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Women with Depression and Anxiety Are Largest Parkinson’s Group with Fibromyalgia, Study Finds

Parkinson's and fibromyalgia

A distinct population of people are diagnosed with both Parkinson’s disease and fibromyalgia, a study in Israel found, noting they tend to be women with mental health issues, such as depression and anxiety, who rely on painkillers more than other Parkinson’s patients.

The study, “Fibromyalgia-Like Syndrome Associated with Parkinson’s Disease—A Cohort Study,” was published in the Journal of Clinical Medicine.

Fibromyalgia is a chronic condition characterized by widespread pain in various parts of the body. Parkinson’s and fibromyalgia share clinical features like muscle stiffness, unusual pelvic and rectal discomfort, poor sleep, fatigue, and depression. Nonetheless, only one case study to date has detailed a patient with both diseases, the researchers said.

“Since PD [Parkinson’s disease] and FM [fibromyalgia] are two relatively common disorders, it is not uncommon for a neurologist, rheumatologist, or a pain specialist to encounter a patient suffering from both illnesses,” they added.

Investigators at the Ben Gurion University sought to retrospectively characterize this specific group of patients, looking at their demographics, comorbidities, and medication use.

The team searched the Clalit Health Services database between the years 2000 and 2015 for people diagnosed with Parkinson’s and fibromyalgia. Researchers identified Parkinson’s patients through the application of a medication tracer algorithm, and those with fibromyalgia based on medical records.

During this 15-year period, 2,606 people (1,220 women and 1,386 men; mean age 67.9) were diagnosed with Parkinson’s and 60 (2.3%) of them also had fibromyalgia (a fibromyalgia-like syndrome associated with Parkinson’s disease, referred to as FLISPAD).

The majority of those with both the neurodegenerative and rheumatic disorders were women (88.3%) diagnosed at a mean age of 63.95 for Parkinson’s, while their age at fibromyalgia diagnosis varied from 51.68 to 76.22 years. A majority — 77% — also received a fibromyalgia diagnosis after that of Parkinson’s disease.

This particular patient population also had a higher prevalence of depression, anxiety, dementia, hypertension, and heart failure.

Compared to those with Parkinson’s, patients with both conditions used different analgesics (painkillers) at higher rates as well as more antidepressants.

“This FLISPAD subgroup of patients are mostly female, younger at PD diagnosis with a higher rate of cigarette smoking, anxiety, and depression,” the researchers wrote. And they “consume more analgesic drugs, both over-the-counter (OTC) and prescription medications, including opioids.”

A diagnosis of depression or use of antidepressants tended to come a mean 3.5 years before a fibromyalgia diagnosis.

Results also showed that Parkinson’s and fibromyalgia patients purchased 21.3% more anti-parkinsonian medications than those who did not have fibromyalgia. Although not significant, this finding achieved borderline statistical significance.

“These patients present a challenge for physicians as they use more analgesics, psychotropic medications, and tend to also use more APDs [anti-parkinsonian drugs] over time. More research is needed to determine the etiology and determinants of this syndrome, the needs of patients and course of treatment, both for PD [Parkinson’s disease] and FM [fibromyalgia] symptoms,” the researchers concluded.

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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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Parkinson’s Medications Relieve Central Pain Better than Other Types of Pain, Study Finds

central pain, Parkinson's therapies

Treatment with standard Parkinson’s therapies, such as levodopa or dopamine agonists, can provide effective relief of central parkinsonian pain, but they may fail to manage motor symptoms in these patients, a study has found.

As many patients with Parkinson’s disease experience some type of pain, these findings suggest that clinicians should take an integrated approach to ensure adequate care for motor and non-motor symptoms in this population.

The study, “Unveiling the Relationship Between Central Parkinsonian Pain and Motor Symptoms in Parkinson’s Disease,” was published in the European Journal of Pain.

Pain is a common non-motor symptom in Parkinson’s patients, but little is known about its clinical characteristics and possible predictors.

Parkinson’s can affect the way patients experience pain, and it can lead to pain even in the absence of any evident cause for it. This is the case of central parkinsonian pain, which is characterized by a constant, aching type of pain affecting most of the body and is caused by Parkinson’s disease itself. This type of pain is poorly understood and can be difficult to treat.

