Study Identifies Biomarkers for Motor, Cognitive Decline in Early Parkinson’s

early Parkinson's biomarkers

Urate, a salt derived from uric acid, and homocysteine, an amino acid, may predict motor and cognitive decline in early Parkinson’s disease, researchers report.

The study with that finding, “Urate and Homocysteine: Predicting Motor and Cognitive Changes in Newly Diagnosed Parkinson’s Disease” was published in the Journal of Parkinson’s Disease.

Low levels of urate have been associated with a higher risk of developing Parkinson’s over the subsequent 15 to 20 years. Low urate plasma concentrations also have been linked to cognitive decline, including poorer performance in attention, executive, and visuospatial functions.

High levels of homocysteine — an amino acid produced by the body, usually as a byproduct of consuming meat — also has been reported to increase the risk of dementia in older adults, suggesting it may play a role in the development of Parkinson’s disease dementia (PDD).

Researchers at Newcastle University, London, England, examined the association between urate and homocysteine levels, disease progression and cognitive status over 4.5 years in early Parkinson’s disease.

A total of 154 recently diagnosed Parkinson’s patients (100 men and 54 women, mean age 66.4 years) and 99 age-matched control subjects (54 men and forty-five women, mean age 67.9 years) underwent medical assessment by a movement disorders specialist. Participants with Parkinson’s disease were evaluated in the “on” motor state (when medication is taking effect and has not worn off) and patients were able to move smoothly.

Data on disease duration, concurrent diseases, medications, smoking history, and alcohol consumption were collected.

Motor symptoms’ severity was quantified using the Movement Disorders SocietyUnified Parkinson’s Disease Rating Scale (MDS-UPDRS) Part III and the Hoehn and Yahr scale. Cognition was assessed using the Montreal Cognitive Assessment (MoCa).

Blood samples were drawn only at the study participants’ initial visit and screened for urate, homocysteine, red cell folate (to measure the body’s store of folic acid) and vitamin B12 (an essential nutrient mainly present in meat and fish). Participants were examined  four times: at the study’s initial visit (baseline) and then at 18, 36 and 54 months.

At the first visit, 73% of Parkinson’s patients were levodopa (L-DOPA) naïve, meaning they were not yet taking prescribed anti-parkinsonian medications. No significant differences were found between treated and levodopa naïve patients regarding serum urate and serum homocysteine levels.

Participants with Parkinson’s disease had significantly lower baseline urate concentrations (302.7 μmol/L) than healthy controls (331.4 μmol/L). This also was true after 18 and 36 months.

On the contrary, plasma homocysteine levels were significantly higher than those observed in healthy controls, both at baseline (11.1 vs. 9.6 μmol/L) and at 18 and 36 months.

Lower urate concentration and higher homocysteine levels were associated with worsening of motor function in early diagnosed Parkinson’s patients. However, only higher homocysteine levels at baseline correlated with worse cognitive scores over 4.5 years of follow-up.

The findings suggest both urate and homocysteine can be biomarkers that help predict motor function decline, while only homocysteine predicts cognitive changes in early Parkinson’s disease.

“These findings lend support to the hypothesis that oxidative stress may play a role in the pathophysiology of PD [Parkinson’s disease] and that motor and cognitive aspects of the disease may have overlapping but separate mechanisms,” researchers wrote.

Of note, oxidative stress is an imbalance between the production of free radicals and the ability of cells to detoxify them, resulting in cellular damage as a consequence of high levels of oxidant molecules.

“In addition to potential disease modification, our findings suggest that determining urate and homocysteine concentration at the outset may have a role in predicting patients with PD [Parkinson’s disease] at greater risk of decline in motor and cognitive function,” they concluded.

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Exercise Improves Cognitive Function in Parkinson’s, Review Finds

Exercise and Parkinson's

Exercise has the potential to improve cognitive function in people with Parkinson’s disease, and has positive effects on motor symptoms, according to a recent literature review study.

“The potential of exercise to improve motor and non-motor symptoms is promising and may help to decelerate disease progression in individuals affected by [Parkinson’s disease],” Tim Stuckenschneider, MA, the study’s first author, said in a press release.

The review, “The Effect of Different Exercise Modes on Domain-Specific Cognitive Function in Patients Suffering from Parkinson’s Disease: A Systematic Review of Randomized Controlled Trials,” was published in the Journal of Parkinson’s Disease.

