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Small talk: Alice in Wonderland Syndrome (Revisited)

Last week, I was contacted by the journalist Abigail Moss about a previous blog that I wrote on Alice in Wonderland Syndrome (AIWS). AIWS is a non-contagious disorientation disorder and refers to when a person’s sense of body image, vision, hearing, touch, space, and/or time are distorted. AIWS sufferers typically experience micropsia (a neurological condition that affects human visual perception in which objects are perceived to be smaller than they actually are and make people feel bigger than they are) or macropsia (a neurological condition that affects human visual perception in which objects are perceived to be larger than they actually are and makes people feel smaller than they actually are).

Moss suffers from AIWS herself and has described her experiences both on camera (for instance in a short YouTube news piece and in numerous news articles such as one in the Daily Mail). Moss also sent me a first-person account of AIWS that she published in the online magazine Planet Ivy. Here are some of the things she recounted:

Extract 1: “When I was about five years old, I started to experience strange visual and sensory hallucinations. My hands and legs would seem too big for my body and the room around me would start to shrink inwards. All movements and sounds would seem extremely fast and hugely exaggerated, giving everything an odd feeling of urgency. This would last about 20 minutes and slowly fade away, and happened about four or five times a week…Luckily, my dad knew exactly what I was describing…He’d experienced the same thing as a kid. I haven’t outgrown it…but it doesn’t happen as often – maybe only five times a year”.

The first doctor suggested she might have a form of epilepsy but after that proved negative she was never diagnosed with anything official. Since then, other medics have suggested that she may have a sleep disorder or some kind of schizophrenia. It wasn’t until she was in her early twenties that she came across something that fitted her symptoms:

Extract 2: “Last year a tiny 50-word inset in a newspaper supplement caught my eye. ‘Alice in Wonderland Syndrome’ the heading read, and underneath it, a perfect description of my experience…I joined a Yahoo forum for ‘AIWS sufferers’…Countless fellow sufferers got in contact, all describing the same thing. Their descriptions were remarkably unvaried and it was immediately obvious this was the same thing I experience: ‘My body felt minuscule’, ‘Sounds were amplified’, ‘Everything was bigger and smaller at the same time’.”

The article outlined the many psychiatrists and psychologists Moss had visited about her condition with all the experts she saw claiming that they had never heard of AIWS. While the condition is rare, the condition has been well documented in the medical and clinical literature (see ‘Further reading’ below) so I was quite surprised that the experts she visited couldn’t have at least spent some time reading up on the syndrome. She then went on to say:

Extract 3: “My brain does something extremely weird, and nobody – not even the world’s leading bodies in the study of brains – can tell me what this is or why it happens. For me, this isn’t a problem, I don’t want to get rid of my episodes – they’re an interesting talking point and everyone knows writers are basically quite boring people. The experience, when it does pop up, doesn’t actually bother me or affect my day-to-day life”.

Moss wanted to ask me a few questions about my understanding of AIWS and how much is now known about it. She knew this wasn’t my primary area of expertise, but said that any opinions I might be able to offer would be invaluable to the article she was writing. I told her that my article on AIWS was written in a journalistic capacity rather from any position of expertise but she still wanted me to answer a few questions. Moss asked me three questions and I thought I would use this blog to share my full answers with my readers.

Question 1: “In my research I’ve found it almost impossible to find solid answers about what causes AIWS. Can you offer a view on what makes this condition so difficult to pin down?”

AIWS has been reported in the psychiatric and psychological literature since the early 1950s. However, since the first papers in the topic less than 20 papers have ever been published and all of them are case reports. Finding ‘solid answers’ based on so few cases is therefore inevitable. The literature is also biased because it is (a) based on those sufferers who seek out medical assistance, and (b) based on those doctors or clinicians that have written the cases for publication. If people don’t seek help and/or there cases remain unwritten, there is little chance if finding ‘solid answers’.

Secondly, the symptoms are not always identical which is why it is referred to as syndrome (that is, a group of symptoms that together are characteristic of a specific disorder or disease, or a predictable, characteristic condition or pattern of behavior that tends to occur under certain circumstances). Syndromes typically have many different causes which again means it is difficult to find ‘solid answers’.

Finally, given that the experiences (like your own) are often short-lived, it is very rare to be able to monitor people neurologically. The few published cases are based on chronic sufferers (who may not be representative of the vast majority of AIWS sufferers). Several neurologists have done M.R.I.s on patients with the condition, though once the bout has passed, there’s usually no sign of unusual brain activity. I read that Dr. Sheena Aurora was the first to scan the brain of someone — a 12-year-old girl — in the middle of an episode. According to Dr. Aurora, electrical activity caused abnormal blood flow in the parts of the brain that control vision and process texture, shape and size.

The case studies that I have read have provided lots of possible reasons for AIWS but there is no consensus and they could all be true (as having the same symptoms doesn’t mean there has to be the same cause). Some research appears to indicate that AIWS can be due to abnormal amounts of electrical activity that causes blood to flow abnormally in the brain areas that process texture and visual perception. AIWS has been associated with migraines, severe depression, and (in extreme cases) brain tumours. Case study research has indicated that AIWS manifestations are due to disturbed function of either medial temporal, hippocampal, tempro-occipital or tempro-parieto-occipital regions of the brain. Unfortunately, chronic AIWS is untreatable and time is the only healer. However, sharing experiences with other sufferers is also thought to be therapeutically beneficial

Question 2: “Is academic disagreement just part and parcel of all psychological conditions or does AIWS seems particularly open to discussion?”

I don’t think there is ‘disagreement’ as no two clinicians or psychiatrists have ever published papers examining the same individuals. They have all published papers based on the AIWS sufferers that they themselves saw and that who came in seeking help. All of the explanations could be correct as syndromes have multiple causes. This is not disagreement. It’s simply a case of multiple possible causes.

Question 3: “I have spoken to a large number of people who also say they also experience AIWS – how useful or valid do you think it would be to think of AIWS as more of a mental phenomenon than a syndrome, comparable with something like déjà vu, for example?”

The word ‘large’ is what we psychologists call a ‘fuzzy quantifier’ as ‘large’ to one individual is small to another. If you have spoken to 100 other sufferers worldwide I would say this is very very small. The condition appears to be rare although in one of my other areas of research, we have demonstrated that a small proportion of video gamers experience disorienting visual effects (that we call game transfer phenomena) like AIWS so such phenomena may be multi-faceted and may arise from specific activities (such as excessive and immersive game playing).

AIWS should not be compared with déjà vu as most scientific evidence suggests that déjà vu is an anomaly of memory and totally different from AIWS on a neurological level (but I’m not an expert on déjà vu and am only basing my opinion on what I have read in the psychological literature). However, there may be some conditions (such as schizophrenia and temporal lobe epilepsy) where individuals may experience both AIWS and déjà vu but these are symptoms of a specific medical disorder. Most individuals that have experienced déjà vu (as many as two-thirds of the population in some studies) and AIWS (very rare) do not have any underlying serious medical conditions.

I don’t know if any of my responses to Moss were of help either in relation to her own experiences or in writing her article but I was pleased with the observations I had made.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Bui, E., Chatagner, A. & Schmitt, L. (2010). Alice in Wonderland Syndrome in major depressive disorder. Journal of Neuropsychiatry and Clinical Neurosciences, 22, 352.e16-352.e16.

Cinbis, M. & Aysun, S. (1992). Alice in Wonderland syndrome as an initial manifestation of Epstein-Barr virus infection (case report). British Journal of Ophthalmology, 76, 316.

Eshel, G.M., Eyov, A., & Lahat, E., et al (1987). Alice in Wonderland syndrome, a manifestation of acute Epstein-Barr virus infection (brief report). Pediatric Infectious Diseases Journal, 6, 68.

Kew, J., Wright, A., & Halligan, P.W. (1998). Somesthetic aura: The experience of “Alice in Wonderland”. The Lancet, 351, 1934.

Kitchener, N. (2004). Alice in Wonderland Syndrome. International Journal of Child Neuropsychiatry, 1, 107-112.

Kuo, Y, Chiu, N.C., Shen, E.Y., Ho, C.S., Wu, M.C. (1998). Cerebral perfusion in children with “Alice in Wonderland” syndrome. Pediatric Neurology, 19, 105-108.

Lahat, E., Eshel, G., & Arlazoroff A (1990). “Alice in Wonderland” syndrome and infectious mononucleosis in children (letter). Journal of Neurology, Neurosurgery and Psychiatry, 53, 1104.

Lambert, M.V., Sierra, M., Phillips, M.L. & David, A.S. The spectrum of organic depersonalization: A review plus four new cases. Journal of Neuropsychiatry and Clinical Neuroscience, 14, 141-154.

Podoll, K., Ebel, H., Robinson, D., & Nicola, U. (2002). Obligatory and facultative symptoms of the Alice in wonderland syndrome. Minerva Medicine, 93, 287-293.

