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How I Steer My Inner Pain Conversation to a Place Where I Can Sleep

conversation

Bad pain day. Trying to keep my mind distracted. Perhaps a good show is on television. Or maybe a movie. The “off” cycle will kick in within a few hours. Pain gets worse. Last medication before bed. Time to be quiet and contemplative, but the pain intrudes upon this space. It’s always murmuring, sometimes shouting, and ever-present. Finding sleep means I need to sit in the “pause between.” I repeat the following mantra to myself:

You can do this. Breathe in: 1, 2. Breathe out: 1, 2.

Let go and allow.

My mind will have nothing to do with this “pause between” nonsense. Waving the imagined finger, my brain’s neocortex, “Neo,” interrupts and says, “How’s that to-do list coming? You’re feeling like you didn’t get much done today. You’re trying to make up for that by working on a new to-do list, but having trouble focusing. This pain sure is annoying.”

Neo continually intrudes on my search for the pause between. He can be more annoying than the pain. I respond flatly, “Yeah, nothing new.” I shift in bed to try to relax as I search for the pause between.

You can do this. Breathe in: 1, 2, 3. Breathe out: 1, 2, 3.

Let go and allow.

Neo pokes a nerve cell. “Remember what the pain was like the other night? Whoo-ee, you were tossing and turning, it felt like we were on a roller coaster!”

My night often starts with thrashing in bed. As I switch positions to find comfort, the covers take on a life of their own, and soon I am entwined by the albino boa constrictor sheets. Waves of pain wash over me as I uncoil the bed linen. Neo didn’t offer any assistance. “Could be a terrible night, you know. It’s surely starting that way. Doesn’t seem to be much you can do about it, huh? You know that each time you try to quieten down to rest, the pain gets louder. I mean, I’m doing what I’m supposed to do, reminding you of the day’s events and whatnot. But it just feels like you’re not trying to fall asleep. You know that you are failing at it.”

The “you’re not good enough” button always hit a tender spot, triggering a surge of anger mixed with worthlessness. I take deep breaths and let out a long sigh of exasperation. Throughout my life this button has been pushed more times than our president has sent a tweet.

Neo pauses for a moment before offering the following, “Lots of memories of pain are connected to punishment, oppression, and self-worth issues. But this is an old familiar path, and you know what will happen if you take that fork in the journey.”

Moving along this well-trodden path, I know that I can tune out those “old voices.” They offer nothing more than the cackling of old hens.

You can do this. Breathe in: 1, 2, 3. Breathe out: 1, 2, 3.

Let go and allow.

Neo jumps in. “We’re not finished here. You have a few things about which to worry. You are trapped in a cycle of heightened emotions, increased pain, and poor sleep.” The logic of his interruption, illustrated with an emotional soundtrack, send me into a worry spin like a dog chasing its tail. The more I worry, the more I became stuck in it. If I keep spinning, I will cross over the “you will never get back to sleep” threshold. I need to return to the pause between.

You can do this. Breathe in: 1, 2, 3, 4. Breathe out: 1, 2, 3, 4.

Let go and allow.

As the first glimmers of change appear, my conversation partner, Neo, warns, “You know the pain is just going to get louder when you do this.”

Very firmly, without anger, I say, “I know that I can move into a pause between and then to a quiet place. I’ve done it before, and I can do it again.”

I can do this. Breathe in: 1, 2, 3, 4. Breathe out: 1, 2, 3, 4.

Let go and allow.

Neo senses the changes. The perceptions of pain and discomfort are slowly lowering. The cool night breezes tuck me into a bed that suddenly feels very embracing. I have no more need to talk about the pain.

Breathe in: 1, 2, 3, 4. Breathe out: 1, 2, 3, 4.

Let go and allow.

Breathe in: 1, 2, 3, 4. Breathe out: 1, 2, 3, 4.

Breathe in.

Breathe out.

Then, 15 minutes later, I am sound asleep.

***

Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Poor Sleep Most Common in Patients with Central Parkinsonian Pain, Study Finds

sleep and pain

People with generalized pain related to their Parkinson’s are prone to disturbed nighttime sleep, a reason these two disease symptoms — central parkinsonian pain and poor sleep — are common together and may imply shared mechanisms, a study reports.