Nuno Vila-Chã, MD, neurologist and researcher at Centro Hospitalar do Porto and the University of Porto, in Portugal, and his collaborators were interested in studying the prevalence and types of pain experienced by people with Parkinson’s. They examined the relationship between central pain and patient characteristics, as well as the impact of Parkinson’s targeted treatments on this type of pain.

They analyzed the clinical records, and performed interviews and neurological examinations of 292 patients with Parkinson’s, aged 63 to 79. The patients’ motor symptoms and degree of independence were assessed using different rating scales, while the patients were on medications (in the morning) or off medications. Anxiety, depression, and impulse control disorders (such as dopamine dysregulation syndrome) were also evaluated through patient-reported questionnaires.

Pain was categorized as central parkinsonian or non-central parkinsonian by a neurologist, based on the patients’ description of their pain. Central parkinsonian pain was defined as “burning, tingling, formication, or ‘neuropathic’ sensations, often relentless and bizarre in quality, not confined to root or nerve territory, and not explained by rigidity, dystonia, musculoskeletal, or internal lesion.”

Except for four patients, all (99%) were taking levodopa alone or combined with a dopamine agonist (taken by 39% of the patients), which included ropinirole (108 patients; brand name Requip, among others), pramipexole (two patients; sold as Mirapex and other names), and piribedil (three patients; sold as Trivastal, among other names).

Most patients (73%) reported feeling some sort of pain, which had lasted for a median time of five years. These patients classified it as either musculoskeletal (in 63% of the patients), dystonia-related (27%), central parkinsonian (22%), and/or radicular or neuropathic (9%).

About one-third (68 or 32%) of the patients reported that the pain developed before their Parkinson’s motor symptoms, and half (105 or 50%) said that they could achieve pain relief with antiparkinsonian therapy.

Many of them (78%) reported to have one type of pain, while some patients (22%) claim to experience two or more forms of pain. Many also complained of feeling pain everyday (63%) and rated it as moderate or severe (83%).

The team found that patients who experienced pain also were the ones with more comorbidities (particularly diseases affecting the bones and joints) and more severe motor symptoms.

These findings “confirmed that pain is a common non-motor symptom in Parkinson’s disease and that the presence of pain is associated with more severe motor manifestations of Parkinson’s,” the researchers wrote.

The researchers found that patients with central pain specifically had certain demographic and clinical characteristics. These patients were significantly younger, and their disease often started earlier, but had fewer comorbidities, compared with patients with non-central pain.

They also showed more disability related to pain and worse non-axial motor symptoms while on medications. Non-axial symptoms include all motor symptoms not related to speech, rigidity of the neck, posture and postural stability, and gait (which are considered axial symptoms).

The patients with central pain reported having greater relief in their pain with the medications they were taking for Parkinson’s, compared with those with non-central pain. Also, there was a tendency for more motor fluctuations in the subgroup of patients who took antiparkinsonian medication to relieve their pain.

“This set of demographic and clinical associations suggests the need for an integrated approach to motor and non-motor symptoms in the clinical care of Parkinson’s patients with central parkinsonian pain,” the researchers stated. Also, the association between pain and mood “appears to be weaker and even more complex in Parkinson’s” than in other diseases, they added.

Future studies should continue to search for a deeper understanding of central pain in Parkinson’s, the team noted, as “the improvement of central parkinsonian pain should be considered as a treatment outcome in Parkinson’s disease.”

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Review Study Provides Update on Treatments for Parkinson’s Non-motor Symptoms

non-motor symptoms, Parkinson's

Although there are now more treatment options available for non-motor symptoms in Parkinson’s disease, a lack of evidence on their effectiveness and safety means that more studies and new therapeutic strategies are needed, according to a review study.

The study, “Update on Treatments for Nonmotor Symptoms of Parkinson’s Disease — An Evidence‐Based Medicine Review,” appeared in the journal Movement Disorders.

The International Parkinson and Movement Disorders Society Evidence-Based Committee reviewed research published from 2011 through 2016 on Parkinson’s non-motor symptoms to help physicians select the most effective treatments and provide an update to a 2011 study.

Two online databases were searched, resulting in the inclusion of 37 studies with 20 patients or more. In all of the included studies, treatment lasted a maximum of six months, except for one low-quality safety study, meaning the recommendations do not cover long-term symptom management, the team noted. The studies included pharmacological, surgical, and nonpharmacological interventions, which had to be available in at least one country.

