The medical records revealed that M.C. had been to the emergency department on three previous occasions:
Four months earlier, he had been admitted for a suicide attempt by heroin overdose. He cited drug use as his stressor and claimed command auditory hallucinations telling him to “end it all.”
A month later, he returned with similar complaints, describing his stressor as being asked to leave the Salvation Army because of drug use and curfew violation.
One week before his presentation, M.C. returned complaining of “bugs crawling out of my skin” for 1 week; the bugs originated from scabs acquired while working as an aluminum press operator. He admitted to a history of crack, cocaine, and heroin use terminating 1 month prior. He received a 10-day course of mupirocin cream and diphenhydramine and a referral to a psychiatry clinic.
At all three visits, the patient’s urine drug screen was positive for cocaine and opiates.
The physical findings included a heart rate of 117 bpm and a blood pressure of 144/90 mm Hg. The patient was noted to be mildly distressed and anxious; he was oriented to person, place, and time and displayed multiple scabs, which he was picking. No bugs or parasites were visible. Additionally, a urine drug screen was positive for cocaine and opiates (Appendix 1). The patient received lorazepam, 1 mg, in the emergency department and agreed to voluntary admission to the psychiatry service for active suicidal ideation.
During his psychiatric interview, M.C. reiterated, “I fell asleep in an abandoned building last week and woke up and found I was infested with bugs.” He complained of “seeing and feeling” bugs on his skin, that his vision was distorted by “bugs in my eyes,” and that “my urine smells funny.” He experienced an urgency to pick the “worms” from his hair follicles, which yielded a sense of relief. He reported no auditory or visual hallucinations but admitted to a depressed mood without neurovegetative symptoms; he had suicidal ideation without a plan, citing a desire “to stop the bugs.” M.C stated he would like admission in order to use social work to regain a place at the Salvation Army. He noted a history of depression and schizophrenia since age 13 with undocumented prior treatment with quetiapine, chlorpromazine, and escitalopram, while reporting no past medical history, specifically HIV or hepatitis. He had no family history of psychiatric illness. For social history, the patient explained that he was staying with his aunt, admitted to using 3–4 bags of heroin intranasally daily, but reported no cocaine or intravenous drug use. M.C. was incarcerated from 2002–2005, during which he abstained from substance use.
Upon examination, M.C. was noted to have scleral injection and at least eight 1-cm round, actively bleeding lesions over his extremities. A mental status examination revealed a well-oriented, agitated man who became frustrated with psychiatric questions because he did not regard them as relevant to his somatic complaints. He was noted to have pressured speech, poor insight and judgment, and poor hygiene. His thought process was intact and goal oriented, but the content was notable for preoccupation with infestation. He received a working diagnosis of substance-induced psychosis and polysubstance abuse (rule out delusional disorder) complicated by poor coping skills. That evening he received diphenhydramine for pruritus and dicyclomine for abdominal cramps; later that night he was noted to be agitated, aggressively scratching himself, and complaining of auditory hallucinations. He subsequently received lorazepam, 1 mg, and quetiapine, 100 mg.
Treatment and Clinical Progression
The following morning, M.C. reported no itching, noting it only occurred at night. Later he recounted “white mites and worms” emerging from his “sores” upon squeezing and agreed to collect a specimen for examination. Clonidine was added for presumptive opiate withdrawal. The patient also requested a nutrition consultation, claiming to have lost 40 lb in 2.5 months (body mass index=22.1 kg/m2). A dermatologist evaluated the patient, during which time the patient asked, “Doc, can’t you see the legs of that bug on my hip?” M.C. denied a “generalized crawling” sensation, insisting he only itched “where the bumps are.” An examination was remarkable for lichenified, excoriated, ecthymatous crusts over his legs, arms, hands, chest, shoulders, and scalp without burrows or webspace involvement. The dermatologist diagnosed him with “delusions of parasitosis aggravated by cocaine,” noting that some lesions may have been secondarily infected and recommended cefuroxime and olanzapine (1).