Various types of exercise — aerobic training, resistance training, forced exercise training, dance and balance training — have been shown to improve motor symptoms in Parkinson’s disease (PD). Those symptoms include tremor, gait disturbances, postural instability, and bradykinesia (the progressive slowness of movement over time).

However, the impact of exercise on Parkinson’s non-motor symptoms is not as clear, especially regarding patients’ cognitive function.

Prior research has shown that aerobic and resistance training, either alone or combined, may improve cognitive function; however, some reports failed to see a positive association.

These conflicting results may be linked with the different types of exercises, but also suggest that the benefits of exercise may be function-specific — linked with attention, processing speed, executive function, memory, or working memory.

Researchers at the Institute of Movement and Neurosciences, German Sport University, Cologne, Germany and colleagues at the School of Health and Sport Sciences, University of the Sunshine Coast, Queensland, Australia, performed a comprehensive literature review of randomized clinical trials that evaluated the effects of various types of exercise — coordination, resistance, and aerobic —on specific cognitive function in people with Parkinson’s.

“Physical exercise is generally associated with increased cognitive function in older adults, but the effects in individuals suffering from PD are not known,” Stuckenschneider said.

Eleven studies comprising 508 patients (mean age 68) were included (trials performed up to March 2018). Patients’ disease severity ranged from mild to severe (scores from 1 to 4 in the Hoehn & Yahr stage scale, which  measures Parkinson’s symptom progression and disability level).

The study’s main outcome was overall cognitive function, which was subcategorized in specific domains, including attention, executive function (cognitive processes necessary to control behavior), speed of processing (the time it takes to do a mental task), and memory. The Unified Parkinson’s Disease Rating Scale (UPDRS), commonly used to assess both motor and non-motor symptoms, was included as a secondary outcome.

Exercise intervention varied between four and 26 weeks, with exercise frequency varying from one to three times a week. Five studies analyzed the effects of aerobic exercises; one the effects of resistance exercises. Five studies analyzed the effects of coordination exercises; three the effects of combining resistance and coordination exercises.

Any form of exercise had a positive effect on executive function, attention and memory compared to no exercise. No benefits were seen for speed of processing. Aerobic exercise, however, tended to best improve memory in Parkinson’s patients.

Global cognitive function also showed a tendency to improve after aerobic, resistance, and combined resistance and coordination exercises, but not after coordination exercises.

Importantly, general exercise tended to improve Parkinson’s symptoms as shown by the UPDRS scores.

Researchers say their “findings suggest that clinicians and researchers should be encouraged to prescribe exercise in individuals with PD; however, further evidence is required to confirm the optimal form of exercise.”

Stuckenschneider said, “Exercise therapy needs to be, and often already is, an essential part of therapy in individuals with PD. However, it is mostly used to treat motor symptoms. As part of a holistic therapy, the potential of exercise to maintain or improve non-motor symptoms such as cognitive function in individuals with PD needs to be acknowledged, and the most effective treatment options need to be defined.

“This will not only help practitioners to recommend specific exercise programs, but also ultimately improve the quality of life of the individual. Our work shows that ‘exercise is medicine’ and should routinely be recommended for people with PD to help combat both the physical and cognitive challenges of the disease.”

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Deep Brain Stimulation May Increase Dementia Risk in Some Parkinson’s Patients, Study Suggests

deep brain stimulation

Parkinson’s disease patients with mild cognitive impairment who undergo deep brain stimulation are at a higher risk of cognitive decline and dementia, a long term “real-life”study suggests.

The study, “Longterm outcome of cognition, affective state, and quality of life following subthalamic deep brain stimulation in Parkinson’s disease,” was published in the Journal of Neural Transmission.

Subthalamic nucleus-deep brain stimulation (STN-DBS) is a surgical treatment for Parkinson’s motor symptoms where a device that generates electrical impulses is implanted into specific regions of the patient’s brain.

Increasing evidence suggests that STN-DBS significantly improves motor symptoms as well as some non-motor symptoms, such as sensory issues and sleep disturbances. However, some reports point to a potential decline in cognition in Parkinson’s patients following STN-DBS.

Researchers here investigated the cognitive status of 104 Parkinson’s patients who received STN-DBS for nine years, from 1997 and 2006, at a single center in Germany.

