The Real Fear of Phobia

For many years psychologists have been aware that our minds are more than capable of producing a real biological reaction to any given situation.

And, so as long as the phobic person ‘believes’ that the object or situation they fear represents danger to them, then they will experience real fear.

The majority of people who do suffer with a phobia understand that their fear is ‘irrational’ but continue to experience it regardless of this knowledge. This is why simply being told to “snap out of it” rarely produces a solution!

What is Bathmophobia?

Introduction

Bathmophobia, or the fear of slopes or stairs, is a somewhat complicated phobia.

It is quite similar to climacophobia, or the fear of climbing stairs, except in its specific focus. If you have bathmophobia, you might panic when simply observing a steep slope, while people with climacophobia typically experience symptoms only when expected to actually climb or descend. The difference is subtle but important, and can only be accurately diagnosed by a trained clinician.

Definition

Bathmophobia is a specific phobia. The word itself defines what it means:

  • ‘Bathmo’ means step in Greek; and
  • ‘Phobia’ means fear in Greek.

Therefore, we have the meaning, which is a fear of steps.

Prevalence

According to the National Institute of Mental Health, approximately 12.5 % of the American population will experience a phobia at some point in their life. Bathmophobia is a specific phobia.

Symptoms

The symptoms of Bathmophobia are very similar to other specific phobias and will often include:

  • Feelings of Panic, Dread or Terror.
  • Inability to Relax.
  • An Impending Sense of Dread.
  • Problems Concentrating.
  • Being quick tempered.
  • Feelings of dizziness.
  • Difficulties in becoming motivated.
  • Prickly sensations like pins and needles.
  • Palpitations.
  • Aches & Pains.
  • Fatigued Muscles.
  • Dry and Sticky mouth.
  • Sweating Excessively.
  • Breathlessness.
  • Migraines and Headaches.
  • Poor Quality of Sleep.

Bathmophobia Symptoms are generally automatic and uncontrollable and can seem to take over a person’s thoughts which frequently leads to extreme measures being taken to avoid the feared object or situation, what are known as ‘safety’ or ‘avoidance’ behaviours. Unfortunately, for the sufferer, these safety behaviours have a paradoxical effect and actually reinforce the phobia rather than solve it!

Bathmophobia may be the result of negative emotional experiences that can be either directly or indirectly linked to the object or situational fear. Over time, the symptoms often become ‘normalised’ and ‘accepted’ as a limiting belief in that person’s life – “I’ve learnt to live with it.”’ In just as many cases, Bathmophobia may have become worse over time as more and more sophisticated safety behaviours and routines are developed.

Causes

Bathmophobia may be caused by a wide range of factors. A particularly common cause is an early negative experience with stairs or a steep hill. If you slipped or fell on steep stairs or watched someone else struggle with shortness of breath while climbing, you may be at a greater risk of developing bathmophobia.

Particularly in children, bathmophobia can also be triggered by negotiating or even just contemplating a particularly scary looking set of stairs. One example is a child involved in a local community theater with stairs leading to the backstage costume loft. The stairs were steep and open at the back so you could see down as you climbed them, and the child could imagine slipping through them, even though they did not ever climb them themself.

Memories of those stairs played into dreams that included struggling to cross a sloped floor that would tilt to near-vertical as they neared their destination in the dreams. They may continue to feel apprehension when confronted with a sloped floor or a tricky set of stairs.

Diagnosis

If your child has a fear of stairs or slopes, keep in mind that fears are a normal part of development. Bathmophobia, as with other phobias, is generally not diagnosed in children or adults unless it persists for more than six months.

Differential Diagnosis

In addition to the above-mentioned climacophobia, bathmophobia may be related to other disorders. Acrophobia, or the fear of heights, is exceptionally common. What appears to be a fear of stairs may, in fact, be a fear of the height that the stairs achieve. Illygnophobia, or the fear of vertigo, can also cause symptoms similar to those of bathmophobia.