Podoll, K. & Robinson, D. (1999). Lewis Carroll’s migraine experiences. The Lancet, 353, 1366.

Rolak, L.A. (1991). Literary neurologic syndromes. Alice in Wonderland. Archives of Neurology, 48, 649–651.

Todd, J. (1955). The syndrome of Alice in Wonderland. Canadian Medical Association Journal, 73, 701–704.

Non-prescription addiction: A brief look at nasal spray dependence

I’m not quite sure about how I came across it, but I unearthed an article on the Discovery Fit and Health website entitled ‘Can nasal sprays be addictive?’ Apparently Oprah Winfrey did a whole episode of her show on the phenomenon (but I must have missed that one). The article noted that nasal sprays (such as Sinex) contain decongestants (such as oxymetazoline, xylometazoline and ephedrine) that constrict the blood vessels inside the nose. More specifically:

“When you have a cold, the flu or allergies, these blood vessels become swollen and dilated. This stimulates the nasal membranes to produce large amounts of mucus. Like stepping on a garden hose, constricting the blood vessels reduces the blood flow to your nostrils. The swollen vessels shrink, and this helps to dry things up. Unfortunately, your nose can become tolerant to the decongestant’s effect if you use it for too long. Tolerance in general happens because your body launches a biological counterattack against the effects of a drug”…You end up using more and more to get rid of your stuffy nose. And each time you sniff more decongestant, your body redoubles its efforts against the resulting constriction”.

The labelling on nasal sprays typically advise not using the product for more than three days in a row because of the diminished effect as the tolerance to the decongestant properties builds up. Anecdotal accounts of ‘nasal spray addiction’ appear quite often in the popular press. For instance, a 2008 story in the Daily Mail recounted the story of 27-year Gloucestershire woman Allyson Forbes, a hay fever sufferer who claimed to be addicted to her nasal spray. Dr George Du Toit, a London-based allergy consultant was interviewed for the story and was quoted as saying:

“These products are not actually addictive in the true sense of the word – you cannot develop a chemical or physical addiction – but they are psychologically addictive because of the initial relief they induce…Patients need increasing doses of the medication to achieve the same response. This rebound condition is called rhinitis medicamentosa (RM), where permanently swollen intranasal tissues can damage the lining of the nose. The products should not be used for longer than seven consecutive days…RM typically occurs after five to seven days of use”.

Another person interviewed for the story was the chemist Sultan Sid Dajani (Royal Pharmaceutical Society) who said:

“People often don’t want to talk about this kind of dependence because they are embarrassed. Chronic abusers who are long-term users of these medications, known as nasodilators, are committing an unwitting form of self-harm and I feel every sympathy for them. On average, I see five people a week who have this problem and I’m an independent chemist, so goodness knows how many there are regularly buying in chains and supermarkets. Addictions to these nasodilators are more common than addictions to over-the-counter medicines, such as codeine”.

Allyson said she had to use her nasal medicine four times a day and says she doesn’t “feel physically addicted” and knows that the addiction is psychologically-based and “is in [her] head”. If you feel you may be suffering from an addiction to nasal sprays are even articles on the internet that claim they can help you such as ‘How do you beat a dependency on nose spray?’ (at the Wiki Answers website). There’s even a totally dedicated website that deals with treating nasal spray addiction (AfrinAddiction.com). Other stories (such as one at the Medical News Today website) sensationally claim that millions suffer from addiction to [over-the-counter] nasal sprays” while a story in the New York Times ran the headline “Nasal sprays can bring on vicious cycle”.

Looking at the psychological and medical literature, there is a lot less that has been published on whether nasal sprays can be addictive. However, there is actually quite an established literature on psychiatric conditions associated with respiratory drugs (including decongestants found in nasal sprays). Dr. Richard Hall and colleagues in a 1985 issue of the journal Psychosomatics reviewed the incidence of psychiatric reactions to medically prescribed and over-the-counter respiratory drugs. The concluded that such psychiatric conditions are most associated with heavy and chronic users of such drugs. However, they also found that toxicity was scarce and poorly defined.

In relation to addiction, I only managed to locate three academic papers that reported ‘addiction’ to nasal sprays. In a 2006 issue of Journal of Investigational Allergology and Clinical Immunology, Dr. J.T. Ramey and colleagues reviewed the literature relating to rhinitis medicamentosa (RM). They noted that:

“Psychological dependence and an abstinence syndrome consisting of headaches, restlessness, and anxiety following discontinuation of nasal decongestants have been reported, leading some authors to use the word ‘addiction’ when describing this syndrome”.

Dr. Ramey and colleagues’ paper based this observation on three case reports published between 1969 and 1984. One case was reported by Dr. M. Pearson and colleagues in a 1969 issue of the American Journal of Psychiatry. They described a man with rhinitis medicamentosa who carried four gallons of phenylephrine aboard a wartime ship because of his addiction to this medication. In another case study reported by Dr S. Snow and colleagues in the British Journal of Psychiatry, toxic psychosis was highlighted in a 26-year old male patient said to be addicted to phenylephrine in nasal spray form. The man was also reported as experiencing tactile and visual hallucinations, visual illusions and paranoid delusions. These papers suggest the possibility of addiction to nasal spray but given the fact so few case studies have been reported in the medical literature, the incidence would appear to be very rare (and certainly not the “millions” reported in some website stories).

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Discovery Fit and Health (2013). Can nasal sprays be addictive? Located at: http://health.howstuffworks.com/mental-health/question546.htm

Estridge, B. (2008). Hay fever has left me addicted to nose spray. Daily Mail, September 6. Located at: http://www.dailymail.co.uk/health/article-1053096/Hay-fever-left-addicted-nose-spray.html

Fleece, L., Mizes, J. S., Jolly, P.A., & Baldwin, R.L. (1984). Rhinitis medicamentosa. Conceptualization, incidence, and treatment. The Alabama Journal of Medical Sciences, 21(2), 205.

Hall, R., Beresford, T., Stickney, S., Nasdahl, C., & Coleman, J. (1985). Psychiatric reactions produced by respiratory drugs. Psychosomatics, 26, 605-616.

Pearson, M.M. & Little, R.B. (1969). The addictive process in unusual addictions: A further elaboration of etiology. American Journal of Psychiatry, 125, 1166-1171.

Ramey, J.T., Bailen, E., & Lockey, R.F. (2006). Rhinitis medicamentosa. Journal of Investigational Allergology and Clinical Immunology, 16(3), 148.

Snow, S.S., Logan, T.P., & Hollender, M.H. (1980). Nasal spray’ addiction’ and psychosis: A case report. British Journal of Psychiatry, 136, 297-299.

Small claims caught: A beginner’s guide to Alice in Wonderland Syndrome

While researching a blog on Cotard Syndrome I came across a case study of Alice in Wonderland Syndrome published by Dr. Eric Bui and his colleagues published in the Journal of Neuropsychiatry and Clinical Neurosciences. They wrote:

“A 74-year-old retired French executive was admitted to hospital for major depressive disorder with psychotic features triggered by prostate surgery 3 months previously…The patient was described by his wife as usually sociable, jolly, scrupulous and a perfectionist. On admission, the patient presented with a depressed mood, loss of pleasure and interest, disordered sleeping, severe fatigue, loss of appetite, psychomotor retardation, and persecutory (being broken into and burgled) as well as somatic (his stools being contaminated) delusions…Ten days after admission, the patient exhibited new delusional symptoms: he believed his hands and feet were shorter than usual and was convinced that his clothes had shrunk. Organic causes (intracranial tumor and infection, thyroid disease, and nutritional deficiency) were ruled out by physiological, laboratory, neurological, and ophthalmological investigations…The patient continued to be delusional and severely depressed…He was discharged on day 45 of hospitalization with complete remission”.

As can be probably be surmised from this brief case study, Alice in Wonderland Syndrome (AIWS) is a non-contagious disorientation disorder and refers to when a person’s sense of body image, vision, hearing, touch, space, and/or time are distorted. AIWS sufferers typically experience micropsia (a neurological condition that affects human visual perception in which objects are perceived to be smaller than they actually are and make people feel bigger than they are) or macropsia (a neurological condition that affects human visual perception in which objects are perceived to be larger than they actually are and makes people feel smaller than they actually are). They may also experience feelings of paranoia.

AIWS has nothing to do with a malfunctioning of the eyes, but is a change in how the world is perceived with those suffering seeing objects the wrong shape or size. Arguably the most disturbing symptom for sufferers is the perceived alteration of their body image. AIWS sufferers become confused about the size and shape of their body (or specific body parts). Time perception may also be affected with many sufferers reporting that time seems to pass incredibly slowly as if they were on an LSD trip. Sufferers (most commonly thought to be children and migraine sufferers) often become very frightened, scared and panic-stricken, although it can often be treated successfully through complete rest and relaxation (and in most cases is a relatively temporary condition). Some research appears to indicate that AIWS can be due to abnormal amounts of electrical activity that causes blood to flow abnormally in the brain areas that process texture and visual perception.

