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Depression Is Risk Factor for Impulse Control Disorders in Parkinson’s Patients, Study Finds

depression

Patients with Parkinson’s are at a greater risk of developing impulse control disorders (ICDs) if they are depressed, according to results from an international study.

The findings also revealed that treatment with dopamine agonists increases this susceptibility, and caution is advised when prescribing such therapies to depressed Parkinson’s patients.

The study, “Depression as a risk factor for impulse control disorders in Parkinson’s disease,” was published recently in the journal Annals of Neurology.

Depression and ICDs are two of the most common non-motor symptoms of Parkinson’s disease. However, while depression often precedes the onset of motor problems, ICDs are related to Parkinson’s treatment, especially to dopamine agonists. “This association with [dopamine agonists] makes ICDs a potentially avoidable disorder,” the researchers wrote.

Prior studies have shown that depression and ICDs often coexist in people with Parkinson’s, but were not able to assess whether depression increases the susceptibility for ICDs.

A team of Spanish researchers used data from the Parkinson’s Progression Markers Initiative, a multi-center clinical trial to identify biomarkers of Parkinson’s progression, to address this gap. A total of 354 patients were included, mostly from specialized university hospitals in the U.S. and Europe. None had ICD at baseline, as assessed with the Questionnaire for Impulsive Compulsive Disorders in Parkinson’s Disease.

ICD and medication use were evaluated at follow-up evaluations every three months initially, and every six months after visit four. The researchers also evaluated anxiety with the State-Trait Anxiety Inventory, apathy with the Movement Disorders Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), and sleep impairments via the REM sleep behavior disorder screening questionnaire.

At baseline, 54.8% of patients were aged between 60 and 75 years and 61.3% were men. The results showed that 68 participants (mean age 60.8 years, 13.3 months since diagnosis) had either depressive symptoms or were diagnosed with depression and taking antidepressants.

The prevalence of depression was higher in women than in men (27.78% vs 15.93%) and depressed patients did not receive dopamine agonists more frequently than non-depressed patients either at baseline or during follow-up.

Also, anxiety and apathy scores were higher in patients with depression (aged 61.6 years, 182 men, 12.7 months since diagnosis).

Over a median follow-up of approximately four years, the patients with depression at baseline showed a nearly two-fold greater risk of developing ICDs, as reflected in an incidence rate of 19.4 cases per 100 patient-years — a measure obtained by multiplying the number of persons at risk over time — compared to 10.3 cases in those without depression.

As shown previously, using dopamine agonists also increased the risk for ICDs. In fact, patients with depression had an ever greater risk of developing ICDs if taking these treatments. Controlling for multiple potential confounding factors — such as age, sex, apathy and anxiety — did not alter these findings.

“Our results show depression acts as a risk factor for the development of ICDs in [Parkinson’s] patients,” the scientists wrote.

“Notably, our results [also] show that the use of [dopamine agonists] in patients with depression is linked to a higher ICD risk,” they added. As such, dopamine should be used with caution in this patient population, the researchers commented.

Importantly, depression should be routinely monitored “to optimize medical decisions regarding the risk of developing ICDs.”

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High Corticosterone Levels a Risk Factor for Parkinson’s, Mouse Study Finds

corticosterone mouse study

High levels of corticosterone — a hormone that regulates energy, immune, and stress responses — is a risk factor for the development and progression of Parkinson’s disease, according to a mouse study.

The study, “Chronic corticosterone aggravates behavioural and neuronal symptomatology in a mouse model of alpha-synuclein pathology,” was published in the journal Neurobiology of Aging.

Parkinson’s disease is a neurodegenerative disorder mainly resulting from the gradual loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for controlling body movements.

This is a consequence of overproduction and misfolding of the protein alpha-synuclein in neurons, which leads to the formation of small toxic deposits called Lewy bodies that gradually damage and kill nerve cells. Growing evidence has demonstrated that these alpha-synuclein aggregates are associated with Parkinson’s onset and progression.

