153  Delusional Parasitosis
Kathryn N Suh, Jay S Keystone
Key features
l An uncommon, unfounded, irrational belief of infestation
that cannot be corrected by reasoning, persuasion, or logic
l More common in women and in older age groups (>50
years)
l Patients may be otherwise highly functional
l Rarely, may be associated with underlying medical or
psychiatric disease, substance abuse, or medications
l Longstanding history of cutaneous complaints and
dermatologic findings, often for months to years before
diagnosis
l Skin lesions are common and often asymmetric, reflecting
the range of the dominant upper limb
l Effective therapies (neuroleptics) are available but often
difficult for patients to accept
l Synonyms: delusional (or delusions of ) infestation;
delusions of parasitosis
l less commonly: chronic tactile hallucinosis, cocaine
bugs, delusional ectoparasitosis, delusory parasitosis,
Ekbom’s syndrome, formication, praeseniler
dermatozoenwahn (presenile dermatozoic delusion),
psychogenic parasitosis
l others: acaraphobia, dermatophobia, entomophobia,
parasitophobia (technically these are not correct since
they indicate a phobia rather than belief )
INTRODUCTION
Delusional parasitosis (DP), first described in 1894, is a disorder in
which affected individuals have a delusion – an unshakeable belief
– that they are infected by “bugs”: parasites, worms, bacteria, mites,
or other living organisms, associated with abnormal cutaneous sensa-
tions. While the disease remains rare, there is increasing awareness of
and advancement in the pharmacologic therapy of DP. However,
recognition and management of this problem continues to be
challenging.
EPIDEMIOLOGY
Delusional disorders are rare, being slightly more common among
women. Their incidence and prevalence were previously estimated to
be 0.7–3.0 and 24–30 cases per 100,000 population, respectively [1].
More recent data suggest that these may be underestimates; in one
1074
Swedish cohort, the lifetime prevalence of delusional disorders was
estimated at 0.30 per 100 population [2].
Rates of DP are difficult to determine. Since patients with DP generally
refuse psychiatric help, the true incidence and prevalence of this dis-
order may be greatly underestimated in the psychiatric literature. In
southwest Germany, the incidence and prevalence of DP were esti-
mated to be 16.6 and 83.2 cases per million population per year,
respectively [3]. In his 1995 review, Trabert [4] had identified a total
of 1223 cases in the literature; as of 2008, reports of over 1400 cases
were published [5]. Most have been reported from North America and
Europe, and recently from most other areas of the world except Africa.
While DP affects adults of all ages, it is much more common in older
age groups (> 50 years). In Trabert’s review, the mean age of onset
was 57 years and 84% of patients were over age 50, with men present-
ing at a slightly younger age than women [4]. Overall, women out-
number men by a 2–3 : 1 ratio [4,6]. Although the sex distribution is
almost equal in early adulthood, the female : male ratio exceeds 3 : 1
in individuals over 50 years of age [4,6].
Patients can be from any socioeconomic background. Many are single
and may be considered “loners”. A higher than expected prevalence
of personality disorders has been observed in some case series [6,7].
However, many affected individuals are both educated and highly
functional; in Lyell’s survey [6], several of the 282 patients described
were professionals, including physicians and psychologists.
NATURAL HISTORY, PATHOGENESIS,
AND PATHOLOGY
In its truest form, DP is a delusional disorder of the somatic type:
“delusions that the person has some physical defect of general medical
condition” [8]. Munro [9] first suggested that DP was a form of
monosymptomatic hypochondriasis or monosymptomatic hypo-
chondriacal psychosis (MHP), a fixed, single hypochondriacal belief
that exists when no other thought disorder is present. Delusions of
parasitosis are the most common form of MHP.
The pathophysiology of somatic delusional disorders is unknown.
Some have theorized that abnormal sensations experienced by
patients (as if something was crawling on the skin) lead to the convic-
tion that parasites are present (that something really is crawling on
the skin). An incident during which exposure to parasites might have
occurred, such as sleeping in unclean bedsheets, borrowing another’s
clothing, or travel to an exotic destination, may be a trigger for DP.