According to their level of evidence, the different approaches were classified as efficacious, likely efficacious, unlikely efficacious, non-efficacious, or with insufficient evidence. To address practice implications, the team also rated the interventions as clinically useful, possibly useful, and unlikely useful, not useful, or investigational.

Christopher G. Goetz, MD, president of the International Parkinson and Movement Disorders Society, noted the differences between this approach and practice guidelines issued by medical associations such as the American Academy of Neurology. In a Neurology Today article written by Susan Fitzgerald, titled “Which are the Most Efficacious Therapies for Nonmotor Parkinson Disease Symptoms?” he said that “guidelines are really culturally based,” and take into account “regulatory issues, access issues, and insurance issues.”

“With evidence-based methodology, we are strictly looking at the published evidence. We don’t tell you whether we recommend it (a specific therapy),” he added.

No clinical trials met the inclusion criteria for the treatment of anxiety disorders, excessive sweating, rapid eye movement behavior disorder, and olfactory or ophthalmologic dysfunction.

Six new studies were reviewed for depression. One addressed venlafaxine, characterized as efficacious, with an acceptable safety risk and no need for specialized monitoring, and clinically useful. This contrasted to amitriptyline, which has insufficient efficacy evidence to treat depression in Parkinson’s patients and was rated as possibly useful. Paroxetine, citalopram, fluoxetine and sertraline, all selective serotonin reuptake inhibitors (SSRIs), were categorized in a similar way.

Rotigotine, marketed as Neupro, was found unlikely efficacious based on the results of one study, and rated as investigational regarding practice implications. Rasagiline, marketed as Azilect, also showed insufficient evidence of efficacy and was classified as investigational as well.

As for nonpharmacological interventions, two studies on repetitive transcranial stimulation showed inconsistent effects on depression. However, its benefits in the general population and in specific measures in people with depression make this approach possibly useful for short-term treatment of Parkinson’s.

Cognitive-behavioral therapy (CBT) could only be rated as likely efficacious and has insufficient safety evidence in the treatment of depression in Parkinson’s due to the lack of replication of its benefits, the investigators cautioned.

Treatments for apathy were also evaluated. Rivastigmine, marketed as Exelon, was found efficacious in one study, but its small group of patients mean that this medication is only possibly useful in the clinic. A similar conclusion was reached for piribedil following deep brain stimulation. In contrast, Neupro was classified as unlikely efficacious based on one trial.

As for the treatment of impulse control disorders, naltrexone, marketed as ReVia, showed insufficient efficacy and safety evidence, while CBT was rated as likely efficacious and possibly useful clinically based on one new study.

Regarding dementia, Aricept (donepezil) and Razadyne (galantamine) still have insufficient efficacy evidence, but were rated possibly useful in clinical practice due to their established benefits outside Parkinson’s.

Both rasagiline and rivastigmine have insufficient efficacy evidence to treat cognitive impairment. A similar conclusion was reached for transcranial direct current stimulation and for cognitive rehabilitation in patients on computer-based cognitive training.

Three new studies were evaluated for psychosis. While olanzapine, marketed as Zyprexa, is not efficacious and therefore not useful from a clinical perspective, Nuplazid (pimavanserin) was characterized as efficacious over six weeks and clinically useful. Seroquel (quetiapine) has insufficient evidence though it is possibly useful in the clinic.

Studies of sleep disorders indicated that Lunesta (eszopiclone) and melatonin have insufficient evidence for the treatment of insomnia, but are possibly useful. Modafinil, marketed as Provigil, is also possibly useful for excessive daytime somnolence and sudden onset of sleep in people with Parkinson’s. Continuous positive airway pressure was considered likely efficacious and possibly useful in lessening daytime sleepiness in patients with obstructive sleep apnea, and Neupro was rated the same for improving sleep quality in Parkinson’s patients.

Assessed treatments of orthostatic hypotension — defined as a drop in blood pressure when standing up — included midodrine and fludrocortisone, marketed as Florinef. Although both have insufficient efficacy evidence, they are classified as possibly useful in the clinic due to benefits seen in clinical trials.

The only trial concerning urinary dysfunction addressed solifenacin, marketed as VESIcare, as a treatment for overactive bladder. It showed that this medication has insufficient evidence on efficacy, but is possibly useful in clinical practice due to benefits observed outside Parkinson’s, while having an acceptable safety risk without specialized monitoring.