“Injection of alpha-synuclein preformed fibrils (PFFs) in different brain regions … induces pronounced alpha-synuclein pathology [aggregate] propagation. Interestingly, in these [mouse] models the amygdala is among the brain regions most severely affected by alpha-synuclein pathology [disease],” the researchers wrote.

The amygdala is an area of the brain involved in memory, decision-making, and emotional responses. Several non-motor symptoms in Parkinson’s, including anxiety and depression, have been linked to structural alterations and functional impairments of the amygdala.

“Similarly, chronic stress and glucocorticoid [imbalance] change amygdala physiology [function], and indeed are involved in the development of anxiety and depression,” they wrote.

The group of researchers from the Brain Mind Institute at the École Polytechnique Fédérale de Lausanne in Switzerland set out to investigate if mood/emotional alterations linked to amygdala dysfunction might accelerate the formation and propagation of alpha-synuclein aggregates associated with Parkinson’s in a mouse model of the disease.

To test their hypothesis, they first treated mice with corticosterone, a glucocorticoid that is normally produced in response to stress, to mimic the effects of depression and chronic stress in the amygdala.

Animals were then injected on one side of the brain’s striatum — a region involved in motor and cognitive control — with either alpha-synuclein preformed fibrils to trigger the formation and propagation of alpha-synuclein aggregates across the whole brain, or with a saline solution (vehicle control).

Chronic treatment with corticosterone triggered depression in animals and had a strong effect on their body shape, fat deposition, body weight, and drinking and eating habits. Injection of alpha-synuclein preformed fibrils had no effects on any of these parameters.

Behavioral tests performed one to two months after the injection of alpha-synuclein showed that animals that had been injected with these fibrils displayed mild anxiety, which was reversed by corticosterone treatment.

However, they found that chronic treatment with corticosterone in animals that had been injected with preformed fibrils led to the accumulation of phosphorylated alpha-synuclein in specific regions of the brain, including the entorhinal cortex, a region involved in memory, spatial navigation, and time perception.

Alpha-synuclein phosphorylation is a chemical modification in which a phosphate group is added to the protein. It is known to occur in Parkinson’s disease, and is thought to be a critical step in disease progression, as it enhances alpha-synuclein’s toxicity, possibly by increasing the formation of aggregates.

They also discovered that treatment with corticosterone in mice that had been injected with alpha-synuclein fibrils increased the loss of dopaminergic neurons.

“We report aggravated alpha-synuclein pathology [disease] and neurodegeneration in mice injected with alpha-synuclein [preformed fibrils] in a condition of heightened corticosterone, suggesting heightened glucocorticoid levels as a risk factor for the development of the neuropathological hallmarks of Parkinson’s disease and potential target for treatment,” the researchers wrote.

“Further studies aimed at elucidating the vulnerability factors of specific brain regions to alpha-synuclein pathology, and why at some point resilience fails and neurodegeneration (such as in the substantia nigra) occurs, are needed and will greatly enhance our understanding of the role of alpha-synuclein pathology in the [development] of Parkinson’s disease and synucleinopathies,” they added.

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Low Vitamin D Levels Linked to Added Falls, More Sleep Problems, Depression, Study Shows

low Vitamin D

Low vitamin D levels are associated with a greater tendency for falls, sleep problems, anxiety, and depression in people with Parkinson’s disease, according to a recent study.

The findings, “Relationship between 25‐Hydroxyvitamin D, bone density, and Parkinson’s disease symptoms,” were published in the journal Acta Neurologica Scandinavia.

Vitamin D deficiency and low bone mass are frequently observed in people with Parkinson’s disease (PD). In fact, one particular study found that lack of this vitamin is more common in people with Parkinson’s (55% of patients) than other populations, such as people with Alzheimer’s disease (41% of patients).

But the relationship between vitamin D levels and Parkinson’s has remained controversial. Some studies suggest that taking vitamin D3 — a form of vitamin D used in supplements — can stabilize the disease, while others see no relation with the risk of Parkinson’s.

