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Neuro-ophthalmology

Ophthalmic Delusional Parasitosis

1. What is Ophthalmic Delusional Parasitosis?

Section titled “1. What is Ophthalmic Delusional Parasitosis?”

Ophthalmic delusional parasitosis (DP) is a subtype of delusional parasitosis. It is a disorder characterized by a fixed and unshakable belief that the eyes are infected with parasites, classified as a monosymptomatic somatic delusional disorder. It is also called Ekbom syndrome or delusional infestation (DI).

In DSM-5, it is classified as a somatic type of delusional disorder, within the schizophrenia spectrum and other psychotic disorders.

  • Incidence: 1.9 per 100,000 person-years2)
  • Prevalence: 27.3 per 100,000 people9), 83.2 per 1,000,000 in Germany7)
  • Age of onset: 50–70 years. Increases after age 402)
  • Sex differences: Nearly 1:1 male-to-female ratio under age 50; women are about 3 times more common than men over age 50
  • Duration of illness: Average 3 years2)
  • Comorbid psychiatric conditions: 74–80% have a history of depression or other psychiatric disorders1)2)
  • Shared delusions: 5–15% of DI patients have shared delusions (folie à deux) among family members9)

Thieberge (1894) and Perrin (1896) first described the clinical picture in detail. Swedish neurologist Ekbom published detailed reports in 1937–1938, and it is also called Ekbom syndrome 5).

Q How is delusional parasitosis distinguished from actual parasitic infection?
A

Actual infection is ruled out by skin scraping tests, biopsy, and ophthalmic examination. An “unshakable belief” that persists despite all negative tests is characteristic of true delusional disorder 9). For details, see the section on Diagnosis and Examination Methods.

  • Fixed belief (unshakable conviction): The belief that the eye is infected with parasites. This belief persists even when all tests are negative9)
  • Pruritus: Itching around the eyes or eyelids
  • Tactile hallucination: Sensation of insects crawling on or biting the eyelids
  • Formication: Sensation of insects crawling on the skin4)
  • Irritation, redness, and tearing: Symptoms associated with excessive scratching

Clinical Findings (Findings Confirmed by the Physician During Examination)

Section titled “Clinical Findings (Findings Confirmed by the Physician During Examination)”
  • Abrasions/ulcers: Skin findings due to self-injury attempting to remove perceived parasites
  • Corneal epithelial defect: Corneal epithelial loss due to excessive scratching
  • Chemical dermatitis/ocular injury: Due to home remedies with acids, alkalis, peroxides, disinfectants, etc. 8)
  • Matchbox sign (specimen sign): Behavior of bringing skin fragments, blood clots, etc. in a container as “evidence” 1)9)
  • Slit-lamp examination: Detection of corneal epithelial defects with fluorescein staining (cobalt blue illumination)
  • Proparacaine eye drops: Local anesthetic may improve itching from true infection but not delusional symptoms. Useful to help rule out primary DP.
  • Eyelid eversion: Examine the eyelid margin, eyelash roots, and upper and lower fornices to rule out true parasitic infection
  • Dilated fundus examination: Evaluate for signs of systemic disease or true parasitosis

The etiology of DP is broadly classified into three categories. In a Mayo Clinic study, only 26% of 54 DP patients had primary disease.

Primary DP

Definition: Delusions occur without any underlying disease. Diagnosis is made after excluding all other causes (diagnosis of exclusion).

Prognosis: Tends to follow a chronic course; prognosis is relatively poor.

Secondary DP (Psychiatric)

Causes: Schizophrenia, depression, anxiety disorder, obsessive-compulsive disorder (OCD), bipolar disorder.

Prognosis: May improve with treatment of the underlying disease3).

Organic DP

Medical factors: Hypothyroidism, diabetes, anemia, vitamin B12 deficiency, folate deficiency.

Infections: Syphilis, tuberculosis, HIV, leprosy.

Neurodegenerative diseases: Parkinson’s disease, multiple sclerosis, Huntington’s chorea, dementia with Lewy bodies5)8).

Drugs and medications: Cocaine, amphetamine, methylphenidate, alcohol (during use and withdrawal); ketoconazole, steroids5).

Brain tumors and cerebrovascular disorders: There are cases where a right frontal meningioma presented as the only symptom of DP5).