M.C. continued to complain of bugs in his skin and frustration that the dermatologist did not provide him with a medication to kill the insects. He continued to endorse suicidal ideation. The patient consented to treatment with cephalexin, 250 mg four times a day for 2 weeks, and olanzapine when it was specifically explained to him that they would help treat the feeling that bugs were infesting his skin.
The patient was noted in the early morning to be lying in his neatly arranged bed complaining of itching and seeing bugs and worms—“their legs coming from bites”—on his arms, neck, torso, and legs. Despite persisting symptoms, M.C. insisted on discharge on the evening of day four because of occupational obligations; he reported no suicidal ideation and contracted for safety, agreeing only to continue cephalexin. An outpatient psychiatric follow-up was advised.
M.C. returned twice to the emergency department:
Six days postdischarge, he returned complaining of skin irritation and itching. He stated he had been diagnosed with scabies and had received permethrin cream from an unknown physician 3 days earlier. He reported no suicidal ideation but admitted to using heroin and cocaine that day. Upon examination M.C. was calm, cooperative, and well oriented. Multiple ulcers were appreciated on his scalp and extremities with blood at the bases. No burrows or other signs of scabies were appreciated. The patient was referred to outpatient dermatology.
Two months after discharge, M.C. was seen for a complaint of “scabies all over me” and considerable itching despite the use of permethrin. He had suicidal ideation and had just been discharged from a local crisis center. He admitted to using heroin earlier in the day. The patient was well oriented and picking at sores. A urine drug screen was positive for benzodiazepines, cocaine, amphetamines, tetrahydrocannabinol, opiates, and barbiturates. He was discharged with permethrin and diphenhydramine.
The patient was ultimately lost to follow-up and as of the writing of this article was incarcerated for possession of crack cocaine.
Diagnosing M.C.’s Chief Complaint
Since appearing in the literature at the turn of the 19th century, delusions of parasitosis—the conviction of infestation with parasites in the absence of objective evidence—has presented dilemmas in diagnosis and management. It has variously been classified as a phobic disorder, delusional disorder, tactile hallucinosis, and monosymptomatic hypochondriacal psychosis (2). Today the classification schema of the symptom complex of delusions of parasitosis consists of three categories: 1) primary psychotic, 2) secondary functional (underlying psychiatric disorder), 3) secondary organic (Appendix 2). The primary form (the most common) (2) is marked by the absence of other disturbances of thought or thought process and is classified under delusional disorder, somatic type, in DSM-IV-TR (3). Notably, delusions of parasitosis occupy the nexus of delusion and hallucination because most patients experience tactile and/or visual and auditory hallucinations of parasites as well as a fixed belief of infestation (4). The DSM-IV specifies that a diagnosis of delusional disorder still applies in this context: “tactile and olfactory hallucinations may be present in Delusional Disorder if they are related to the delusional theme” (5).
Delusions of parasitosis occur most often in patients over 50, with an equal sex ratio for patients younger than 50 and a 2:1 female predominance in those over 50; men commonly present at an earlier age. Bimodal peaks occur at 20–30 years and greater than 50. The prevalence is higher in patients with less education and of lower socioeconomic status. Around 10% of cases present as folie á deux (shared psychotic disorder). Because the American literature on delusions of parasitosis consists mainly of case reports and series, the incidence of the disorder is unknown but considered extremely low. For example, the incidence of delusions of parasitosis in southwest Germany was estimated at 83.2 per million per year. The incidence of past psychiatric disorders is actually low in delusions of parasitosis patients, and a small percentage of patients have a history of dermatologic conditions (6, 7).