However, most studies have focused on limited aspects of the disease and did not include important outcomes — notably, non‐motor symptoms.

Vitamin D has a vital role in bone health, since it promotes calcium absorption and bone mineralization, which keeps bones strong and healthy. It also blocks the release of parathyroid hormone (PTH), an hormone that promotes bone tissue reabsorption and bone thinning.

Some studies support that lack of vitamin D results in a greater risk of falls and fractures in Parkinson’s patients, which can increase hospitalization and even fatal disability. Its levels also have been associated with cognition and mood, as well as stomach malfunction, in people with the disease.

While it is possible that deficits in this vitamin impact several symptoms of PD, the connection remains unclear.

To shed light on this relationship, researchers at the Second Affiliated Hospital of Soochow University and Soochow University, in China, set out to determine if vitamin D levels correlated with bone mineral density (BMD) and non‐motor symptoms in Parkinson’s patients.

The team measured blood levels of 25-hydroxyvitamin D, or 25(OH)D — a precursor of the active form of vitamin D and the most accurate indicator of vitamin D levels in the body — and performed extensive clinical evaluations in 182 Parkinson’s patients as well as 185 healthy people (controls).

Participants were recruited from the Second Affiliated Hospital of Soochow University from March 2014 to December 2017.

Bone mineral density — a measure of bone mass and health — was measured at the lumbar spine and the top of the femur (thigh bone) by bone densiometry, which measures bone loss.

The data showed that people with Parkinson’s had significantly lower vitamin D levels in the blood compared with healthy controls — an average of 49.75 versus 43.40 nanomol per liter of 25(OH)D.

In agreement, low levels of vitamin D (below 50 nmol/l) also were more common in Parkinson’s patients (68.68%) than controls (54.05%).

People with lower vitamin D levels were more likely to fall and experience sleep problems, including difficulty in falling asleep (insomnia). They also had significantly more depression and anxiety.

Mean bone densities in both the spine and femur were lower in PD patients, however no correlation was seen between the levels of BMD and vitamin D.

“Together, these results indicate that vitamin D deficiency may play a role in PD pathogenesis [disease manifestations], while vitamin D supplementation may be used to treat the non‐motor symptoms of PD,” the researchers  said.

“As various non-motor symptoms place a burden on individuals with Parkinson’s disease and their caregivers, vitamin D might be a potential add-on therapy for improving these neglected symptoms,” study’s senior author Chun Feng Liu, MD, PhD, said in a press release.

However, the researchers stressed that future studies with a larger sample size are necessary to clarify the role of vitamin D in Parkinson’s disease.

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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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Panic Attacks Can Go Hand-in-Hand with Parkinson’s Disease

panic attacks

Twice in the past month I have had what I am calling panic (anxiety) attacks, which are something I had never experienced before. I had shortness of breath and my heart was beating much faster than normal. Since the only activity I was involved in at the time was trying to go to sleep, it concerned me. It scared me enough that I told my husband about it the following day.

I consulted Dr. Google and here’s what I found:

A study showed that panic attacks in Parkinson’s disease could possibly be a long-term complication of levodopa therapy. The keyword here is “possibly,” which isn’t definitive enough for me, plus the study is from 1993. I skipped that one and continued my search.

Dr. Google led me to the Parkinson’s Foundation, which stated, “Anxiety is a common non-motor symptom of PD. It is important to note that anxiety is not simply a reaction to the diagnosis of Parkinson’s, but is instead a part of the disease itself, caused by changes in the brain chemistry of the brain.”

It went on to say that, “Anxiety (or panic) attacks usually start suddenly with a sense of severe physical and emotional distress. Individuals may feel as if they cannot breathe or are having a heart attack. They may feel they are experiencing a medical emergency. These episodes usually last a few minutes to an hour, particularly when associated with ‘off’ periods, though they can last for longer periods of time.” 

Several different sources agree that some of the symptoms of a panic attack can be trouble sleeping, heart palpitations, hyperventilating, uncontrollable worry, chest pain, dizziness, tunnel vision, and hot or cold flashes.