Medical causes must also be considered. True vertigo is a medical disorder of the balance system that causes a feeling of spinning or dizziness. The term is also applied medically to similar symptoms that are not caused by a balance disorder. Both types can be worsened by even minor changes in height. By definition, a fear that is reasonable due to an existing medical condition cannot be called a phobia.

Treatment

The good news is that the vast majority of people who suffer from Bathmophobia will find a course of psychotherapy helps enormously. Almost every phobia responds well to psychological interventions.

If your clinician determines that your symptoms are caused by bathmophobia, you are likely to receive cognitive behavioural therapy (CBT). The goal of this type of therapy is to help you replace your fearful thoughts and behaviours with more rational alternatives. You will be taught relaxation exercises to help you remain calm, and slowly introduced to the object of your fear through a process known as systematic desensitisation.

Although it takes time, therapy has an excellent success rate in treating this type of phobia. Choosing a therapist that you trust is an essential component in working through your fear.

Did You Know?

  • Bathmophobia can be seen in both children and adults.
  • If you have medical vertigo, fearing that stairs and slopes may trigger your symptoms does not mean that you also have bathmophobia.
  • It is also fairly common among animals, particularly household pets.
  • Dogs trained as service animals may be rejected because of their fear of stairs.
  • Donald Trump has a fear of stairs.

Further Reading

Do Psychiatric Conditions Shift Over Time?

Diagnoses for mental health conditions often morph into each other, suggesting that psychiatry’s reliance on specific diagnoses may be misguided.

A team led by Avshalom Caspi and Terrie Moffitt (2020) at Duke University, North Carolina, analysed data from the Dunedin Birth Cohort Study, which follows a nationally representative group of more
than 1,000 New Zealanders born in 1972 and 1973.

As the participants in the Dunedin Study have grown up, they have been assessed nine times to measure aspects of their health and behaviour, including their mental health. Caspi and Moffitt’s team found that by the age of 45, 86% of participants had met the criteria for at least one psychiatric diagnosis in one assessment. This did not mean that they had received a psychiatric diagnosis, but if they had seen a psychiatrist, they could have been given one.

A third of the cohort met the criteria for a psychiatric diagnosis before they reached the age of 15. Yet over time, people’s mental health usually shifted into a different category of psychiatric conditions.

This could suggest that an excessive focus on a current diagnosis is short-sighted and that therapy should not just address the presenting disorder, but must build fundamental skills for maintaining general mental health.

However, one must caution against ditching diagnostic categories as some disorders are linked to specific causes and respond better to certain treatments than others. It could do harm to ignore these distinctions, at least in some cases.

Reference

Caspi, A., Houts, R.M., Ambler, A., Danese, A., Elliott, M.L., Hariri, A., Harrington, H., Hogan, S., Poulton, R., Ramrakha, S., Rasmussen, L.J.H., Reuben, A., Richmond-Rakerd, L., Sugden, K., Wertz, J., Williams, B.S. & Moffitt, T.E. (2020) Longitudinal Assessment of Mental Health Disorders and Comorbidities Across 4 Decades Among Participants in the Dunedin Birth Cohort Study. JAMA Network Open. 3(4), pp.e203221. doi:10.1001/jamanetworkopen.2020.3221

Is Schizophrenia Associated with Urbanisation?

Research Paper Title

Association of Urbanicity with Schizophrenia and Related Mortality in China.

Background

Although higher prevalence of schizophrenia in Chinese urban areas was observed, studies focused on the association between schizophrenia and urbanicity were less in China. Using a national representative population-based data set, this study aimed to investigate the relationship between urbanicity and schizophrenia and its related mortality among adults aged 18 years old and above in China.

Methods

Data were obtained from the Second China National Sample Survey on Disability in 2006 and follow-up studies from 2007 to 2010 each year. The researchers restricted their analysis to 1,909,205 participants aged 18 years or older and the 2,071 schizophrenia patients with information of survival and all-caused mortality of the follow-up surveys from 2007 to 2010.Schizophrenia was ascertained according to the International Statistical Classification of Diseases, 10th Revision.

