or kidney function but not the details of what is or isn’t happening regarding the blood supply to our brain that we are conscious with?

Now, someone can be told they had a “small” stroke, but that is like saying I only got shot with a small gun versus a big gun. A .22 in the head is a great tool of the assassin and a .44 magnum bullet shot into your foot by Dirty Harry is problematic but theoretically you could still run a marathon after it healed. Like real estate, it is all about location, location, location.

A “small” stroke in your brainstem can kill you or devastate you. A “small” stroke in your speech center can prevent you from understanding language or speaking language forever.

If you have ANY stroke, of ANY size, you are definitively more likely to have more strokes unless something changes… so ANY stroke to me is LARGE in its implication. And TIAs are associated with a much higher risk of subsequent stroke within the following hours, days, and months, so calling either of these phenomenon “mini-strokes” does the patient a severe disservice.

In summary:

A stroke is permanent and is a big deal no matter how big or small it is.

A TIA is NOT a mini-stroke; it is a NON-permanent lack of blood flow that did NOT permanently damage the brain but suggests you are HIGHLY likely to have a stroke in the near future if something isn’t done.

There is no such thing as a mini-stroke in my book.

Thursday, October 1, 2015

Sleep Murder..... A Sleep Entry For the Month of Halloween

A very disconcerted patient of mine sent me the above clipping. She has Parkinson's Disease and REM Behavior Disorder (RBD) as a part of her symptoms overall. And now this sweet, older woman is terrified that she is going to "sleepwalk strangle" her grandchildren when she babysits. When she babysits her grandchildren overnight, she has come up with an ingenious solution and wants my approval: She plans to lock herself in her master bedroom at night, and her husband of 50+ years will sleep in the guestroom outside the locked room in case the grandchildren needed something in the middle of the night. She has asked my approval of the overall plan's logistics and on the specific sliding bolt lock she has found at Home Depot and whether she will open this lock in her sleep (versus an alternative combination lock-bolt system she found). 

I felt very bad for her situation, or her perspective, rather. 
I was trying to imagine this future situation where "scary" grandma locks herself in her room at night as though she were a werewolf or some other Wes Craven creature of the night. Definitely something more frightening than my grandmother's pantry of eternal cookies. 

First of all, parasomnia is the term for abnormal sleep behavior in all its forms (other than things like epileptic events and movement disorders, etc... which aren't really called behaviors). We are referring to complex motor events resembling what someone might do while awake. Parasomnia literally means "next-to-sleep," like paranormal means "next-to-normal" or in this case, behavior outside of normal sleep behavior, or in the latter, something happening outside of the normal. Parasomnia come in two broad flavors: NREM and REM parasomnias. Either you do this during non-dreaming sleep (NREM sleep), or while you're dreaming (REM sleep--Rapid Eye Movement).

The actual prevalence of all parasomnic behavior happening sometime over a lifetime (ALL SPECTRUM AND FORMS OF BEHAVIOR, from soft mumbling to eating a stick of butter or driving a car) is quite variable, as high as 67% of the population in some studies, so it's relatively common. Actual lifetime sleep walking behavior is as high as 22% and at any given time affects 1.7% of the population, which is heavily skewed toward kids who make up a majority of these walkers. More complex behavior like eating in one's sleep (4.5%) and sexual behavior (7%) is relatively rare and more likely in the adult population. 

For self-injurious behavior, the current prevalence in the population is only 0.9% and injuring someone else is only 0.4%.  And of all self-injurious behaviors and injuries to someone else, almost 99.99% of reported incidents involved accidental quick punching out/thrusting out/kicking out/falling off the side of bed/tripping on something in one's sleep, or other such simple, abrupt, relatively non-complex behaviors. AND, these latter, injurious-type behaviors are more common in person's with co-morbid psychiatric disorders such as active depression, anxiety, PTSD, etc. which skews the probability this direction. 

So I reassured the patient that probability is in her favor, since her grossest probability of even attempting the type of aggressive behavior she is concerned about is 4 x 10 to the negative 4th power in logarithmic terms, and there is lots of wiggle room for poor math which would push the probability to even lesser degrees. Even if we use this number, she still would have to attempt this behavior without the child waking up and waking her in the process; have to negotiate her house without accidental self-injurious behavior in the process such as tripping or bumping herself awake; not wake her likely curious husband while getting up; and assume that she will have a directed effort again the children as opposed the man with whom she's had 50+ years of marital arguments with. And... we are treating her with medication, since parasomnias are treatable, so she would have to fail this too. 

