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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.

Double trouble: Syndrome of subjective doubles‬

In a previous blog on Delusional Misidentification Syndromes, I briefly mentioned the rare syndrome of ‘subjective doubles’ (SSD). Also known as Christodoulou syndrome (after the Greek psychiatrist Dr. George Nikos Christodoulou who first wrote about the syndrome), SSD refers to individuals who have the belief that there are (one or more) doubles of themselves (i.e., doppelgangers) that carry out actions and behaviours independently and lead a life of their own but that have part or sometimes all of the SDD sufferer’s personality. If the sufferer believes that (some or all of) their personality has been transferred to their doppelganger, they may also experience depersonalization (i.e., a problem of self-awareness in which individuals feel they have little control over social situations and feel they are watching themselves act in a vague and dreamlike state. As with other DMSs, subjective doubles syndrome typically arises as a consequence of a mental disorder, brain injury (typically the right central hemisphere) or a neurological disorder. The Wikipedia entry on SSD cited the case of a man who became depersonalized after an operation and was convinced his brain had been placed into someone else’s head and then claimed he recognized the other person.

In the original paper on SSD in a 1978 issue of the American Journal of Psychiatry, Dr. Christodoulou described the case of a young 18-year-old woman who claimed that a female neighbour had (via an “elaborate transformation” involving “metapmophosis”) acquired all of her physical characteristics (“same face, same build, same clothes, same everything’) and become an identical double. To become her double, the female case study believed her doppelganger had used a mask, wig, and special makeup. Her female neighbour wasn’t the only doppelganger as the woman also claimed at least one other woman had become her doppelganger. In rare instances, there may be comorbidity with the Capgras delusion (another misidentification syndrome) and is then referred to ‘subjective Capgras syndrome’. In fact, there are a number of different sub-types of SDD. As the online Dictionary of Hallucinations notes:

A subdivision of the syndrome of subjective doubles yields a ‘Capgras type’ (characterized by the delusional conviction that unseen doubles are active in the affected individual’s environment), an ‘autoscopic type’ (in which doubles of the self are perceived, ‘projected’ onto other people or objects, as in pareidolia), and a ‘reverse type’ (in which the affected individual believes to be an impostor or to be about to be replaced by someone else). The syndrome of subjective doubles is associated with various psychiatric disorders (notably the group of so-called schizophrenia spectrum disorders) and neurological disorders (notably disorders of the right parieto-temporal lobe). Conceptually and phenomenologically, the syndrome of subjective doubles constitutes the counterpart of a syndrome called ‘mirrored self-misidentification’, in which the affected individual is unable to identify his or her mirror image as oneself”.

Although most sources cite Dr. Christodoulou’s paper in the American Journal of Psychiatry as the first recorded case of SSD, he actually published a paper a year earlier in a 1977 issue of Acta Psychiatrica Belgica on the treatment of the syndrome of doubles. In this paper, Christodoulou used biological methods to treat 20 psychiatric patients with SDD or the related syndromes (Frégoli, intermetamorphosis, Capgras) aged 17 to 67 years of age. His patients were treated with ECT, antidepressants, neuroleptics, and antiepileptics (in some cases given singly whereas others were in combination). It was reported that:

“Results show that (a) the syndrome of doubles responded to various biological treatment methods; (b) in depression, it responded to tricyclic antidepressants; (c) in schizophrenia or organic psychosis, it usually responded to neurolytics; (d) in schizophrenia, it had more chances of responding to trifluoperazine given alone or in association with other psychopharmacological drugs; and (e) in certain cases, combination of antipsychotic treatment with treatment of coexisting organic dysfunctions appeared to be important”.