The patients’ confidence in their delusional system often manifests in the “matchbox sign”—patients bring in particles of lint, skin, paper, or food for inspection by health professionals—and the fact that 90% of the patients present for nonpsychiatric care, generally refusing subsequent psychiatric evaluation. Many patients describe detailed lifecycles for their parasites and are able to draw the organisms, even in the absence of visual hallucinations. Reports describe patients developing elaborate cleansing rituals and self-mutilation to remove the parasites (6). Before modern psychopharmacology, the remission rate for delusions of parasitosis was 33.9%; more recent data cites a rate of 51.9%, with relapse remaining common (7).
Addressing the differential diagnosis
The first step in approaching a patient with apparent delusions of parasitosis is to assess for objective evidence of infection (especially scabies) or other skin conditions such as Grover disease (transient acantholytic dermatosis). Next, the strength of the patient’s conviction should be assessed to distinguish delusions of parasitosis from hypochondriasis or obsessive-compulsive disorder, in which patients generally maintain relative insight regarding their conditions. Once the patient is deemed truly delusional, an attempt should be made to discern between primary and secondary delusions of parasitosis and to assess the degree of functional impairment. Patient rapport is critical to successful treatment and compliance.
It is important then to investigate potential medical conditions that may underlie the delusions. Specifically, conditions marked by symptoms of itching or abnormal skin perception (8), including liver failure, obstructive jaundice, renal failure, anemia, vitamin deficiencies, and HIV/AIDS, are vital to consider because they represent potentially treatable underlying etiologies. In M.C.’s case, though, clinical and laboratory evaluation uncovered cocaine use as the only suspicious secondary organic cause.
Formication, a tactile hallucination of something creeping or crawling on or under the skin, is often referenced and is reported by 13%–32% of cocaine abusers (“cocaine bugs”). Formication is hypothesized to result from parietal lobe stimulation (8). It is important, though, to recognize that delusions of parasitosis in younger patients are more likely to have an underlying cause and not to dismiss prematurely M.C.’s symptoms as substance-induced psychosis. Most cocaine users are familiar with formication, maintain cognizance of it as a hallucination, and do not go on to form delusions (9). Although reports suggest that most cocaine psychoses abate within 24–48 hours of discontinuation (10, 11), M.C. came to the emergency department with a systematized delusion about his infestation, including an attributional narrative (sleeping in an abandoned house, preexisting work-related lesions), that was stable over at least 1 week. However, reports, although uncommon, exist of chronic psychoses in long-standing, heavy users (12, 13). Given his suicidal ideation and history of attempt, it was critical to approach his chief complaint with caution and seriousness because it may have signaled a psychiatric emergency; it is not uncommon for patients with delusions of parasitosis to experience depression and suicidal ideation with the motivation to end infestation, and there is at least one report of fatal delusions of parasitosis in which a 40-year-old man completed suicide during treatment (14). Finally, because M.C. agreed to admission to the voluntary psychiatric service for the stated purpose of using social work services, malingering must be considered.
M.C. was diagnosed with cocaine- and/or schizophrenia-related delusions of parasitosis, although a primary delusional disorder, exacerbated by cocaine use, remained under consideration.
How This Case Fits Into the Literature
In M.C.’s case, as in many delusions of parasitosis cases, confident categorization of his symptoms is challenging given his inconsistently self-reported psychiatric history (none, schizophrenia, and depression) and positive drug screens. In particular, case reports have linked cocaine psychosis with delusions of parasitosis (distinct from classic formication) (15); delusions of parasitosis have also been reported in the context of schizophrenia (3, 16). Taken together, suspicion is high for a secondary organic and/or functional etiology. The potential interaction between multiple secondary factors in delusions of parasitosis is unknown. A secondary etiology would help explain M.C.’s younger age (the mean is the sixth decade of life), earlier presentation in disease course (the mean is 1 year), and unusual claim of ocular involvement (7, 17). Although inadequate follow-up complicates interpretation, M.C.’s apparent co-occurring somatic delusions of weight loss and urine odor represent interesting phenomena; one other report exists of delusions of parasitosis with the delusion of body odor in a schizophrenic patient (16). Phenomenologically, though, M.C.’s insistence of a dermatologic condition with detailed delusions, his skepticism of psychiatric involvement, and the persistence of the condition comport with current reports.