Neuropsychological data from before the surgery were available for 79 of the patients, of whom 37, diagnosed with Parkinson’s for more than 11 years, were followed long term for a median of 6.3 years after surgery. During this time, they underwent several neuropsychological and motor tests.

In the remaining 42 patients, no follow-up was possible due to patients’ death (21 of the cases), loss of contact (nine patients) and patients’ refusal to undergo follow-up (12 patients).

Researchers measured patients’ dementia rate (using the Mattis dementia rating scale) and cognitive status, focusing on five domains — memory, executive function, language, attention, and working memory — mood (depression and anxiety), and quality of life using the Parkinson’s Disease Questionnaire and the 36-item Short-Form Health Survey.

Motor function was assessed using several motor tests, including the Unified Parkinson Disease Rating Scale motor subscore (UPDRSm) and Hoehn and Yahr Stage, a widely used clinical rating scale, with broad categories of motor function in Parkinson’s.

Prior to the surgery, 28 patients (75.7%) had mild cognitive impairment, while nine patients (24.3%) had normal cognitive function. Moreover, no patients showed signs of Parkinson’s-related dementia.

Patients in the two groups — with and without mild cognitive impairment — showed no differences in age, disease duration, response to treatment, and dosage with levopoda, motor function, and education. Mood and quality of life were also similar.

Patients’ verbal intelligence, measured by a multiple choice word test, and memory were lower in the mild cognitive impairment group.

After undergoing STN-DBS, 18.9%, or seven, of the patients had no cognitive impairment, while the remaining patients (41%) were diagnosed with either mild cognitive impairment (15 patients) or dementia (15 patients).

Mild cognitive impairment has been previously identified as a risk factor for dementia in Parkinson’s patients. Twenty-eight patients categorized as having mild cognitive impairment before STN-DBS developed dementia within 6.3 years after surgery.

Researchers observed a trend, although not statistically significant, between mild cognitive impairment before STN-DBS and progression to dementia according to the patients’ age, sex, and education at the beginning of the study.

Compared with non-demented Parkinson’s patients, those with dementia had longer disease duration (15 years versus 20.2 years, respectively) and more severe motor impairments (UPDRSm score of 23.7 versus 36.1), with demented patients showing a faster progression of several typical Parkinson’s symptoms — bradykinesia (slowness of movement), rigidity, impaired speech, posture, gait, and postural stability.

In general, researchers observed a decline in cognition, including memory and language, in all STN-DBS-treated patients in the 6.3 years after surgery. However, partial working memory (also referred to as short-term memory) was preserved and slightly improved in some cases.

Disease duration, but not age, at the time of DBS surgery had a significant relation to the risk of developing dementia.

“This observational, ‘real-life’ study provides long-term results of cognitive decline in STN-DBS-treated patients with presurgical [mild cognitive impairment] possibly predicting the conversion to dementia,” the researchers wrote.

“Although, the present data is lacking a control group of medically treated PD [Parkinson’s disease] patients, comparison with other studies on cognition and PD do not support a disease-modifying effect of STN-DBS on cognitive domains,” they concluded.

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Subjective Cognitive Decline Could Help Predict Parkinson’s Dementia, Study Contends

cognitive decline

Subjective cognitive decline in Parkinson’s disease could predict the development of dementia. As such, a suitable cognitive screening test could help provide an accurate diagnosis and prognosis.

The study with those findings, “Subjective cognitive decline and progression to dementia in Parkinson’s disease: a long-term follow-up study,” was published in Journal of Neurology.

Even during the early stages of disease, mild cognitive impairment can affect non-demented Parkinson’s patients, and is considered a risk factor for the development of dementia (PDD).

In fact, the prevalence of PDD increases as the disease progresses: from 28% after five years of evolution to 80% after 20 years of the disease.

Subjective cognitive decline — self-reported acquired difficulties with cognitive functioning — is common in the elderly and can be used as a predictor of dementia. In Alzheimer’s disease, subjective cognitive decline has been linked to disease-related tissue/molecular changes and a higher risk for dementia development. However, the predictive value of this type of cognitive status impairment has not been demonstrated yet in Parkinson’s disease.

Scientists from the University of La Laguna, Spain, investigated the neuropsychological profile of subjective cognitive decline in Parkinson’s disease and explored which components could better predict the development of PDD. The team also compared different screening tests to assess subjective cognitive complaints.