The degree of urbanicity and the region of residence were used to be the proxies of urbanicity. Of these, the degree of urbanicity measured by the ratio of nonagricultural population to total population and the region of residence measured by six categorical variables (first-tier cities, first-tier city suburbs, second-tier cities, second-tier city suburbs, other city areas, and rural areas).

Logistics regression models and restricted polynomial splines were used to examine the linear/nonlinear relationship between urbanicity and the risk of schizophrenia. Cox proportional hazards regression models were used to test the role of urbanicity on mortality risk of schizophrenia patients.

Results

10% increase in the degree of urbanicity was associated with increased risk of schizophrenia (OR = 1.44; 95% CI, 1.32 to 1.57). The nonlinear model further confirmed the association between the degree of urbanicity and the risk of schizophrenia. This association existed sex difference, as the level of urbanicity increased, schizophrenia risk of males grew faster than the risk of females. The hazard ratio (HR) of mortality in schizophrenia patients decreased with the elevated of urbanicity level, with a HR of 0.42 (95% CI, 0.21 to 0.84).

Conclusions

This research suggested that incremental changes in the degree of urbanicity linked to higher risk of schizophrenia, and as the degree of urbanicity elevated, the risk of schizophrenia increased more for men than for women. Additionally, we found that schizophrenia patients in higher degree of urbanicity areas had lower risk of mortality.

These findings contributed to the literature on schizophrenia in developing nations under a non-Western context and indicates that strategies to improve mental health conditions are needed in the progress of urbanicity.

Reference

Luo, Y., Pang, L., Guo, C., Zhang, L. & Zheng, X. (2020) Association of Urbanicity with Schizophrenia and Related Mortality in China. Canadian Journal of Psychiatry. doi: 10.1177/0706743720954059. Online ahead of print.

Major Depressive Disorder: Childhood Trauma

Research Paper Title

Major depressive disorder with childhood trauma: Clinical characteristics, biological mechanism, and therapeutic implications.

Background

Major depressive disorder (MDD) is a main type of mood disorder, characterised by significant and lasting depressed mood.

Until now, the pathogenesis of MDD is not clear, but it is certain that biological, psychological, and social factors are involved.

Childhood trauma is considered to be an important factor in the development of this disease.

Previous studies have found that nearly half of the patients with MDD have experienced childhood trauma, and different types of childhood trauma, gender, and age show different effects on this disease.

In addition, the clinical characteristics of MDD patients with childhood trauma are also different, which often have more severe depressive symptoms, higher risk of suicide, and more severe cognitive impairment.

The response to antidepressants is also worse.

In terms of biological mechanisms and marker characteristics, the serotonin transporter gene and the FKBP prolyl isomerase 5 have been shown to play an important role in MDD and childhood trauma.

Moreover, some brain imaging and biomarkers showed specific features, such as changes in gray matter in the dorsal lateral prefrontal cortex, and abnormal changes in hypothalamic-pituitary-adrenal axis function.

Reference

Guo, W., Liu, J. & Li, L. (2020) Major depressive disorder with childhood trauma:Clinical characteristics, biological mechanism, and therapeutic implications. Zhong nan da xue xue bao. Journal of Central South University. 45(4), pp.462-468. doi: 10.11817/j.issn.1672-7347.2020.190699.

What is Capgras Delusion?

Introduction

Capgras delusion, also known as Capgras syndrome. is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical impostor.

It is named after Joseph Capgras (1873-1950), a French psychiatrist.

The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been “warped” or “substituted” have also been reported.

The delusion most commonly occurs in individuals diagnosed with:

  • Paranoid schizophrenia, but has also been seen in;
  • Brain injury;
  • Dementia with Lewy bodies; and
  • Other dementia.

It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks.

In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine.

It occurs more frequently in females, with a female to male ratio of approximately 3 to 2.

Brief History

Capgras syndrome is named after Joseph Capgras, a French psychiatrist who first described the disorder in 1923 in his paper co-authored by Jean Reboul-Lachaux, on the case of a French woman, “Madame Macabre,” who complained that corresponding “doubles” had taken the places of her husband and other people she knew. Capgras and Reboul-Lachaux first called the syndrome “l’illusion des sosies”, which can be translated literally as “the illusion of look-alikes.”

