This happened to my poor husband and me, as it does to nearly 1/2 of the bed partners of PD patients around the world since REM Behavior is reported to occur in about 47% of Parkinson’s patients….
I have been having vivid dreams and talking in my sleep for years, I would not be a good secret agent as per my husband. My sleep talking (about 70% of individuals have somniloquence-talk in sleep in some point in their lives without being aware) drives my husband crazy because I usually speak in my native tongue. As my Parkinson’s disease has advanced, my dreams have become more vivid more frequent thought the night and my sleep talking has increased. However, over the last few months I noticed that my sleep talking had become louder to the point of awakening me. Then one morning I awoke to find my husband had built a wall of pillows between us for “protection,” he said.
“Against whom?” I asked.
“You, of course! I always knew that you were lethal. But, now I have confirmation!” He stated in a jokingly matter. ( I guess I picked up a thing or two watching all the boxing matches with my dad who was an avid boxer and boxer aficionado!)
A few days later in the middle of the night, I again awoke flinging my arms in the air and talking. Later the same night, I awoke because I felt hit something hard. Apparently, I had punched my husband and was pulling his t-shirt. He was desperately pushing me away without trying to hurting me. “Sorry,” I muttered and fell asleep rather quickly.
Next day, at bed time he was building a bigger barrier.
“It’s amazing how you can’t throw a punch to save your life when awake,” he said “but people better what out if they try to mess with you when you are asleep. You throw a big punch that leaves a sting like ALi.”
After laughing, I apologized feeling really guilty. I told him that I was now having REM behavior ( RDB) due to my PD which was not only causing me to ‘act out’ my wild dreams but was awaking me from sleep frequently since I was beginning to hear myself talk, punch and flail my arms in the air repeatedly.
“You are dangerous,” he commented. “If this keeps up, I may have to start sleeping in another room for my own safety.”
Others had broken bones from suddenly jumping out of bed and tripping on objects near bed. While other patients of mine had injured themselves on open chest drawers nearby. these scenarios were causing many partners to seek separate beds at night for fear of being assaulted by Manny Pacquiao’s and Floyd Mayweather’s and other famous boxer’s impersonators everywhere. Even frail and weak appearing PD individuals can develop the strength of 100 men when in violent rage awake or asleep. I know I have seen it first hand as a doctor, a caregiver and a patient.
Thus, not wanting to continue 1) injuring my husband; 2) risking hurting myself; 3) continuing experiencing restless nights and chronic fatigue from lack of sleep; I increased my dopamine dose and started melatonin at night. I am sleeping better once more. My husband’s barricade has decreased and he no longer sleeps on the edge of the bed but still keeps a pillow nearby for protection just in case.
Few days ago, I asked him if I was still spilling state secrets. He answered in the affirmative, I surely would make a horrible spy I thought to just myself; but at the moment it appears that my boxing days and extreme fighting in bed at least for now appear to be behind me. I feel well rested and my dreaming although vivid has quieted down.
Things to know about REM behavior:
Sleep disorders is one of the most common non motor Parkinson’s symptoms that can precede motor symptoms of Parkinson’s many years before tremors and stiffness become noticeable. They can also occur in various forms ranging from insomnia, RLS, REM behavior (RDB) as the disease progresses. REM behavior is also known as “dream enacting behavior.”
Typically in REM sleep, which is part of deep sleep, our brains are very active and we experience a lot of dreaming while our bodies remain paralyzed. We usually go through this stage many times during the course of the night. About 20% of our sleep is spent in this stage which usually occurs more commonly in the second part of the night. REM behavior is more common in men over age 50 but more women are experiencing this phenomena (perhaps this goes along with the new trend of young women developing PD). This sleep disorder is very common in neurodegenerative diseases like Parkinson’s, MSA and dementia of Lewy body (LBD); it is also seen in narcolepsy. It can be the initial symptom of PD and MSA as well as that of dementia of Lewy Body.
Dream enactment differs from night terrors by way that people if awoken from an episode of REM Behavior they are fully awake not confused and remember details of the dream unlike those with night terrors who have no recollection and are not fully awake.
Symptoms of REM Behavior include :
- arm flailing,
- shouting profanity
- at times emotional out cries.