In some, newly acquired knowledge or awareness of a disease (through
heightened public health or media interest, or the internet, for
example) can amplify and perpetuate new or pre-existing symptoms;
reasons for this symptom amplification are unclear. Stress can also
exacerbate somatic complaints, and the stress induced by the severity
of the perceived illness may augment symptoms further.
It has also been suggested that DP may be due to central nervous
system abnormalities. Response of many patients to the dopamine
 D e l u s i o n a l Parasitosis 1075

BOX 153.1  Diagnostic Criteria for TABLE 153-1  Some Medical Conditions and
Delusional Disorder Medications Associated With Delusions of Parasitosis

1. Non-bizarre delusions involving situations that occur in real

Neurologic Dementia
life, lasting >1 month disorders Head trauma
2. Does not meet all criteria for diagnosis of schizophrenia Infarction
(see text) Infection
3. Function is otherwise not markedly impaired Multiple sclerosis
Multiple system atrophy
4. Mood episodes, if concurrent, are of brief duration com- Postoperative complication of neurosurgery
pared with duration of delusions Tumors of the central nervous system
5. Substance abuse, medication side effects, and general
Endocrine Diabetes mellitus
medications must be ruled out
disorders Hyperthyroidism
Adapted from American Psychiatric Association. DSM-IV-TR. Diagnostic and Hematologic Severe anemia
Statistical Manual of Mental Disorders, 4th edn, Text Revision. Washington, disorders Leukemia
DC: American Psychiatric Association, 2000;323–9. Polycythemia vera
Infectious HIV infection
diseases Leprosy
antagonist pimozide supports the theory that DP results from excess Tuberculosis
extracellular dopamine within the striatum of the brain [10]. In some Prior infestation
patients, structural abnormalities in the basal ganglia, in particular
Malignancy Lymphoma
the putamen and caudate nucleus, have been documented [11,12]; Solid organ: breast, colon, lung
most of these patients also responded favorably to dopamine antago-
nists. Such findings must be interpreted with caution, however, given Nutritional B12, folate, thiamine deficiency
the small number of patients studied and the lack of comparison with deficiency Pellagra
age-matched normal controls.
Drugs or toxins Alcohol
Amphetamines, including methylphenidate
CLASSIFICATION OF   Cocaine
DELUSIONAL PARASITOSIS Heroin
Prescription Amantadine
No definite classification of DP exists. Broadly speaking, three differ-
medications Ciprofloxacin
ent forms can be described. Corticosteroids
Ketoconazole
PRIMARY DELUSIONAL PARASITOSIS Pargyline
Pegylated interferon-alpha
Primary DP is a somatic delusional disorder (Box 153.1). Patients
Phenelzine
with delusional disorders do not meet the diagnostic criteria for Topiramate
schizophrenia or other psychiatric disorders. Specifically, hallucina-
tions, disorganized speech, schizophrenic behavior, and other “nega- Adapted from Slaughter JR, Zanol K, Rezvani H, et al.: Psychogenic parasitosis: a
tive” symptoms are absent, although hallucinations that are secondary case series and literature review. Psychosomatics 1998;39:491–500; and
to the delusional theme (i.e. tactile hallucinations) may be present. Johnson GC, Anton RF: Delusions of parasitosis: differential diagnosis and
Similarly, anxiety or depression secondary to the delusional disorder treatment. South Med J 1985;78:914–18.
may be present.

SECONDARY DELUSIONAL PARASITOSIS

ASSOCIATED WITH UNDERLYING
PSYCHIATRIC DISEASE
Delusions of parasitosis may be a manifestation of an underlying
psychiatric illness, such as schizophrenia, anxiety, depression, obses-
sive compulsive disorder, schizophreniform disorder, bipolar disor-
der, or post-traumatic stress disorder. It is essential to distinguish this
form of DP from primary DP as the management differs, but this may
be challenging, particularly for the non-psychiatrist physician who is
most likely to encounter such patients.
