PTEN-induced putative kinase 1 (PINK1) mutations result in young onset recessively inherited, levodopa responsive parkinsonism [1]. A 59-year-old lady, homozygous for PINK1, with onset of parkinsonism at age 29 years was treated initially with anticholinergic then dopaminergic medication from the age of 33 years. She remained well controlled on levodopa. She discontinued oral agonist therapy after a short trial in her 40s because of worsening dyskinesias. By 2006, age 54 years she was taking Stalevo 100, six times daily, Sinemet 125 mg once daily and Amantadine 100 mg once daily (Levodopa equivalent units, LEU, 900 mg). In 2007, age 55 years, she was started on a continuous jejunal levodopa infusion (Duodopa) because of motor fluctuations and peak dose dyskinesia. She responded very well to low-moderate infusion rates over the next 3 years (30–60 mg/h, LEU 600–900). In 2009 she reported pins and needles. Neurophysiological testing confirmed a sensory axonal polyneuropathy. She was found to be vitamin B6 deficient and her symptoms improved on replacement. Between 2009 and 2011, she was noted to be requiring increased infusion rates and was self-administering 3–4 bolus doses of 40 mg/day (LEU *1,200 mg/24 h). She developed dyskinesias and the hourly rate was reduced. In 2011, 4 years after starting Duodopa therapy, and whilst living with her sister in stable circumstances, she was admitted to hospital because of a change in her behaviour. Her older sister (also homozygous for PINK1 and with a 35-year history of parkinsonism) reported that whilst she had always been a little stubborn with mild obsessional tendencies, she had purchased a new computer and had been spending increasing amounts of time ‘‘working’’ on researching her condition. She stayed up later into the night and kept her Duodopa pump running for longer periods until eventually keeping it infusing for 24 h a day over a 2-week period. During this time she spent £700 on printer cartridges and other stationery. Based on the amount stored in the home, as described by her sister, this was excessive to the amount of stationery required as a result of the ‘‘punding’’ behavior, suggesting compulsive buying, an impulse control disorder (ICD). She was markedly dyskinetic, had paranoid delusions and delusions of grandeur and hyper-religiosity. She developed derailment of her thought processes and did not sleep for 2–3 days at a time. The Duodopa infusion was stopped and oral levodopa instigated at a lower total daily dose (LEU 150 mg daily). She remained unwell with similar behavioural disturbances and dyskinesias despite this marked reduction in the administered levodopa dose and surreptitious self-administration was suspected. After two searches of her room, a hidden supply of levodopa was discovered. Quetiapine was prescribed, increasing over a 3–4 week period to 450 mg. Her thought disorder, delusions and sleep improved but motor symptoms of freezing and akinesia were more pronounced. She experienced increased levels of anxiety and depression in her off state. The oral levodopa dose was cautiously increased (to LEU 4–500 mg over 3 months) but motor fluctuations, unpredictable freezing and dyskinesia were all re-emergent. Her family history includes an older brother and two nephews with young onset parkinsonism as well as an D. C. Paviour (&) M.-H. Marion Department of Neurology, Atkinson Morley Wing, St George’s Hospital NHS Trust, London SW17 OQT, UK e-mail: dpaviour@doctors.org.uk