In another 1978 paper (in the Journal of Nervous and Mental Disease), Dr. Christodoulou described the course and prognosis of 20 patients with the syndrome of doubles (including Capgras syndrome, Fregoli syndrome, intermetamorphosis syndrome, and SDD – and presumably the same cases reported in the 1977 paper). He reported that the onset of the syndromes occurred either synchronously or at a later stage than the onset of the associated psychosis. In seven of the 20 cases, the syndrome failed to remit. In the remaining 13 cases, remission occurred either synchronously with or later than the remission of the basic psychosis. In all cases where there was comorbid depression, the syndromes cleared shortly after the successful treatment of the depressive illness. It was also noted that relapse of the basic psychotic condition in the setting of which the syndrome had originally developed was usually accompanied by the syndrome reappearing. In one of his most recent papers (from a 2009 issue of Current Psychiatry Reports), Christodoulou and three of his colleagues noted that:

“The delusional misidentification syndromes [including SDD] are rare psychopathologic phenomena that occur primarily in the setting of schizophrenic illness, affective disorder, and organic illness. They are grouped together because they often co-occur and interchange, and their basic theme is the concept of the double. They are distinguished as hypoidentifications (Capgras’ syndrome) and hyperidentifications (the other three syndromes [including SDD]).,,[We] propose that the appearance of these syndromes must alert physicians to investigate the existence of possible organic contributions”.

Compared to other misidentification syndromes, SDD appears to be relatively rare and is often comorbid with other similar conditions. For instance, in a 1986 issue of the Journal of Clinical Psychiatry, Dr. A.B. Joseph described the case of a 30-year old white male who had SDD along with paranoid schizophrenia, Cotard’s syndrome, Capgras delusion, and palinopsia (visual perseveration). Joseph concluded that cerebral dysfunctions in the confluence of the parietal, temporal, and occipital regions of the brain appeared to account for the disorders. Similarly, a 1996 paper in the journal Australasian Psychiatry, Dr. S. Atwal and Dr. M. Khan reported an unusual case of Capgras syndrome coexisting with three related syndromes (Fregoli syndrome, intermetamorphosis syndrome, and SDD).

In a more recent 1991 paper in the journal Psychological Medicine, Dr. H. Forstl and his colleagues examined the psychiatric, neurological and medical aspects of 260 cases suffering misidentification syndromes. Among the sample SDD was relatively rare as 174 cases had a Capgras syndrome misidentifying other persons, 18 a Fregoli syndrome, 11 intermetamorphosis, 17 reduplicative paramnesia and the rest had other forms or combinations of mistaken identification (including SDD). The most common comorbid disorders among those who misidentified themselves or other were schizophrenia (n=127; mostly paranoid schizophrenia), affective disorder (n=29), and organic mental syndromes including dementia (n=46). The authors reported that:

“The misidentification of persons can be a manifestation of any organic or functional psychosis, but the misidentification of place is frequently associated with neurological diseases, predominantly of the right hemisphere. Misidentification syndromes show a great degree of overlap and do not represent distinctive syndromes nor can they be regarded as an expression of a particular disorder. These patients deserve special diagnostic and therapeutic attention because of the possible underlying disorders and their potentially dangerous behaviour”.

Finally, I thought I would leave you with a paper from a 2005 issue of the journal Psychopathology that reported some extreme cases involving delusional misidentification syndromes (DMS) and the danger associated with them. Dr. M. Aziz and his colleagues reported on three cases with histories of paranoid schizophrenia tall of who developed DMSs:

“Two of them acted out on delusional thinking toward their sons. Case 1 managed to kill her son and Case 2 was caught twice trying to choke him. Our case reports suggest that the degree of threat perceived by the patient from the delusionally misidentified object is the most important factor in determining the patient’s response to the delusions. Alcohol and substance intoxication facilitated the patients’ acting out on their delusions, but did not explain the genesis of the delusions. There is a need to continue to study patients with DMS in order to provide opportunity for greater understanding of the psychopathology of DMS”.

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

Further reading

Atwal, S., & Khan, M. H. (1986). Coexistence of Capgras and its related syndromes in a single patient. Australasian Psychiatry, 20, 496-498.

Aziz, M.A., Razik, G.N., & Donn, J.E. (2005). Dangerousness and management of delusional misidentification syndrome. Psychopathology, 38(2), 97-102.