SECONDARY DELUSIONAL PARASITOSIS
ASSOCIATED WITH UNDERLYING
MEDICAL CONDITIONS
Although up to 25% of cases of DP have been attributed to underlying
medical conditions [4,7], in our experience this is remarkably rare.
Delusional parasitosis has been attributed to diseases of most organ
systems, most commonly the central nervous system (Table 153-1).
Substance abuse should be considered, especially when DP presents
in younger age groups. Numerous prescription medications have
been implicated in DP; in such cases, symptoms generally resolve
once the offending drug is discontinued. Documented parasitic infec-
tion rarely (2% of all cases) precedes the development of DP [6].
CLINICAL FEATURES
Patients with DP have unfounded, irrational beliefs of infestation that
cannot be corrected by reasoning, persuasion or logic. Symptoms and
beliefs are variable, ranging from a non-disruptive feeling of infesta-
tion to delusions that may interfere with daily activities. Patients with
primary DP generally have intact mental function, lack other mani-
festations of psychiatric disease, and have otherwise normal behavior.
Their delusions are limited in scope and usually do not interfere with
personal and professional aspects of their lives. Although they initially
cannot appreciate their delusional state, it may subsequently become
evident to them during therapy. Patients with secondary DP may have
signs and symptoms of underlying disease. Younger patients are more
likely to have DP associated with head injuries, substance abuse and
schizophrenia, and are more likely to be involved in shared delusions
[6,13]. Delusions due to substance abuse are usually transient and of
inadequate duration to meet the criteria for delusional disorder.
Longstanding dermatologic complaints are common, including
rashes, pruritus, and sensations of stinging, biting and formication.
1076 HUNTER’S TROPICAL MEDICINE AND EMERGING INFECTIOUS DISEASE
Most patients have chronic symptoms, at least 6 months in duration
and often longer, before the diagnosis is established. The median and
average duration of symptoms before diagnosis in Trabert’s study was
1 year and 3 years, respectively [4]. Patients may have received
repeated courses of dermatologic and antiparasitic therapies despite
the lack of an objective diagnosis. They frequently bring in specimens
for examination which they have picked from their skin – the “match-
box” or “Ziploc® bag” sign [14,15] – and which typically contain
normal skin flakes or dust, hair, or occasionally parts of non-
pathogenic insects. Patients may produce bizarre and exhaustive
descriptions and diagrams of the parasites and their reproductive
cycles. Patients who attribute their disease to household pets may
have visited veterinarians repeatedly, seeking treatment for their pets.
Consultation with pest-control services and exterminators, and use of
potentially toxic pesticides (on themselves and their belongings), may
be attempted. Those driven to extremes may move, or rid themselves
of their belongings. For some, fear of transmission of their “infection”
to others may cause them to be socially isolated, even from family
members. Recently, as a result of web searches, some believe that they
have “Morgellons disease”, an unexplained condition characterized
by diverse cutaneous symptoms, foreign material (e.g. fibers) on the
skin, and skin lesions.
Others, particularly family members, may occasionally be drawn into
the patient’s delusional system, usually by a woman [16]. Between
8% and 25% of delusions of parasitosis are shared [6,7,16], most
often with one other person (folie à deux), usually a partner or spouse
(less commonly offspring). On occasion, trios (folie à trois), or even
larger groups, may be involved.
PATIENT EVALUATION, DIAGNOSIS,
AND DIFFERENTIAL DIAGNOSIS
Delusional parasitosis should be suspected when an individual
presents with an irrational, fixed belief that he or she is infected with
internal or external parasites in spite of reassurance and ample evi-
dence to the contrary. It is important to determine the following: 1)
is the belief founded in reality, and the patient truly infected; 2) if
infection can be excluded, is the patient truly delusional, or is the
patient hypochondriacal and the belief “shakeable”; and 3) if the
patient is delusional, what form of DP is present? The optimal therapy
differs depending on the answers to these questions. If an organic
cause can be ruled out, the major challenge is then to determine
whether the patient is suffering from a primary delusional disorder
or has an underlying psychiatric illness. A psychiatric opinion is inval-
uable in such instances, but most patients with DP will refuse a
psychiatric assessment.