One other study addressed erectile dysfunction. Viagra (sildenafil) was considered efficacious and clinically useful, with data in the general population indicating an acceptable safety risk.

Similar efficacy and clinically utility conclusions were presented for botulinum toxin B as a therapy for drooling. Both botulinum toxin type A and B should be administered by well-trained physicians with access to specialized monitoring tools, the researchers emphasized.

Three studies evaluated approaches for gastrointestinal dysfunction. Results of one trial led to lubiprostone, marketed as Amitiza, being considered likely efficacious and possibly useful to treat constipation in people with Parkinson’s. Its safety data in the general and elderly populations indicate that lubiprostone has an acceptable risk in Parkinson’s patients.

Probiotics were categorized as efficacious and clinically useful, which support their over-the-counter use and lack of safety concerns. In contrast, abdominal massages with lifestyle advice have insufficient evidence on safety and efficacy to ease constipation.

Rasagiline was also evaluated as an approach for fatigue, considered efficacious and possible useful based on one small study. One trial analyzed acupuncture in Parkinson’s, but although benefits were found, this approach still has insufficient efficacy evidence.

For pain, prolonged-release oxycodone-naloxone has insufficient evidence, but is possibly useful for Parkinson’s patients with chronic pain, with an acceptable safety risk without specialized monitoring. Rotigotine also has insufficient evidence as a way to lessen pain in Parkinson’s patients, despite benefits seen in one trial.

Overall, despite the substantial growth in the evidence base of approaches for non-motor symptoms in Parkinson’s, this update shows that treatment options remain limited, making the development and testing of new therapies “a top priority,” the team said.

According to Daniel Weintraub, MD, research on Parkinson’s psychiatric and cognitive symptoms is key due to the specificity of the disease compared with the same manifestations found in the general population. He also said this update may help investigators spot areas in need of clinical trials, such as anxiety.

Laura Marsh, MD, a professor of psychiatry and neurology at Baylor College of Medicine, cautioned that although the new review provides “a useful analysis for clinicians to consider,” they still have to practice “the art of medicine.” This involves challenges such as evaluating if dopaminergic therapies for motor function are causing non-motor side effects and what symptom to address first in people with more than one of these complications, she said.

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Parkinson’s Medicines May Contribute to Somatosensory Deficits, Study Finds

Somatosensory deficits

Antiparkinsonian medicines may cause Parkinson’s patients to develop abnormal sensitivity to temperature, touch and pain, according to a recent study.

The study, “Quantitative Sensory Testing (QST) in Drug-Naïve Patients with Parkinson’s Disease” was published in the Journal of Parkinson’s Disease.

The somatosensory system is composed of neurons that make the conscious perception of touch, pressure, pain, temperature, position, movement, and vibration possible.

Evidence supports that Parkinson’s patients have somatosensory deficits, including perception of temperature, touch and one’s body position in space. Moreover, and although there is still no clear physiological explanation for it, most Parkinson’s patients experience pain before motor symptoms’ onset.

However, most studies on this matter have been performed on medicated patients and have generated inconsistent results, which seems to imply that dopaminergic medication — the gold-standard Parkinson’s treatment — may influence patients’ somatosensory abilities.

To assess whether dopaminergic medication contributes to sensory processing abnormalities, researchers from the University Medical Center Hamburg-Eppendorf and the University Hospital Essen in Germany set up to investigate sensitivity to temperature, touch, and pain in Parkinson’s patients who had never taken antiparkinsonian drugs.

To do so, they used the well-established quantitative sensory testing (QST) protocol. Quantitative sensory testing determines the sensation and pain thresholds for cold and warm temperatures, and the vibration sensation threshold by stimulating the skin and comparing the results to normative values.

Researchers assessed 13 somatosensory parameters including cold and warm detection thresholds, perception of changing temperatures from warm to cold and vice versa, perception of cold as heat, cold and heat pain thresholds, mechanical detection and mechanical pain thresholds, sensitivity to pinprick stimuli, pressure pain threshold, vibration detection thresholds, experience of pain during innocuous dynamic tactile stimulation and temporal summation of pain (i.e. increased perception of pain to repetitive painful stimuli).

Nineteen dopaminergic, drug-naïve Parkinson’s patients (ages 42–82) and 19 age, sex and dominant hand-matched healthy subjects were examined.