AIWS was named after the 1865 book Alice’s Adventures in Wonderland by Lewis Carroll, but is also known as Todd Syndrome named after the psychiatrist who first wrote about the condition in a 1955 issue of the Canadian Medical Association Journal. (Interestingly, a short article by Dr. Klaus Podoll and Dr. Derek Robinson in The Lancet from 1999 highlighted that Carroll was a migraine sufferer and that his book may have been inspired by his own personal experiences!). Todd’s original paper reported five patients (of which four were female) all of who suffered from severe migraines. All of these patients described their body, body parts and/or objects around them changing in size (with two of them also having time disorientation too). On the basis of these five cases, Todd coined the term ‘Alice in Wonderland Syndrome’ (although such hallucinations had been noted three years prior to this by Dr. C.W. Lippman in a 1952 paper on certain hallucinations peculiar to migraine”).

The condition has also been associated with other medical conditions besides migraines, including (mononucleosis) infections, and severe depression, and (in extreme cases) brain tumours. A paper by Dr. Nabil Kitchener in a 2004 issue of the International Journal of Child Neuropsychiatry also noted that AIWS can also be the presenting manifestations in some patients with epilepsy, hyperpyrexia (i.e., extremely elevated body temperatures), typhoid encephalopathy, and other psychiatric disorders. In a 2005 paper in the journal European Neurology, Dr. Valmantas Budrys also reported that AWS could occur in hypnagogic, delirious states, encephalitis, cerebral lesions, drug intoxication, and schizophrenia.

In a literature review on organic depersonalization in the Journal of Neuropsychiatry and Clinical Neuroscience, Dr. Michelle Lambert and her colleagues examined the literature on AIWS. The noted that since Todd’s case studies were published, the subsequent published case reports of body image distortion associated with AIWS, often included depersonalization and/or derealization. They suggested that such symptom were consistent with parietal lobe pathology. More specifically, they argued that the frequent accompanying symptoms of fear, anxiety, and panic implicate the role of the temporal lobe. Dr. Kitchener’s 2004 paper also concludes that AIWS manifestations are due to disturbed function of either medial temporal, hippocampal, tempro-occipital or tempro-parieto-occipital regions of the brain based on the research of Dr. Kuo and colleagues published in a 1998 study in the Pediatric Neurology journal.

However, the case study published by Dr. Bui and his colleagues that I began this blog suggested that AIWS may be similar to Cotard Syndrome (CS). As the authors noted, that:

“Cotard Syndrome comprises any one of a series of delusions ranging from the belief that one has lost organs to the conviction that one is dead. Since Cotard’s syndrome is also usually associated with severe depression and improves rapidly with ECT [electro-convulsive therapy], it is possible that the somatic delusions experienced by our [AIWS] patient were a variant of this syndrome. According to our observations, the psychotic features of major depressive disorder might present in the form of Alice in Wonderland syndrome although the relationship between this syndrome and Cotard’s syndrome remains to be determined”.

Depending upon co-morbid conditions, medical treatments include beta blockers, anti-depressants, and anti-convulsants, AIWS has also been reported in both the Pediatric Infectious Diseases Journal (1987) and British Journal of Ophthalmology (1992) as one of the early signs of the Epstein-Barr Virus, one of the most common human viruses and of the herpes family. Most commonly it causes glandular fever but is associated with various forms of cancer including Hodgkin’s lymphoma. Chronic AIWS is untreatable and time is the only healer. Sharing experiences with other sufferers is also thought to be therapeutically beneficial (although I know of no clinical support for the claim).

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Budrys, V. (2005). Neurological eponyms derived from literature and visual art. European Neurology, 53, 171-178.

Bui, E., Chatagner, A. & Schmitt, L. (2010). Alice in Wonderland Syndrome in major depressive disorder. Journal of Neuropsychiatry and Clinical Neurosciences, 22, 352.e16-352.e16.

Cinbis, M. & Aysun, S. (1992). Alice in Wonderland syndrome as an initial manifestation of Epstein-Barr virus infection (case report). British Journal of Ophthalmology, 76, 316.

Eshel, G.M., Eyov, A., & Lahat, E., et al (1987). Alice in Wonderland syndrome, a manifestation of acute Epstein-Barr virus infection (brief report). Pediatric Infectious Diseases Journal, 6, 68.

Kew, J., Wright, A., & Halligan, P.W. (1998). Somesthetic aura: The experience of “Alice in Wonderland”. The Lancet, 351, 1934.

Kitchener, N. (2004). Alice in Wonderland Syndrome. International Journal of Child Neuropsychiatry, 1, 107-112.

Kuo, Y, Chiu, N.C., Shen, E.Y., Ho, C.S., Wu, M.C. (1998). Cerebral perfusion in children with “Alice in Wonderland” syndrome. Pediatric Neurology, 19, 105-108.

Lahat, E., Eshel, G., & Arlazoroff A (1990). “Alice in Wonderland” syndrome and infectious mononucleosis in children (letter). Journal of Neurology, Neurosurgery and Psychiatry, 53, 1104.

Lambert, M.V., Sierra, M., Phillips, M.L. & David, A.S. The spectrum of organic depersonalization: A review plus four new cases. Journal of Neuropsychiatry and Clinical Neuroscience, 14, 141-154.

Lippman, C.W. (1952). Certain hallucinations peculiar to migraine. Journal of Nervous and Mental Diseases, 116, 346-351.

Podoll, K., Ebel, H., Robinson, D., & Nicola, U. (2002). Obligatory and facultative symptoms of the Alice in wonderland syndrome. Minerva Medicine, 93, 287-293.

Podoll, K. & Robinson, D. (1999). Lewis Carroll’s migraine experiences. The Lancet, 353, 1366.

Rolak, L.A. (1991). Literary neurologic syndromes. Alice in Wonderland. Archives of Neurology, 48, 649–651.

Todd, J. (1955). The syndrome of Alice in Wonderland. Canadian Medical Association Journal, 73, 701–704.

Cock tales: A brief look at Penile Dysmorphic Disorder

In a previous blog, I examined Body Dysmorphic Disorder (BDD). At its simplest level, BDD is a distressing, handicapping, and/or impairing preoccupation with an imagined or slight defect in body appearance that the sufferer perceives to be ugly, unattractive, and/or deformed. BDD sufferers can think about their perceived defect for hours and hours every day. The International Classification of Diseases (ICD-10) criteria for BDD is:

  • Persistent belief in the presence of at least one serious physical illness underlying the presenting symptom(s), even though repeated investigations and examinations have identified no adequate physical explanation, or a persistent preoccupation with a presumed deformity or disfigurement.
  • Persistent refusal to accept the advice and reassurance of several different doctors that there is no physical illness or abnormality underlying the symptoms.

One particular body part that has been the focus of some research in the BDD field is that of genitalia. Many men worry about the size of their penis and think it is too small. This is perfectly normal and the worry or concern is highly unlikely to be a symptom of BDD. In a 2004 issue of the Postgraduate Medical Journal, British psychiatrist Dr David Veale reported that although there are broad similarities between the genders in BDD, there are some differences. For instance, men with BDD show a greater preoccupation with their genitals, and women with BDD are more likely to have a co-morbid eating disorder. Dr. David Sarwer (writing in a 2006 issue of Plastic and Reconstructive Surgery) asserted that the rate of body dysmorphic disorder should be examined among patients re-questing atypical procedures and cites the example of those individuals requesting genital surgery.

Back in 2008, Channel 4 in the UK had a television series called Penis Envy. The first episode (The Perfect Penis) featured a US psychology student who paid $4000 to have his penis lengthened by cutting the ligament in his pubis. Such actions might be indicative of BDD but the programme didn’t explore this facet. Following such operations, men then have to spend the following weeks suspending a weight from their penis for at least eight hours a day. For all the financial and physical burdens faced, the average increase in length is only 0.5-3cm (with official statistics being closer to 0.5cm than 3cm). Other methods of increasing genital size include the injection of silicon into the penis (although this is dangerous and can result in a silicon embolism).

Dr. Stephen Snyder (Associate Clinical Professor of Psychiatry, Mount Sinai School of Medicine, New York, US) was interviewed about (so-called) ‘Penile Dysmorphic Disorder’ (PDD) in an online Psychology Today article. He was quoted as saying:

I don’t know of any statistics on [PDD]. Anxiety or insecurity about penis size is extremely common in men. It would be difficult to determine how frequently the more serious condition of penis-focused BDD occurs. People with BDD tend to avoid mental health specialists…It’s much more likely I think that a man with penile BDD will purchase penis enlargement equipment or consult a surgeon than consult someone like me…Some people seem to have an innate tendency for obsessive thinking. Why some of these people develop BDD, and others OCD or Anorexia Nervosa is unknown…A man who begins to obsess about the size of his penis may begin to compulsively and repeatedly measure his erections, and to avoid dating because he’s convinced he’ll be humiliated. Then the whole thing can spiral out of control, until ultimately he’s online studying penis enlargement techniques”.