The initial assessment(s) should focus on the patient’s primary com-
plaints, eliminating both true infection and an organic disease(s) as
causes of their symptoms. A thorough history to elicit symptoms of
underlying disease, and use of prescription and illicit drugs, should
be obtained; important clues about underlying medical or psychiatric
illness can be discovered by thorough careful questioning and listen-
ing. A complete physical examination is essential, looking for findings
of underlying conditions and paying particular attention to the skin,
since most patients have cutaneous symptoms. Ulcers, scratches,
denuded skin and scars may be present from attempts to remove the
organisms from the skin by using fingernails, knives, pins, duct-tape
or other objects. Lesions are often absent in the upper back where the
patient cannot reach. Contact or irritant dermatitis may be present
from excessive cleaning or the use of abrasive soaps or chemicals.
Evaluation by a dermatologist can be beneficial and may reassure
the patient that his/her symptoms are being taken seriously. If the
patient has brought his/her own specimens, reassure the patient that
these will be sent to a proper laboratory and/or entomologist for
examination. The patient should be provided with specimen bottles
containing preservative to collect additional specimens, thereby
reducing the chance that parasites will be missed because of improper
collection and reassuring the patient that you “believe” him/her. Skin
biopsies are rarely required. Negative results, especially from repeated
BOX 153.2  Suggested Initial Investigations
in Patients with Delusional Parasitosis
In all patients:
l Complete blood count and differential
l Electrolytes, urea, creatinine
l Liver function tests and enzymes
l Fasting blood sugar
l Thyroid-stimulating hormone level
l B12 and folate levels
l Calcium and magnesium
l Erythrocyte sedimentation rate and C-reactive protein
l Chest radiograph
Based on the individual’s risk factors  
and symptoms:
l Drug and toxin screen
l Serology for HIV infection and syphilis
l Tuberculin skin test
l Additional radiologic imaging (e.g. computerized tomogra-
phy or magnetic resonance imaging of the brain)
examinations of submitted specimens, can eliminate the possibility
of a real parasitic infection. Appropriate initial investigations should
be obtained (Box 153.2).
Follow-up visits fulfill multiple needs. In addition to providing more
opportunity for the patient to develop trust in the physician, serial
examination of skin lesions during repeat visits can be performed and
additional specimens (or other investigations) obtained as required.
Repeated assessments may also be helpful in determining whether the
patient has a shakeable belief (hypochondriasis) rather than true
delusions, if this remains unclear. Since most patients will not agree
to psychiatric care, long-term follow-up with the primary care physi-
cian may be most appropriate.
PSYCHIATRIC ASSESSMENT
Secondary DP associated with underlying psychiatric disorders is best
managed by a psychiatrist. Some suggest that most patients with DP
should be managed by primary care physicians, dermatologists, or
infectious disease consultants for fear of losing them to medical care
altogether by suggesting they see a psychiatrist, while others recom-
mend that a psychiatrist be at least consulted at some point in the
patient’s care. However, many healthcare practitioners are not trained
or prepared to provide the pharmacotherapy that can benefit the
patient with DP.
Convincing patients with DP of the need for and importance of a
psychiatric referral is extremely difficult. The treating physician’s cred-
ibility often dissipates and trust is lost at the mere mention of the
need for psychiatric consultation or therapy; there is a significant risk
of losing the patient altogether. Gradual introduction of the topic over
the course of several visits, emphasizing the need for expert guidance
to manage the effects that DP has had on the patient’s life (such as stress
or depression) may result in greater success. In some situations it may
be helpful to discuss the case with a psychiatrist prior to commencing
therapy.