The syndrome was initially considered a purely psychiatric disorder, the delusion of a double seen as symptomatic of schizophrenia, and purely a female disorder (though this is now known not to be the case) often noted as a symptom of hysteria. Most of the proposed explanations initially following that of Capgras and Reboul-Lachaux were psychoanalytical in nature. It was not until the 1980s that attention was turned to the usually co-existing organic brain lesions originally thought to be essentially unrelated or accidental. Today, the Capgras syndrome is understood as a neurological disorder, in which the delusion primarily results from organic brain lesions or degeneration.

Signs and Symptoms

The following two case reports are examples of the Capgras delusion in a psychiatric setting:

Mrs. D, a 74-year-old married housewife, recently discharged from a local hospital after her first psychiatric admission, presented to our facility for a second opinion. At the time of her admission earlier in the year, she had received the diagnosis of atypical psychosis because of her belief that her husband had been replaced by another unrelated man. She refused to sleep with the impostor, locked her bedroom and door at night, asked her son for a gun, and finally fought with the police when attempts were made to hospitalise her. At times she believed her husband was her long deceased father. She easily recognised other family members and would misidentify her husband only. )Passer and Warnock, 1991).

Diane was a 28-year-old single woman who was seen for an evaluation at a day hospital program in preparation for discharge from a psychiatric hospital. This was her third psychiatric admission in the past five years. Always shy and reclusive, Diane first became psychotic at age 23. Following an examination by her physician, she began to worry that the doctor had damaged her internally and that she might never be able to become pregnant. The patient’s condition improved with neuroleptic treatment but deteriorated after discharge because she refused medication. When she was admitted eight months later, she presented with delusions that a man was making exact copies of people – “screens” – and that there were two screens of her, one evil and one good. The diagnosis was schizophrenia with Capgras delusion. She was disheveled and had a bald spot on her scalp from self-mutilation. (Sinkman, 2008).

The following case is an instance of the Capgras delusion resulting from a neurodegenerative disease:

Fred, a 59-year-old man with a high school qualification, was referred for neurological and neuropsychological evaluation because of cognitive and behavioural disturbances. He had worked as the head of a small unit devoted to energy research until a few months before. His past medical and psychiatric history was uneventful. […] Fred’s wife reported that about 15 months from onset he began to see her as a “double” (her words). The first episode occurred one day when, after coming home, Fred asked her where Wilma was. On her surprised answer that she was right there, he firmly denied that she was his wife Wilma, whom he “knew very well as his sons’ mother”, and went on plainly commenting that Wilma had probably gone out and would come back later. […] Fred presented progressive cognitive deterioration characterised both by severity and fast decline. Apart from [Capgras disorder], his neuropsychological presentation was hallmarked by language disturbances suggestive of frontal-executive dysfunction. His cognitive impairment ended up in a severe, all-encompassing frontal syndrome. (Lucchelli and Spinnler, 2007).

Causes

It is generally agreed[14] that the Capgras delusion has a complex and organic basis (caused by structural damage to organs) and can be better understood by examining neuroanatomical damage associated with the syndrome.

In one of the first papers to consider the cerebral basis of the Capgras delusion, Alexander, Stuss and Benson pointed out in 1979 that the disorder might be related to a combination of frontal lobe damage causing problems with familiarity and right hemisphere damage causing problems with visual recognition.

Further clues to the possible causes of the Capgras delusion were suggested by the study of brain-injured patients who had developed prosopagnosia. In this condition, patients are unable to recognize faces consciously, despite being able to recognize other types of visual objects. However, a 1984 study by Bauer showed that even though conscious face recognition was impaired, patients with the condition showed autonomic arousal (measured by a galvanic skin response measure) to familiar faces, suggesting that there are two pathways to face recognition – one conscious and one unconscious.