  • Social isolation: The increase in cases during the COVID-19 pandemic suggests the involvement of isolation2)8)
  • Advanced age: Risk increases after age 40
  • Cognitive decline9)
  • Stressful life events
  • DP by proxy: Cases where caregivers perform unnecessary treatments on children, people with dementia, or individuals with intellectual disabilities
Q Can family members have the same symptoms?
A

Shared delusions (folie à deux) are observed in 5–15% of DI patients 9). Caregivers or cohabiting family members may share the same delusion. Separation of the primary and secondary patients may be a treatment option.

The diagnosis of DP is one of exclusion, and it is essential to rule out true parasitic infection and organic causes.

DSM-5 Diagnostic Criteria (Delusional Disorder, Somatic Type)

Section titled “DSM-5 Diagnostic Criteria (Delusional Disorder, Somatic Type)”
  • Delusion present for at least 1 month
  • Does not meet diagnostic criteria for schizophrenia
  • Functioning is not markedly impaired, apart from the direct impact of the delusion
  • If manic or depressive episodes have occurred, they are brief relative to the delusional period
  • Not caused by substance use, medical condition, or another mental disorder

The following tests are performed to rule out organic causes.

Test ItemPurpose
CBC (including eosinophils) and IgEParasitic infection screening
CMP (glucose, BUN, liver function), HbA1cMetabolic diseases, diabetes
TSH, vitamin B12, folateEndocrine disorders, nutritional deficiencies
Syphilis, HIV, tuberculosis testsInfectious diseases
Urine drug screeningDrug use
  • Imaging: Contrast/non-contrast brain and orbital MRI to rule out organic causes such as brain tumors or cerebrovascular disorders. Neuroimaging is particularly recommended for new-onset cases in patients aged 40 years or older5)
  • Skin examination: Skin scraping with mineral oil and biopsy to rule out true parasitic infection
  • Ophthalmic examination: Slit-lamp examination (fluorescein staining), dilated fundus examination, and eyelid eversion
  • Psychiatric evaluation: Screen for comorbid conditions such as depression, anxiety disorders, and schizophrenia1)
  • True parasitic infections (scabies, helminths, dermatophytes, etc.)
  • Psychiatric disorders such as schizophrenia and depression
  • Symptoms due to drug use or withdrawal
  • Morgellons disease: a condition involving the belief that fibers, etc., emerge from the skin1)9)
  • Oral cenesthopathy: complaining of foreign body sensation in the mouth without dental or medical evidence8)

The most important aspect of treatment is building a therapeutic alliance with the patient. Only 8% of DP patients accept a psychiatric referral, making a non-judgmental attitude essential 9). Explaining that a medication is “for reducing itch, not for schizophrenia” improves medication adherence. A multidisciplinary approach (primary care, psychiatry, dermatology, ophthalmology, infectious disease) is recommended 1).

Atypical antipsychotics are first-line treatment.

  • Risperidone: Has fewer extrapyramidal symptoms and is considered first-line 1)
  • Olanzapine: 10–15 mg/night is a common dose1)2)3)
  • Aripiprazole: relatively mild side effect profile2)6)
  • Quetiapine: start at 25 mg/day5)
  • Amisulpride2)

Typical antipsychotics are also an option.

  • Pimozide: a classic option but requires caution regarding cardiac side effects1)4)
  • Haloperidol, Sulpiride, Perphenazine2)

Treatment outcomes: Antipsychotics achieve partial to complete remission in 60–100% of patients5)6).

Adjunctive pharmacotherapy:

  • SSRIs (fluvoxamine, sertraline, etc.): Used for comorbid depression or compulsive scratching behavior6)7)8)
  • Benzodiazepines (alprazolam, lorazepam, etc.): Used to relieve anxiety symptoms2)4)
  • CBT (cognitive behavioral therapy): May be a first-line option in DP patients with comorbid mild depression 1)8). However, the efficacy of psychotherapy alone is only 10% 1).
  • ECT (electroconvulsive therapy): Considered in treatment-resistant cases where multiple drugs have failed. A report describes partial improvement after 9 ECT sessions in an 82-year-old treatment-resistant patient 2).

Symptomatic treatment with topical steroids, NSAIDs, etc., for itching and pain is performed concurrently. In mild cases, improvement may occur with therapeutic relationship building and symptomatic treatment alone.

Q Why do patients often refuse psychiatric treatment?
A

Because the delusion is strong, the patient is convinced that “there really are bugs” and does not recognize it as a mental illness. The acceptance rate for psychiatric referral is reported to be only 8%. It is important to interact with a non-judgmental attitude, neither denying nor affirming the delusion9).