TREATMENT
Psychotherapy, psychosurgery, and electroconvulsive therapy have
met with little success in the treatment of DP, with low cure rates
comparable to the rate of spontaneous resolution (17). Antidepres-
sant and anxiolytic medications may improve secondary mood dis-
orders but generally have no role in the treatment of primary DP.

A strong therapeutic relationship with the patient is critical. A sympa-
thetic, non-judgmental approach, acknowledgment that patients’
symptoms are real (and, if necessary that they are not mentally ill),
and empathetic exploration into the effects their symptoms have had
on their daily lives can instill a sense of trust into the relationship. A
conservative, non-confrontational approach is recommended [17–
19]. Use of phrases such as “I cannot see any parasites today” rather
than “There are no parasites” [6], and acknowledgment that their
problem may have resulted from a previous infection may accomplish
this, while further gaining the patient’s trust. It is important not to
dismiss patients’ complaints as trivial, even when they are clearly
delusional, but equally important not to openly support their beliefs
and feed into their delusional system. Reassurance that they can be
helped is also valuable.
In spite of the limited evidence of their efficacy, with few clinical trials
and no substantial randomized controlled trials conducted, antipsy-
chotic medications have become the mainstay of therapy for DP [20].
The goal of therapy should be improvement in the patient’s symp-
toms, and not necessarily cure. Convincing patients to take antipsy-
chotic agents poses another significant obstacle, however. Even if
patients do agree to start medication, adherence may be an issue. How
does one convince psychotic patients who steadfastly believe that they
are not psychotic to take antipsychotics? One strategy that we have
used with considerable success is the approach that “the parasitic
infection” is no longer present, but symptoms continue as a result of a
“biochemical imbalance” resulting from the initial infestation. Introducing
the need for an antipsychotic is accomplished by indicating that
although the drug was originally designed for schizophrenia (“but of
course, you are not schizophrenic”), it is being used for another purpose,
i.e. to rebalance body chemistry. This statement should be followed
by examples of other medications that have more than one use, such
as aspirin for pyrexia and coronary artery disease, or amitriptyline for
depression and neuritis. Patients are much more likely to agree to take
medication for treatment of a “chemical imbalance” than for a psy-
chiatric problem. Some patients may be persuaded if they are told
that patients with a similar condition have experienced great relief in
their symptoms using similar medications. Bargaining with a patient
is fraught with potential problems; however, the physician may agree
to a patient’s request (for example, treatment with an antiparasitic
agent) on the condition that the patient also begin an antipsychotic
medication.
Efficacy comparisons of different agents are hindered by publication
bias, the paucity of controlled trials, the inclusion of patients with
both primary and secondary DP in many studies, and the lack of
standardized criteria for assessing response to therapy.
First-Generation Antipsychotic Agents
While many first-generation antipsychotics have been used success-
fully for treatment of DP, pimozide has been the most extensively
studied, with the highest reported success rate. Case series from the
late 1990s reported response rates of up to 87% (33% to 52% com-
plete, 28% to 35% partial) [21,22], and two small double-blind trials
both demonstrated efficacy of greater than 90% [23,24].
Pimozide selectively blocks dopamine type 2 receptors. It has minimal
effect on other central nervous system neurotransmitters, although its
antagonistic effects on opiate receptors may also reduce sensations of
pruritus and formication [23]. The most common adverse effects are
extrapyramidal reactions (tremor, bradykinesia, shuffling gait), which
occur in up to 15% of patients [13].
Doses between 1 and 12 mg daily are usually effective for treatment
of DP. An initial dose of 0.5 to 1 mg daily can be increased gradually
(e.g. by 1 mg weekly) either to the maximum daily dose of 20 mg, or
until the desired clinical effect has been achieved, which may take
several weeks. Most patients respond to doses much lower than 10 mg
per day. Once a satisfactory response has been obtained, the patient
should be maintained on the same dose for several months, and the
dose can then be tapered gradually (by 1 mg every 1 to 2 weeks) until
the drug is discontinued [13,25]. If relapses occur, they often respond
D e l u s i o n a l Parasitosis 1077
to re-institution of the drug. Some patients will require prolonged or
indefinite therapy in order to control their symptoms.