Christodoulou, G.N. (1977). Treatment of the syndrome of doubles. Acta Psychiatrica Belgica, 77(2), 254-259.

Christodoulou, G.N. (1978). Syndrome of subjective doubles. American Journal of Psychiatry, 135, 249-251.

Christodoulou, G.N. (1978). Course and prognosis of the syndrome of doubles. Journal of Nervous and Mental Disease 166, 73-78.

Christodoulou, G.N., Margariti, M., Kontaxakis, V. P., & Christodoulou, N. G. (2009). The delusional misidentification syndromes: strange, fascinating, and instructive. Current Psychiatry Reports, 11(3), 185-189

Dictionary of Hallucinations (2013). Syndrome of subjective doubles. Located at: http://hallucinations.enacademic.com/1828/syndrome_of_subjective_doubles

Enoch, D., Ball, H. (2001). Uncommon Psychiatric Syndromes (Fourth Edition). London: John Wright & Sons.

Forstl, H.A.N.S., Almeida, O. P., Owen, A. M., Burns, A., & Howard, R. (1991). Psychiatric, neurological and medical aspects of misidentification syndromes: A review of 260 cases. Psychological Medicine, 21, 905-910.

Joseph, A.B. (1986). Cotard’s syndrome in a patient with coexistent Capgras’ syndrome, syndrome of subjective doubles, and palinopsia. Journal of Clinical Psychiatry, 47, 605-606.

Identity marred: A ‪beginner’s guide to Delusional Misidentification Syndrome‬s

Some of the strangest mental and neurological syndromes that exist involve delusional misidentification. There are many different types and they all come under the umbrella term Delusional Misidentification Syndrome (DMS)‬. It was Dr. Nikos Christodoulou who introduced the term in his 1986 edited collection The Delusional Misidentification Syndromes. All DMSs involve a belief by the affected individual that the identity of something (i.e., a person, place, object, etc.) has altered or changed in some way. There are many variants of DMS, and in most cases the delusion is monothematic (i.e., it only concerns one particular topic). Here is a brief summary of the different types:

The Fregoli delusion: This refers to an individual who has the belief that more than one person that they have met is the same person in more than one disguise. The disorder is named after Leopoldo Fregoli an Italian theatre actor who was known for his remarkable ability to quickly change his physical appearance while on stage. The first reported case was in 1927 (by Dr P. Courbon and Dr. G. Fail in a French psychiatry journal) when a female schizophrenic (aged 27 years) claimed that she was being persecuted by two actors that she had seen at the theatre. According to the woman the actors “pursued her closely, taking the form of people she knows or meets”. Compared to other forms of delusional misidentification, the Fregoli delusion is thought to be the least common.

The Capgras delusion: This refers to an individual who has the belief that someone (typically a spouse or close relative) has been replaced by an identical-looking imposter. The delusion was named in 1923 after a French psychiatrist (Dr. Joseph Capgras) reported the case of a French woman who believed that her husband (and some other people she knew) had been replaced by identical looking doubles. Females are slightly more likely than males to have the delusion (approximately 60% females and 40% males). The disorder is most likely to found in individuals that have a brain injury, schizophrenia and/or dementia, but has also been associated with other medical conditions including hypothyroidism, diabetes, and migraines. There was also a case study published in a 2010 issue of the journal Biological Psychiatry (by Dr. P.R. Corlett and colleagues) who reported that the delusion had been induced by a psychologically healthy following the taking of the drug ketamine.

Subjective doubles (aka Christodoulou syndrome): This refers to individuals who have the belief that there are (one or more) doubles of themselves (i.e., doppelgangers) that carry out actions and behaviours independently and lead a life of their own. The disorder was first identified by Dr. Nikos Christodoulou in a 1978 issue of the American Journal of Psychiatry. As with other DMSs, subjective doubles syndrome typically arises as a consequence of a mental disorder, brain injury (typically the right central hemisphere) or a neurological disorder. In rare instances, there may be comorbidity with the Capgras delusion and is then referred to ‘subjective Capgras syndrome’.