A total of 43 Parkinson’s patients and 20 healthy subjects were subjected to neuropsychological examination using a battery of cognitive tests. All patients were being medicated for Parkinson’s and were evaluated during their “on” state — when they are responding to medication and have reduced symptoms.

Subjective cognitive decline was diagnosed using two distinct approaches. A semi-structured interview in which the patient provided his/her subjective opinion on his/her attention, memory, spoken language, naming, written language, visuospatial skills and executive functions; diagnosis was considered when the patient had at least one cognitive complaint. Additionally, a subjective cognitive decline diagnosis also was established on the basis of the interview question concerning memory complaint.

For a mild cognitive impairment diagnosis, investigators followed the criteria proposed by the Movement Disorder Society (MDS)

Based on the results of the interview and on the MDS Task Force criteria, patients were diagnosed as having either subjective cognitive decline or mild cognitive impairment. Of the 43 patients, 13 (30.2%) were diagnosed with subjective cognitive decline, 22 (51.2%) with mild cognitive impairment and 8 (18.6%) had no subjective cognitive complaints. Difficulties in naming and memory were the most frequent cognitive complaints.

Based on memory complaints alone 10 patients (23.25%) were diagnosed with subjective cognitive decline. Interestingly, 10 of the 22 (45.45%) who had been diagnosed with mild cognitive impairment reported no memory complaints.

Mild cognitive impairment subjects performed poorer in the processing speed (the time it takes a person to do a mental task), executive functions (a set of mental skills that helps with organization and regulation), visuospatial skills, memory, and language domains, compared to the other groups.

There were no significant differences between healthy participants (controls)  and Parkinson’s disease patients with subjective cognitive decline in any of the neuropsychological measures.

The team also assessed how many patients diagnosed with subjective cognitive decline progressed to dementia after a mean follow-up of 7.5 years. Fifty percent of mild cognitive impairment patients, 33.3% of individuals diagnosed with subjective cognitive decline, and 14.3% of patients without subjective cognitive complaints developed dementia, which was found to be associated with a poor performance in verbal and visuospatial memory and naming at the beginning of the study.

Additionally, both the language and memory domains were good predictors of dementia development.

“These results are highly relevant for future investigations and also for clinicians: the [subjective cognitive decline] assessment is frequently the first step of cognitive examination and can influence future decisions (e.g., to administer a screening test or a comprehensive neuropsychological assessment),” researchers wrote.

“Assessments that do not include procedures to adequately explore cognitive complaints may underestimate the proportion of [Parkinson’s-related subjective cognitive decline] and, therefore, [mild cognitive impairment] and thus misclassify patients as [Parkinson’s disease] with normal cognition, especially when brief cognitive examinations are chosen,” they concluded.

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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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Changes in Gait, Cognition May Be Early Signs of Idiopathic Parkinson’s, Research Suggests

gait and Parkinson's

Changes in gait and cognition precede a diagnosis of idiopathic (without known cause) Parkinson’s disease, and may occur earlier than typical non-motor symptoms, a study has found.

The study, “Prediagnostic markers of idiopathic Parkinson’s disease: Gait, visuospatial ability and executive function,” was published in Gait & Posture.

Motor symptoms in idiopathic Parkinson’s disease (IPD) are identified relatively late in the disease course, reducing the odds of neuroprotective benefit from available treatment options. Identifying individuals during the prodromal (early) period that precedes motor symptoms could be of great use for clinical studies seeking new therapies to prevent or delay disease progression.

A team of French researchers sought to determine the existence of any subtle gait disorders or other signs that precede the diagnosis of IPD, based on data from a long-standing study of human aging across the adult lifespan: the Baltimore Longitudinal Study of Aging (BLSA).

Conducted by the National Institute on Aging (NIA) Intramural Research Program, the BLSA continuously enrolls healthy volunteers age 20 and older who are followed throughout their life independently of the development of age-related diseases.

Ten pre-diagnosed IPD patients (eight men and two women) and 30 healthy control subjects were chosen for this study.

Subjects were assessed for the disease approximately 2.6 years before diagnosis. Clinical examination included gait speed, spatio-temporal gait parameters, balance, upper-limb motor skills, neuropsychological profile, and non-motor symptoms.

In comparison to the control group, IPD patients had shorter step length and reduced gait speed in a usual gait speed testing condition. Despite also having shorter step length when testing maximum gait speed, no differences between the IPD and control samples were found in walking speed.