A controversial phenomenon possibly related to delusions of parasitosis inspiring discussion and media attention is Morgellons’s disease. As in delusions of parasitosis, patients describe insects/parasites crawling on or under the skin, are convinced they are infested and contagious, and produce physical “evidence” of infestation. In particular, though, patients complain of fibers extruding from the skin; such particles produced for examination have been variously identified as cellulose, fibers with “autofluorescence,” fuzz balls, specks, granules, Strongyloides stercoralis, Cryptococcus neoformans, “alternative cellular energy pigments,” and various bacteria. In no case, however, has an infectious etiology for these mysterious symptoms been confirmed. Morgellons’s disease is largely regarded in the dermatology literature as a manifestation of delusions of parasitosis (and potentially a means of promoting patient rapport through destigmatization), despite the efforts of the Morgellons Research Foundation to promulgate an infectious rather than a neuropsychiatric etiology. Until a treatable infectious component is identified, patients can continue to be treated with neuroleptics—pimozide, risperidone, aripiprazole—which have been reportedly effective (18, 19).
Current Etiologic Hypotheses
The debate over the classification and etiology of delusions of parasitosis has revolved around a central question: do delusions of parasitosis reflect a delusional system that arises in response to anomalous sensory perceptions (sensorial view), or does a primary delusion “induce” supporting hallucinations (cognitive view) (4, 8)? Etiologic hypotheses have arisen addressing this paradox, and it now appears likely that both mechanisms contribute in different patients, suggesting that delusions of parasitosis are not a homogenous entity. For years, the dopamine D2 receptor has been implicated in the genesis of psychotic symptoms, including the characteristic of delusions of parasitosis. Involvement of the D2 receptor in the mesolimbic system could account for the successful use of typical and atypical antipsychotics in treating the primary delusional disorder (6). This has been traditionally viewed as support for the cognitive view of delusions of parasitosis. However, it is now believed that pimozide, a highly potent typical antipsychotic and the classic treatment for delusions of parasitosis, antagonizes central opiate in addition to D2 receptors, which may mitigate pruritus and formication that underlie/accompany the delusion of infestation (6, 20). In fact, pimozide has effectively treated formication in the absence of delusion (e.g., in delirium tremens). Furthermore, naloxone, an opioid receptor antagonist (21), has been used to treat cases of delusions of parasitosis, supporting the sensorial view.
A recently proposed hypothesis focuses on the decreased function of the striatal dopamine transporter. This presynaptic protein is responsible for dopamine reuptake and hence modulates the concentration of synaptic dopamine and the duration of synaptic signals. It follows that decreased functioning of the transporter results in dysregulation of extracellular dopamine concentration. The authors propose that both primary and secondary delusions of parasitosis develop because of dysfunctional striatal dopamine transporter (3). Primary forms result from an exaggeration of age-related striatal dopamine transporter density decrease (there is a mean physiologic decrease in striatal dopamine transporter density of 6%–8% per decade), which would help explain the prevalence of cases in patients over 50 (3, 6). Secondary etiologies of delusions of parasitosis affect the striatal dopamine transporter through a variety of mechanisms (Table 1). Psychostimulants, for example, are known to inhibit the striatal dopamine transporter, resulting in increased dopamine levels. Psychiatric disorders such as schizophrenia and depression are thought to decrease striatal dopamine transporter binding (3).
Other studies offer a connection between delusions of parasitosis and cerebral hypoperfusion documented by single photon emission computed tomography. It has been found that active delusional thought is associated with hypoperfusion of the left temporal and parietal lobes. Blood flow normalizes with the resolution of the delusion (22). Some argue that successful treatment of delusions of parasitosis with paroxetine and clomipramine, which may restore blood flow to hypoperfused regions by increasing serotonin levels, supports this hypothesis (22, 23).
