Tag Archives: neuropsychology

Misophonia and Me

Misophonia is a term (first coined in 2003 by Pawel J. Jastreboff, Margaret M. Jastreboff 1) given to describe a relatively unexplored condition that causes a person to experience an involuntary fight of flight reaction to innocuous repetitive, unpredictable, sounds and in some cases small repetitive movements. This immediate autonomic arousal is described by those with the condition as being akin to intense anger, panic and anxiety. Often it affects their ability to complete every day tasks and stops them from engaging in normal and healthy social interactions. (Edelstein et al. 20132) The types of sound that most typically ‘trigger’ this reaction in misophonic patients are eating sounds, breathing sounds, nasal and sniffing sounds, coughing, tapping, clicking and whistling or humming.

Due to the nature of these ‘trigger’ sounds, it is extremely difficult for a person with misophonia to avoid coming in to contact with them in their every day life. As such they might withdraw from social activities, eat in isolation, avoid public transport and face difficulties in their work place.

It is not conjecture to suppose that people who suffer with this condition over a number of years may begin to develop other psychological issues ranging from social anxiety disorder to depression, although further research would be needed to verify this suggestion.

There currently exist only two peer reviewed papers that focus on this condition. The first was published in January this year by a group of Dutch researchers who’s area of expertise was OCD and other psychiatric disorders. They outline the condition based on 42 participants who were referred to or got in contact with their clinic. (Schro, Vulink & Denys, 2013 3.)

They propose that the condition be treated as a discrete psychiatric disorder as it has unique qualities, which mean that none of the symptoms of misophonia can be classified in the current DSM-IV (DSM-V) or ICD-10 systems. In their paper they also outline a diagnostic criteria that might be implemented in the future to help with diagnosis and encourage further research.

Whilst we welcome this study and it’s identification of Misophonia as a separate condition that does not share it’s qualities with other more readily diagnosed disorders, it should be noted that the focus on the condition being psychiatric does not mean that it has not got a neurological cause.

The more recent study by Edelstein et al. 20132, which I refer too most often as ‘San Diego’ paper, can be seen to be a more neurological and physiological investigation. In this study they looked at misophonia with comparisons to another neurological phenomena called ‘synethesia’, which is a condition where a certain stimulus, either visual or auditory causes an incongruent sensory reaction from what is normally expected from such inputs. For a basic example synesthetes might see a color when they hear a particular word or see a certain number.  The suggestion being that the sensory misdirection present in synethesia might be comparable to that in misophonia. They were able to identify statistically significant differences in stress responses (measured by SCR, skin conductivity response, a bit like a lie detector test)  between misophonic patients, synesthetes and ‘normal’ control subjects in their physiological reaction to trigger sounds and visual triggers. Importantly this means that they have provided the first evidence to support the severity of the condition beyond the anecdotal evidence that already exists. (For more details please find a link to their study at the end of this post).

Whilst it is very important to aknowledge how great it is that this work is being conducted and that misophonia is slowing gaining recognition in the scientific community, what remains a concern to me is that the anecdotal evidence suggests that this condition is not very responsive to popular treatment methods such as CBT, and in some cases the has caused peoples reactions to become more intense and even increases the number of ‘trigger’ sounds. Often people are being prescribed anti anxiety drugs to help combat the response to triggers but these also seem to be having limited success amongst patients who have sought help. The only methods of ‘treating’ the condition that seem to offer relief come from avoidance techniques, or using headphones to block out the sounds, which ultimately might lead to more damage than good. Internet forums are a buzz with information and reports of less well known therapies being of some help to them, such as neuro-feedback and schema retraining. Time and greater levels of research will be needed to verify or find suitable treatment options.

I think at this point it is import to be clear about exactly how severe these reactions are so that there is not the common misunderstanding that those with misophonia simply find these sounds ‘annoying’. I can not think of a feeling that is further removed from ‘annoyance’ as my reaction to these ‘trigger’ sounds is. It’s fair to say that everyone gets irritated to some degree with a ‘noisy’ eater or that person at the cinema who just won’t stop rustling their popcorn as they moronically shovel it into their mouths without taking their eyes off the screen ahead. Misophonia is not that feeling.