Moreover, patients had worse mental rotation ability (the ability to rotate mental representations of two-dimensional and three-dimensional objects, which is related to the brain’s capacity for visual representation), and impaired ability to name different examples that could be inserted into a category (for instance, naming all types of flowers one can think of in one minute).

Compared to control subjects, IPD patients had no changes in upper-limb motor function, no depression, no sleep disturbances, no urinary symptoms, and no orthostatic hypotension (when blood pressure suddenly drops when standing up quickly).

Researchers concluded that the observed “changes might serve as markers to improve the early detection of IPD patients, who could then benefit from pharmacological neuroprotection trials and/or prevention trials of lifestyle-related interventions in order to delay, or even prevent, clinical manifestations.”

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How to Use Computer Gaming as Therapy for Parkinson’s Disease

Computer Gaming

The brain is a plastic organ continually reshaping itself in response to the stimuli it receives and the way those stimuli are processed. The old adage “use it or lose it” applies even in the face of a challenging disease like Parkinson’s.

Computer gaming can help with brain training by exercising the brain to help moderate the effects of PD. For computer gaming to be efficacious as therapy, it must be implemented with careful attention to finding the right fit between the demands of the game and the therapeutic needs of the PD patient.

Recent research on video gaming and treatment for PD shows it can help with physical issues such as gait and balance.

The key to successfully using computer gaming is to find the right match of game for each person, as well as the appropriate difficulty level. The game must be challenging, but not so challenging that it becomes discouraging. It also must be rewarding and enjoyable. (There is that dopamine factor to consider.) Gaming has a “sweet spot,” like Goldilocks, in which you find just the right fit. I found this balance in the game “Shroud of the Avatar,” which I recommend for people with PD.

It took me a while to find the right video game — years, actually. “Shroud of the Avatar,” or “SotA,” is that game! It can be played at various levels. Not only can you find the sweet spot for your own style of playing, but also you can move that spot around depending on whether it is a good day or a bad day.

The game has a solid ethical foundation built on virtue and clean gameplay (no foul language). Playing SotA for 10 to 20 hours a week exercises the brain and the body — use it or lose it — while having a good time doing it.

SotA is just the right game for those with PD. It offers exercise for geographical memory, hand-eye coordination, speech, and problem-solving (scenario looping) at a variety of levels. It is a place where impulsivity can be applied with fewer consequences than in the real world. It is a place where the grouch can go when T.O.O.T.S. needs to be applied.

Have the urge to buy? Then earn virtual money and buy virtual things. Frustrated? Then enter the virtual world and work it out on some monsters. Have pain with your PD (a difficult problem for me)? Spend time in the virtual world of SotA to help manage the pain with less medication. Want a sense of accomplishment? Help build a community while also making yourself a strong avatar.

I have built a “sanctuary” for Parkinson’s folks inside SotA. It is a place where your avatar will find support and fellowship. Within this sanctuary is a place where you can find that sweet spot while contributing to building a support community. You can find this virtual sanctuary inside SotA in a town called Grumridge, just east of the city Aerie. You can see it on the map shown in the cover art of this column.

It may seem counterintuitive to say that fighting skeletons and building a virtual community is relaxing, but this has been my experience. Conversations I have had with others indicate that this experience is common. I often have clarity of mind while playing, and some of the ideas for these columns pop up in the middle of the game. That dopamine effect happens when successful within SotA, and the game offers many ways to experience success. You can’t get much better than having good, clean fun while slowing down the progression of PD!

One more note: I do use adaptive equipment to help me play the game. I have a large trackball on my dominant hand and a keypad with a thumb joystick on my other hand. You can see this illustrated in the cover art. It takes a little while to learn how to use this equipment, but the reward is a greater success rate inside the world of SotA (more dopamine!).

I also have a headset with a microphone. Plenty of opportunities exist to speak with others within the world of SotA, and the community of players is the best I have encountered in the gaming world. As far as I know, this is the first time a virtual support community within a game was developed for people with PD. Oh — and the game is free!

I look forward to seeing you there. My avatar name is Dr. Wiz. Let us build something special together.

PS: Thanks to the all the avatars (especially Ajumma Kim) and the game developers for their help building the Grumridge sanctuary.