An Integrated, Individualized Model of the Formation of Delusions of Parasitosis
The majority of case reports and reviews of delusions of parasitosis have concentrated on defining a demographic profile, investigating associated conditions, describing response to treatment, and suggesting neurophysiologic etiologies. Given the growing evidence and interest for cognitive and affective models of delusion formation, maintenance, and content (24), an integrated, neuropsychiatric narrative of M.C.’s delusions of parasitosis is fruitful and contextualizes the particular presentation and course of illness.
First, it is reasonable to regard M.C. as a psychosis-prone individual. Although it remains undocumented, his stated history of schizophrenia is supported by complaints of command auditory hallucinations and prior treatment with antipsychotics. It is not possible to determine with confidence the etiology of M.C.’s past psychiatric history due to presumed long-term drug use. Indeed, it is well-documented that cocaine increases the risk for psychotic experiences (one of Freud’s patients treated with cocaine developed delusions of parasitosis) (25). The most common form of cocaine-induced psychosis is paranoid delusions. Studies have identified risk factors for true psychosis formation in cocaine users as male sex, lower body mass index, earlier initiation of regular use, and greater degree of use (12).
It seems intuitive that M.C.’s psychosis proneness and substance use contributed in concert to the development of his delusions of parasitosis. It has been found that in schizophrenic patients, chronic substance abuse correlates with significantly increased rates of visual and olfactory hallucinations (Table 2). Furthermore, substance abuse is associated with decreased medication responsiveness in schizophrenic and bipolar patients with auditory and tactile hallucinations (26). Perhaps this is related to the previously discussed findings that schizophrenia and cocaine act at the striatal dopamine transporter in distinct ways to increase dopamine levels (3). In addition, it has been posited that auditory and tactile hallucinations are associated with changes in the superior and inferior temporal lobes in schizophrenia patients; drug use may contribute to the development of psychosis in these compromised individuals by accelerating brain tissue loss (26).
How exactly these biologic findings lead to psychosis formation remains unclear. Growing evidence for cognitive dysfunction and bias in delusions has led to a number of cognitive models describing delusion formation. Significantly, cognitive models help explain why delusions, which make sense for the believer and are held to be evidentially true, are often resistant to change despite psychopharmacologic treatment (24). Over the last decade, research has unveiled a number of cognitive biases in those prone to psychosis. Patients with auditory hallucinations have been shown to have impaired source monitoring (the ability to discriminate between one’s internal verbal thoughts and other stimuli) (27). Source monitoring in psychosis-prone patients has also been shown to be excessively influenced by external factors and suggestion (28).
Cognitive theories have also been posed to account for the formation of delusional thoughts in addition to that of hallucinations, and one could easily apply these theories to the formation of delusions regarding hallucinations. One early study showed that delusional patients showed a “jumping-to-conclusions” reasoning bias, whereby initial probabilistic estimates and subsequent revision of hypotheses were made based on less evidence than in control subjects, a finding that is stronger when reasoning regarding emotional material (24). In the formation of paranoid delusions, significant attention has been paid to attributional biases in delusion-prone individuals. Most people are neither rational nor fair minded when generating and selecting causal explanations for events, demonstrating a “self-serving bias” toward internal (self) blame for positive events and external blame for negative events. Paranoid patients have an exaggerated self-serving bias (27). Although incompletely understood, it has been shown that when cognitive resources are taxed or individuals feel threatened, people tend to resort to external attribution. Finally, studies have found that latent inhibition is particularly disrupted in acute psychosis and suggest that an impairment in attentional filtering might underlie symptom development (e.g., M.C. preferentially attended to threatening tactile stimuli) (24).
A number of current models approach delusion formation as a variation of normal belief formation. It has been argued that perceptual disturbance is a necessary “first factor” in delusion formation and that cognitive biases influence the content of hypothesis generation. A necessary “second factor” accounts for how unusual hypotheses result in full-blown delusions (i.e., how does M.C. go from feeling like he has bugs on his skin to a deeply held conviction of infestation?); this factor is thought to be a deficit in the rational evaluation of candidate hypotheses (24).