Second-Generation Antipsychotic  
(SGA) Agents
Many psychiatrists today would choose a newer atypical antipsychotic
over pimozide, particularly in the elderly and those with known
cardiac disease, because of the better safety profile, greater tolerability,
and more specific actions. In a recent retrospective case series of
patients with primary and secondary DP treated with various SGAs,
partial or full remission was achieved in 37% and 38% of 63
cases, respectively, and overall, SGAs were felt to be as effective as
traditional first-generation drugs, albeit with a lower rate of complete
remission [26].
Risperidone is considered by some to be the first-line therapy for DP.
Risperidone has been effective for some patients who have failed
therapy with pimozide [26,27]. Risperidone preferentially blocks
serotonin receptors while still maintaining some activity against
dopamine receptors. Between 0.25 and 8 mg daily, administered in
one or two doses, are required for clinical response, although most
patients require 2–4 mg [26]. Adverse effects, including extrapyrami-
dal reactions, can occur. A possible increased risk of cerebrovascular
accidents in dementia patients receiving risperidone [28] has not been
reported in patients with delusional disorders.
Olanzapine at doses of 2.5 to 20 mg daily also appears to be effective,
but its use has been reported less frequently [26]. Success has also
been reported with many other SGAs.
OUTCOME AND PROGNOSIS
Delusional parasitosis was previously considered a progressive disor-
der with only a 10% to 30% chance of spontaneous remission [11,17].
Antipsychotic therapy has resulted in markedly improved outcomes.
Prognostic factors include the type of DP (primary versus secondary),
duration of illness prior to therapy, and the duration of therapy. In
patients treated with SGAs, the time to onset of any effect and to
maximal effect was shorter, and response rates higher (80% versus
68%) in secondary DP compared with primary DP, but these differ-
ences were not statistically significant [26]. Maximum effects of
therapy were generally noted by 10 weeks in responders, suggesting
that a lack of response by this time should prompt a change in treat-
ment. The duration of symptoms may also affect outcome. In Trabert’s
study [4], the likelihood of a full remission was inversely correlated
with the duration of symptoms, although this was not observed in
patients treated with SGAs [26]. Sustained therapy of at least 8 weeks’
duration and treatment supervision by a psychiatrist may also be
associated with improved response rates [26]. Relapse rates are diffi-
cult to determine; they appear to be common and tend to respond
well to re-institution of therapy, regardless of the antipsychotic agent
used [6,15].
REFERENCES
1. Kendler KS. Demography of paranoid psychosis (delusional disorder): a
review and comparison with schizophrenia and affective illness. Arch Gen
Psychiatry 1982;39:890–902.
2. Bogren M, Mattisson C, Isberg PE, Nettelbladt P. How common are psychotic
and bipolar disorders? A 50-year follow-up of the Lundby population. Nord
J Psychiatry 2009;63:336–46.
3. Trabert W. Zur Epidemiologie des Dermatozoenwahns. Nervenarzt 1991;
62:165–9.
4. Trabert W. 100 years of delusional parasitosis: meta-analysis of 1,223 case
reports. Psychopathology 1995;28:238–46.
The earliest and largest case series in the literature which provides many observations
about many features of DP.
5. Freudenmann RW, Lepping P. Delusional infestation. Clin Microbiol Rev
2009;22:690–732.
A recent, very thorough review of all aspects of DP as they are currently understood.
6. Lyell A. Delusions of parasitosis. Br J Dermatol 1983;108:485–99.
1078 HUNTER’S TROPICAL MEDICINE AND EMERGING INFECTIOUS DISEASE
7. Skott A. Delusions of infestation. Reports from the Psychiatric Research
Center. No. 13. Göteborg, Sweden: St. Jörgen’s Hospital, University of Göte-
borg, 1978.
8. American Psychiatric Association. DSM-IV-TR. Diagnostic and Statistical
Manual of Mental Disorders, 4th edn, Text Revision. Washington, DC: Ameri-
can Psychiatric Association, 2000;323–9.