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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DBS Linked to Distinct Motor and Cognitive Pathways in Brain, Finding That May Improve Its Use

deep brain stimulation

The benefits of deep brain stimulation (DBS) on motor function in Parkinson’s patients are mediated by a different brain pathway than the one involved in the procedure’s unwanted cognitive effects, according to a new study.

This finding may help improve the effectiveness and safety of DBS use in patients with Parkinson’s disease.

The research, “Functional segregation of basal ganglia pathways in Parkinson’s disease,” was published in the journal Brain.

DBS is an efficient alternative surgical procedure to treat Parkinson’s motor symptoms, such as tremor, rigidity, stiffness and slowed movement, in patients with an inadequate response to medications.

The treatment targets the subthalamic nucleus (STN), a brain region that is hyperactive in Parkinson’s patients. Besides its role in motor control, the STN is also involved in cognitive processes such as decision-making.

Prior research has shown that the STN is part of a brain pathway linking the striatum — a key region in movement and cognition — to the thalamus, which relays motor and sensory signals. This pathway is affected by loss of the neurotransmitter dopamine in the striatum due to Parkinson’s.

The STN is also involved in a brain pathway connecting motor-related areas in the cerebral cortex with the globus pallidus, a major component of the basal ganglia, which is mainly implicated in the control of movement and posture. The STN has been proposed to act through this pathway to delay, and thereby optimize, behavioral responses.

Although researchers suggest that DBS may alter the activity of both these brain pathways, no study had assessed the treatment’s effects on cognition and movement control in an integrated perspective.

A research team from Charité – Universitätsmedizin Berlin, in Germany, combined behavioral experiments with clinical observations, brain mapping and computer-based modeling. The study involved 20 Parkinson’s patients (18 men, mean age 63) undergoing STN-DBS, and 20 controls given a tracking task that required normal (automatic) and controlled reach movements.

Improvements in motor function — such as in movement velocity — were independent from unwanted cognitive effects, such as premature actions taken in situations requiring deliberation and decision-making. These motor and cognitive effects were independently mediated by the striatum-thalamus and the cortex-globus pallidus pathways, respectively.

“Our findings integrate with previous reports regarding cognitive and clinical implications of distinct pathway effects in Parkinson’s,” the researchers wrote.

Besides a better understanding of the neuronal networks affected by Parkinson’s, the findings also shed light on the workings of DBS.

“Only an improved understanding of the treatment’s mechanism of action will allow us to make [DBS] more effective,” Wolf-Julian Neumann, MD, the study’s first author, said in a press release.

As such, the results “may inspire new innovative pathway-specific approaches to reduce side effects and increase therapeutic efficacy of neuromodulation in patients with Parkinson’s,” the researchers wrote.

The team is now planning to use measurements of neural activity to differentiate patients and healthy individuals.

“This will allow us to adapt brain stimulation treatments according to the needs of the individual patient and in real time,” said Andrea A. Kühn, MD, the study’s senior author. “It is an important step on the way to developing an intelligent, personalized and demand-adapted treatment.”

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Source: Parkinson's News Today

The ABCs of Parkinson’s Disease: The Letter C


Sherri Journeying Through

Third in a series. Read part one and two.

In this column, the letter C is for cognitive changes and caregiving.

Cognitive changes

Some possible Parkinson’s disease symptoms are obvious because they are visible: tremors, abnormal gait, a non-swinging arm. You can see them. Others can see them. But some symptoms are not so obvious because they are invisible: internal tremors, dystonia (muscle cramping/twisting), and pain in many and various places.

Other invisible symptoms are cognitive changes (brain symptoms such as disturbance of memory, thinking and language abilities). These changes can range from mild (feelings of distraction or disorganization, finding it difficult to plan and accomplish tasks) to more severe (such as Parkinson’s dementia).

The struggle to remember certain things — such as dates, directions, or where your glasses or car keys are hiding — may be a clue that your cognitive functions are faltering. Or it may be just a case of forgetfulness. It is best to seek out your doctor’s expert advice.