The study, “Sleep disturbances in Parkinson’s disease are associated with central parkinsonian pain,” was published in the Journal of Pain Research.

Most Parkinson’s patients experience disease-related non-motor symptoms that often precede the onset of hallmark motor problems. Non-motor symptoms can include anxiety, mood changes, cognitive impairment, sleep disturbances and pain, all affecting patients’ quality of life.

Depending on its origin, pain in Parkinson’s can be classified into five distinct subtypes. One, called central parkinsonian pain, is believed to be the only subtype directly caused by the disease, resulting from abnormal pain information processing (the way the body perceives pain) that leads to pain sensations even though no anatomic or physiological reason can be found. As such, it is considered a neuropathic pain.

Evidence suggests pain is associated with sleep disturbances in a bidirectional manner, with pain disrupting sleep and sleep deprivation increasing pain. But the link between central parkinsonian pain and sleep disturbances has not been explored.

Researchers set out to identify predictors of sleep disturbances and to investigate the relationship between sleep disorders and pain in Parkinson’s disease.

Their study enrolled 229 people (122 men and 107 women, mean age 69) diagnosed with Parkinson’s and with a mean disease duration of nine years. Each had their level of sleep disruption, pain complaints, anxiety, depression, motor symptoms, and functional independence assessed by clinically validated scales.

Results showed that 33% of patients had clinically relevant sleep disturbances, 57% had motor fluctuations, and 71% experienced pain. “Of those with pain, 38 (24%) had central parkinsonian pain,” the study stated.

Patients with sleep disturbances experienced more pain and had more severe motor symptoms, lesser independence in daily activities, more evidence of anxiety and depression, and poorer quality of life.

Those with central parkinsonian pain were more likely to have disturbed sleep — even after considering the possible influence of motor symptoms, motor fluctuations, pain intensity, and symptoms of anxiety and depression — than were patients with other types of pain.

“The study results also demonstrate that the association between quality of sleep and pain in PD depends on pain subtype,” the researchers wrote.  Musculoskeletal and dystonia-related pain “were the most common subtypes of pain … [but] only central parkinsonian pain was significantly related to an increased risk of sleep disturbances.”

General population studies show that sleep deprivation alters pain processing and increases sensitivity to pain, while a healthy nighttime sleep routine can reduce pain perception.

The close relationship between central parkinsonian pain and sleep disturbances in PD [Parkinson’s disease] raises the possibility of common pathophysiological mechanisms,” the team concluded, adding this may relate to the loss of dopamine caused by the disease.

Further research is necessary to better understand the relationship between sleep disturbances and central parkinsonian pain, and may help doctors trying to manage these symptoms in patients.

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Sleep Deprivation May Amplify Cognitive and Emotional Issues in Parkinson’s, Study Finds

sleep deprivation studied

Not getting enough sleep may cause memory defects and emotional changes in Parkinson’s disease due to changes in dopamine metabolism, according to a study of zebrafish.

The study, “Sleep Deprivation caused a Memory Defects and Emotional Changes in a Rotenone-based Zebrafish Model of Parkinson’s Disease,” was published in Behavioural Brain Research.

Most Parkinson’s patients experience disease-related non-motor symptoms often preceding the onset of hallmark motor signs. Some of Parkinson’s non-motor symptoms include anxiety, apathy, mood changes, cognitive impairment and emotional disorders, which individually or taken together eventually affect patients’ quality of life.

“In addition to cognitive and emotional disorders, sleep abnormalities are also prevalent in [Parkinson’s disease],” the researchers wrote. “The problem of sleep is not only the characteristics of the disease itself, but also related to medication and dyskinesia such as tremor and rigidity.”

Sleep is an essential physiological process, and lack or shortage of sleep time causes fatigue, increase of mood swings, and can affect learning and memory. Some studies have shown that sleep deprivation can result in emotional and cognitive impairments.

Now, a team of Chinese researchers investigated the effects of sleep deprivation on locomotor activity, memory and emotional behavior in a zebrafish model of Parkinson’s disease.