Compared to the control group, somatosensory processing of drug-naïve patients was normal. However, previous research showed medicated Parkinson’s patients have increased sensitivity to temperature and pain plus reduced sensitivity to touch. Therefore, considering the results of non-medicated subjects, researchers assume the possibility of a role for dopaminergic medication in somatosensory disability.

Investigators also tested differences between the more affected body side and the less affected one, but no significant changes were observed. In addition, no relevant alteration was found in somatosensory characteristics of patients with or without disease-specific chronic pain and with distinct disease subtypes (tremor-dominant, akinetic-rigid or mixed).

However, age, but not disease severity, was negatively associated with warm and mechanical detection thresholds, suggesting a decrease in patients’ ability to sense temperature and touch with increasing age. Although less pronounced, these findings were also observed in elderly controls.

Of note, this study’s small sample size with an average disease duration of almost two years (a range of 6–67 months) could constitute a selection bias toward patients with less severe disease (because disease severity progresses with age/disease duration), which could in turn influence the analysis.

“[S]omatosensory abnormalities previously reported in medicated [Parkinson’s disease] patients might rather be a result of dopaminergic medication or may occur later in the course of the disease or with increasing age,” researchers said.

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Finding Words to Describe Parkinson’s Pain

pain

Parkinson’s disease (PD) pain is unique, so finding words to describe it is difficult. Not all those with a diagnosis experience pain. But for some, like me, pain is the major, disabling symptom. It is important to find words that describe the pain experience as clearly as possible. There is no “grin and bear it,” nor is this “a pity party.” Instead, this is a search for accurate articulation of the pain experience to help maintain quality of life.

Pain may be an early symptom of PD, according to a study presented at the 2018 World Congress on Parkinson’s Disease and Related Disorders titled “Pain: A marker of prodromal Parkinsons disease?” The American Parkinson Disease Association published research that supports the connection of pain with Parkinson’s, suggesting that if the pain is relieved with dopaminergic medication and the patient has a pattern of painful sensations that correlate to “off” episodes, more credence can be given to the idea that the pain is PD-related.

PD pain can resemble pain from other disease processes, especially as the patient ages and faces a multitude of other pain-causing conditions such as arthritis, spine degeneration, poor muscular conditioning, and such. In my case, PD pain is distinguished by the following:

  • The progression of body pain correlated with the progression of the disease over time.
  • Levodopa, a dopaminergic therapy, successfully reduces the pain.
  • The pain is worse during “off” periods.

My PD pain also has a particular characteristic: stinging (sometimes knife-jabbing), irritating tingling, burning, and muscle heaviness with increased pain on movement. This pain happens over large regions of the body and varies in severity. At its worst, it can last several days and reach level 7, inducing spontaneous tears.

PD with episodic chronic pain is disabling in several ways. First, high levels of pain obstruct clear thinking. Second, high levels of pain induce the fight-or-flight response, which interferes with emotion management. Third, the amount of energy necessary to manage it is very tiring (even more so in the face of the deep fatigue associated with PD). Chronic PD pain entails much more than body symptoms.

Parkinson’s pain is a total experience that touches thoughts, feelings, and relationships. Even when it’s a struggle, finding the words to describe pain experiences is imperative to maintaining quality of life in the face of a difficult diagnosis. Finding the right words helps one communicate the pain experience to care providers, family, and friends — a network of relationships that help form the foundation for quality of life. By communicating the pain, those close to me are more understanding of why I act the way I do, which helps to maintain those relationships.

Over the years, I have watched my PD progression. I have taken the warrior stance to do all I can to slow the progression. My hardest battle is with the total experience of chronic PD pain. Large blocks of time disappear into the fog of war. Over time, I have learned the importance of communicating about the pain daily, sometimes multiple times a day. My partner asks, “Where are you today?” I will say, “I’m at level 5,” followed by a quick mention of the most bothersome symptoms. In the past, I kept track of the pain levels throughout several months to create benchmarks. This is all part of finding the words to describe the Parkinson’s pain experience.

I have been a “communicator” most of my life, but it remains a struggle to find words that describe the unique character of PD pain. If you experience PD pain, please share your descriptors in the comments. Together we may find a common dialogue that will help others.