One area that doesn’t get enough attention is caregiving. Sooner or later the Parkinson’s patient will need help, and those tasks will most likely fall upon family members. Whether you are a family member or a good friend, offering your time and extending your love to care for your loved one is a tiring, wearisome task. It takes a lot of energy and time. To prevent burnout, it is important that the caregiver takes time for themselves to keep from becoming resentful and exhausted. Some suggestions include:

  • Have lunch with an encouraging friend who knows your situation
  • Join a support group for caregivers, a book club, or an exercise or dance class
  • Take daily walks
  • Listen to encouraging music
  • Start a game night with some friends
  • Go to church
  • Begin a new hobby

The sky’s the limit, but as a caregiver, you are limited in what you can personally give. Try to share the load. Ask a friend if they can sit in for you once in a while when you need to go to the store or grab a hamburger and sit in the parking lot to read a book. You won’t do your “patient” any good if you become resentful for the time it is taking to care for them and lose sight of the fact that they really aren’t trying to make life more difficult for you. It’s just called Parkinson’s disease, and unfortunately, you or your loved one has it. But don’t forget, we’re in this together.


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.

The post The ABCs of Parkinson’s Disease: The Letter C appeared first on Parkinson’s News Today.

Source: Parkinson's News Today

Anti-Parkinson’s, Other Anticholinergic Therapies Increase Risk of Dementia, Study Shows

dementia risk

Anticholinergic medications used to treat depression, urinary incontinence, or Parkinson’s disease increase the risk of dementia, even if the therapy was taken 20 years before diagnosis of cognitive impairment, a study has found.

The study, “Anticholinergic drugs and risk of dementia: case-control study,” was published in The BMJ.

Anticholinergic medications are designed to prevent the activation of nerve cells by the signaling molecule acetylcholine. Depending on the site where the treatment acts, it can be used to prevent several responses such as tremors in Parkinson’s or respiratory reactions. This class of medicines is also widely used to treat depression and gastrointestinal disorders, among others illnesses and conditions.

Their potential to affect cognition has been previously reported, and guidelines suggest avoiding use in frail older people. However, until now, the long-term effects of anticholinergic medications on cognitive function was not fully realized.

Researchers at the University of East Anglia in the U.K. conducted a large-scale, retrospective study to compare the use of anticholinergic medications among 40,770 people who were diagnosed with dementia and 283,933 individuals without cognitive impairment (EUPAS8705).

Patients’ clinical information was collected from the Clinical Practice Research Datalink, which covers more than 11.3 million patients from across 674 primary care practices in the U.K. The study included patients 65 years or older, who had been diagnosed with dementia between April 2006 and July 2015.

Of the five most common anticholinergic therapies used by participants in the study, 29% took amitriptyline (brand names Endep, Lentizol, Saroten, Tryptanol, and Tryptizol), 16% dosulepin (brand name Prothiaden), 8% paroxetine (brand names Paxil and Seroxat), 7% oxybutynin (brand names Ditropan, Lyrinel XL, Lenditro, Driptane, and Uripan), and 7% tolterodine (brand names Detrol and Detrusitol).

The team found that the use of anticholinergic treatments was linked to a 10-11% increased risk of dementia. When they analyzed the data according to drug indication, they found that dementia was more common among patients who had been prescribed antidepressants, anti-Parkinson’s therapies, and urological medications. No association was found with antispasmodic, antipsychotic, antihistamine, or other treatments.

This increased risk was found to persist even if the medications had been prescribed several years before the dementia diagnosis. In fact, patients who had been treated with anti-Parkinson’s therapies 10 to 15 years before diagnosis had a 54% increased risk of having dementia. For antidepressants, the risk was 19% and for urological therapies, 27%, when taken 15 to 20 years before diagnosis.

“These findings make it clear that clinicians need to carefully consider the anticholinergic burden of their patients and weigh other options,” Malaz Boustani, MD, co-author of the study and a researcher at Indiana University Center for Aging Research in the U.S., said in a press release. “Physicians should review all the anticholinergic medications — including over-the-counter drugs — that patients of all ages are taking and determine safe ways to take individuals off anticholinergic medications in the interest of preserving brain health.”

It is still unclear why these medications have such an adverse effect, and additional studies are needed to fully address the risks linked to their use. Still, these findings highlight not only the short-term effects of anticholinergic therapies but also long-term adverse effects on cognitive function.

“With many medicines having some anticholinergic activity, one key focus should be de-prescribing. Clinical staff, patients and carers need to work together collaboratively to limit the potential harm associated with anticholinergics,” said study co-author Ian Maidment, PhD, a senior lecturer in clinical pharmacy at Aston University in the U.K.

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Source: Parkinson's News Today