A heuristic model for the acute development of delusions of parasitosis in M.C. can be derived from a synthesis of the two-factor cognitive model of Bell et al. (24) and some of what is known about the neurobiology of psychosis and substance use. Consistent with such a model would be a situation in which M.C. woke up on the morning of admission experiencing formication related to cocaine use and/or opiate-induced pruritus. He regarded this as an anomalous, threatening experience, and in the context of the stressor of losing his housing, preferentially attended to this aversive stimulus. The disorientation of unfamiliar surroundings as well as his cognitive and attributional strategies that constituted his psychosis proneness biased hypothesis generation toward externalization and concretization. An error in probabilistic reasoning resulted in delusion formation of parasitosis, a hypothesis that comports with M.C.’s persistent denial of cocaine use. Factors that favor maintenance of the delusion include cognitive reinforcement (e.g., the literature recommends against empirically diagnosing or treating delusions of parasitosis patients for scabies) (9, 29) and continued “anomalous” sensory perception with resumption of drug use. Such a heuristic model generates implications for designing therapeutic intervention. Rigorous attention should be invested in M.C.’s housing troubles, and of course, intensive treatment of his substance use is critical. Furthermore, once the patient’s baseline cognitive strategies removed from substance use become clearer, appropriate attempts at disrupting the maintaining factors of the delusion could be made, including education and long-term antipsychotics as needed.
Considerations for the Future
This case highlights some important gaps in our current understanding of delusional parasitosis. First, in Trabert’s 1995 meta-analysis of delusions of parasitosis (7), substance-induced cases were excluded, resulting in a dearth of information regarding these particular cases. Specifically, very little has been written about the appropriate management of delusions of parasitosis in the context of substance use other than that it is notoriously difficult. Are the same antipsychotic medications used for primary delusions of parasitosis effective for substance-related delusions of parasitosis? Will they shorten the disease course or help mitigate symptom severity as part of a harm-reduction strategy? Similarly, when delusions of parasitosis occur in the context of schizophrenia, how should management be adjusted to address these symptoms? Although studies are difficult because of the condition’s rarity, a closer examination of delusions of parasitosis and their associated conditions as well as a multicenter randomized clinical trial are needed to better understand delusions of parasitosis and the mechanisms of delusion formation in general.
Received March 2, 2007; revision received May 8, 2007; accepted May 17, 2007 (doi: 10.1176/appi.ajp.2007.07030381). From the Department of Psychiatry, UMDNJ–Robert Wood Johnson Medical School. Address correspondence and reprint requests to Dr. Dunn, Department of Psychiatry, UMDNJ–Robert Wood Johnson Medical School, Cooper University Hospital, One Cooper Plaza, Camden, NJ 08103; email@example.com (e-mail).
All authors report no competing interests.