In a 1990 paper published in the British Journal of Psychiatry, psychologists Hadyn Ellis and Andy Young hypothesised that patients with Capgras delusion may have a “mirror image” or double dissociation of prosopagnosia, in that their conscious ability to recognise faces was intact, but they might have damage to the system that produces the automatic emotional arousal to familiar faces. This might lead to the experience of recognising someone while feeling something was not “quite right” about them. In 1997, Ellis and his colleagues published a study of five patients with Capgras delusion (all diagnosed with schizophrenia) and confirmed that although they could consciously recognise the faces, they did not show the normal automatic emotional arousal response. The same low level of autonomic response was shown in the presence of strangers. Young (2008) has theorised that this means that patients with the disease experience a “loss” of familiarity, not a “lack” of it. Further evidence for this explanation comes from other studies measuring galvanic skin responses (GSR) to faces. A patient with Capgras delusion showed reduced GSRs to faces in spite of normal face recognition. This theory for the causes of Capgras delusion was summarised in Trends in Cognitive Sciences in 2001.

William Hirstein and Vilayanur S. Ramachandran reported similar findings in a paper published on a single case of a patient with Capgras delusion after brain injury. Ramachandran portrayed this case in his book Phantoms in the Brain and gave a talk about it at TED 2007. Since the patient was capable of feeling emotions and recognising faces but could not feel emotions when recognising familiar faces, Ramachandran hypothesises that the origin of Capgras syndrome is a disconnection between the temporal cortex, where faces are usually recognized (see temporal lobe), and the limbic system, involved in emotions. More specifically, he emphasises the disconnection between the amygdala and the inferotemporal cortex.

In 2010, Hirstein revised this theory to explain why a person with Capgras syndrome would have the particular reaction of not recognising a familiar person.

Furthermore, Ramachandran suggests a relationship between the Capgras syndrome and a more general difficulty in linking successive episodic memories because of the crucial role emotion plays in creating memories. Since the patient could not put together memories and feelings, he believed objects in a photograph were new on every viewing, even though they normally should have evoked feelings (e.g., a person close to him, a familiar object, or even himself). Others like Merrin and Silberfarb (1976) have also proposed links between the Capgras syndrome and deficits in aspects of memory. They suggest that an important and familiar person (the usual subject of the delusion) has many layers of visual, auditory, tactile, and experiential memories associated with them, so the Capgras delusion can be understood as a failure of object constancy at a high perceptual level.

Most likely, more than just an impairment of the automatic emotional arousal response is necessary to form the Capgras delusion, as the same pattern has been reported in patients showing no signs of delusions. Ellis suggested that a second factor explains why this unusual experience is transformed into a delusional belief; this second factor is thought to be an impairment in reasoning, although no definitive impairment has been found to explain all cases. Many have argued for the inclusion of the role of patient phenomenology in explanatory models of the Capgras syndrome in order to better understand the mechanisms that enable the creation and maintenance of delusional beliefs.

Capgras syndrome has also been linked to reduplicative paramnesia, another delusional misidentification syndrome in which a person believes a location has been duplicated or relocated. Since these two syndromes are highly associated, it has been proposed that they affect similar areas of the brain and therefore have similar neurological implications. Reduplicative paramnesia is understood to affect the frontal lobe, and thus it is believed that Capgras syndrome is also associated with the frontal lobe. Even if the damage is not directly to the frontal lobe, an interruption of signals between other lobes and the frontal lobe could result in Capgras syndrome.

Diagnosis

Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on a psychiatric evaluation of the patient, who is most likely brought to a psychiatrist’s attention by a family member or friend believed to be an imposter by the person under the delusion.

Treatment

Treatment has not been well studied and so there is no evidence-based approach. Treatment is generally therapy, often with support of antipsychotic medication.

Cultural References

In the Memoirs Found in a Bathtub novel by the Polish writer Stanisław Lem, first published in 1961 the narrator inhabits a paranoid dystopia where nothing is as it seems, chaos seems to rule all events, and everyone is deeply suspicious of everyone. In the end, it is revealed that the world is filled by phantom body doubles.

A central character in Richard Powers’s 2006 novel The Echo Maker suffers from Capgras Delusion subsequent to traumatic brain injury.

