Delusional infestation caused by pramipexole

Delusional infestation (DI) is a rare psychiatric condition in which the patient has the fixed belief of being infested with parasites, insects or even inanimate objects (Morgellons disease), despite no dermatological evidence of their presence.1 DI can be primary, or, more rarely, drug‐induced. DI has been reported very rarely in patients with Parkinson disease (PD) treated with antiparkinsonian medications, including amantadine, levodopa, anticholinergics and dopamine agonists (ropirenole, cabergoline, pergolide).2 3 We provide the first report, to our knowledge, of a patient who developed DI that was probably induced by pramipexole, a dopamine agonist of the nonergoline class. A 65‐year‐old man with a 5‐year history of PD presented with skin complaints. He was being treated with carbidopa/L‐dopa 25/100 mg three times daily, selegiline 5 mg three times daily and pramipexole 1 mg/day. Two months after his pramipexole dose had been increased to 3 mg/day to obtain better control of his PD symptoms, he started to experience the firm belief of being infested by ‘small shrimp‐like insects’ that were crawling and burrowing under the skin of the face, trunk and limbs. Physical examination showed only dry skin and excoriations with no evidence of infection or infestation. The patient's motor symptoms were controlled and his cognitive assessment was normal. During the examinations, he attempted to dig these ‘creatures’ out with his fingernails to demonstrate how real they were and to avoid them reaching the examiner. DI secondary to antiparkinson drugs was suspected, and this information was sent to the patient's neurologist. The pramipexole dose was then reduced to 1.5 mg/day, and the delusional symptoms disappeared in a few weeks. Delusions, hallucinations, sleep disturbances and cognitive impairment may develop in up to 30% of patients with PD receiving antiparkinsonian medications.2 The frequency of such symptoms is increased in older patients taking higher doses, DI is much rarer, with only 11 cases reported to date. It has been suggested that decreased function of the striatal dopamine transporter may be involved in DI.4 Treatment of psychosis in patients with PD can be complex. The first step of treatment is to eliminate triggering factors other than anti‐PD drugs, such as infections, metabolic disorders, subdural haematoma and hallucinogenic drugs.5 Drugs should be discontinued staring with those with the greatest psychosis‐inducing potential and the least antiparkinsonian activity: first, the anticholinergics, amantadine and selegiline; second, the dopamine agonists; and finally levodopa/carbidopa.5 If this is insufficient, atypical antipsychotics such as clozapine or quetiapine can be added.6 In the present case, pramipexole was suspected of inducing the delusional episode because its dose had recently been increased and the delusional symptoms cleared after dose reduction. Nevertheless, the possibility of an interaction between the antiparkinsonian medications such as pramipexole and carbidopa/L‐dopa causing the symptoms cannot be totally excluded. Patients with DI usually present to a dermatologist rather than a psychiatrist because they are convinced that their symptom is primarily skin‐related. Dermatologists must be aware that DI can rarely be drug‐induced and that dose reduction may be sufficient to improve symptoms. Conflict of interest: the authors declare that they have no conflicts of interest.