Bingo. They hit that nail on the head.

The list goes on and it can be hard to diagnose what is happening, as the symptoms mimic other possibilities of what could be going on. 

When I identified what I believed to be the culprit (a panic attack), I made a note to bring it up at my upcoming appointment with my neurologist. Until then, I decided to rely on the hope and faith I had within me. I forced myself to breathe normally and drew deep upon that faith. The attack finally subsided and I was able to quit worrying about getting the porch fixed and the gate repaired and the shower installed and the sink replaced and …

Here I go again … 

This time I’m diving deep into that faith before the panic kicks in. 

***

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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Yoga Decreases Anxiety and Depression More Than Resistance Training, Study Finds

yoga, mindfulness

Mindfulness yoga seems to be better than conventional exercise at alleviating depression and anxiety in people with Parkinson’s disease, according to a recent study.

The study with that finding, which was published in the journal JAMA Neurology, is titled, “Effects of Mindfulness Yoga vs Stretching and Resistance Training Exercises on Anxiety and Depression for People With Parkinson Disease.”

It’s well-established that exercising regularly has a multitude of health benefits for people with Parkinson’s. Exercising also is known to have psychological benefits, particularly when a mindfulness component is incorporated.

In the study, the mental health effects of mindfulness yoga and more conventional stretching and resistance training exercises were compared head-to-head.

Researchers recruited 138 adults with Parkinson’s disease at four community rehabilitation centers in Hong Kong, between Dec. 1, 2016, and May 31, 2017. All patients had a clinical diagnosis of idiopathic (of unknown cause) Parkinson’s disease and were able to stand unaided and walk with or without an assistive device.

Individuals were assigned randomly to participate in mindfulness yoga (71 people) or resistance exercises (67 people). A slim majority (52.9%) of the participants were female, the average participant age was 63.6 years, and both groups were similar in terms of demographics, etc., although slightly more in the yoga group were less educated and lived at home.

Both interventions consisted of weekly classes offered once per week, with participants encouraged to practice at home, too. Average attendance rates for the eight-week intervention were 6.1 classes for both groups, and about three-quarters of participants in both groups reported actually practicing at home. Over the course of the study, some participants dropped out for reasons that included disinterest and scheduling conflicts; dropout rates were comparable between the two groups.

Before and after the intervention, depression and anxiety were measured using the Hospital Anxiety and Depression Scale.

In the yoga group, anxiety scores decreased from 6.32 before the intervention to 3.04 afterward; this decrease was significantly larger than the decrease seen in the resistance exercise group (5.66 to 4.95). Similarly, depression scores in the yoga group decreased significantly more than those in the conventional exercise group (6.69 to 3.53 vs. 6.16 to 6.00).

Motor skills also were assessed (via the MDS-UPDRS), and similar improvements were observed in both groups: a decrease from 34.90 to 22.41 in the yoga group, and from 31.64 to 23.25 in the resistance exercise group. Of note, higher MDS-UPDRS scores reflect worse motor capacity.

The data suggest that, while both interventions provide comparable physical benefits, the mental health benefits of mindfulness yoga are superior to those of stretching and resistance training exercises.

A few instances of mild knee pain in both groups were the only adverse side effects reported; these were resolved without medical intervention.

“These findings suggest that mindfulness yoga is an effective treatment option for patients with [Parkinson’s disease] to manage stress and symptoms,” the researchers concluded in their paper, adding that “[f]uture rehabilitation programs could consider integrating mindfulness skills into physical therapy to enhance the holistic well-being of people with neurodegenerative conditions.”

Limitations of this study include the small sample size and the fact that participants were fully aware of which group they were put into, so it’s possible that participant bias may have influenced the results.

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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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Are You the Light in Someone’s Darkness?

