Detecting anxiety in individuals with Parkinson disease: A systematic review

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Wednesday, 13 December 2017

Detecting anxiety in individuals with Parkinson disease: A systematic review

This is a new systematic review of studies assessing the diagnostic accuracy of anxiety scales in people with PD. It is important because anxiety is a common feature of Parkinson's both before and after the diagnosis. The authors found that overall 30% of people with Parkinson's meet the criteria for anxiety, but I have to say that in my experience I would put it closer to 50%. Maybe this reflects a bias in the patients I see??

The properties of the scales available for assessing anxiety are important. At the beginning of PREDICT-PD, we went through a pain-staking process of selection and in the end arrived at the Hospital Anxiety Depression Scale (HADS). In fact, at that time we knew that it was not the very best Anxiety scale or the very best Depression scale in terms of diagnostic accuracy, but it did combine assessment of both problems in one validated questionnaire, it was feasible to self-administer and it was relatively short. Nearly seven years on I am still happy with that decision but we may now test other scales within the PREDICT-PD programme too. Depression and anxiety are two features that are likely to pre-date a diagnosis of PD by a long time and it is critically important to be using the best tools to identify them both. They also have a dramatic impact on quality of life and are treatable, which are two good reasons to be trying to pick them up in people that don't have a diagnosis because there are likely to be significant health benefits...

Alastair Noyce

Neurology. 2017 Dec 6. pii: 10.1212/WNL.0000000000004771. doi: 10.1212/WNL.0000000000004771. [Epub ahead of print]
Mele B, Holroyd-Leduc J, Smith EE, Pringsheim T, Ismail Z, Goodarzi Z.

http://n.neurology.org/content/early/2017/12/06/WNL.0000000000004771.long

OBJECTIVE: To examine diagnostic accuracy of anxiety detection tools compared with a gold standard in outpatient settings among adults with Parkinson disease (PD).

METHODS: A systematic review was conducted. MEDLINE, EMABASE, PsycINFO, and Cochrane Database of Systematic Reviews were searched to April 7, 2017. Prevalence of anxiety and diagnostic accuracy measures including sensitivity, specificity, and likelihood ratios were gathered. Pooled prevalence of anxiety was calculated using Mantel-Haenszel-weighted DerSimonian and Laird models.

RESULTS: A total of 6,300 citations were reviewed with 6 full-text articles included for synthesis. Tools included within this study were the Beck Anxiety Inventory, Geriatric Anxiety Inventory (GAI), Hamilton Anxiety Rating Scale, Hospital Anxiety and Depression Scale-Anxiety, Parkinson's Anxiety Scale (PAS), and Mini-Social Phobia Inventory. Anxiety diagnoses made included generalized anxiety disorder, social phobia, and any anxiety type. Pooled prevalence of anxiety was 30.1% (95% confidence interval 26.1%-34.0%). The GAI had the best-reported sensitivity of 0.86 and specificity of 0.88. The observer-rated PAS had a sensitivity of 0.71 and the highest specificity of 0.91.

CONCLUSIONS: While there are 6 tools validated for anxiety screening in PD populations, most tools are only validated in single studies. The GAI is brief and easy to use, with a good balance of sensitivity and specificity. The PAS was specifically developed for PD, is brief, and has self-/observer-rated scales, but with lower sensitivity. Health care practitioners involved in PD care need to be aware of available validated tools and choose one that fits their practice.

ASMR

reposted from  thanks Allen for the tip

ASMR

Published by Steven Novella under Neuroscience 
Comments: 77

You can find almost anything on YouTube. I can imagine a future historian analyzing the millions of videos from a certain period of time, using it as a window into our contemporary society. I further imagine some videos would be quite mysterious, however. For example, why is there a video of a person whispering Genesis in Latin? Another video is a static picture of a wrapped present with the sound of someone wrapping presents (several people apparently loved this). There is also video of is a real people getting eye exams. This seems ordinary enough – but there is a strange connection between the eye exam videos and the previous two.

The phenomenon is called autonomous sensory meridian response (ASMR). I have been reading about this for a short time, it seems to be a growing subculture on the internet and is just peaking through to mainstream awareness.

