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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.

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.

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.