The protagonist in the movie Synecdoche, New York, who is named Caden Cotard (played by Philip Seymour Hoffman), goes to see his ex-wife at her apartment, and, as he enters the building, one of the resident call boxes is taped with the name “Capgras”. He is then misidentified as his ex-wife’s cleaning lady, Ellen Bascomb, as he tries to enter the apartment, and, later in the film, he actually comes to play the role of Ellen Bascomb in his own play. Throughout the film, Cotard enlists actor-doubles to play actors, and, as the film progresses, the actor-doubles are in turn then given actors-doubles.

Addictions: Broken Brain Model vs Systems-Level Perspective

Research Paper Title

Curing the broken brain model of addiction: Neurorehabilitation from a systems perspective.

Background

The dominant biomedical perspective on addictions has been that they are chronic brain diseases.

While the authors acknowledge that the brains of people with addictions differ from those without, they argue that the “broken brain” model of addiction has important limitations. They propose that a systems-level perspective more effectively captures the integrated architecture of the embodied and situated human mind and brain in relation to the development of addictions. This more dynamic conceptualisation places addiction in the broader context of the addicted brain that drives behaviour, where the addicted brain is the substrate of the addicted mind, that in turn is situated in a physical and socio-cultural environment.

From this perspective, neurorehabilitation should shift from a “broken-brain” to a systems theoretical framework, which includes high-level concepts related to the physical and social environment, motivation, self-image, and the meaning of alternative activities, which in turn will dynamically influence subsequent brain adaptations. The authors call this integrated approach system-oriented neurorehabilitation.

They illustrate their proposal by showing the link between addiction and the architecture of the embodied brain, including a systems-level perspective on classical conditioning, which has been successfully translated into neurorehabilitation. Central to this example is the notion that the human brain makes predictions on future states as well as expected (or counterfactual) errors, in the context of its goals.

The authors advocate system-oriented neurorehabilitation of addiction where the patients’ goals are central in targeted, personalised assessment and intervention.

Reference

Wiers, R.W. & Verschure, P. (2020) Curing the broken brain model of addiction: Neurorehabilitation from a systems perspective. Addictive Behaviors. doi: 10.1016/j.addbeh.2020.106602. Online ahead of print.

Misophonia: Quirk of Human Behaviour or Mental Health Condition?

Introduction

By analogy with misogyny and misanthropy, misophonia ought to mean hatred of noise.

In fact, it is a recent coinage used to label the phenomenon of strong aversive reactions to sounds originating in other people’s oral or nasal cavities, such as chewing, sniffing, slurping, and lip smacking.

A report of a large series of cases seen in the Netherlands suggests that misophonia is well on its way to becoming a new psychiatric disorder (see below) (Jager et al., 2020).

Some commentators have expressed concern at the creeping medicalisation of quirks of human behaviour (BMJ, 2020).

What is Misophonia?

  • It is also known as Selective Sound Sensitivity Syndrome.
  • Misophonia is a disorder in which certain sounds trigger emotional or physiological responses that some might perceive as unreasonable given the circumstance.
  • Those who have misophonia might describe it as when a sound “drives you crazy.”
  • Their reactions can range from anger and annoyance to panic and the need to flee.

Research Paper Title

Misophonia: Phenomenology, comorbidity and demographics in a large sample.

Objective

Analyse a large sample with detailed clinical data of misophonia subjects in order to determine the psychiatric, somatic and psychological nature of the condition.

Methods

This observational study of 779 subjects with suspected misophonia was conducted from January 2013 to May 2017 at the outpatient-clinic of the Amsterdam University Medical Centres, location AMC, the Netherlands. The researchers examined DSM-IV diagnoses, results of somatic examination (general screening and hearing tests), and 17 psychological questionnaires (e.g. SCL-90-R, WHOQoL).