A misophonic reaction is so strong and so instantaneous that, honestly, the only other emotion I can compare it to is that moment when someone tells you that a person you love has died. That gut wrenching, heart stopping, shortness of breath feeling, that you can not possibly control or stop from occurring. This is how intense the reaction to hearing a trigger sound can be. However, instead of that hollow grief that comes from such news, it is instead a burning anger, a completely alien level of rage. I am not a violent person (if you exclude the tantrums I had as a very small child) and I would never dream of hitting a person or causing them harm, but a trigger will make me want to lash out, my cognitive processes go from perfectly normal to phrases such as ‘I wish you’d just die’ or ‘why the hell are you making that noise, I’ll make you stop’… along with some often very violent imagery. There is nothing normal about this at all, and I can’t express enough how this is not just ‘being annoyed’ at someone eating rudely or loudly. Quite often the way in which a person is eating or the volume level has no significant impact at all on whether a trigger is better or worse. Though I would never actually hit anyone, I have to employ ‘coping’ mechanisms to deal with hearing these noises. My first response is often to try to leave the room if I can (this can lead to some very annoying train journeys where I have been known to move carriages 7 times in a half hour journey, or being incredibly rude at family dinners – Christmas time being the worst of course). Or I have to mimic the person eating, pretending to chew when they do (but this often just makes me look a little crazy so over the years I have tried to stop doing this if I can help it). I have tried humming to myself, or clicking my fingers to try and distract myself from the noise. But inevitably the aftermath of any of these attempts to lessen my reaction of ‘fight or flight’ is of course immense feelings of shame, guilt and embarrassment.

The reactions individuals report tend to be more intense depending on their physical situation and emotional state. For example being in an enclosed space, such as on public transport or a lift where there is no easy escape heightens the reaction. (This makes sense if considering the reaction to be fight or flight). Unsurprisingly being stressed or tired also is reported to make the reactions worse, either more intense or more likely to happen.

What concerns me most of all is that it appears that over time trigger sounds spread. Looking at the hundreds of posts written on the facebook site people say their reactions typically starting between the ages of 8-13, and initially were isolated to one particular individual being a ‘trigger’ (usually a close family member) before becoming more widely applied to close friends, extended family, work colleagues and then strangers. They might also begin as being eating sounds or breathing sounds but overtime it appears many people find their triggers extend to noises such as keyboards typing, pens clicking, packets rustling, dogs barking and whistling. There are people who have had misophonia for over 40 years and yet no one has ever been able to help them with their condition.

What is clear is that this is a condition that affects hundreds of people, social media sites and support groups are seen to have over 1000 members and the UK misophonia website has had over 100,000 hits. Little is understood about it’s origin, prognosis or treatment options and there is essentially a whole condition waiting to be uncovered.

It is my ambition to be the person to study this condition, to uncover it’s secrets and hopefully work towards finding a successful treatment plan for those who have suffered with it for longer than I have. If the doctors can’t help me, I will help myself and all the others too.

 

1.Pawel J. Jastreboff, Margaret M. Jastreboff (April 2003). “Tinnitis retraining therapy for patients with tinnitus and decreased sound tolerance”. Otolaryngol Clin. 36(2): 321–36.

2. Misophonia:physiological investigations and case descriptions Miren Edelstein, David Brang, Romke Rouw and Vilayanur S.Ramachandran Frontiers in Human Neuroscience June 2013 | Volume 7 | Article 296

3. Misophonia: Diagnostic Criteria for a New Psychiatric Disorder. Arjan Schroder, Nienke Vulink and Damiaan Deny* PLOS ONE | January 2013 | Volume 8 | Issue 1 | e54706

If you are a researcher who is particularly interested in this topic I would be very keen to hear from you. I have a background in Psychology and a MSc in Neuroscience and want to study misophonia as part of a PhD project, preferably starting in 2014 and based in the UK. I am currently actively seeking a potential supervisor for such a project and can be contacted at oggie114@hotmail.com

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Let There Be Light! A breakthrough in microtechnology that is giving blind people back some sight.

I couldn’t imagine loosing any of my senses, least of all my sight. To go blind slowly over time must be one of the most challenging illnesses a person can have to face. Knowing that there is nothing that can stop a hereditary degeneration of your sight must be heartbreaking, to say the least. Just imagine having the memory of what a flower covered in morning dew looked like as a sunbeam touched the tip of the petal, or being able to recall how you used to look in a mirror but can no longer see yourself, to know that there are wonders beyond most peoples own imaginations that are possible to observe in a sunset and to have all of that knowledge, that discover, taken from you along with your independence has to be one of life’s most unfair consequences of genetic illnesses.

Like any disability that worsens over time you’d hold on to the hope that one day science will find a cure, but it would seem an unfathomable wish for them to cure blindness. This is why the news that came out this week of a microchip that has the potential to restore at least the basic functions of sight seems almost too good to be true.

Some forms of blindness are caused by a degeneration of the photo-receptors within the eye. These are the cells that allow us to interpret light signals into meaning, by building on signals received about colour and brightness. With this information our brain is then able to construct the images that allow us to perceive the world around us. Clever, clever nature.