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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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How to Get Through the Cold of Winter

cold

Sherri Journeying Through

Winter has just about landed upon us, and it’s getting to be that time of year when we hang up garden tools, freeze-proof the outside water spigots, and pull out the heavy sweaters and rain boots. For many of us, it also means trying to get warm and comfortable with our Parkinson’s disease while freezing as we watch the snow fall outside our windows.

One of the inconveniences of Parkinson’s is that changes in temperature outside can create pain and discomfort.

When winter slowly creeps upon us, our symptoms can slowly intensify. Sometimes it’s hard to link the weather to our discomfort until one day we realize the seasons have definitely merged from one into another.

The crisp, cool days of autumn are just about over, and the frosty, frigid days of winter are almost here to stay.

Does the cold make your PD more unbearable? Most people with Parkinson’s would respond with a resounding yes. If you aren’t one of those people, be grateful. If you are, by now you’ve probably noticed more stiffness, especially in the evenings as the warmth of whatever sun remains slowly hides behind the horizon.

The winter months can cause your tremors to worsen. They can contribute to an increase in gait problems as well as problems with balance and stiffness. Pain can become your closest friend. 

How can you survive another winter?

When sleeping, try an electric blanket, which hopefully will eliminate the cold that often permeates the body and causes aches. Throw blankets used for the couch now come in heated varieties that make reading or watching TV more pleasant.

If you’re shopping for a new car, don’t forget to check out the heated seat option. They make trips, short or long, easier to bear.

To alleviate stiffness, arnica gel and magnesium spray have worked well for me to loosen up muscles.

Keep your feet warm and wear a sweater or sweatshirt. Layer up. Once you get a chill in your bones, it’s hard to get warm. When you go outside, put on some tights to give you an added layer of warmth. Warm up on the inside with a cup of tea or hot chocolate. And don’t forget the oldest remedy: Snuggle up with a good book in front of a roaring fireplace. If you don’t have a fireplace, light a candle and pretend.

Merry winter!

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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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Chronic Pain Common in Parkinson’s Patients and Weighs Heavily on Quality of Life, Study Reports

Chronic pain is prevalent in Parkinson’s disease patients and its severity considerably impacts their daily life, work, and social relationships, a  study aiming to guide physicians in better managing this symptom reports. It also links chronic pain to such psychological ills as depression, low self-esteem, frustration and sleep deprivation.
The study, “Negative impact of severity of pain on mood, social life and general activity in Parkinson’s disease,” was published in the journal Neurological Research.
Parkinson’s non-motor symptoms are often reported prior to a definitive diagnosis, and become more frequent and severe with disease progression.
Several studies have shown that many Parkinson’s patients have abnormal pain processing that could be affected by levodopa treatment. Pain is also believed to be associated with the reappearance of motor symptoms when the effects of levodopa wear off. However, the characteristics of pain associated with Parkinson’s disease, its causes and underlying mechanisms, and its psychological impact have not been thoroughly analyzed.
Previous research revealed that neurons involved in pain processing, mood, and motor functions may be connected, suggesting a higher prevalence of fibromyalgia — a chronic rheumatic condition that causes widespread pain — and chronic pain in Parkinson’s patients.
Researchers in Canada and Pakistan conducted a case control study to assess patients’ perception of pain, as well as its impact on their quality of life, measures in terms that included daily activities, mood, and social relationships.
The study included 100 Parkinson’s patients (mean age, 70.4) and 100 healthy age- and gender-matched controls (mean age, 69.4) visiting a community-based movement disorders clinic between June 2011 to June 2012. Patients with dementia and/or atypical Parkinson’s were excluded.
Chronic pain between the two groups was assessed using the Brief Pain Inventory (BPI), which measures pain severity (pain right now, pain at its worst and least since the last week), pain interference (disrupting  general activities, mood, walking ability, normal work environment, relationships with others, sleep and enjoyment of life) and pain frequency. A qualitative description of pain was also conducted.
Patients described pain as “exhausting,” “tiring,” “penetrating,” “miserable” and “unbearable” significantly more often than controls.
Among patients, those with depressive symptoms — as evidenced by a score of eight or higher in the Hospital Anxiety and Depression Scale (HADS) — reported pain as tender more frequently than those without depression. Controls with depressive symptoms were more likely to report pain as stabbing, tender and tiring compared to those without evidence of depression.
“These descriptions indicate a significant impact of pain on the psychological well-being of the patient,” the researchers wrote.
Subsequent analysis showed that patients overall scored higher than controls in “worst pain felt since last week” and in global pain severity. Among all participants with depressive symptoms, those with Parkinson’s had higher scores of worst pain felt and average pain felt since last week, as well as higher reported pain levels at the time of assessment and global pain severity than those in the control group.
Pain among Parkinson’s patients also interfered most with life quality, showing a greater impact that among controls on general activity, mood, walking ability, work, sleep, social relationships, and enjoyment. In agreement, these