To mimic the neurodegenerative disorder, animals were given rotenone — a pesticide that inhibits function of mitochondria (cells’ powerhouses) — which leads to cellular death and onset of parkinsonian features. People who come in contact with rotenone are at an increased risk of developing Parkinson’s disease.

Zebrafish were deprived of sleep for four weeks by being in an aquarium with around-the-clock lighting. Of note, fish usually are exposed to 10 hours of “lights off” a day. Rotenone-treated and sleep-deprived animals’ results were compared to control animals who were not given rotenone.

Rotenone-treated zebrafish exhibited parkinsonian-like symptoms, particularly slowness of movement. Motor symptoms’ progression was not aggravated by sleep deprivation.

Rotenone treatment alone impaired the zebrafishs’ memories. Compared to control animals, animals treated with rotenone that were sleep deprived had trouble memorizing and discerning similar objects that were presented to them, suggesting sleep deprivation further damages short-term cognitive deficits.

Not getting enough sleep also was found to worsen anxiety and depression-like behavior in the rotenone treated animals.

Scientists then sought to understand if the observed behavioral changes could  be related to the metabolism of dopamine – the chemical messenger that’s in short supply in Parkinson’s disease.

When compared to control animals, those treated with rotenone had lower levels of dopamine in the brain. However, sleep deprivation did not decrease dopamine concentrations any further. DOPAC, the principal metabolite (i.e., product of metabolism) of dopamine, which was reduced after rotenone treatment alone, had its levels restored upon sleep deprivation.

High levels of two types of dopamine receptors (to which dopamine binds), specifically D2 and D3, were observed in rotenone-treated zebrafish, in comparison to the control group. Interestingly, the levels of those same receptors significantly decreased after sleep deprivation.

Dopamine metabolism appears to be altered in rotenone-treated animals and sleep deprivation seems to play a part in such alteration, however there is not a clear understanding as to how this happens yet.

“[Z]ebrafish displayed an anxiety-depressed mood and a decline in memory after [exposure] to Rotenone, and sleep deprivation caused more severe phenotype [disease characteristics] in this model via altering the [dopamine] metabolism and D2 and D3 receptors,” the researchers wrote. “Our studies not only provided the understanding the roles of [sleep deprivation] in PD non-motor dysfunctions, but also provided a useful model for future pathogenesis and therapeutic studies,” they concluded.

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Study Cites Factors Associated With Sleep Benefit In Parkinson’s Disease

sleep study

Parkinson’s patients who have had the disease for a long time, who do not sleep very efficiently, and have higher motor impairment are more likely to experience sleep benefit — the phenomenon in which Parkinson’s patients wake up feeling better before taking medication.

The study with that finding, “The related factors of sleep benefit in Parkinson’s disease: A systematic review and meta-analysis,” was published recently in PLOS One.

Sleep benefit is, as the investigators wrote, “a fascinating, but mysterious phenomenon.” It is reported to happen in between a third and half of Parkinson’s patients.

The phenomenon is essentially when a person wakes up from sleep and feels better, with fewer disease symptoms. This is particularly puzzling for clinicians because, at least in theory, just waking up is often when a person has no medications helping them along. So, what could cause sleep benefit?

Researchers still are not sure. Some reports suggest that, although patients may report feeling better, they do not actually perform better on objective motor control tests. aAs such, it might all be psychological.

Still, the team wondered whether patient characteristics — from age and sex to sleep patterns and disease score — might predict which patients would experience sleep benefit.

After a search of the existing scientific literature, the investigators identified seven studies reporting on sleep benefit that included more than 1,300 Parkinson’s disease patients. Using the data from these studies, the authors looked for statistical trends to see which patient traits might be associated with experiencing sleep benefit.

Most of the factors they looked at, including sex, age at diagnosis, and sleep length, did not have a significant association with sleep benefit. However, the investigators did identify three factors that were predictive of experiencing sleep benefit: having had Parkinson’s for a long time; having a low sleep efficiency; and having a high score on the MDS-UPDRS-Ⅲ, a scale used to assess the severity of Parkinson’s motor symptoms, while on medication.