Results

The diagnosis of misophonia was confirmed in 575 of 779 referred subjects (74%). In the sample of misophonia subjects (mean age, 34.17 [SD = 12.22] years; 399 women [69%]), 148 (26%) subjects had comorbid traits of obsessive-compulsive personality disorder, 58 (10%) mood disorders, 31 (5%) attention-deficit (hyperactivity) disorder, and 14 (3%) autism spectrum conditions. 2% reported tinnitus and 1% hyperacusis. In a random subgroup of 109 subjects the researchers performed audiometry, and found unilateral hearing loss in 3 of them (3%). Clinical neurological examination and additional blood test showed no abnormalities. Psychological tests revealed perfectionism (97% CPQ>25) and neuroticism (stanine 7 NEO-PI-R). Quality of life was heavily impaired and associated with misophonia severity (rs (184) = -.34 p = < .001, p = < .001).

Limitations

This was a single site study, leading to possible selection–and confirmation bias, since AMC-criteria were used.

Conclusions

This study with 575 subjects is the largest misophonia sample ever described.

Based on these results the researchers propose a set of revised criteria useful to diagnose misophonia as a psychiatric disorder.

References

BMJ 2020;369:m1843.

Jager, I., de Koning, P., Bost, T., Denys, D. & Vulink, N. (2020) Misophonia: Phenomenology, comorbidity and demographics in a large sample. PloS One. https://doi.org/10.1371/journal.pone.0231390.

Misophonia: Quirk of Human Behaviour or Mental Health Condition?

Introduction

By analogy with misogyny and misanthropy, misophonia ought to mean hatred of noise.

In fact, it is a recent coinage used to label the phenomenon of strong aversive reactions to sounds originating in other people’s oral or nasal cavities, such as chewing, sniffing, slurping, and lip smacking.

A report of a large series of cases seen in the Netherlands suggests that misophonia is well on its way to becoming a new psychiatric disorder (see below) (Jager et al., 2020).

Some commentators have expressed concern at the creeping medicalisation of quirks of human behaviour (BMJ, 2020).

What is Misophonia?

  • It is also known as Selective Sound Sensitivity Syndrome.
  • Misophonia is a disorder in which certain sounds trigger emotional or physiological responses that some might perceive as unreasonable given the circumstance.
  • Those who have misophonia might describe it as when a sound “drives you crazy.”
  • Their reactions can range from anger and annoyance to panic and the need to flee.

Research Paper Title

Misophonia: Phenomenology, comorbidity and demographics in a large sample.

Objective

Analyse a large sample with detailed clinical data of misophonia subjects in order to determine the psychiatric, somatic and psychological nature of the condition.

Methods

This observational study of 779 subjects with suspected misophonia was conducted from January 2013 to May 2017 at the outpatient-clinic of the Amsterdam University Medical Centres, location AMC, the Netherlands. The researchers examined DSM-IV diagnoses, results of somatic examination (general screening and hearing tests), and 17 psychological questionnaires (e.g. SCL-90-R, WHOQoL).

Results

The diagnosis of misophonia was confirmed in 575 of 779 referred subjects (74%). In the sample of misophonia subjects (mean age, 34.17 [SD = 12.22] years; 399 women [69%]), 148 (26%) subjects had comorbid traits of obsessive-compulsive personality disorder, 58 (10%) mood disorders, 31 (5%) attention-deficit (hyperactivity) disorder, and 14 (3%) autism spectrum conditions. 2% reported tinnitus and 1% hyperacusis. In a random subgroup of 109 subjects the researchers performed audiometry, and found unilateral hearing loss in 3 of them (3%). Clinical neurological examination and additional blood test showed no abnormalities. Psychological tests revealed perfectionism (97% CPQ>25) and neuroticism (stanine 7 NEO-PI-R). Quality of life was heavily impaired and associated with misophonia severity (rs (184) = -.34 p = < .001, p = < .001).

Limitations

This was a single site study, leading to possible selection–and confirmation bias, since AMC-criteria were used.

Conclusions

This study with 575 subjects is the largest misophonia sample ever described.

Based on these results the researchers propose a set of revised criteria useful to diagnose misophonia as a psychiatric disorder.

References

BMJ 2020;369:m1843.

Jager, I., de Koning, P., Bost, T., Denys, D. & Vulink, N. (2020) Misophonia: Phenomenology, comorbidity and demographics in a large sample. PloS One. https://doi.org/10.1371/journal.pone.0231390.