Traveling through Parkinson's

I attend my boxing class twice a week. Regardless of whether she is having a good or not-so-good day, Kathy, another woman in my class, will be smiling. Not only will she be smiling, but she will be giving away words of encouragement. I often hear her thanking one of the coaches or the occasional volunteers for something they have done — not for her, necessarily, but for the entire class, like showing up for us.

It’s not that the rest of us aren’t thankful or don’t appreciate what is done for us, but Kathy goes a step further and thanks them — every time. She is illuminating the journey to being found.

What do I mean by that?

Panorama: The Journal of Intelligent Travel introduced its fifth issue, titled “Lost,” by saying, “The word lost originates from the Old English losian, meaning to perish. While this collection features many narratives of loss, it also illuminates the journey to being found.”

Having Parkinson’s disease can feel like being lost. It can sometimes feel as if you are all alone, wandering by yourself on a journey of endless twists and turns, unable to see what is coming around the next bend. You feel like you are slowly fading from who you once were into someone you no longer recognize.

You may have once been calm, while now you are anxious. At one time, you may have been a great orator, whereas now you fret over holding a simple conversation with a friend. You may have won medals for being the fastest runner on your college track team, but now you don’t dare go anywhere without your cane to stabilize you.

It’s hard to come to terms with something like Parkinson’s disease, and it’s easy to feel lost and misplaced. To feel like you’re living someone else’s life and not the one you thought you’d be living. It’s hard to go around greeting people cheerfully while you’re dealing with a disease you’d rather not have. 

Let’s just say it, shall we? Let’s just be honest. Sometimes, we don’t just feel lost, we feel as if we are perishing faster than we’d hoped and in a manner we never dreamed of. But there were people who found us slumped over alongside the path we have found ourselves on with this disease. They sat down beside us, told us they’ve “been there, too,” and helped us get back up. They brought light to our dark world and showed us we can smile and be thankful once again.

Is there someone who is a light in your life? Someone who illuminated your path while you felt lost and alone? Pay it forward. Be a Kathy, a light in their darkness.

***

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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You’re Not a Pack Mule: Release Your Burdens

Sherri Journeying Through Parkinson's

I was reading through some forums for Parkinson’s disease recently and came across one that was talking about stress. I am a fairly calm, even-keeled person who handles stress pretty well.

I thought so anyhow.

The woman who brought up the topic of stress said she had felt like her “meds were not working.” 

Check. That has been my story for the past week.

Then she had her regular Parkinson’s exam and found out she was actually doing quite well. Her movement disorder specialist, after further testing, said that this woman’s anxiety was what was making her feel “like crap.”

The other night, I had my boxing class. What started out well ended up badly — in my mind, anyhow. My meds wore off much too soon. They’ve been fizzling out at about the three-hour mark lately, but I was lacking coordination at only an hour and a half into my last dose. 

This isn’t good, I thought to myself, while punching out my frustrations on one of the jelly bags.

That night, I cried myself to sleep over all the things I had been worrying about lately. Most of these things will probably never happen, but try telling that to someone who is stuck in her head, and her head keeps telling her that they might happen. As I lay there, it became harder to breathe. My legs began to ache, and rigidity set in. It was a long night.

The next morning, my husband and I went for a walk at the mall. We stopped for coffee and had a heart-to-heart talk. All my worries began to pour out of me. And just when he and I thought that was it — that there was nothing more to say — there was plenty more. But you know how much better you can feel after a good cry, even if everyone sitting around you wonders why you’re blubbering at the table? You feel as if your burdens have been lifted.

Lifting something is raising it to a higher level, and the only higher level I know or put my hope in is God. I believe my burdens are raised to someone who can actually help. I pictured my husband unlocking the clasps that had held those burdens tightly to my back and saw God lift up and off what was weighing me down recently. The minute I felt my worries and cares leave, peace and calm settled back within me.

A woman who responded to the original forum post said something like, “Stress is our enemy [of Parkinson’s disease] and hope is our ally.”

How very true. 

Hope is here for today. For you. For me.

That heavy pack of burdens that is strapped to your back is not a permanent accessory for your journey with this disease.