Source: Parkinson's News Today

Parkinson’s Patients Have Greater Incidence, Duration, and Intensity of Low Back Pain, Study Reports

low back pain

Patients with Parkinson’s disease have a higher incidence, longer duration, and greater severity of low back pain than individuals without the disease, according to a study.

These findings also show that Parkinson’s patients with low back pain have a greater disability correlated with the severity of motor impairments.

The study, “The prevalence of chronic low back pain and lumbar deformities in patients with Parkinson’s disease: implications on spinal surgery,” appeared in the European Spine Journal.

Pain is a typical non-motor symptom of Parkinson’s disease, and has been regarded as one of the most troublesome. Skeletal and joint deformities are possible causes of pain in Parkinson’s patients. In particular, the lumbar region is more involved in musculoskeletal pain in these individuals.

Back pain seems to be a common and early symptom in Parkinson’s disease, and patients appear to be more often troubled by chronic low back pain, possibly due to a combination of altered posture, abnormal muscle tone, and truncal dystonia — uncontrollable muscle contractions in the trunk.

German researchers conducted an observational study to explore the association between low back pain and Parkinson’s by analyzing its prevalence, its underlying skeletal changes in the spine, and the relationship between spinal deformities and Parkinson’s-specific symptoms.

A total of 97 Parkinson’s patients at a mean age of 67.7 years, including 60 men, and 97 individuals used as controls at a mean age of 67.5 years, including six men, without the disorder or other neuromuscular diseases, filled out a questionnaire on the intensity of local lumbar back pain. The intensity of leg radicular pain — caused by inflammation and/or injury to a spinal nerve root – was quantified by the visual analogue scale (VAS) — a continuous scale used to measure pain intensity.

In addition, the participants’ permanent functional disability was assessed via the Oswestry Low Back Pain Disability Questionnaire (ODI) — a self-completed questionnaire that includes 10 different topics: intensity of pain, lifting, ability to care for oneself, ability to walk, ability to sit, sexual function, ability to stand, social life, sleep quality, and ability to travel.

Patients were further asked to describe the painful sensation they experience as pricking, tingling, burning, paresthesia — often described as feelings of pins and needles, or numbness — or other.

The team also assessed Parkinson’s duration, medications being used, severity of motor symptoms — as assessed by the Unified Parkinson’s disease rating scale part III (UPDRS III) — and the Hoehn and Yahr (H&Y) stage, which is a system used to assess symptom progression.

Low back pain was significantly more frequent (87.6%) and lasted longer (16 years) in Parkinson’s patients than in controls (64.9%, 11.8 years). Additionally, in patients with low back pain, the pain was more frequently (87.3%) located in the lumbar region compared with controls with low back pain. Lumbar pain intensity was also higher in Parkinson’s patients.

No differences were found on radicular leg pain frequency and intensity. The distribution of participants describing the sensation they felt as pain, pricking, tingling, burning, paresthesia or other was also not different between Parkinson’s patients and controls. Functional disability was also not different between the two groups.

According to the ODI results, minimal disability was reported by 43.8% of Parkinson’s patients, moderate disability by 27.5%, severe disability by 22.5%, and “crippled” by 6.3%.

Parkinson’s patients with or without low back pain did not differ in disease duration, H&Y stage, UPDRS III motor score, or medications. Higher ODI scores correlated with higher (worse) H&Y stages and UPDRS motor scores.

Patients with hypokinetic Parkinson’s — slow or reduced movement — experienced higher intensities of lumbar and radicular pain than those with tremor.

Fifty-four patients with low back pain had an X-ray of the lumbar spine. Of these, 43 (79.6%) showed arthritic changes, 21 (38.8%) had scoliosis — curvature of the spine — and 13 (24.1%) had spondylolisthesis, which refers to slippage or displacement of one vertebra.