In people with degenerative eye conditions such as retinitis pigmentosa (RP) the optic nerve is left mostly intact. There are two ‘treatment’ options available at the moment, the first involves forms of gene therapy and other protective factors, which have been shown to slow degeneration in people with this and similar conditions. However, this has to be received at an early enough stage of the degeneration.  The second option is what this current research focused on, and sounds more like something from a science fiction film than reality. They invoke electrical stimulation of the surviving retinal networks to try to produce some form of visual experience in people who’s level of degeneration is beyond that which might be helped by the other form of ‘treatment’. More specifically in this case a microchip is implanted under the transparent retina to act as electronic man-made ‘replacement’ photoreceptors.

The chips are able to sense light and create signals from this at many pixel locations. This is achieved using “microphotodiode arrays” or MPDA’s.  There are 1500 pixel generating arrays on a chip, and each acts independently as a light sensitive electrode, this is subsequently able to provide an electrical stimulus to the neurons nearby. In this way it is unique to other approaches, within each element is the electrode set allowing for the electrical stimulation of neurons to be caused by the reception of light. There are also photodiodes found within the chip which allow for varied amplifications to be transmitted based on the level of light reception.

With the chip in place within the eye, the photodiodes are able to capture an image each, several times a second, simultaneously.

Illustration from the original paper found here . It gives a better demonstration of the set up of the microchip with the electrodes and MPDAs, and also a nice picture of an eye is always a winner. (I can remember dissecting an eye in alevel bio, it was fascinating)

It’s enough to make your head hurt to think about, I mean really. There are 1500 elements able to transmit signals from the photodiodes, which are able to capture an image in a ridiculously small time frame and transfer this into meaningful information by way of electrical impulses to the bipolar cells that would have originally received information from the rods and cones of the eye. With the amount of current that is sent by each electrode determinable by the brightness recorded by each photodiode.  Oh, did I also forget to mention that the chip that all of this occurs on is a mere 4mm square in size!

In this trial study of ‘the chip’ three people with hereditary degenerative blindness were given the implant. They were tested 7 to 9 days after the implant with some psycho-physical tests. If they achieved well on these they went on to be tested for recognition of everyday objects. Due to the electrical nature of the chip it was possible for two test conditions to be employed for all these tests, a chip ‘on’ and chip ‘off’ baseline condition, which allowed for statistically significant results to be acquired.

All three patients were able to detect single electrode single pulse simulations, the perception of this varied slightly between patients but they all reported seeing the stimuli.

They went on to distinguish letters from one another, patient one begin able to tell the difference between U and I, and patient three going further by successfully distinguish four letters presented at random. Patients were also tested on pattern recognition, two of the three were able to correctly distinguish the direction of grid patterns, showing that the chips have high spatial resolution capacities.

Patient two show better recognition in further tests, and interestingly was the only patient of the three to have the chip placed in a slightly different part of the eye. In these cases the patient, identified as Miikka, was able to name objects presented in an unknown dining table situation, including distinguishing between a fork and spoon, as well as an apple and banana.  In subsequent optional tests he went on to read his name (a clip that many will have seen on the news) and pointed out the fact that they’d made a spelling mistake!

The fact that they’d only had the chips in place for just over a week and this was having an impact on their perception of light is impressive enough, but for one participant to go on to read their own name is quite incredible for a first trial.

It’s difficult to find fault in this study, you could say it only worked very successful on one subject, but that wouldn’t be fair at all. It seems promising that all of the patients were able to respond to light stimuli in the first instances.  There are any number of individual differences that might account for the relative different levels of impact that the chip had on all three participants.  One might try to say the media exaggerated the findings in some way but the majority of the reports I saw were very careful to give a full background of the type of blindness that this is appropriate for, as well as the fact that it is very new technology and that it doesn’t ‘restore full sight’.

No questioning then that the results are truly remarkable, and although the success wasn’t replicated in all three subjects, all involved had slight improvements above the level of vision that they had previous to the implant. This research is clearly going to continue to develop into something more and more complex throughout its research future and I hope it can go on to be offered to people with RP more widely in years to come.

It is not often that there is a developement of such magnitude that I’d feel comfortable ending on such a hopeful and positive note but I really do think that this will one day be able to improve the everyday lives of those who have degenerative eye sight. I hope that it’ll go on to allow them to regain the independence that has been taken from them by their conditions and also relieving some of the demands on the carers who have to become their replacement eyes at the moment.