9. Munro A. Monosymptomatic hypochondriacal psychosis manifesting as delu-
sions of parasitosis. A description of four cases successfully treated with
pimozide. Arch Dermatol 1978;114:940–3.
10. Huber M, Kirchler E, Karner M, Pycha R. Delusional parasitosis and the
dopamine transporter. A new insight of etiology? Med Hypotheses 2007;
68:1351.
11. Huber M, Karner M, Kirchler E, et al. Striatal lesions in delusional parasitosis
revealed by magnetic resonance imaging. Prog Neuropsychopharmacol Biol
Psychiatry 2008;32:1967–71.
12. Narumoto J, Ueda H, Tsuchida H, et al. Regional cerebral blood flow changes
in a patient with delusional parasitosis before and after successful treatment
with risperidone: a case report. Prog Neuropsychopharmacol Biol Psychiatry
2006;30:737–40.
13. Driscoll MS, Rothe MJ, Grant-Kels JM, Hale MS. Delusional parasitosis: a
dermatologic, psychiatric, and pharmacologic approach. J Am Acad Dermatol
1993;29:1023–33.
14. [Anonymous]. The matchbox sign [letter]. Lancet 1983;2:261.
15. Zanol K, Slaughter J, Hall R. An approach to the treatment of psychogenic
parasitosis. Int J Dermatol 1998;37:56–63.
16. Musalek M, Kutzer E. The frequency of shared delusions in delusions of
infestation. Eur Arch Psychiatr Neurol Sci 1990;239:263–6.
17. Wykoff RF. Delusions of parasitosis: a review. Rev Infect Dis 1987;9:433–7.
18. Lynch PJ. Delusions of parasitosis. Semin Dermatol 1993;12:39–45.
19. Winsten M. Delusional parasitosis: a practical guide for the family practi-
tioner in evaluation and treatment strategies. J Am Osteopath Assoc
1997;97:95–9.
20. Lepping P, Russell I, Freudenmann RW. Antipsychotic treatment of primary
delusional parasitosis: systematic review. Br J Psychiatry 2007;191:198–
205.
A review of the literature focusing on therapy with both traditional and atypical
antipsychotic agents. Publications included here are limited non-randomized studies
(crossover studies and case series) as no randomized clinical trials have been
performed.
21. Bhatia MS, Jagawat T, Choudhary S. Delusional parasitosis: a clinical profile.
Int J Psych Med 2000;30:83–91.
22. Zomer SF, de Wit FRE, van Bronswijk JEH, et al. Delusions of parasitosis: a
psychiatric disorder to be treated by dermatologists? An analysis of 33
patients. Br J Dermatol 1998;138:1030–2.
23. Ungvari G, Vladar K. Pimozide treatment for delusions of infestation. Act
Nerv Super (Praha) 1986;28:103–7.
24. Hamann K, Avnstorp C. Delusions of infestation treated by pimozide: a
double-blind crossover clinical study. Acta Derm Venereol 1982;62:55–8.
25. Koo J, Gambla C. Delusions of parasitosis and other forms of monosympto-
matic hypochondriacal psychosis: general discussion and case illustrations.
Dermatol Clin 1996;14:429–38.
26. Freudenmann RW, Lepping P. Second-generation antipsychotics in primary
and secondary delusional parasitosis: outcome and efficacy. J Clin Psychop-
harmacol 2008;28:500–8.
The largest case series of patients with DP treated with second-generation (atypical)
antipsychotic agents.
27. Wenning MT, Davy LE, Catalano G, Catalano MC. Atypical antipsychotics in
the treatment of delusional parasitosis. Ann Clin Psychiatry 2003;15:
233–9.
28. Mazzucco S, Cipriani A, Barbui C, Monaco S. Antipsychotic drugs and cere-
brovascular events in elderly patients with dementia: a systematic review. Mini
Rev Med Chem 2008;8:776–83.