A 2006 study led by Dr. J. Lever and published by Psychology of Men and Masculinity reported that in an online survey of over 52,000 participants, most male participants rated their penis as average (66%) and only 22% as large and 12% as small. Among the female participants, around 85% of women were satisfied with their partners’ penile size, while only 55% of men were satisfied, with 45% wanting to be larger (and 0.2% to be smaller).

Just recently, Dr. Warren Holman highlighted the case of ‘Sam’, a 17-year-old white male from a middle-class Jewish family living in Midwest USA with penile dysmorphic disorder (in a 2012 issue of Social Work in Mental Health). As Dr. Holman reported:

“Sam had stopped attending school several weeks earlier, and on many days would not even leave his home. He said he wanted to remain at home and away from school because, ‘My penis is shrinking and people can tell.’ Sam reported he had had his anxiety about his penis for about a year, but until recently had been able to reason himself out of it…Sam was well related, and his mental status was unremarkable except for his belief about his penis”.

Dr. Holman believed that Sam’s conviction that his penis was shrinking (and people could tell) suggested three possible diagnoses (i.e., social phobia; BDD and/or delusional disorder of the somatic type; or schizophrenia). Holman eventually reached the conclusion that Sam’s beliefs were due to BDD although did say that it “may be in a prodromal phase of schizophrenia”. Sam was treated via a form of psychodynamic counselling (which much to the disappointment of Holman ultimately failed perhaps because of initial misdiagnosis).

In 2007, British urologists Dr. Kevan Wylie and Dr. Ian Eardley published a review on penile size in BJU International. They summarized all of the studies on penile size that have examined flaccid penis length, stretched penis length, erect penis length, flaccid penis girth and erect penis girth. They reported that:

“Stretched penile length in these studies was typically 12–13 cm, with an erect length of 14–16 cm. For girth, there was again remarkable consistency of results, with a mean girth of 9–10 cm for the flaccid penis and 12–13 cm for the erect penis…Concern over the size of the penis, when such concern becomes excessive, might present as the ‘small penis syndrome’ [SPS], an obsessive rumination with compulsive checking rituals, body dysmorphic disorder, or as part of a psychosis”.

However, they did also assert that more research was required on the effects of race and age on penile length. Wylie and Eardley speculate that SPS (or ‘locker room syndrome’ as they also call it) originates in childhood following the sight of their father’s, elder sibling’s and/or older friend’s penis. This appears to have support from a 2005 study (also published in BJU International). Dr. N. Mondaini and Dr. P. Gontero surveyed men who thought they had a small penis at an andrology clinic and reported that nearly two-thirds said their SPS had begun in childhood (63%) with the rest saying it began in adolescence (37%).

Wylie and Eardley also examined the treatment options of men with SPS and also examined the evidence of commercial penis extending techniques. They concluded that:

“It is recommended that the initial approach to a man who has SPS is a thorough urological, psychosexual, psychological and psychiatric assessment that might involve more than one clinician…Conservative approaches to therapy, based on education and self-awareness, as well as short-term structured psychotherapy [cognitive-behavioural therapy] are often successful, and should be the initial interventions in all men. Of the physical treatments available, there is poorly documented evidence to support the use of penile extenders. More information is need on the outcomes with these devices. Similarly, there is emerging evidence about the place of surgery and there are now several reports suggesting that dividing the suspensory ligament can increase flaccid penile length”.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Goodman, M.P. (2009). Female Cosmetic Genital Surgery. Obstetrics and Gynecology, 113, 154-159.

Holman, W.D. (2012). “My Penis Is Shrinking and People Can Tell”: A Confusing Case of Apparent Body Dysmorphic Disorder. Social Work in Mental Health, 9, 319-335.

Morrison, T.G., Bearden, A., Ellis, S.R. & Harriman, R. (2005). Correlates of genital perceptions among Canadian post- secondary students. Electronic Journal of Human Sexuality, 8. Located at: http://www.ejhs.org/volume8/GenitalPerceptions.htm

Lever, J., Fredereicjk, D.A. & Peplau, L.A. (2006). Does size matter? Men’s and women’s views on penis size across the lifespan. Psychology of Men and Masculinity, 3,129-143.

Mondaini, N. & Gontero, P. (2005). Idiopathic short penis: myth or reality? BJU International, 95, 8–9.

Sarwer, D.B. (2006). Body Dysmorphic Disorder and cosmetic surgery. Plastic and Reconstructive Surgery, December, 168e-180e.

Snyder, S. (2011). When size obsession gets out of hand. Psychology Today, June 11. Located at: http://www.psychologytoday.com/blog/sexualitytoday/201106/when-size-obsession-gets-out-hand

Sondheimer, A. (1988). Clomipramine treatment of delusional disorder-somatic type. Journal of the American Academy of Child and Adolescent Psychiatry, 27, 188-192.

Veale, D. (2004). Body dysmorphic disorder. Postgraduate Medical Journal, 80, 67-71.

Wylie, K.R. & Eardley, I. (2007). Penile size and the ‘small penis syndrome’. BJU International, 99, 1449–1455.

Making the cut: A beginner’s guide to Klingsor Syndrome

In one of my previous blogs, I looked at one of the world’s rarest behaviours – male genital self-mutilation (GSM). As I noted in that article, there have only been about 125 cases ever recorded in the clinical and/or medical literature. (Having said that, it may be that this number of cases relates to those published in the English language as I did come across a Japanese case study of male GSM by M. Tomita and colleagues published in 2002 in the Japanese journal Hinyokika Kiyo, that noted that their case study was the 24th case of male GSM in the Japanese scientific literature). A 1988 study by Dr. C. Tobias and colleagues published in the South Medical Journal reported that self-mutilators (including all types of self-mutilation not just GSM) were most likely to suffer from schizophrenia, religious preoccupation, substance abuse, and/or social isolation.

Today’s blog specifically looks at genital self-mutilators who engage in the behaviour because of a religious belief, and are typically diagnosed as having Klingsor Syndrome. The name of the syndrome was derived from the character Klingsor in Parsifol (a Wagner opera) who engaged in an act of self-castration to gain entry into the Brotherhood of the Knights of the Holy Grail.

In a 1990 issue of the Australian and New Zealand Journal of Psychiatry, Dr. I. Schweitzer wrote a paper called ‘Genital self-amputation and the Klingsor syndrome’. In his paper, he described two psychotic individuals, who had carried out GSM on themselves (one of which had done it in an attempt to kill himself). He noted that those most at risk from committing GSM were similar to self-mutilators more generally and comprised:

“Psychotic patients with delusions (often religious), sexual conflict associated with guilt, past suicide attempts or other self-destructive behaviour and depression, severe childhood deprivation, and major premorbid personality disorder”.

Dr. Schweitzer tried to argue that ‘Klingsor syndrome’ should be applied to anyone that carries out GSM as a result of psychotic illness and not just those with religious delusions. However, this does not appear to have been taken up that widely in more recent published case studies. A couple of (seemingly) genuine cases of the ‘archetypal’ Klingsor Syndrome, were reported in the Indian Journal of Psychiatry. The first one was by Malay Dave and colleagues in 1997, and described the case of a 22-year old unmarried schizophrenic Muslim male:

“[He] was admitted in the urology department with self-inflicted traumatic amputation of the penis At that time some Muslim men accosted him and told him not to be seen in that locality again. After this incident the patient became fearful, started hearing voices belonging to the devil and Allah which would tell him that he was not… At the initial interview the patient was uncommunicative and rapport was difficult to establish. He had a perplexed affect…As the patient gradually became more controlled delusions of persecution, reference and control were elicited along with thought insertion and broadcast. His concept formation was average and auditory hallucinations (2 voices belonging to the God and the devil talking amongst themselves and to him, saying derogatory things) were elicitable. These voices had initially commanded the patient to cut off his penis”.

The second one was published in 2001 by Dr. Subhash Bhargava and colleagues. They wrote that:

A 25-year old unmarried male presented to the emergency services as he had severed off his penis with a knife. Patient reported of feeling no pain at that time and explained this act as carrying out the orders given to him by the goddess. The voice had assured him that by doing so his sins would be expiated and that he would attain sainthood. His family reported that he had disturbed sleep, a decline in work performance, increased talking, mainly religious in content and disinhibited behaviour off and on for the past seven months…Mental status examination revealed bizarre sexual and religious delusions and auditory hallucinations. The latter were accusatory as well as commanding in nature and mainly religious in content. A diagnosis of schizophrenia was made”.