Q How effective are antipsychotic medications?
A

Antipsychotics achieve partial to complete remission in 60–100% of patients5)6). However, medication adherence is a major challenge, and caution is needed for relapse of delusions due to self-discontinuation6).

6. Pathophysiology and Detailed Mechanisms

Section titled “6. Pathophysiology and Detailed Mechanisms”

The dopamine hypothesis proposed by Huber et al. is the main pathophysiological hypothesis of DP. It is thought that decreased function of striatal dopamine transporter (DAT) receptors leads to elevated extracellular dopamine, triggering delusional symptoms.

Conditions that reduce DAT function—cocaine use, alcohol use, schizophrenia, Parkinson’s disease, Huntington’s disease—are all known causes of secondary DP, supporting this hypothesis. The efficacy of atypical antipsychotics (dopamine receptor antagonists) is also consistent with this hypothesis.

Involvement of the striatum-thalamus-parietal circuit has been suggested2). The following lesion sites have been reported in the development of organic DP.

  • Right frontal meningioma: Developed as the sole symptom of DP, with delusions disappearing 7 days after tumor removal5)
  • Left cerebral infarction and left posterior thalamic hematoma: Association with the development of oral DP has been reported1)
  • Occipital lobe cerebrovascular disorder: Association with DP development has been reported6)

SARS-CoV-2 has a high affinity for the ACE2 receptor, which is highly expressed in the central nervous system. This may cause cerebrovascular disorders, seizures, and encephalopathy, and is attracting attention as a pathway that exacerbates existing psychiatric disorders and induces secondary DP3).


7. Latest Research and Future Perspectives (Investigational Reports)

Section titled “7. Latest Research and Future Perspectives (Investigational Reports)”

Wang et al. (2024) reported a case of new-onset DP in a patient with pre-existing psychiatric illness after COVID-19 infection3). Head CT showed no structural abnormalities, suggesting a possible unknown pathway by which COVID-19 exacerbates psychiatric illness without brain structural changes.

Frewen et al. (2022) reported that among 381 DI patients across multiple UK centers, 12 (3%) were healthcare professionals (HCPs)7). The treatment engagement rate among HCPs with primary DI was remarkably low at 20%. Factors cited include stigma of mental illness, resistance due to medication knowledge, and difficulty building therapeutic relationships with peers, highlighting the need for new intervention strategies for HCPs.

Romine et al. (2023) reported a longitudinal course of shared DI among family members (wife, husband, granddaughter) over 12–15 months 9). After multiple emergency visits, the patient was hospitalized in psychiatry, but there was no record of antipsychotic medication, and the delusions persisted after hospitalization. In shared delusions, separation of the pair may be a treatment option.

Alsafwani et al. (2022) reported 4 cases of oral DI during a 12-month period in the COVID-19 pandemic 8). This was more frequent than usual, possibly triggered by social isolation and limited psychiatric support. The pandemic situation as a contributing factor to the onset of DI requires further investigation.


  1. Alhendi F, Burahmah A. Delusional parasitosis or Morgellons disease: a case of an overlap syndrome. Case Rep Dent. 2023;2023:3268220.
  2. Suparmanian A, Cardona NJ. A longitudinal perspective case study of delusional parasitosis in a geriatric psychiatry unit. Cureus. 2023;15(5):e39434.
  3. Wang J, Kato B, Li S, Agustines DA. Delusional parasitosis in a patient with a history of COVID-19 and substance use disorder. Perm J. 2024;28:24.006.
  4. Tumbi A, Mistry A, Le BA, Lippmann S. Can you properly manage delusional parasitosis? Innov Clin Neurosci. 2025;22(7-9):40-41.
  5. Konnakkaparambil Ramakrishnan K, Mohan L, Jacob JJ, Gopinath R. Right frontal meningioma presenting as delusional parasitosis. BMJ Case Rep. 2021;14:e245249.
  6. Armin S, LaPointe G, Jacob R. Importance of early recognition and management of delusional parasitosis. Proc (Bayl Univ Med Cent). 2022;35(2):256-258.
  7. Frewen J, Lepping P, Goulding JMR, Walker S, Bewley A. Delusional infestation in healthcare professionals: outcomes from a multi-centre case series. Skin Health Dis. 2022;2(4):e122.
  8. Alsafwani Z, Aljishi M, Shiboski C, Jordan R, Villa A. Oral manifestations of delusional infestation: a case series. BMC Oral Health. 2022;22:652.
  9. Romine D, Winston Bush S, Reynolds JC. A longitudinal case of shared delusional infestation. Cureus. 2023;15(2):e34546.

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