Intermetamorphosis: This refers to an individual who has the belief that people in their immediate vicinity change identities with each other but keep the same appearance. The disorder was first reported in 1932 by Dr. P. Courbon and Dr. J. Tusques (again in a French psychiatry journal), and again shares comorbidity with mental and/or neurological disorders. An interesting case study was published in a 2002 issue of the journal Cognitive Neuropsychiatry by Dr. M.F. Shanks and Dr. A. Venneri. They described a man with Alzheimer’s disease who mistook his wife for his dead mother and (at a later date) his sister. He later mistook his son for his brother and his daughter for another sister. As the delusion occurred when speaking on the telephone to these misidentified individuals he was not diagnosed with either visual agnosia (i.e., an inability of the brain to recognize or understand visual stimuli) or prosopagnosia (i.e., ‘face-blindness’ – the inability to recognize faces).

There are also some other conditions that could feasibly be classed as DMSs including (i) mirrored-self misidentification, (ii) reduplicative paramnesia, (iii) delusional companion syndrome, (iv) clonal pluralization of the self, and (v) the Cotard delusion (which I covered in a previous blog). Very briefly:

  • Mirrored-self misidentification: This refers to an individual who has the belief that when they look in the mirror they see someone else.
  • Reduplicative paramnesia: This refers to an individual who has the belief that something (e.g., a person, a body part, an object, or a place has been duplicated.
  • Delusional companion syndrome: This refers to an individual who has the belief that inanimate objects are actually alive.
  • Clonal pluralization of the self: This refers to individuals who have the belief that there are multiple copies of themselves (both physically and psychologically identical).
  • The Cotard delusion: This refers to an individual who has the belief that they are dead, don’t exist and/or immortal.

There are some cases reported where individuals have more than one DMS simultaneously. For instance, in very rare cases, a person may suffer from both the Fregoli delusion and the Capgras delusion at the same time. Such individuals often experience both depersonalization and derealization and typically co-occur with other mental disorders such as bipolar disorder, schizophrenia, obsessive-compulsive disorders, and/or other mood disorders. In general, DMS is thought to arise because of a dissociation between identification and recognition processes. The Wikipedia entry on the Fregoli delusion (which also examines other DMSs) concludes:

“The study of DMS currently remains controversial…Although there is a plethora of information on DMS, there are still many mysteries of the physiological and anatomical details of DMS. An accurate semiological analysis of higher visual anomalies and their corresponding topographic sites may help elucidate the aetiology of Fregoli’s and other misidentification disorders”.

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

Further reading

Christodoulou G.N. (1986). Delusional Misidentification Syndromes. Basel: Karger.

Christodoulou G.N. (1977). The syndrome of Capgras, British Journal of Psychiatry, 130, 556.

Christodoulou G.N. (1978). Syndrome of subjective doubles. American. Journal of Psychiatry, 135, 249.

Corlett, P.R., D’Souza, D.C. & Krystal, J.H. (2010). Capgras Syndrome induced by ketamine in a healthy subject. Biological Psychiatry, 68(1), e1–e2.

Ellis HD, Luauté JP, Retterstøl N (1994). “Delusional misidentification syndromes”. Psychopathology 27 (3-5): 117-120.

Benson DF, Gardner H, Meadows JC (February 1976). Reduplicative paramnesia. Neurology 26, 147-151.

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

Shanks MF, Venneri A (2002). The emergence of delusional companions in Alzheimer’s disease: An unusual misidentification syndrome. Cognitive Neuropsychiatry, 7, 317-328.

Vörös, V., Tényi, T., Simon, M. & Trixler, M. (2003). Clonal pluralization of the self: A new form of delusional misidentification syndrome. Psychopathology 36, 46-48.

Sno, H.N. (1994). A continuum of misidentification symptoms. Psychopathology, 27, 144-147.

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.

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.