The original paper is:

Subretinal electronic chips allow blind patients to read letters and combine them to words

Eberhart Zrenner, Karl Ulrich Bartz-Schmidt, Heval Benav, Dorothea Besch, Anna Bruckmann, Veit-Peter Gabel, Florian Gekeler, Udo Greppmaier, Alex Harscher, Steffen Kibbel, Johannes Koch, Akos Kusnyerik, Tobias Peters, Katarina Stingl, Helmut Sachs, Alfred Stett, Peter Szurman, Barbara Wilhelm, Robert Wilke.

and a full free PDF can be found here !

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Barley Eating – Video

My mom managed to capture the last 30 seconds of Barley eating. I think it’s interesting how she’s trying to completely clear her bowl (in the side that she is already eating from) so one might suggest she is still feeling hungry when she walks away from the bowl, presumably because she ‘thinks’ it is empty!

The saga continues…

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Barley’s forgotten her food again. Hemispatial neglect symptoms in dog continue.

More images of Barley eating, these are from the 6th September, this time she didn’t eat her whole bowl and again ate only from the right hand side.

So the left hemispace neglect symptoms seem to still be present. I’m working on getting a video and mom has said she’ll try to get the vet to maybe get a scan of barley’s brain so will post those if/when they happen.

Have been in touch with a researcher in my dept at Royal Holloway who forwarded the info on to a researcher at UCL’s NIC. He seems very interested in it, and pointed out that Balint induced neglect symptoms in a dog in his early studies on neglect.

Again, anyone with any information that might be useful please get in touch with me. I should get back to writing up my research project, draft is due in next week and I’ve not written a great deal so far.

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Update: Apparent symptoms of neglect in Barley

It’s difficult for me to write with 100% accuracy about her progress as I am at university 80 miles away from home so am relying on interpretations from emails/photographs and updates via the phone from my mom (who is being incredibly helpful, so big thanks is due!).

But Barley’s most recent progress seems quite promising. My mom said she’d noticed Barley’s ‘fussy eating’ (as she calls it) about 2/3 weeks ago after what was likely to have been another stroke since her first major stroke just over a month ago, which left her with a strong left side weakness which she is now recovering from. The photo’s she has sent today indicate that if she is showing  signs of neglect or another similar neurological condition that these  symptoms are beginning to subside. However, I still think that they way in which she is eating is still very interesting, see the below photos for an illustration.

There seems to be a definite right side preference for the food bowl, (image one) and she clears a whole half almost down a straight line bisection before she moves across to the second ‘half’ of the bowl on her left hand side (image 3). The fourth picture seems to indicate she has changed position slightly, as in the previous photos she is standing right in front of the bowl and in this image she seems to be at it’s side. Again I’ll stress that I do not know precisely how she is eating, I keep trying to get my mom to work out video on her photo so we can have a more accurate step by step portrayal of this.

The fact that she’s managing now to eat her entire bowl without promting is a nice postive sign, I suppose as cool as it is that she’s showing these signs of a neglect I do really want her to get better and make a good recovery. I’m not all about ‘the science’.

I’ll end with this image of Barley being looked after by our new Puppy called Moya (who’s in training to be a dog for the disabled for my mom who has a degenerative spinal condition. I love Moya, she is awesome even if she ate my teddy bear last time I went home!)

Thanks to all of you who’ve seen the post about Barley and have shared it around. If anyone has any suggestions as to how I might better test for neglect signs other than with her food bowl please don’t hesitate to put them forward! I’m also not sure how long neglect can last in a dog when it hasn’t been induced medically for scientific research purposes. So I’d be most grateful for any info from those with veterinary science backgrounds or experience with such things as well. All other information about this condition that anyone may have would be really great to see too!

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My dog has unilateral neglect!

So I really thought that I’d written a post about Unilateral Neglect before but apparently I’m just imagining that! Perhaps my confusion is because I did write an essay about it for the first course I took last year, and hence forth I’ve become all muddled and confuddled that I can no longer differentiate from the work I ‘have to do’ and the blog posts I enjoy doing…

Anyway, this is the most perfect time for me to write about unilateral (or hemispatial) neglect, as my dog appears to be displaying the symptoms! Brilliant isn’t it? I shouldn’t be this excited but I can’t help it.

Meet Barley:
She is a 16 year old Whippet x. Lurcher who used to spend her days chasing bunnies and sometimes catching them, but now just potters about the place and would rather just stare at a field of rabbits and keep walking than bother to do anything about them. A few months ago Barley had a stroke, she suffered severe left side weakness and although has gained a lot of mobility back still has a slightly wonkey head. I believe she is still having small strokes and that she must have had one about a fortnight ago that affected her posterior parietal cortex. My reasons for suspecting this are outlined below, after my brief explanation of unilateral neglect symptoms in humans.