A 2010 paper in the Israel Journal of Psychiatry and Related Sciences by Turkish clinicians led by Dr. Erol Ozan outlined four cases of GSM (three schizophrenics, and one with psychotic bipolar depression) forwarded some other symptoms that appear to put men at risk of GSM including (i) failures in the male role, (ii) problems in the early developmental period, (iii) such as experiencing difficulties in male identification and persistence of incestuous desires, (iv) depression, and (v) having a history of GSM. They also proposed a new concept in formulating religiously themed psychotic male GSM – atonement.

Another more recent (2012) paper in the Israel Journal of Psychiatry and Related Sciences by Indian researchers Dr. Ranjan Bhattacharyya and colleagues described a case of male GSM who was a paranoid schizophrenic who castrated himself at a time when no psychotic symptoms were present (but were enacted during a period of what the authors described as “post-psychotic depression”). Following a review of the psychological literature on male GSM, they considered that their case “best [fitted] the description for Klingsor Syndrome” probably because their case study was of a man “recovering from a psychotic episode with possible sexual guilt, religiosity and intense hatred towards women”. The religiosity in this case didn’t seem to be as pronounced as the two cases published in the Indian Journal of Psychiatry (outlined above). Given the rarity of any kind of GSM, it would appear that Klingsor Syndrome is arguably one of the world’s rarest syndromes. Every new case study appears to add to our knowledge of this strange (and potentially life threatening) behaviour.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Ajape, A.A., Issa, B.A., Buhari, O.I.N., Adeoye, P.O., Babata, A.L. & Abiola, O.O. (2010). Genital self-mutilation. Annals of African Medicine, 9, 31-34.

Bhargava, S.C., Sethi, S., & Vohra, A.K. (2001). Klingsor syndrome: a case report. Indian Journal of Psychiatry, 43, 349-350

Bhattacharyya, R., Sanyal, D. & Roy, K. (2011). A case of Klingsor Syndrome: when there is no longer psychosis. Israel Journal of Psychiatry and Related Sciences, 48, 30-33.

Dave, M., Apte, J., Dhavale, H.S. & Pinto, C. (1997). The Klingsor Syndrome. Indian Journal of Psychiatry, 39, 341-342.

Martin, T. & Gattaz, W.F. (1991). Psychiatric aspects of male genital mutilations. Psychopathology, 24, 170.

Murota-Kawano, A, Tosaka, A. & Ando, M. (2001). Autohemicastration in a man without schizophrenia. International Journal of Urology, 8, 257-259.

Ozan, E., Deveci, E., Oral, M., Yazici, E., & Kirpinar, I. (2010). Male genital self-mutilation as a psychotic solution. Israel Journal of Psychiatry and Related Sciences, 47, 297-303.

Rao, K.N., Bharathi, G., & Chate S. (2002). Genital self-mutilation in depression: A case report. Indian Journal of Psychiatry. 44, 297-300.

Russell, D.B., McGovern, G. & Harte, F.B. (2005). Genital self-mutilation by radio frequency in a male-to-female transsexual. Sexual Health, 2, 203-204.

Schweitzer, I. (1990). Genital self-amputation and the Klingsor syndrome. Australian and New Zealand Journal of Psychiatry, 24, 566-569.

Stunnell, H., Power, R.E., Floyd, M., & Quinlan, D.M. (2006). Genital self-mutilation. International Journal of Urology, 13, 1358-1360.

Tobias, C.R., Turns, D.M., Lippmann., S., Pary, R. & Oropilla, T.B. (1988) Evaluation and management of self-mutilation. South Medical Journal, 81(10), 1261-1263.

Tomita, M., Maeda, S., Kimura, T., Ikemoto, I. & Oishi, Y. (2002). [A case of complete self-mutilation of penis]. Hinyokika Kiyo, 48, 247-249.

Waugh, A.C. (1986). Autocastration and biblical delusions in schizophrenia. British Journal of Psychiatry, 149, 656-658.

What’s bugging you? A beginner’s guide to Ekbom’s syndrome

It was only a few months ago that I watched the 2006 film Bug for the very first time. Directed by William Friedkin, it tells the story of a mentally ill drifter called Peter Evans (with a great performance by Michael Shannon). Evans ends up having a sexual relationship with Agnes White, a bisexual alcoholic junkie (played surprisingly well by Ashley Judd). During the film, Peter confides in Agnes his belief that he has a colony of microscopic bugs infested one of his molar teeth (and then in one ‘memorable’ scene starts pulling his own teeth out). Evans’ paranoia becomes increasingly erratic and becomes a shared belief with White (who also comes to believe that they are both infested with microscopic bugs; this sharing of a delusional belief is known as a ‘folie à deux’ [French for ‘a madness shared by two people’, a shared psychosis] and would make a good blog topic). However, today’s blog focuses on imagined bug infestation (i.e., delusional parasitosis) that is known in psychological and psychiatric terms as Ekbom’s syndrome (named after the Swedish neurologist Karl Ekbom who first described the condition in a number of published papers in the late 1930s).

As you have probably gathered from my quick film synopsis above, Ekbom’s syndrome (ES) is a type of psychosis in which sufferers have a vehement delusional belief that they are infested with parasites that those affected describe as bugs or insects crawling around under their skin (when in reality they simply do not exist). I ought to add that the characters in Bug also appeared to be suffering from ‘delusory cleptoparasitosis’ (DC) another type of insect psychosis in which the sufferer thinks the place where they live is infested with parasites (rather than from within their body). As a consequence, both ES and DC sufferers are more likely to seek the help of skin specialists (e.g., dermatologists) and insect specialists (e.g., pest control, entomologists) than psychologists.

In essence, ES is a tactile hallucination and is also known as ‘formication’ (which is the word that describes the feeling of insects crawling and/or burrowing underneath the skin’s surface. Formication is also one form of parasthaesia (of which other examples include the ‘pins and needles’ tingling sensations that many people experience regularly). Parasthaesia includes any non-permanent skin sensation including tickling, pricking, tingling, numbness, and/or burning. ES sufferers will focus on any unusual body mark on their skin as ‘evidence’ that they have a parasitic infection. It is not uncommon for obsessive and/or compulsive checking of the body to occur. The prevalence of ES is unknown although Dr. J. Koo and Dr. C. Gambla reported in the journal Dermatologic Clinic that they see around 20 new cases per year in the large US referral clinic.

In some psychological circles, ES has been used synonymously with Wittmaack-Ekbom syndrome that is more associated with ‘restless leg syndrome’ (RLS; something that I myself have suffered from due to a chronic spinal condition that I have). When I get my bouts of RLS, it really does feel as though I have tiny insects moving about inside my right leg. The difference between ES and RLS is that RLS is a real physical condition that has bona fide physical basis whereas the basis for ES is an imaginary delusion. Clinical and medical research has shown that ES is associated with a number of comorbid conditions including affective psychosis, paranoid schizophrenia, organic brain disease, neurosis, and anankastic/paranoid personality disorder. It has also been reported in some people undergoing alcohol withdrawal, cocaine misuse, cerebrovascular disease, senile dementia, and thalamic brain lesions.

There can also be medical complications for ES sufferers. The fictional example of someone pulling their teeth out is not unknown although the gouging or digging out of the perceived parasites is more common. However, a paper by Dr. M. Nel and colleagues in the Journal of the South African Veterinary Association, most ES sufferers are able to function normally in all other aspects of their lives, in spite of their fixed parasitic delusions. They also noted that:

“The typical history often describes numerous attempts at eradicating the infestation. These could include taking medication, applying topical treatments, using pesticides, making use of exterminators, discarding clothing and possessions and even relocatingIn a study of 94 patients (Ohtaki, 1991), most patients complained of itching and/or a tickling sensation. In order to rid themselves of the so-called parasites, patients often scratch, pick and wash frequently or use caustic agents on their skin, almost invariably leading to traumatic skin lesions”.

According to one meta-analytic study of 1,223 ES cases (published by Dr. W. Trabart in the journal Psychopathology), the occurrence of ES as a shared psychotic disorder is an uncommon phenomenon. He reported only about 5-15% of such cases were found. It was also reported that ES was more common amongst females (two-thirds female, one-third male), and is more prevalent in those over the age of 40 years. The symptoms had lasted three to four-and-a-half years. ES can be classified into three sub-types (primary; secondary-functional; and secondary-organic) based on the presenting symptoms:

  • Primary ES refers to individuals that have the delusional parasitic infestation but no other comorbid conditions (i.e., other mental functioning is normal). Those where ES occurs by suggestion from another individual (e.g., the folie a deux case mentioned above) would be included in this ES sub-type. (It’s also worth noting that at least three studies have reported either the folie à deux or folie à trois among family members or loved ones including papers in the British Journal of Psychiatry and Dermatologica). Treatment is usually pharmacotherapy-based and utilizes drugs that are used in the treatment of other delusional-based syndromes (e.g., atypical antipsychotic drugs such as risperidone and olanzapine.
  • Secondary-functional ES refers to individuals that have the delusional parasitic infestation and are associated with another psychiatric condition (e.g., clinical depression, schizophrenia).
  • Secondary-organic ES refers to individuals that have the delusional parasitic infestation that is caused by another medical illness (e.g., cancer, diabetes, tubercolosis, hyperthyroidism, vitamin deficiency, cerebrovascular disease, neurological disorders). Other conditions can also facilitate ES including drug abuse (including stimulant psychosis), various allergies, and the menopause). Treating the primary disorder will often lead to a reduction or elimination of the ES symptoms.