By the way – this is perhaps another phenomenon worth pointing out, the internet allowing for previously personal and hidden experiences to come to general awareness. Human communication has been increased to the point that people who have what they think are unique personal experiences can find each other, eventually bringing the phenomenon to general awareness, giving it a name and an internet footprint. Of course, such phenomena are not always real – sometimes a real pattern emerges from the internet, sometimes illusory or misidentified patterns, the cultural equivalent of pareidolia.

But I have left you waiting long enough – what is ASMR? It is described as a pleasurable and calming tingling sensation in the back of the head. It is often called a brain orgasm, or braingasm (which I think is a bit misleading, since the regular kind of orgasm occurs in the brain with some peripheral manifestations). This experience can be triggered by a variety of odd sensations. The ASMR Research and Support website (you knew that had to exist) gives a list:

- Exposure to slow, accented, or unique speech patterns
- Viewing educational or instructive videos or lectures
- Experiencing a high empathetic or sympathetic reaction to an event
- Enjoying a piece of art or music
- Watching another person complete a task, often in a diligent, attentive manner – examples would be filling out a form, writing a check, going through a purse or bag, inspecting an item closely, etc.
- Close, personal attention from another person
- Haircuts, or other touch from another on head or back

This is a diverse list of triggers, but I can see what they all have in common. They all seem to engage the same networks of the brain – that part of us that interacts carefully and thoughtfully with our environment or with other people.  There is something calmly satisfying about such things. (Total aside – this reminds me of an episode of Spongebob in which he confessed he loves the sound that two pickles make when you rub them together.)

But of course not everyone gets a definite tingling sensation in their head and spine as a result of this soft satisfaction. I always start my investigations of such phenomena by asking the most basic question – is it real? In this case, I don’t think there is a definitive answer, but I am inclined to believe that it is. There are a number of people who seem to have independently (that is always the key, but it is a recent enough phenomenon that this appears to be true) experienced and described the same syndrome with some fairly specific details. In this way it’s similar to migraine headaches – we know they exist as a syndrome primarily because many different people report the same constellation of symptoms and natural history.

Another way to address this question is to ask how plausible the phenomenon is. For reasons I will get into below, I think it is entirely plausible, or at least this is no obstacle to acceptance of ASMR as real.

So, with the small caveat that we are not completely sure at this time, it seems reasonable to proceed with the working assumption that ASMR is a real thing. If it is, then what’s going on. That is a matter for research. While there are references to research on the internet, it seems if any is happening at this time it is entirely descriptive. A PubMed search for ASMR (the full name, not the acronym) yielded exactly zero results. This could mean that there is a more technical term for ASMR and  I need to find out what that is, but I have not been able to find any other terms for ASMR. So if there is real research going on nothing has been published in the peer-reviewed literature so far.

Nicholas Tufnell wrote about his own experience with ASMR at the Huffington Post, and his description seems typical. I have never experienced this myself. I listened to the whispering in Latin video, which was eerily intimate at first, and then just a bit weird, although I always love listening to Latin. But I experienced no tingling or euphoria. The only thing in my life that I can relate to this is when I was a child very occasionally listening to a certain frequency of tapping, just about two per second, like a relentless monotonous beat, would “resonate” in my brain. I basically grew out of these experiences and have not had them for decades.

Looking back as a neurologist I have wondered what they were. They could even have been little seizures.  Seizures can be triggered by auditory stimuli. Perhaps ASMR is a type of seizure. Seizures can sometime be pleasurable, and can be triggered by these sorts of things.

Or, ASMR could just be a way of activating the pleasure response. Vertebrate brains are fundamentally hardwired for pleasure and pain – for positive and negative behavioral feedback. We are rewarded with a pleasurable sensation for doing things and experiencing things that increase our survival probability, and have a negative or painful experience to make us avoid harmful behavior or warn us about potential danger or injury. Over evolutionary time a complex set of reward and aversion feedbacks have developed.