1.Meehan WJ, Badreshia S, Mackley CL: Successful treatment of delusions of parasitosis with olanzapine. Arch Dermatol 2006; 142:352–355
2.Slaughter JR, Zanol K, Rezvani H, Flax J: Psychogenic parasitosis: a case series and literature review. Psychosomatics 1998; 39:491–500
3.Huber M, Kirchler E, Karner M, Pycha R: Delusional parasitosis and the dopamine transporter: a new insight of etiology? Med Hypotheses 2007; 68:1351–1358
4.Baker PB, Cook BL, Winokur G: Delusional infestation: the interface of delusions and hallucinations. Psychiatr Clin North Am 1995; 18:345–361
5.American Psychiatric Association: Diagnostic and Statistical Manual, Fourth Ed., Text Revision. Washington, DC, APA, 2000
6.Wenning MT, Davy LE, Catalano G, Catalano MC: Atypical antipsychotics in the treatment of delusional parasitosis. Ann Clin Psychiatry 2003; 15:233–239
7.Trabert W: 100 years of delusional parasitosis: meta-analysis of 1,223 case reports. Psychopathology 1995; 28:238–246
8.de Leon J, Antelo RE, Simpson G: Delusion of parasitosis or chronic tactile hallucinosis: hypothesis about their brain physiopathology. Compr Psychiatry 1992; 33:25–33
9.Koo J, Lee CS: Delusions of parasitosis: a dermatologist’s guide to diagnosis and treatment. Am J Clin Dermatol 2001; 2:285–290
10.Harris D, Batki SL: Stimulant psychosis: symptom profile and acute clinical course. Am J Addict 2000; 9:28–37
11.Adler LE, Olincy A, Cawthra E, Hoffer M, Nagamoto H, Amass L, Freedman R: Reversal of diminished inhibitory sensory gating in cocaine addicts by a nicotinic cholinergic mechanism. Neuropsychopharmacology 2001; 24:671–679
12.Thirthalli J, Benegal V: Psychosis among substance users. Curr Opin Psych 2006; 19:239–245
13.Boutros NN, Bowers MB Jr: Chronic substance-induced psychotic disorders: state of the literature. J Neuropsychiatry Clin Neurosci 1996; 8:262–269
14.Monk BE, Rao YJ: Delusions of parasitosis with fatal outcome. Clin Exp Dermatol 1994; 19:341–342
15.Elpern DJ: Cocaine abuse and delusions of parasitosis. Cutis 1988; 42:273–274
16.Tenyi T, Trixler M: Coexistence of the delusions of infestation and body smell in schizophrenia: a case report. Psychopathology 1993; 26:292–293
17.Sherman MD, Holland GN, Holsclaw DS, Weisz JM, Omar OH, Sherman RA: Delusions of ocular parasitosis. Am J Ophthalmol 1998; 125:852–856
18.Koblenzer CS: The challenge of Morgellons disease. J Am Acad Dermatol 2006; 55:920–922
19.Murase JE, Wu JJ, Koo J: Morgellons disease: a rapport-enhancing term for delusions of parasitosis. J Am Acad Dermatol 2006; 55:913–914
20.Johnson GC, Anton RF: Pimozide in delusions of parasitosis. J Clin Psychiatry 1983; 44:233
21.Botschev C, Muller N: Opiate receptor antagonists for delusions of parasitosis. Biol Psychiatry 1991; 30:530–531
22.Hayashi H, Oshino S, Ishikawa J, Kawakatsu S, Otani K: Paroxetine treatment of delusional disorder, somatic type. Hum Psychopharmacol 2004; 19:351–352
23.Wada T, Kawakatsu S, Nadaoka T, Okuyama N, Otani K: Clomipramine treatment of delusional disorder, somatic type. Int Clin Psychopharmacol 1999; 14:181–183
24.Bell V, Halligan PW, Ellis HD: Explaining delusions: a cognitive perspective. Trends Cogn Sci 2006; 10:219–226
25.Becker HK: Carl Koller and cocaine. Psychoanalytic Q 1963; 32:309–373
26.Sokolski KN, Cummings JL, Abrams BI, DeMet EM, Katz LS, Costa JF: Effects of substance abuse on hallucination rates and treatment responses in chronic psychiatric patients. J Clin Psychiatry 1994; 55:380–387
27.Bentall RP: Abandoning the concept of schizophrenia: the cognitive psychology of hallucinations and delusions, in Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. Edited by Read J, Mosher LR, Bentall RP. New York, Brunner-Routledge, 2004, pp 195–208
28.Young HF, Bentall RP, Slade PD, Dewey ME: The role of brief instructions and suggestibility in the elicitation of auditory and visual hallucinations in normal and psychiatric subjects. J Nerv Ment Dis 1987; 175:41–48
29.Gould WM, Gragg TM: Delusions of parasitosis: an approach to the problem. Arch Dermatol 1976; 112:1745–1748