The most recent review of the literature I came across was by Dr. Andrea Boggild and colleagues, and published in a 2010 issue of the International Journal of Infectious Diseases, they concluded that:

“In summary, [delusional parasitosis] is one of the more challenging entities that infectious diseases specialists will be enlisted to help treat. Unfortunately, optimal therapeutic regimens leading to sustained remission are lacking, and assurances on the part of the clinician do little to ameliorate patient suffering”.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Berrios GE (1985). Delusional parasitosis and physical disease. Comprehensive Psychiatry 26, 395-403.

Boggild, A.K., Nicks, B.A., Yen, L., Voorhis, W.V., McMullen, R., Buckner, F.S., & Liles, W.C. (2010). Delusional parasitosis: six-year experience with 23 consecutive cases at an academic medical center. International Journal of Infectious Diseases, 14, e317–e321.

Bourgeois, M.L., Duhamel, P. & Verdoux, H. (1992). Delusional parasitosis: Folie à deux and attempted murder of a family doctor. British Journal of Psychiatry, 161, 709-711.

Frances, A. & Munro, A. (1989). Treating a woman who believes she has bugs under her skin. Hospital and Community Psychiatry, 40, 1113–1114.

Freinhar, Jack P (1984). Delusions of parasitosis. Psychosomatics, 25, 47-53.

Gieler, U. & Knoll, M. (1990). Delusional parasitosis as ‘folie à trois’. Dermatologica, 181, 122-125.

Goddard J (1995). Analysis of 11 cases of delusions of parasitosis reported to the Mississippi Department of Health. Southern Medical Journal 88, 837-839.

Gould, W.M. & Gragg, T.M. (1976). Delusions of parasitosis. Archives of Dermatology 112, 1745–1748.

Grace, K.J. (1987). Delusory cleptoparasitosis: Delusions of arthropod infestation in the home. Pan-Pacific Entomologist, 63, 1-4.

Koblenzer, C.S. (1993). The clinical presentation, diagnosis and treatment of delusions of parasitosi: A dermatologic perspective. Bulletin of the Society of Vector Ecologists 18, 6-10.

Koo, J. & Gambla, C (1996). Delusions of parasitosis and other forms of monosymptomatic hypochondriacal psychosis. General discussion and case illustrations. Dermatologic Clinic, 14, 429-438.

Morris, M. (1991). Delusional manifestation. British Journal of Psychiatry, 159, 83-87.

Hinkle, N.C. (2000). Delusory parasitosis. American Entomologist 46, 17-25.

Ohtaki, N. (1991). Ninety four cases with delusions of parasitosis. Japanese Journal of Dermatology, 101, 439-446.

Rasmussen, J.E. & Voorhees, J.J. (1990). Psychosomatic dermatology. Archives of Dermatology, 126, 90-93.

Nel, M., Schoeman, J.P. & Lobetti, R.G. (2001). Delusions of parasitosis in clients presenting pets for veterinary care. Journal of the South African Veterinary Association, 72, 167-169.

Trabert, W. (1995). 100 years of delusional parasitosis. Meta-analysis of 1,223 case reports. Psychopathology, 28, 238-46

Webb, J.P. (1993). Case histories of individuals with delusions of parasitosis in southern California and a proposed protocol for initiating effective medical assistance. Bulletin of the Society of Vector Ecologists 18, 16-24.

An eye for an I! A beginner’s guide to auto-enucleation

I have to say that I have no idea what it must be like to lose an eye (i.e., enucleation) but one thing I can’t possibly begin to imagine is what it must like is to remove my own eye (i.e., auto-enucleation). However, there are many clinical and medical reports of people that self-mutilate by stabbing or removing their eye(s). Arguably the most infamous auto-enucleator was Oedipus (in Sophocles’ play) who removed both his eyes after he realized he had unwittingly slept with his own mother and killed his own father.

The psychiatrist Dr. Armando Favazza defines self-mutilation as “the deliberate, direct, non-suicidal destruction or alteration of one’s body tissue”. Dr. Niraj Ahuja and Dr. Adrian Lloyd writing in the Australian and New Zealand Journal of Psychiatry also add that self-mutilation relates to bodily self-damage without wishing to die. Dr. Favazza also believes there are three fundamentally different types of self-mutilation. Enucleation is included in the first type (major self-mutilation) and is the least common. Other forms of self-mutilation in this category include self-castration, penectomy (cutting off one’s own penis) and self-limb amputation.

The second type includes “monotonously repetitive and sometimes rhythmic acts such as head-banging, hitting, and self-biting” (which according to Dr Favazza occur mostly in “moderate to severely mentally retarded persons as well as in cases of autism and Tourette’s syndrome”). The final and most common forms of bodily self-mutilation are moderately superficial and include a compulsive sub-type (e.g., hair-pulling, skin scratching and nail-biting), as well as an episodic/repetitive sub-type (e.g., skin-cutting, skin carving, burning, needle sticking, bone breaking, and wound picking). Many of these self-harming behaviours are a symptom and/or an associated feature in a number of mental personality disorders (e.g., anti-social, borderline, and histrionic personality disorders).

Reports of auto-enucleation in the medical literature were first described in the 1840s. By the early 1900s, the act of removing one’s own eye was actually termed ‘Oedipism’ by Blonel. Auto-enucleation is (of course) exceedingly rare although a couple of studies in the American Journal of Ophthalmology (in 1984) and an analysis of 1,146 enucleations between 1980 and 1990 in the British Journal of Ophthalmology (in 1994) estimated there were 2.8 to 4.3 per 100,000 in the population. However, some papers (such as those by Dr. Favazza) on major self-mutilation have put the incidence as low as one in 4 million.

Enucleators are also known to be at increased risk of further self-harming, and (predictably) are more likely to be living in psychiatric institutions when the auto-enucleation event occurs. They are also at increased risk of removing the second eye at a later date if they didn’t pull out both eyes to start with. A review by Dr. H.R. Krauss and colleagues in a 1984 issue of the Survey of Opthalmology examined 50 cases of self-enucleation and reported that 19 of them had bilateral auto-enucleation (i.e., had removed both of their eyes). A 2007 paper by Dr. Alireza Ghaffari-Nejad and colleagues in the Archives of Iranian Medicine examined the many theories behind self-harming behaviour. They briefly overviewed theories ranging from Fruedian psychoanalytic theory to biologically-based theories. They wrote:

Psychoanalytically self-injurious behaviour has been linked to castration and explained as a process of failure to resolve oedipal complex, repressed impulses, self punishment, focal suicide and aggression turned inwards especially in cases of depression. [Other authors] have postulated interpersonal loss preceding self-injurious behaviour and linked it to rejection sensitivity…Biologically serotonergic depletion preceding self-mutilation has been linked to aggression and depression…Some authors have claimed strong moral, religious and delusional component”

A recent literature review by Dr. Alexander Fan in the journal Psychiatry reported that the vast majority of auto-enucleation cases suffer from psychotic illness (particularly schizophrenia) although other medical and/or psychiatric conditions associated with auto-enucleation include obsessive-compulsive neuroses, severe depression, post-traumatic stress disorders, drug-induced psychoses, bipolar mania. There are also case studies where auto-enucleation has been linked with structural brain lesions, Down Syndrome, epilepsy, neurosyphilis, and Lesch-Nyhan syndrome (juvenile gout). These are similar to other forms of extreme self-mutilation. For instance, self-mutilation in schizophrenia in response to auditory hallucinations has often been described as Van Gogh Syndrome (in reference to the painter’s self-excision of his own left ear)

Other reviews of the psychiatric literature have reported that those who remove their own eyes commonly have delusions (typically sexual and/or religious) and that when asked about motivations for self-harming include reasons such as guilt, atonement, sin, evil, etc. Although some authors have noted that enucleators with religious beliefs are often Christian, other case studies have made reference to other religious faiths (e.g., Muslims). Finally, another paper by Favazza in Hospital and Community Psychiatry concluded that:

“Males in a first episode of a schizophrenic illness that is characterized by delusions associated with a body part or religious delusions are at the greatest risk for MSM [major self-mutilation]. However, MSM of this severity is so rare that it cannot be predicted accurately unless there has been a previous attempt at self-injury or the patient has spoken about wanting to remove or injure an organ. Threatened ocular mutilation deserves special mention because it may occur in a hospital setting, and the case histories suggest that one-to-one nursing is not always be sufficient to prevent enucleation”.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Berguaa, A., Sperling, W. & Kuchlea M. (2002). Self-enucleation in drug-related psychosis. Ophthalmologica, 216, 269-271.

