Effective control of catatonia in Parkinson’s disease by electroconvulsive therapy: a case report

Catatonia is a psychomotor syndrome, including mutism, immobility, rigidity, negativism, catalepsy and echophenomena. Although catatonia has been reported to occur in many illnesses [1], there have been few reports in the literature of catatonia in Parkinson s disease (PD). We describe a rare case of a patient with PD who developed catatonia during the course of the disease. The patient was a 75-year-old woman. At age 71 years, she was diagnosed with idiopathic PD and treatment with levodopa/carbidopa (300 mg/day) and cabergoline (4 mg/day) initiated. At age 74 years, levodopa/carbidopa was increased to 400 mg/day and cabergoline was switched to pramipexole (3 mg/day) because of motor fluctuations, and talipexole (0.4 mg/day) was added at bedtime to control sleep disturbance [2] as well as nocturnal akinesia. At age 75 years, she experienced hallucinations and complained of dyspnoea with anxiety in the off state. Subsequently, the patient was admitted to our hospital for adjustment of her medications. Neurological examination showed that she was alert with somatic and persecutory delusion in addition to visual, auditory and olfactory hallucinations, which appeared to be late complications of PD [3]. She had no dementia. Hoehn and Yahr stage was 3 and 4 in the on and off state, respectively. To control the psychiatric disorders and motor fluctuations, the dose of levodopa/ carbidopa was increased to 650 mg/day and entacapone (700 mg/day) was added, while pramipexole and talipexole were withdrawn. Several days after altering the medication, the patient went into a peculiar state in which she did not follow any commands in the morning. The status included mutism, immobility, rigidity, negativism and catalepsy. She readily recovered from the status after administration of levodopa via a nasogastric tube, although she was unable to take levodopa orally in a standard way because of the immobility and negativism. Based on the characteristic phenomenology, we diagnosed the disorder as catatonia. Neuroleptic malignant-like syndrome or acute akinesia was ruled out in the absence of fever, infection, dehydration, perspiration, creatine phosphokinase (CPK) elevation and refractoriness to administration of levedopa [4]. A trial of therapy aimed at stimulating various receptors such as droxydopa, clonazepam, donepezil and paroxetine was ineffective for catatonia. Because the use of an indwelling nasogastric tube is unpleasant and impractical at home, we decided to use electroconvulsive therapy (ECT). Two successive ECT alleviated the catatonia as well as the psychiatric problems and motor fluctuations. Although the pathomechanism of catatonia remains poorly understood, dysregulation of dopaminergic system could play a role [5]. Alleviation of catatonia by levodopa in our case might provide support to this hypothesis. In the only previously reported PD case with catatonia other than our patient, catatonia occurred following administration of neuroleptics for psychosis [6], further supporting the possible role of dopaminergic hypoactivity in catatonia at least in PD. Neurologists are often in a dilemma when treating PD patients with psychosis, i.e. dopaminergic treatment for parkinsonism can result in exacerbation of psychosis. In this context, ECT can be a promising therapeutic option, which has been reported to be effective for motor symptoms in PD and psychiatric comorbidity [7]. Although the mechanism by which ECT exhibits its effectiveness still remains elusive, neurologists should consider ECT as a therapeutic option when they encounter dilemmatic PD patients, that is, those with psychiatric comorbidity including catatonia.