Let it go. You were never meant to carry it alone. Let it be lifted up and off of you. 

Now, doesn’t that feel better?

***

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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Mindfulness Exercises Lessen Stress, Anxiety Symptoms Among Caregivers of Veterans, Study Shows

mindfulness therapy

Mindfulness-based interventions can improve mental health status, including reduction of stress and anxiety levels, in family caregivers of veterans with Parkinson’s disease and other health issues, a study shows.

The study, “A Pilot Randomized Controlled Trial of a Mindfulness-Based Intervention for Caregivers of Veterans,” was published in the journal Mindfulness.

Beyond combat-related physical injuries, U.S. military veterans often suffer from a wide variety of mental health issues, including Parkinson’s disease. In most cases, responsibility of daily care of these patients lies on informal caregivers, typically family members, who are the backbone of long-term care.

Recognizing the challenges and difficulties that are associated with caregiving, U.S. federal legislation was introduced to provide caregivers with financial and emotional support in the form of mentoring, support groups, and respite care. However, these strategies may fall short, as respondents from a Patient Aligned Care Team (PACT) survey reported a lack of focus on caregiver mental health outcomes.

“While the Veterans Administration, the Dole Foundation, and other organizations are providing services, there’s research to suggest that some services often don’t match caregivers’ needs,” Sandraluz Lara-Cinisomo, PhD, said in a press release written by Sharita Forrest. Lara-Cinisomo is an assistant professor at the University of Illinois at Urbana–Champaign and lead author of the study.

“Furthermore, there’s been little research that has evaluated the effectiveness of current caregiver services,” she added.

In fact, compared with caregivers in the general population, informal caregivers of veterans are reported to have poorer mental health, as shown by higher levels of psychological distress and “caregiver burden,” highlighting the emotional, physical, and financial strains of caregiving. Moreover, evidence suggests that the physical and stressful demands experienced by those caring for military veterans are double those of other caregivers.

This underscores the need for more effective interventions to improve mental health outcomes among informal caregivers of veterans.

Researchers evaluated the potential of mindfulness-based intervention at improving perceived stress, depressive symptoms, anxiety, and worry among caregivers of veterans.

The pilot study recruited 23 caregivers, the majority being women caring for their spouses. They were randomized to undergo mindfulness intervention or to be included in a control waitlist group.

The majority of the participants had been caregiving for more than nine years, spending between 21 to 30 hours per week focused solely on the veterans’ needs, Lara-Cinisomo said. Also, 78% of the caregivers showed signs of moderate-to-extreme emotional stress resulting from their caring activities.

Participants underwent the mindfulness program for eight weeks, which included a weekly class of mindfulness exercises, such as sitting, walking, body scans, hearing and seeing meditations, and mindful stretching. They also were encouraged to practice these exercises at home during 30 to 40 minutes daily, with the help of an audio CD, until the next class.  They spent on average 19 minutes per week performing the mindfulness activities at home.

Caregivers in the waitlist control group did not receive any instructions or educational materials during the eight-week intervention time, but were offered mindfulness instructions following that period.

Overall, the mindfulness program was found to have a significant positive effect on caregivers’ perceived stress, anxiety, and worry compared to those in the waitlist group. Specifically, 91% of the caregivers in the mindfulness group reported less perceived stress and anxiety, and 73% experienced less depressive symptoms and worry.

“Despite our small numbers, we were able to show that mindfulness helps and that it should be pursued not only by researchers, but by practitioners and those providing services to this population,” Lara-Cinisomo said.

In contrast, only 42% of caregivers in the control group reported a reduction in perceived stress, depressive symptoms, and worry, while anxiety symptoms were lessened in 33% of them.

“Given these promising results, policymakers, health practitioners, and veteran-related programs should increase efforts to provide caregivers of veterans with mindfulness-based interventions to improve mental health outcomes,” researchers wrote.

Researchers plan to explore other potential benefits of mindfulness for this population, such as whether mindfulness-based interventions also may improve caregivers’ and veterans’ quality of sleep.

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