Eric, J.C., Nevitt, M.P., Hodge, D. &  Ballard, D.J. (1984). Incidence of enucleation in a defined population. American Journal of Ophthalmology, 113, 138-44.

Fan, A.H. (2007). Autoenucleation: A case report and literature review. Psychiatry, October, 60-62.

Favazza, Armando (1998) ‘Introduction’, in Marilee Strong A Bright Red Scream: Self-mutilation and the Language of Pain. New York: Viking.

Favazza, A. & Rosenthal R. (1993). Diagnostic issues in self-mutilation. Hospital and Community Psychiatry, 44, 134-140.

Field, H. & Waldfogel, S. (1995). Severe ocular self-injury. General Hospital Psychiatry, 17, 224-227.

Gamulescu, M.A., Serguhn, S., Aigner, J.M., Lohmann, C.P., & Roider J. (2001). Enucleation as a form of self-aggression, two case reports and review of the literature. Klin Monatsbl Augenheilkd, 218, 451-454.

Ghaffari-Nejad, A., Kerdegari, M., & Reihani-Kermani, H. (2007) Self-mutilation of the nose in a schizophrenic patient with Cotard Syndrome. Archives of Iranian Medicine, 10, 540-542.

Gottrau, P., Holbach, L.M. & Nauman, G.O. (1994). Clinicopathological review of 1,146 enucleations (1980-90). British Journal of Ophthalmology, 78, 260-5.

Jeffreys, S. (2000). ‘Body art’ and social status: Cutting, tattooing and piercing from a feminist perspective Feminism and Psychology, 10, 409-429.

Krauss, H., Yee, R. & Foos, R. (1994). Autoenucleation. Survey of Ophthalmology, 29, 179-87.

MacLean, C. & Robertson, B.M. (1976). Self enucleation and psychosis. Archives of General Psychiatry, 33, 242-249.

Patil, B. & James, N. (2004). Bilateral self-enucleation of eyes. Eye, 18, 431-432.

Patton N. (2004). Self-inflicted eye injuries: A review. Eye, 18, 867-872.

Rao, K.N. & Begum, S. (1996) Self enucleation in depression; A case report. Indian Journal of Psychiatry, 38, 267-70

Witherspoon, D., Feist, F., Morris, R. & Feist, R. (1989). Ocular self-mutilation. Annals of Ophthalmology, 21, 255-259.

Lovestruck: A brief look at de Clérambault’s Syndrome

In previous blogs I have looked at both love addiction and obsessional love. Since writing my blog on obsessional love and noting that it is also known as erotomania, I have received a couple of emails from clinicians saying that obsessional love is not necessarily erotomania by definition. The problem with the wider area of obsessions, compulsions and addiction more generally is that academics and clinicians have different definitions of what it is to be obsessed or addicted to something.

In clinical circles, erotomania is known as de Clérambault’s syndrome (DCS), and was named after a paper published in 1921 (Les Psychoses Passionelles) by the French psychiatrist Gaëtan de Clérambault. Those with DCS typically have a delusional belief that another person (typically someone famous, high status and/or a stranger) is in love with them. Some of the scientific literature suggests that DCS sufferers may have experienced loss of people that were emotionally close to them, and that therefore they may feel emotionally and psychologically safer by attaching themselves to people who are unattainable. Such actions prevent any further losses. In a 1983 issue of Psychological Medicine, Dr. P. Taylor and colleagues described the main components of DCS:

  • The presence of a delusion that the individual (usually described as a female) is loved by a specific man;
  • The woman has had little or no contact with the man;
  • The man is unattainable in some way, because he is already married or because he has no personal interest in her;
  • The man is perceived as watching over, protecting or following the woman;
  • Despite the erotic delusion, the woman remains chaste.

One of the reasons I am personally interested in DCS is that back in the early 1990s, my then girlfriend (who was – and still is – a clinical psychologist) was the object of affection by a DCS sufferer. The man who fell in love with my girlfriend was slightly brain damaged following a bad motorcycling accident. The accident had also left him paralyzed and had to use a wheelchair. As part of her job, my girlfriend worked with the charity Headway (a brain injury association), and it was when she was caring for this head injured and paralyzed man that he fell in love with her and believed that the feelings were reciprocal. The condition was so intense that he even booked a wedding date, sent out wedding invitations, and told all his family and friends that he was marrying my girlfriend. I even started to question my girlfriend’s fidelity because I couldn’t comprehend that someone could organize a whole wedding if nothing had ever happened between them. (Even though I was a psychologist when this happened I had never come across DCS).

The research literature on DCS suggests that the delusional behaviour is usually part of psychotic behaviour (typically schizophrenia, bipolar disorder, or borderline personality disorder) and can therefore be treated using atypical anti-psychotics (however, most DCS sufferers do not ask for help or seek treatment as they don’t believe they are doing anything wrong). According to the Wikipedia entry on DCS (and based on a paper published in a 1998 issue of the Journal of Neuropsychiatry and Clinical Neuroscience by Dr. C. Anderson and colleagues):

“During an erotomanic episode, the patient believes that a ‘secret admirer’ is declaring his or her affection to the patient, often by special glances, signals, telepathy, or messages through the media. Usually the patient then returns the perceived affection by means of letters, phone calls, gifts, and visits to the unwitting recipient. Even though these advances are unexpected and unwanted, any denial of affection by the object of this delusional love is dismissed by the patient as a ploy to conceal the forbidden love from the rest of the world”.

In a 2002 issue of the journal History of Psychiatry, Dr. German Berrios and Dr. N. Kennedy describe four convergences in the history of erotomania.

  • Convergence 1: From classical times to the early eighteenth century, erotomania was viewed as a ‘general disease caused by unrequited love’.
  • Convergence 2: During the nineteenth century, erotomania was viewed as a disease of ‘excessive physical love (nymphomania)’
  • Convergence 3: During the twentieth century, erotomania was viewed as a form of ‘mental disorder’
  • Convergence 4: Currently, erotomania is viewed as a ‘delusional belief of being loved by someone else’.

Berrios and Kennedy also note that there are differences between Anglo-Saxon and French views surrounding the meaning or coherence of “the much-abused English eponym ‘de Clérambault syndrome’. Erotomania is a construct, a mirror reflecting Western views on spiritual and physical love, sex, and gender inequality and abuse. On account of this, it is unlikely that there will ever be a final, ‘scientific’ definition rendering erotomania into a ‘natural kind’ and making it susceptible to brain localization and biological treatment”.

Empirical research suggests that women are more likely than men to suffer from DCS, and that DCS sufferers tend to have social and intimacy difficulties, and are therefore typically loners. Developmentally, they are likely to have a poor sense of self and may have suffered abuse during childhood and/or adolescence. Much of the published theorizing about erotomania is from a psychodynamic perspective or genetic/neurochemical presispositions. I’m far more eclectic in my approach to understanding human behaviour and believe that environmental, psychological, pharmacological and physiological factors most likely trigger a predisposed person into developing DCS. It’s also been speculated that learning through the media (television, radio, books, etc.) has influenced the development of DCS.

Dr. Louis Schlesinger in his 2004 book Sexual Murder: Catathymic and Compulsive Homicides writes about DCS sufferers in relation to possible stalking behaviour. He notes that: “some stalkers are unable to give up a prior intimate relationship (Zona, Sharma, and Lane, 1993). Some develop delusional beliefs about the target (Goldstein, 1987), while others develop strong obsessional thoughts about virtual strangers (Spitzberg and Cupach, 1994). Meloy (1992) and Kienlen (1998) believe that a disturbance of attachment begins in the offender’s early childhood and stalking starts when some type of loss in adulthood resurrects these early conflicts”

In some individuals, DCS can remain with the person for a long time. For instance, Dr. Harold Jordan and colleagues published a paper in a 2006 issue of the Journal of the National Medical Association. They reviewed two cases of DCS that they had followed for over 30 years making these some of the longest, single-case longitudinal studies yet reported”. They noted that DCS remains a “ubiquitous nosological psychiatric entity with uncertain prognosis”. De Clerambault’s original paper presented the case of a woman whose chronic, erotic delusion remained with her for 37 years, and the cases reported by Dr. Jordan and his colleagues also demonstrated that the delusion can remain unchanged for decades. I have yet to come across any research that estimates the prevalence of DCS among the general population but given most published papers are clinical case reports, it suggests the disorder is relatively rare.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Anderson CA, Camp J, Filley CM (1998). Erotomania after aneurismal subarachnoid hemorrhage: Case report and literature review. Journal of Neuropsychiatry and Clinical Neuroscience, 10, 330-337.

Berrios G.E. & Kennedy, N. (2002). Erotomania: a conceptual history. History of Psychiatry, 13, 381-400.