Okay, so here goes the ‘science’. Hemispatial neglect can occur following damage to the right or left posterior parietal cortex, most commonly occurring however in the right and usually as a result of a stroke. The form of neglect can be both extrapersonal, representational and/or personal. In right hemispherical damage the effects tend to be longer lasting and more severe, though most patients do recover over time.

Extrapersonal Neglect

In cases of extrapersonal neglect patients fail to be aware of objects on the contralateral side of their lesion, in most cases this means that they neglect objects in the left side of space. For patients to be diagnosed with hemispatial neglect no other explanation such as a motor or sensory deficit can be present (Vallar, 1998). This form of neglect can involve near space (or peripersonal space) or far space, or both. Often patients will recover over time from hemispatial neglect syndrome. It’s common for these patients to fail to draw the left hand side of a picture, as illustrated below, or for them to even eat food only from the right hand side of their plate and not realise that there is still food on the left to be eaten.

Figure illustrates the left side neglect of a patient.

Representational Neglect
In these cases patients neglect the contralesional space in their memories and imagination of places, objects and people. Representational neglect is far more common to right hemispherical damage and is found in conjunction with the extrapersonal visuospatial neglect described above (Bartolomeo, D’Erme, & Gainotti, 1994).

Personal Neglect
Personal neglect differs in that the patient fails to recognise or use parts of their own body that are on contralateral side of their brain damage. Patients are reported to be unaware of their own limbs, claiming for example that the left leg attached to them belongs to somebody else and is not theirs. This form of neglect is less common than that of extrapersonal neglect, and may involve additional regions of damage. Right personal neglect following a left sided lesion is extremely rare although some cases have been reported (see Peru & Pinna, 1997).

Now of these three forms of neglect I believe it is quite likely that my dog Barley is suffering from extrapersonal neglect following some sort of damage to her Posterior Parietal Cortex in her right hemisphere. The photographs below show my reasons for thinking this is likely. (Thanks go to my Mom for taking these photographs and emailing them to me!)

First image

Number One. Bowl still relatively full of food.

Number Two. Barley eating her food.

Number Three. Barley thinks she has finished eating.

It is pretty clear from these images that she’s really neglecting to ‘see’ the food that is in her left visual field! If mom turns the bowl around so that the food is then on the right hand side of the bowl she continues to eat, albeit a little confused as to where this food has magically appeared from but still.

I hope that these images and experiences of Barleymow have helped illustrate this neurological disorder well, and I will keep tracks on how Barley is doing over time and write about anything new or interesting that happens.

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The Curious Case of Phineas Gage.

Aged 25 and working on the US railroad in Vermont in 1848, Phineas Gage was lucky to survive when a three foot long, tampering iron was propelled through his skull! The blast was caused by Gage neglecting to place a layer of protective sand between the fuse of the dynamite and the tampering pole. Remarkably Gage survived, at the time of his injury he remained conscious and did not even report any pain. He was treated by Dr. John Martyn Harlow, who cared for him during his recovery.

Whilst Gage was recovering well physically, Dr. Harlow noticed changes in his demeanour. An extract from the Doctor’s medical notes reads,

Gage was fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operations, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man. Previous to his injury, although untrained in the schools, he possessed a well-balanced mind, and was looked upon by those who knew him as a shrewd, smart businessman, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and acquaintances said he was ‘no longer Gage’.

It appeared that post his brain injury Gage quite literally became a new man, and this was not a change for the better. Gage died aged 37 after the onset of severe epileptic seizures, no examination of his brain took place at his death. However, his body was exhumed in order that his skull could be examined. From this it has been possible to deduce which brain areas were more likely to have been damaged, which might have implications for the role of particular areas involving personality.
It is likely that the anterior frontal cortex was most significantly damaged. It was the first real case that gave strong evidence that frontal lobes are likely to be important in aspects of human nature such as personality, decision making, and moral approach.

It seems likely now given some recent evidence that Gage did learn to adapt to the changes in his personality and those aspects reported by Harlow might have been only short term. This would be expected as generally adaptation occurs following brain injury, the brain is highly plastic in its nature, which means that even the most severe of injuries can become less impacting on mental and physical wellbeing over time.

It’s important that we remember that this is a single case study, based on evidence from well over one hundred years ago. It makes a nice story to tell in class and keeps people interested, but we aren’t studying history. There was never any real information collected based on the actual physical injuries to Gages brain, if this type of injury occurred today they could have popped him into an MRI scanner and had a proper look at what was going on. Alas, psychologists have relied on mere speculation to develop their theories of brain and personality based on Gage’s case. It is pretty bloody cool though.

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