These results might let researchers determine which patients are most likely to experience sleep benefit, though what causes this phenomenon is still pretty much unknown.

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Cognitive Performance in Parkinson’s Linked to Sleep Efficiency, Study Shows

sleep study

University of São Paulo researchers have found that Parkinson’s patients with dementia sleep less and less efficiently, which affects their overall cognitive performance.

The study with that finding, “Global cognitive performance is associated with sleep efficiency measured by polysomnography in patients with Parkinson’s disease,” was published in Psychiatry and Clinical Neurosciences.

Non-motor complications associated with Parkinson’s disease, including cognitive impairment and sleep disturbances, can drastically affect patients’ quality of life.

Evidence suggests an interaction between sleep disorders and cognition. For instance, sleep after learning helps memory consolidation.

In addition, people with obstructive sleep apnea syndrome or chronic insomnia have cognitive abnormalities, which could be reversed after proper treatment of the underlying sleep disturbance.

Although there is still no consensus about whether sleep disorders are associated with cognitive dysfunction, studies suggest an association and add that rapid eye movement (REM) sleep behavioral disorder may be associated with increased risk for cognitive decline. REM is a sleep stage in which the eyes move rapidly in various directions.  During sleep, the body cycles between intervals of basic states: REM sleep and non-REM sleep.

Researchers in Brazil now examined a possible association between clinical variables, cognitive status and the presence of sleep abnormalities and symptoms in Parkinson’s patients.

Investigators performed detailed clinical and cognitive assessment in 79 patients. Participants were mostly men (61%), 51-72 years old, and a disease duration varying between 3.9 and 13.9 years.

Based on cognitive diagnosis, researchers categorized patients as those with normal cognition (29 patients), mild cognitive impairment (39 patients) or dementia (11 patients).

Within two weeks after initial medical evaluation, participants were submitted to an overnight polysomnography, meaning they had their brain waves, blood oxygen level, heart rate, breathing patterns, and eye and leg movements monitored while they were asleep.

Compared to Parkinson’s patients with normal cognition, the dementia group was older, had more severe disease, and more difficulty performing daily activities. Dementia patients also took higher daily levodopa-equivalent dose than participants without abnormalities.

Patients with dementia had lower sleep efficiency, less total sleep time and lower number of sleep state changes, in comparison to the normal cognition group.

Researchers also found an association between sleepiness, measures of obstructive sleep apnea and sleep symptoms, which were assessed by the Parkinson’s Disease Sleep Scale and the Pittsburgh Sleep Quality Index.

“Concerning sleep disorders and sleep symptoms, [there was] no significant differences between groups in the proportion of cases with obstructive sleep apnea, chronic insomnia, [REM sleep behavioral disorder] and [restless legs syndrome]. We also did not observe significant differences between scores of patients in the three groups about excessive daytime sleepiness, quality of sleep and general sleep-related symptoms. There was also no significant differences in the number of sleep disorders between the groups,” authors wrote.

There was a significant association between overall (aka “global”) cognitive performance and wakefulness and the number of sleep state changes during sleep.

“However, we did not find any other association between sleep disorders or symptoms and cognitive status or cognitive performance of patients with Parkinson’s,” researchers wrote.

The team believes the association with the number of state changes during sleep may be because Parkinson’s disease patients with dementia slept less than the other subsets and as such, had less time to change between sleep states.

“We hope that, in the near future, new prospective controlled studies, with more significant numbers of patients, could evaluate, in detail, the relationship of different variables related to sleep with cognitive functions in this specific population,” researchers concluded.

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Parkinson’s Study Analyzes Levodopa‐induced Dyskinesia’s Effect on Sleep

sleep study

When a person is awake, brain circuit activity is constantly “on.” This activity needs to be normalized during sleep. Researchers now report that neuronal activity in Parkinson’s disease patients with levodopa-induced dyskinesia fails to decrease during sleep.

The study, “Levodopa-induced dyskinesia in Parkinson’s disease: sleep matters,” was published in Annals of Neurology.

The brain’s structure and functional networks are constantly changing/evolving in a biological process scientists call “neuronal plasticity,” which affects the brain’s learning and memory abilities.