- increasing dopamine dosage,
- intake of small doses of klonopin is highly effective in most patients up to 90% with doses of .25 mg; it has complete effect in 79% of patients and the great thing about it is that it appears to do so without building tolerance or abuse.
- The other extremely effective medication is over the counter melatonin in doses 3-12 mg taken at dinner around 5-6 pm.
- tegretol ( carbamazepine) has also been shown to help
- Mattress should be placed on floor
- Put alarms in beds
- remove potentially hazardous objects from around bed. One patient broke his lamp because he picked it up as sword, fortunately his spouse awoke him before he struck her with it!
Okay, don’t panic you come to the right place!
First of all, Parkinsonism simply means you have features of Parkinson’s disease (PD) but not the entire clinical picture based on the UK a brain criterion which includes 4 main symptoms: rest tremor; rigidity (stiffness); bradykenisia (slowness); and gait abnormality. Usually people labeled ‘parkinsonian’ have two or three of these features.
What Causes This?
3 scenarios are possible for why this occurs.
1) You either have an underlying illness which affects the basal ganglia – structure involved in PD – which then mimics PD. Things that affect these structures of the brain whether it’s through blood loss, loss of oxygen, pressure, swelling from trauma or infection can then mimic symptoms of Parkinson’s because remember the basal ganglia is important in movement, learning and balance. So common primary neurological diseases like strokes, multiple sclerosis, brain tumors must be ruled out and can be a reason why you have received a diagnosis of Parkinsonism. Non- neurological causes which can affect the brain are things like lupus which cause brain inflammation and other types of infections such as lymes disease or syphilis, and HIV. NPH (Normal pressure hydrocephalus) and lower body parkinsonism caused by multiple strokes (considered to be its own disease type) can be other less known causes of parkinsons-like symptoms in an individual. This is why we often order an MRI of the brain at time of diagnosis as well as lumbar puncture / spinal tap to make sure no infections are present.
2) Your Parkinson’s disease is very early in its presentation at time of first evaluation and has not developed all of its features; this is especially common in younger people with YOPD who may present usually with dystonia (abnormal contraction of muscles) along with more non- motor symptoms in conjunction with stiffness and slowness. I have had many young patients take 5 years or longer to present with full blown PD symptoms- initially receiving diagnosis of Parkinsonism or focal even segmental dystonia. I myself did not start having rest tremors till 7 years after onset of other PD symptoms; even now my rest tremors are not very prominent. They are more pronounced in my toes than in my hands which is not very common or typical.
3) You may have an atypical Parkinson’s syndrome or Parkinson’s plus disease such as Lewy body dementia (LBD), corticobasalganglia degeneration (CBGD), progressive supranuclear palsy (PSP), multi system atrophy (MSA) which could either be Shy-drager or olivopontocerebellodegeneration or atrophy (OPCA). All of these “atypical” PD illnesses take time to develop into full blown disease that can be recognized sometimes even by experts if the right “key” feature is not present from the beginning like “alien-hand” is characteristic of CBGD. Plus we must remember there are many other hereditary illnesses which are less typical and common that can present this way some of which may not have characteristic imaging findings and can’t be recognized unless an expert does a specific blood test such as SCA6 . However, because we don’t have a diagnostic blood test or an objective way of differentiating among the various types of Parkinson’s we must rely on the ability of MDS doctors to recognize the other clinical signs which point to the fact that one is not dealing with ‘typical’ Parkinson’s disease. The signs and symptoms such as dementia, memory loss, personality changes, or apathy from the beginning of disease, bladder issues severe and out of proportion for time of other symptoms like tremors, stiffness .as well as greater swallowing difficulties, increase falling, speech impediments, difficulty with coordination or action tremors are all signs that we are dealing with a Parkinson’s plus syndrome. In this category, a good MDS can be of great benefit. He or she should be able to tell that your Parkinsonism is due to an atypical syndrome as opposed to a secondary cause like in 1. However, knowing a person has a Parkinson’s plus syndrome and being able to pinpoint with 100% certainty which one may still require frequent visits with your physician.
Getting A Dat scan does not help in these situation because all it can tell you is that there is a dopamine problem if normal it would only point to a non -dopaminergic cause and if MRI normal- NPH, infection (individual would be sick with fevers, rash etc), and even psychogenic causes need to be entertained.