Jordan, H.W., Lockert, E.W., Johnson-Warren, M., Cabell, C., Cooke, T., Greer, W. & Howe, G. (2006). Erotomania revisited: Thirty-four years later. Journal of the National Medical Association, 98, 487-793.

Schlesinger, L.B. (2004). Sexual murder: Catathymic and compulsive homicides. London: CRC Press.

Taylor, P., Mahendra, B. & Gunn J. (1983). Erotomania in males. Psychological Medicine, 13, 645-650.

Zona, M., Sharma, K., and Lane, J. (1993). A comparative study of erotomania and obsessional subjects in a forensic sample. Journal of Forensic Sciences, 38, 894–903.

Dead man walking: A beginner’s guide to Cotard’s Syndrome

One of the strangest and rarest mental disorders that has been studied academically is Cotard’s Syndrome (CS), and also known as the Cotard Delusion, the Nihilistic Delusion, and the Walking Corpse Syndrome, CS is where individuals hold the delusional belief that they are dead (figuratively or literally) and do not exist. Alternative versions of CS involve the individual believing they are putrefying and/or have lost their blood and/or internal organs. In even rarer instances the condition may include delusions of immortality. Unsurprisingly, CS is often found in psychotic individuals with schizophrenia but has also presented itself following adverse reactions to the anti-viral drug acyclovir (typically used in the treatment of herpes simplex virus). Some research has also indicated that individuals with impaired renal function are also at a higher risk of displaying CS symptoms.

CS is named after the 19th century French neurologist Jules Cotard who first described the condition in 1880. Cotard named the disorder the ‘negation delerium’ (le délire de négation). The severity of the disorder can differ between individuals (i.e., mild to severe). The characteristics of CS include despair and self-loathing at one end through to intense delusions and chronic depression at the other. The original case described by Cotard was a female given the pseudonym ‘Mademoiselle X’. She eventually died of starvation (because she believed she didn’t need to eat and denied that some parts of her body even existed) and believed she was eternally damned.

According to Yamada and colleagues in a 1999 issue of Acta Psychiatrica Scandinavica, CS has three distinct stages (i.e., germination, blooming and chronic). The first (germination) stage comprises psychotic depression and hypochondria. The second (blooming) stage comprises the full development of the syndrome and the delusions of negation. In the final (chronic) stage comprises severe delusions and chronic depression, and leads to a completely distorted view of the world in which they live. They also become socially withdrawn, completely neglect their hygiene, and cannot make sense of reality. As far back as 1921, Tissot described two components of the syndrome – an affective component associated with anxiety and a cognitive component associated with the presence of delusion.

Here are a couple of examples from the clinical literature.

  • Example 1: In 1996, Dr. A.W. Young and Dr. K.M. Leafhead reported a case of CS in a Scottish man who suffered brain injury following a motorcycling accident. Following his discharge from hospital, he was taken to South Africa by his mother and became convinced that he had died of septicaemia or AIDS and had gone to hell.
  • Example 2: A case study reported by Dr. D.N. Mendhekar and Dr. N. Gupta in a 2005 issue of the Indian Journal of Pediatrics described CS in a 14-year-old male epileptic. He had a history of depression, social withdrawal, talking about death, and disturbed biological function. His CS episodes occurred around twice a year (lasting 1-3 months each time). During each affected episode, the child believed that he and everyone around was dead.

Recently, Hans Debruyne and colleagues wrote an excellent review of CS in a 2011 issue of Mind and Brain, and wrote what they believed is a “classical description” of CS:

“In its early stages, Cotard’s syndrome is characterized by a vague feeling of anxiety, with a varying time span from weeks to years. This anxious state gradually augments and can result in nihilistic delusions where denial of life or denial of body parts are the prominent features. The patient loses sense of reality. Despite the delusion of being dead, these patients show an increased tendency to automutilation or suicidal behavior. Additional symptoms may include analgesia and mutism. The core symptoms always reflect a preoccupation with guilt, despair, and death”.

In the same 2011 review, the authors examined all the epidemiological studies and summarized the findings:

“The prevalence and incidence of this rare syndrome is not known. Only one study reported on prevalence in a selected psychogeriatric population in Hong Kong. In 2 out of 349 patients, Cotard’s syndrome was diagnosed suggesting a prevalence of 0.57% in this population. A prevalence of 3.2% was reached when severely depressed elderly were included. A recent study found 0.62% (n=3) of patients in a Mexican sample (screened over a 2-year period) of primary psychiatric patients having Cotard’s syndrome. Using the same methodology they found also 0.11% (n=1) having Cotard’s syndrome in a sample of neurological patients with mental disturbances”.

In 1995, Dr. G.E Berios and Dr. R. Luque (University of Cambridge, UK) carried out a statistical analysis of 100 cases of CS. They reported no differences between men and women with CS, and age appeared to increase the likelihood of someone developing CS. In relation to affective disorders and mood state, the authors reported that CS sufferers experienced depression (89%), anxiety (65%) and guilt (63%). In relation to delusions, CS sufferers experienced hypochondriacal delusions (58%) and delusions of immortality (55%). The most common nihilistic delusions concerned the body (86%) and existence (69%). The authors also carried out exploratory factor analysis and reported that the factors appeared to suggest three types of CS (i.e., Psychotic Depression Type; Cotard Type I; and Cotard Type II) and that each type may need to be treated differently and have different therapeutic implications.

  • The Psychotic Depression type includes individuals with melancholia and a few nihilistic delusions.
  • The Cotard Type I includes individuals with no depression or other disease and comprises a “pure” CS whose nosology is closer to delusional disorders (rather than the affective disorders).
  • The Cotard Type II includes individuals with anxiety, depression and auditory hallucinations and comprise a mixed group.

Neurologically, CS is thought to be related to the Capgras Syndrome (i.e., a disorder in which an individual has the delusion that someone close to them – partner, friend, or family member – has been replaced by an identical-looking imposter). Both syndromes are thought to originate from a disconnection between the areas of the brain that recognize faces and the areas that associate emotional content with such facial recognition. This can lead to feelings of derealization (i.e., an alteration in experience or perception of the external world so that it seems unreal). Brain scans show that those displaying CS often have lesions in the parietal lobe and greater brain atrophy than those in control groups. There are several reports of successful treatment in the psychiatric literature with ant-depressants, anti-psychotics, and various mood stabilizers. Therapeutic interventions such as electro-convulsive therapy have also been used to positive effect. In their 2011 review, Debruyne and colleagues concluded:

“Despite that Cotard’s syndrome was first described more than a century ago, literature on this topic remains restricted to case reports. Although the syndrome is rare, more larger scale research is needed to further clarify the pathophysiologic underpinnings of the disease and its relation to other delusions of misidentification such as Capgras syndrome”.

Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK

Further reading

Berrios G.E. & Luque R. (1995) Cotard’s delusion or syndrome? Comprehensive Psychiatry, 36, 218-223.

Berrios G.E. & Luque R. (1995) Cotard Syndrome: clinical analysis of 100 cases. Acta Psychiatrica Scandinavica,  91, 185-188.

Berrios G.E. & Luque R. (1999) Cotard’s ‘On hypochondriacal delusions in a severe form of anxious melancholia’. History of Psychiatry, 10, 269-278.

Cohen, D. & Consoli, A. (2006). Production of supernatural beliefs during Cotard’s syndrome, a rare psychotic depression. Behavioral and Brain Sciences, 29, 468-470.

Debruyne H, Portzky M, Peremans, K. & Audenaert K (2011). Cotard’s syndrome. Mind and Brain, 2, 67-72.

Debruyne H, Portzky M, Van den Eynde F. & Audenaert K (2009). Cotard’s syndrome: a review. Current Psychiatry Reports, 11, 197-202.

Mendhekar, D. N., & Gupta, N. (2005). Recurrent postictal depression with Cotard delusion. Indian Journal of Pediatrics, 72, 6, 529-31.

Pearn, J. & Gardner-Thorpe, C (2002). Jules Cotard (1840-1889) His life and the unique syndrome that bears his name. Neurology, 58,1400–3.

Tissot F. (1921). De lire des negations termine par guerison. Cosiderations sur l’hypochondrie et la melancholie. Ann Med Psychol, 79, 321-328.

Yamada, K., Katsuragi, S. & Fujii, I. (1999). A case study of Cotard’s syndrome: stages and diagnosis. Acta Psychiatrica Scandinavica, 100, 396-399.

Young, A.W., Robertson, I.H., Hellawell, D.J., de, P.K.W., & Pentland, B. (1992). Cotard delusion after brain injury. Psychological Medicine, 22, 799-804.

Young, A.W. & Leafhead, K.M. (1996) Betwixt life and death: Case studies of the Cotard Delusion. In P.W. Halligan & J.C. Marshall. (Eds.), Method in Madness: Case studies in Cognitive Neuropsychiatry). Hove: Psychology Press.