No, I think they are quite safe. But I still thought you might find this interesting all the same.

Thursday, May 8, 2014

Do Statins (anti-cholesterol medications) Cause Nerve Damage or Muscle Damage?

A patient of mine brought this in and I thought it should be shared because I field questions about it all the time.

 The summary of the question/answer article above is essentially: 
My primary care doctor put me on a statin medication. My cholesterol improved but was replaced with "peripheral neuropathy" in my fingers & toes to the point that I had difficulty gripping things. The primary doctor and one of my fellow neurologists reportedly found no cause, and told the patient suck it up (but hopefully in a more eloquent manner). The patient stuck to their guns, and with their doc's blessing, tried a few weeks off the statin with rapid improvement of the numbness.

Peripheral neuropathy is not a specific term. It literally means, "pathology of the nerve," or "nerve-something-wrong-with." You can imagine that coming to your doctor with that complaint is inherently ambiguous, even if your concern is specifically troublesome. 

The hard part is that "peripheral neuropathy" causes in people of an age advanced enough to start statin medications (as opposed to, say, an 8 year old with neuropathy), is a very long list. I started counting truly unique potential causes in one of my neuropathy textbooks here in my office (yes, I have multiple 300+ page textbooks dedicated to neuropathy alone), and stopped when I hit over 101 causes, because I kept wanting to read about some of the more esoteric causes and the digressions were eating into my other work responsibilities.

So, because a statin-relationship to neuropathy is actually rare, and the other common and not-so-common causes as a group much more likely, it is relatively easily to miss this tree among the forest of other potential causes. 

But to expand the statin concern:

Statins currently include simvastatin, atorvastatin, pravastatin, fluvastatin, lovastatin, pitavastatin, and rosuvastatin, commonly known respectively as Zocor, Lipitor, Pravachol, Lescol, Mevacor, Livalo, and Crestor, with the bold ones most commonly seen by me in my patients.

They ALL inhibit an enzyme Beta-hydroxy-Beta-methylglutaryl-CoA reductase which is essential in the formation of cholesterol. It is already well established that they can cause myalgias (muscle pain & tenderness) and myopathy (actual muscle breakdown & weakness), and this is one of the reasons someone would be switched from one of these to another. Sometimes multiple ones have to be tried before a "good" one is found that both lowers one's cholesterol and doesn't cause significant myalgias or myopathy.

More controversial, however, is the potential claim of toxicity to the actual nerves. Some studies show a definitive effect in people and many studies do not. And the question is whether it is direct or indirect. For instance, we know that eating lead paint or being exposed to frostbite causes DIRECT damage to nerves. But with statins, we know that some/many people have some slight increase in their triglycerides, and we know that other people with unusually high triglyceride levels can have damage to their nerves from that... so is the cause in some people indirectly through the slight bump in triglycerides? Who knows--no one for sure yet.

If you undergo a nerve conduction study (NCS) to characterize the neuropathy, the type of neuropathy is usually an axonal sensorimotor neuropathy (which, by the way, also includes such common causes as thyroid disease, B vitamin deficiencies, other medications, diabetes, too much alcohol, HIV, kidney disease... lots of stuff essentially). 

Just to make things harder, the onset of neuropathy if actually due to the statin medication, can start 1 to 7 years AFTER starting and continuing the medication, so think of what other things can enter someone's life over that period of time. BUT the good news is that it should resolve or improve dramatically and relatively quickly after you stop the medication.

So what does all this mean? It means that IF you get a neuropathy, and IF it is the specific kind which RARELY CAN be associated with statin use, then if you aren't in desperate need of uninterrupted statin therapy because you've had a heart attack or stroke or are teetering on the cusp of one, then, WITH YOUR PRIMARY DOCTOR'S BLESSING, you could try to come off the statin for 2 to 3 weeks, to see if things improve before wading into the deeper waters of more exotic workup of causes.

Tuesday, May 6, 2014

Migraineurs have a different intracranial vascularity than people who don't get migraines.

This study, while interesting, told neurologists something already known, or at least strongly suspected by most. It does support, however, our thoughts that there is a significant vascular cause behind migraines, and especially some of the asymmetry associated with them. We knew it was true at the microscopic and less-microscopic level, but this little study supported the suspicion at even the larger-vessel suspicion as well.