Add to this the notion of neurodiversity – the fact that all of our human brains are not clones or copy cats, but vary in every possible way they can vary. We have a range of likes and dislikes, and there are individuals and even subcultures that seem to have a different pattern of pleasure stimulation than what is typical. (Perhaps in some cases this is largely cultural, not neurotypical.) S&M comes to mind. If reports are accurate, there are some people who experience pain as pleasurable and erotic.

Admittedly it gets very difficult teasing out learned associations and behaviors from innate hardwired ones, and all this applies to ASMR as well.

In any case it is plausible that a subset of the population has a particular pattern of neural hard wiring so that when they experience certain things that are typically quietly satisfying they get a little extra shot to their pleasure center. Once they experience this then they seek out greater and greater triggers of this response, and perhaps then a learning or conditioning component kicks in. Tufnell even describes getting a little addicted to seeking out ASMR stimuli.

What we need at this point are functional MRI and transcranial magnetic stimulation studies that look at what is happening in the brains of people while experiencing ASMR, vs typical controls. Are their brains really different, and in what way? I also wonder if the same or similar experience can be artificially induced in typical (non-ASMR) people.

This is just another example of how our brains are fantastically complex and weird. How else can you explain the existence of videos of whispering Latin and wrapping paper noise on YouTube.

———-

Thanks to kwilliams1 for suggesting the topic.

Risk of Parkinson's disease following anxiety disorders: a nationwide population-based cohort study

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Risk of Parkinson's disease following anxiety disorders: a nationwide population-based cohort study

Consistent with the results of previous observational studies and a dose dependent effect as well...

Eur J Neurol. 2015 May 29. doi: 10.1111/ene.12740. [Epub ahead of print]

Lin CH, Lin JW, Liu YC, Chang CH, Wu RM.

BACKGROUND AND PURPOSE:

Anxiety is potentially a pre-motor symptom of Parkinson's disease (PD). Our aim was to investigate the association between anxiety and subsequent PD risk in a population-based sample.

METHODS:

A total of 174 776 participants, who were free of prior PD, dementia and stroke, were enrolled from Taiwan National Health Insurance Research Database between 1 January 2005 and 31 December 2005. The association between anxiety at the beginning of the study and the incidence of PD was examined using a Cox regression model. Information regarding comorbidities, especially depression, and concomitant medication use was adjusted in the proportional hazards models.

RESULTS:

Over an average follow-up of 5.5 years, 2258 incident PD cases were diagnosed. After adjusting for age, sex, comorbidities and concomitant medication use, patients with anxiety were more likely to develop PD than subjects without anxiety [adjusted hazard ratio (HR) 1.38; 95% confidence interval (CI) 1.26-1.51]. Anxiety severity was dose-dependently associated with increased likelihood of PD: crude HR 1.27 (95% CI 1.11-1.44) for mild anxiety, 1.35 (95% CI 1.19-1.53) for moderate anxiety and 2.36 (95% CI 2.13-2.62) for severe anxiety (P < 0.0001). Results were similar after adjustment for age, sex, comorbid depression and other PD risk factors, and in the sensitivity analyses excluding participants with comorbid depression or with a PD diagnosis <3 years after anxiety diagnosis, and controlling for Charlson's scores.

CONCLUSIONS:

The likelihood of developing PD was greater amongst patients with anxiety than patients without anxiety, and the severity of anxiety correlated with risk of PD.

Depression and subsequent risk of Parkinson disease: A nationwide cohort study

reposted from

Thursday, 28 May 2015

Depression and subsequent risk of Parkinson disease: A nationwide cohort study

Interesting stuff indeed...dose dependent effect and significance differences observed up to two decades prior to diagnosis. To my knowledge this is the first study that has suggested depression precedes PD by this length of time but anxiety has been shown to antedate PD by a similar length of time...

Neurology. 2015 May 20. pii: 10.1212/WNL.0000000000001684. [Epub ahead of print]

Gustafsson H, Nordström A, Nordström P.

http://www.neurology.org/content/early/2015/05/20/WNL.0000000000001684.short?rss=1

OBJECTIVE:

To investigate the long-term risk of Parkinson disease (PD) after depression and evaluate potential confounding by shared susceptibility to the 2 diagnoses.