At this point since we do not have an assortment of drugs to treat different types of Parkinsonism or to treat even between the different subtypes of PD the treatment is always Levodopa! All types of Parkinsonism except psychogenic requires levodopa. However, the prognosis for each and the amount of response vary on the type and underlying cause. The best response to levodopa is with typical PD- a big clue for physicians.
The key to successful treatment is early initiation of medication independent of cause except psychogenic/stressed induced. Since if its early PD – the sooner the treatment the better the prognosis and greater quality of life, if its Parkinson’s plus it will initially give quality but because of nature of disease it will progress independent of medication and will not lose anything by starting dopa early. In the one’s caused by an underlying disease, patients will fell symptomatically better but once underlying disease or culprit found they may or may not need further dopa but if they do unlike the other dopaminergic illnesses there will not be a need for escalation of does and medications because symptoms are for the most part static.
Nevertheless, all Parkinsonism patients will benefit from a neurologist care. Those with Parkinson’s and those with Parkinson’s plus syndromes need a movement disorder specialist which can manage the subtleties as well as coordinate a team care approach. Those with Parkinsonism due to other underlying cause need to seek care from a specialist in that area such as stroke doctor, MS specialist, or rheumatologist. In some cases, the Parkinsonism can resolve completely once cause is identified like treating infection or NPH.
This is why it is extremely important to seek initial treatment with a neurologist and follow- up with the same person consistently in order to increase as well as expedite accurate and proper diagnosis.
“Smell is a potent wizard that transports you across thousands of miles and all the years you have lived.” -Helen Keller
Imagine not being able to smell your favorite food, perfume, or flower in my case the star-gazer lily. Smell is intricately connected to our memories. Have you ever walked into a place and immediately transported to a bye gone era simply by an aroma?
Smell is a huge component of our everyday life, as I first discovered as an undergraduate when we did an experiment in which we were asked to drink of a substance while holding our nose tightly….after sipping the clear substance, we all unanimously hailed it as water. But after, the professor asked for us to drink the same liquid without holding our nose our astonishment was evident—-it was LEMONADE! A simple pinching of our nose had altered our perception of the world!
Loss of smell can be one of the earliest signs of Parkinson’s disease. It is believed that the olfactory bulb impairment is due to clumping of alpha synuclein…. (a normal protein found abundantly throughout the brain and in smaller amounts in heart, muscles and other tissues- believed to be an important player in maintaining synaptic vesicles in pre-synaptic terminals- these are the ones responsible for release of neurotransmitters like dopamine).
Recent data suggests that >95% of Parkinson’s patients present with significant loss of smell. This may be supportive of new theory that Parkinson’s disease starts in the olfactory bulb and not in basal ganglia as previously believed.
Besides helping us with survival by avoiding harmful substances like toxic gases or rotten foods the olfactory system help us to maintain personal hygiene, which allows us to interact with others socially.
Loss of smell has been linked to cognitive decline and loss because of that primitive connection to our memory banks; therefore it should come as no surprise that this is a harbinger of dementia –olfactory loss being one of the first symptoms and signs of Alzheimer’s and PD. Loss of smell has also been linked to psychiatric problems such as depression another common symptom of PD.
However, most people don’t really notice a loss of smell per say but rather a loss or change in taste because as I mentioned earlier taste is directly linked to our ability to smell. So food begins tasting bland and sometimes even foul. But when formerly tested using a Snell smell test, PD patients show deficits in discrimination, detection, and identification of odors.
At this time there is no known cure for hyposmia (decrease ability to smell) or anosmia (complete loss of smell or inability to smell). Smell problems are often overlooked in the medical community since they are not deemed critical to living yet they have a great impact upon our lives as I stated before. Much research is needed in this field particularly if it has potential to alter our moods and cognition.
However, the best we can do is try to augment gustatory strategies and be cognizant of potential hazards and install protective measures such as fire alarms- since smoke may not be detected. Make sure inspect expiration dates of food carefully. Simulated odors are available to use while cooking for those of us who cannot smell to increase sensation of flavor. However, these odors are quiet pungent to normal smelling people so would not advice using if there are people who have normal smell in family.
Other ways to circumvent this is by enhancing gustatory senses via creative cooking such as preparing and eating foods which are spicy, crunchy, and full of aromatic herbs, as well as adding color and textures to your foods in order to engage your other senses like sight and make your whole mouth titillate and vibrate with joy….. Bon Appetite!