What is the Circle of Willis? Below is a picture of it by itself and what it looks like perched on the underbelly of the brain. In summary, you have four main arteries coming from the heart to supply the brain. The two in front are the carotid arteries and the two in back are the vertebral arteries. The Circle of Willis is essentially the anatomy of how these "trunks" branch into the various recesses of the brain.

In this picture, the Internal carotid artery on one side is labeled, and the Vertebral arteries are NOT labeled but you can see them at the very bottom, joining together as an upside down "V" to make the labeled Basilar artery.

Now, this study was unique in that it looked at these larger vessels for differences in anatomy between different types of migraine patients. As I was saying before, what neurologists have always known however is that that the tiny branches everywhere from a tenth of mm in size (smaller than this period:  .  ) to a mm in size (about the width of this n)-- that these billions of blood vessels that imbue every nook & cranny of your brain are also different by design in some manner, and more likely to show some damage at a greater frequency than other people just like you who don't have migraines. There is something different about a migraineur's brain vasculature. That being said, there are numerous studies (especially in the psychology and psychiatric journals) showing that there is no long-term negative cognitive changes (thinking problems) associated with these small vascular changes, and many non-migraineurs ALSO have this same thing to some degree or another but for other reasons.

Anyway, if you have migraines and you have an MRI showing something like "non-specific T2 changes," or "subtle white matter changes consistent with small vessel disease," or the like, you should know it is a relatively common finding, is a relatively underwhelming finding, not associated with any changes in thinking, and that this below is often what it looks like:

The two white spots toward the front on your left (perhaps a subtle third spot just above can also be seen)

Sunday, March 30, 2014

Melatonin for High Altitute Sleep.... What can we down here learn from it?

This was presented at the 27th annual meeting of the Associated Professional Sleep Societies LLC (June 4, 2013), as an abstract, also published as an online supplement in the journal SLEEP.

The official title of the abstract was
“Melatonin as a countermeasure to the effects of high altitude on sleep and cognition on North America’s highest peak,”

The study only involved 13 people (climbers). 2 were women.
Average age: 34
The were climbing at14,200 feet on North America's highest peak, Denali, in Alaska.
Keep in mind that 140 MILLION people live among 8,000 feet and many ski resorts in the contiguous United States have people skiing precariously on them greater than 10,000 feet.

They each were given melatonin or placebo on 2 consecutive nights. Neither they nor the person who gave them the pill at that time knew which night they were getting the melatonin versus the placebo, so they couldn't "predict" how well they should sleep or perform the next day on a test.
They took the medication 1.5 hours before bed.
They wore a wireless sleep monitoring device (polysomnogram) to help judge how much they slept.

The amount of time they slept was judged, as well as how they performed on the Stroop test the next day.... as a hopeful, indirect sign they actually got more sleep and would therefore have better cognitive acuity as a result.
-On average they fell asleep in 20 minutes (with melatonin) versus 44 minutes with placebo. They also had less wake after sleep onset time.
-The next day they also performed better on the Stroop test, which is a mark of reaction time, judging how fast one can correctly name a series of colors who's name (in word form) is different than the color you are to name. There are other variations on this test as well.


Things I believe you should take away from this study:
-Melatonin should be taken not just before bed (as many people are tempted to do) but at least 1.5 hours before bed.
-Melatonin helps with sleep solidarity and time to sleep onset, and does so without being a prescription, without as many side effects of the prescription sleep aids, and without the reliance & habituation which can come from regular prescription sleep aid use.

Things this study doesn't tell you:
-What dose will work for you personally
-Melatonin works best if you take it EVERY night at the SAME TIME before bed as part of regular pre-sleep ritual. Melatonin does not work like Ambien/Sonata/Lunesta, etc. Melatonin encourages the orchestra of sleep, but by itself cannot force sleep.You really need to use it regularly for some period of time to see a more robust positive & sustained effect.
-Whether other supplements could be just as effective or was it specific to melatonin's affect on a specific location within the brain or because of its affects on the circadian rhythm

Problems with the study: 
-It might lead someone to believe, erroneously, that the medication could or should work one night at a time, when melatonin is NOT designed to be a "rescue" medication.
-The wireless sleep study hardware/software could only offer a limited assessment. It was not as good as in-lab study, and it may be missing some key information.
-These were fit 34 year-olds... We don't know what type of implication the medication would have for older or younger people...
                       ...or people who snore or have apnea (Could melatonin make it worse by having them sleep more deeply and not protect their airway?)
-Small study: 13 people. How well can we extrapolate to a large population from that?
-We don't know what happens with longer use.