Levodopa (L-Dopa), one of the main therapies used to treat Parkinson’s symptoms, “successfully controls motor symptoms for several years and then induces motor fluctuation and abnormal involuntary movements, i.e. levodopa-induced dyskinesias (LIDs),” researchers wrote.

This long-term, therapy-related complication results in important functional disability, often requiring complex pharmacological or surgical interventions.

Although LDIs are believed to be associated with changes in neuronal plasticity in the striatum — a brain area involved in multiple aspects of cognition — studies have demonstrated abnormal motor cortex plasticity in LID patients. The motor cortex is the brain area involved in the planning, control, and execution of voluntary movements.

In addition, changes in cortical slow wave activity (SWA) — the major characteristic of deep sleep key for both cortical restructuring and functioning, which, in turn, supports cognition — have been described in animal models of Parkinson’s disease with LID.

SWA increases with wake duration, peaks in early sleep, and declines in late sleep. Animal studies have shown that “rodents exposed to combined levodopa treatment and sleep deprivation developed earlier and more severe LID than animals that were not sleep deprived,” authors noted.

The team at Neurocenter of Southern Switzerland investigated if sleep could influence clinical presentation of Parkinson’s in humans, as previously observed in animals.

A total of 27 Parkinson’s patients (50-65 years old) were divided into three groups:

  • de novo: seven recently diagnosed patients who had received only azilect (rasagiline, by Teva) as dopaminergic therapy;
  • advanced: nine subjects without LID using their usual therapy, but demonstrating the end-of-dose or wearing-off phenomenon;
  • dyskinetic: 11 advanced patients with LID.

Seven healthy and age-matched participants also were recruited as controls.

Researchers evaluated subjects’ mood and sleep complaints as well as their Parkinson’s motor symptoms, using a series of rating scales, and asked them to maintain regular sleep-wake schedules.

A wristwatch-like device was attached to individuals’ non-dominant wrist to monitor their sleep/wake cycles for one week. This method is known as actigraphy. Because of technical failure, one patient from each of the Parkinson’s groups could not undergo rest/activity cycles monitoring.

Additionally, participants were submitted to whole night video polysomnography-high-density electroencephalogram (EEG) recording, meaning those studied had their brain waves, blood oxygen level, heart rate, breathing patterns, eye and leg movements monitored while they were asleep. Recording data was corrupted by artifacts in two de novo patients and one dyskinetic participant, and as a result was excluded from the SWA analysis.

Subjects were followed for at least six months.

Results showed there was a decline in SWA in the de novo, advanced and control groups, but not in dyskinetic patients, who had their SWA persistently elevated during the night.

In accordance, all groups except the dyskinetic one, manifested a significant decrease in SWA between early and late sleep, further supporting the investigators’ hypothesis that dyskinetic patients have their much-needed overnight brain activity normalization process compromised.

In all Parkinson’s patients, total sleep time and sleep efficiency were negatively correlated with disease duration, which is consistent with previous studies.

However, “while the correlation between [deep sleep] and disease duration was positive in both [de novo and advanced] patients, it was surprisingly negative in [dyskinetic] patients,” researchers wrote.

A possible explanation is there may be biological compensatory mechanisms in the de novo and advanced sample that can be compromised in the dyskinetic one, making dyskinetic patients unable to sleep efficiently as disease progresses.

Because levodopa dose influences dyskinesia onset, investigators performed a correlation analysis between sleep parameters and levodopa-equivaled daily dose.

A negative correlation of total sleep time and sleep efficiency with levodopa-equivalent daily dose was observed in all patients with motor fluctuations, i.e., in both advanced and dyskinetic groups. Importantly, slow wave (or deep) sleep was negatively correlated with levodopa-equivalent daily dose only in patients  experiencing LID.

“In conclusion, these results support our preclinical findings of a clear association between sleep and LID at the electrophysiological, behavioral, and biochemical levels,” researchers wrote.

“Although our findings do not imply a causative role for the lack of SWA reduction in the emergence of LID … they do suggest an association between sleep and some clinical [features] of PD and suggest a relationship between sleep disruption and LID,” they concluded.

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