METHODS:

The nationwide study cohort included 140,688 cases of depression, matched 1:3 using a nested case-control design to evaluate temporal aspects of study parameters (total, n = 562,631). Potential familial coaggregation of the 2 diagnoses was investigated in a subcohort of 540,811 sibling pairs. Associations were investigated using multivariable adjusted statistical models.

RESULTS:

During a median follow-up period of 6.8 (range, 0-26.0) years, 3,260 individuals in the cohort were diagnosed with PD. The multivariable adjusted odds ratio (OR) for PD was 3.2 (95% confidence interval [CI], 2.5-4.1) within the first year of depression, decreasing to 1.5 (95% CI, 1.1-2.0) after 15 to 25 years. Among participants with depression, recurrent hospitalization was an independent risk factor for PD (OR, 1.4; 95% CI, 1.1-1.9 for ≥5 vs 1 hospitalization). In family analyses, siblings' depression was not significantly associated with PD risk in index persons (OR, 1.1; 95% CI, 0.9-1.4).

CONCLUSIONS:

The time-dependent effect, dose-response pattern for recurrent depression, and lack of evidence for coaggregation among siblings all indicate a direct association between depression and subsequent PD. Given that the association was significant for a follow-up period of more than 2 decades, depression may be a very early prodromal symptom of PD, or a causal risk factor.

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2-Jan-2014

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Contact: Cody Mooneyhan
cmooneyhan@faseb.org
301-634-7104
Federation of American Societies for Experimental Biology 

Want a good night's sleep in the new year? Quit smoking

New research in The FASEB Journal identifies the mechanism by which tobacco smoke affects the expression of clock genes in the lung and resets levels of locomotor activity in the brain

As if cancer, heart disease and other diseases were not enough motivation to make quitting smoking your New Year's resolution, here's another wake-up call: New research published in the January 2014 issue of The FASEB Journal suggests that smoking disrupts the circadian clock function in both the lungs and the brain. Translation: Smoking ruins productive sleep, leading to cognitive dysfunction, mood disorders, depression and anxiety.

"This study has found a common pathway whereby cigarette smoke impacts both pulmonary and neurophysiological function. Further, the results suggest the possible therapeutic value of targeting this pathway with compounds that could improve both lung and brain functions in smokers," said Irfan Rahman, Ph.D., a researcher involved in the work from the Department of Environmental Medicine at the University of Rochester Medical Center in Rochester, N.Y. "We envisage that our findings will be the basis for future developments in the treatment of those patients who are suffering with tobacco smoke-mediated injuries and diseases.

Rahman and colleagues found that tobacco smoke affects clock gene expression rhythms in the lung by producing parallel inflammation and depressed levels of brain locomotor activity. Short- and long- term smoking decreased a molecule known as SIRTUIN1 (SIRT1, an anti-aging molecule) and this reduction altered the level of the clock protein (BMAL1) in both lung and brain tissues in mice. A similar reduction was seen in lung tissue from human smokers and patients with chronic obstructive pulmonary disease (COPD). They made this discovery using two groups of mice which were placed in smoking chambers for short-term and long-term tobacco inhalation. One of the groups was exposed to clean air only and the other was exposed to different numbers of cigarettes during the day. Researchers monitored their daily activity patterns and found that these mice were considerably less active following smoke exposure.

Scientists then used mice deficient in SIRT1 and found that tobacco smoke caused a dramatic decline in activity but this effect was attenuated in mice that over expressed this protein or were treated with a small pharmacological activator of the anti-aging protein. Further results suggest that the clock protein, BMAL1, was regulated by SIRT1, and the decrease in SIRT1 damaged BMAL1, resulting in a disturbance in the sleep cycle/molecular clock in mice and human smokers. However, this defect was restored by a small molecule activator of SIRT1.

"If you only stick to one New Year's resolution this year, make it quitting smoking," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Only Santa Claus has a list longer than that of the ailments caused or worsened by smoking. If you like having a good night's sleep, then that's just another reason to never smoke."

###

Receive monthly highlights from The FASEB Journal by e-mail. Sign up athttp://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is among the most cited biology journals worldwide according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century.