Of the 85 Parkinson’s patients with low back pain, 20 (23.5%) were being treated by an orthopedic specialist, nine of whom had lumbar spine surgery, four received local injections or infiltrations, and seven were continuously treated with oral pain medications. The low number of patients undergoing surgery reflects the difficult surgical management of Parkinson’s patients with spinal deformities, according to the researchers.

Of the 63 controls with low back pain, 24 (38%) received orthopedic treatment. This greater percentage of treated controls compared with Parkinson’s patients supports the previous characterization of low back pain as an underestimated issue in the disease, the scientists observed.

“[Low back pain] and lumbar degeneration are common in [Parkinson’s disease]. Both are related to movement disorder symptoms. The knowledge about musculoskeletal conditions in Parkinson’s disease is important for an interdisciplinary conservative or operative treatment decision of [low back pain],” the researchers concluded.

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Source: Parkinson's News Today

Study Reveals Mechanisms Underlying Pain Processing in Parkinson’s Disease

pain, subthalamic nucleus

A novel pain-sensing brain network links pain in Parkinson’s disease to a specific region of the brain, called the subthalamic nucleus, an animal study has found.

The findings illustrate why this specific brain region is a potential target for pain relief in Parkinson’s, as well as in Huntington’s disease, and other neurodegenerative disorders.

The study, “Revealing a novel nociceptive network that links the subthalamic nucleus to pain processing,” was published in the journal eLIFE.

Pain is one of Parkinson’s non-motor symptoms and may manifest as burning, stabbing, aching, itching or tingling sensations. Scientists believe that these symptoms, which are not directly related to the pain caused by the disorder’s motor symptoms, result from dysfunction of the central nervous system.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN), a brain area involved in motor function that is hyperactive in Parkinson’s patients, is an effective technique to ease motor dysfunction. This surgical treatment also has been shown to weaken pain intensity, but the mechanism underlying this benefit remains unclear.

Early studies have indicated that the STN could be part of a network involved in pain perception, but little is known about the type of sensory stimulus activating this brain area.

“We set out to determine whether the [STN] is involved in translating a harmful stimulus such as injury into pain, and whether this information transmission is altered in [Parkinson’s],” Arnaud Pautrat, the study’s lead author, said in a press release.

The research team from France and the U.K. conducted electrophysiology (electrical activity) experiments in rats subjected to a shock to the hind paw. This showed that neurons in the STN could be separated into three groups, depending on whether their electrical activity increased, decreased or was unchanged upon being shocked. Most of the responsive cells changed their activity specifically after pain stimulation and not other types of stimuli.

Then, the team explored if damage to the STN changed these responses. Results showed that rats with lesions in this brain area took much longer to manifest discomfort in comparison to controls.

Subsequent experiments in a rat model of Parkinson’s revealed that neurons in the STN had higher firing rate (greater activity) and exhibited bigger and longer responses to pain than healthy animals. According to researchers, these findings suggest that Parkinson’s-associated pain is caused by impaired pain processing in this brain area.

To understand where pain signals in the STN could come from, the team focused on the superior colliculus and the parabrachial nucleus, two brain areas that relay damage signal originating from the spinal cord.

Blocking the activity or damaging these regions changed the number of STN cells responding to pain, revealing the key role of both regions. Also, researchers found that the parabrachial nucleus and the STN are directly connected.

“We have found evidence that the [STN] is functionally linked to a pain-processing network and that these responses are affected in Parkinsonism,” said Veronique Coizet, PhD, the study’s senior author. Of note, Parkinsonism is a general term for neurological disorders that cause movement problems similar to those of Parkinson’s patients.

Overall, the team believes this network is possibly implicated in the pain relief achieved with DBS in Parkinson’s patients. Coizet noted that more work is necessary to fully characterize the effects of DBS on the STN in animal models.

“The STN-DBS technique can thus be considered in the future as a new target for the treatment of pain in pharmaco-resistant patients suffering from previously described neurodegenerative disease, but also, for example, in chronic pain disease or pharmaco-resistant patients with certain form of migraine,” researchers wrote.

“Further experiments are now needed to fully characterize the effects deep brain stimulation on this brain region in our experimental models, with a view to finding ways to optimize it as a treatment for pain caused by Parkinson’s and other neurological diseases,” Coizet added.

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Source: Parkinson's News Today