FASEB is composed of 27 societies with more than 110,000 members, making it the largest coalition of biomedical research associations in the United States. Our mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

Details: Jae-Woong Hwang, Isaac K. Sundar, Hongwei Yao, Michael T. Sellix, and Irfan Rahman Circadian clock function is disrupted by environmental tobacco/cigarette smoke, leading to lung inflammation and injury via a SIRT1-BMAL1 pathway. FASEB J. January 2014 28:176-194; doi:10.1096/fj.13-232629 ; http://www.fasebj.org/content/28/1/176.abstract

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reported from here

Where and how are fear-related behaviours and anxiety disorders controlled?

21.11.2013 - PRESS RELEASE

Neurosciences, cognitives sciences, neurology and psychiatry

A team of researchers at Inserm led by Cyril Herry (Inserm Unit 862, “Neurocentre Magendie,” Bordeaux) has just shown that interneurons located in the forebrain at the level of the prefrontal cortex are heavily involved in the control of fear responses. Using an approach combining in vivo recordings and optogenetic manipulations in mice, the researchers succeeded in showing that the inhibition of parvalbumin-expressing prefrontal interneurons triggers a chain reaction resulting in fear behaviour. Conversely, activation of these parvalbumin interneurons significantly reduces fear responses in rodents. 

This research is published in the journal Nature

Some traumatic events may lead to the development of severe medical conditions such as anxiety disorders or posttraumatic stress disorder (PTSD).

Anxiety disorders have a prevalence of approximately 18% worldwide.

Despite successful treatments, some patients relapse, and the original symptoms reappear over time (fear of crowds, recurring nightmares, etc.). An understanding of the neuronal structures and mechanisms involved in this spontaneous recovery of traumatic responses is essential.

All observations made by researchers indicate that fear behaviours are controlled in the forebrain at the level of the dorsomedial prefrontal cortex. This control of fear behaviour is based on the activation of neurons in the prefrontal cortex that are in contact with specific areas of the amygdala.

Using an innovative approach combining electrophysiological recording techniques, optogenetic manipulations and behavioural approaches, the researchers were able to demonstrate that fear expression is related to the inhibition of highly specific interneurons—the parvalbumin-expressing prefrontal interneurons.

More specifically, inhibition of their activity disinhibits the activity of the prefrontal projection neurons, and synchronises their action.

Synchronisation of the activity of different neuronal networks in the brain is a fundamental process in the transmission of detailed information and the triggering of appropriate behavioural responses. Although this synchronisation had been demonstrated as crucial to sensory, motor and cognitive processes, it had not yet been examined in relation to the circuits involved in controlling emotional behaviour.

“Our results identify two complementary neuronal mechanisms mediated by these specific interneurons, which accurately coordinate and increase the neuronal activity of prefrontal projection neurons, leading to fear expression,” explains Cyril Herry. 

The identification and better understanding of these neuronal circuits controlling fear behaviour should allow the development of new treatment strategies for conditions such as posttraumatic stress disorder and anxiety disorders. “We could, for example, imagine the development of individual markers for these specific neurons, or the use of transmagnetic stimulation approaches to act directly on excitatory or inhibitory cells and reverse the phenomena.”

How is fear analysed in an animal?

From an experimental standpoint, the classic Pavlovian conditioning procedure involves associating one stimulus, such as a sound, with another, unpleasant stimulus, such as a small electric shock. This first step allows the animal to establish a persistent aversive memory. In other words, the animal comes to remember and learn that the sound is associated with an unpleasant state, and an immobility response is routinely triggered, which is a good indication of fear in an animal.

In the second step, the extinction procedure involves repeated presentation of the sound alone, inducing a temporary inhibition of the conditioned fear responses. This inhibition is only temporary, as the mere passage of time favours the spontaneous recovery of the conditioned fear responses, which, from the clinical standpoint, may be associated with the phenomenon of relapse into traumatic responses seen following the treatment of posttraumatic stress disorder using exposure-based therapies.

TO CITE THIS PAGE :
Press release – Inserm press room – Where and how are fear-related behaviours and anxiety disorders controlled?

Link :
http://presse-inserm.fr/en/where-and-how-are-fear-related-behaviours-and-anxiety-disorders-controlled/10232/