Aripiprazole monotherapy in the treatment of vascular parkinsonism
Version of Record online: 17 OCT 2011
© 2011 The Authors. Psychiatry and Clinical Neurosciences © 2011 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 65, Issue 6, page 607, October 2011
How to Cite
Ishitobi, M., Kosaka, H., Takahashi, T., Oonuma, M., Murata, T. and Wada, Y. (2011), Aripiprazole monotherapy in the treatment of vascular parkinsonism. Psychiatry and Clinical Neurosciences, 65: 607. doi: 10.1111/j.1440-1819.2011.02263.x
- Issue online: 17 OCT 2011
- Version of Record online: 17 OCT 2011
- Received 21 June 2011; revised 29 July 2011; accepted 8 August 2011.
VASCULAR PARKINSONISM (VP) is characterized by poor response to levodopa. In contrast, reduced presynaptic dopaminergic activity, the main pathology of Parkinson's disease (PD), is not suggested in VP.1 Dopamine D2 partial agonists have been suggested as a potential therapeutic approach to the treatment of the motor symptoms of PD that may avoid common dopaminergic side-effects including dyskinesia and psychosis.2 We report a first case of antiparkinsonian agent-refractory VP in which both psychosis and parkinsonism were treated successfully using aripiprazole monotherapy.
A 75-year-old woman with an 8-year history of antiparkinsonian agent-refractory VP was admitted to Department of Neuropsychiatry, Fukui University Hospital for treatment for psychosis. On admission, treatment consisted of 400 mg/day of l-dopa/carbidopa, 100 mg/day of droxidopa, and 100 mg/day of amantadine. The patient had showed postural tremor, gait disorder, and pyramidal signs with lower-body predominance and mild cognitive impairment (Mini-Mental State Examination: 22/30). The severity score on the Unified Parkinson's Disease Rating Scale (UPDRS) was 118. The illness stage according to the Hoehn and Yahr scale was IV. The patient exhibited frank psychosis with vivid visual hallucinations and fearful delusions of persecution (severity score on the Brief Psychiatric Rating Scale [BPRS] was 96). Results of laboratory tests, electrocardiography, and electroencephalography were normal. Myocardial 123I-metaiodobenzylguanidine indicated a normal heart to mediastinum ratio; cranial magnetic resonance imaging showed multiple deep subcortical lesions. Antiparkinsonian medications were gradually tapered off with no apparent clinical changes of parkinsonism. Her psychotic symptoms improved to a large extent (BPRS score, 52) on day 20, but visual hallucinations persisted. On day 34, aripiprazole monotherapy was started at 3 mg/day and increased by 3 mg every week up to 9 mg. Her psychosis gradually improved (BPRS score, 32), with dramatic amelioration of parkinsonism (UPDRS score, 43), especially in activities of daily living and motor examination items of UPDRS. Using the same regimen, no worsening of psychiatric or neurological symptoms had occurred 7 months after discharge.
In the present case, aripiprazole improved pharmacologically paradoxical symptoms such as psychosis and parkinsonism by the stabilization of dopaminergic activity through dopamine D2 partial agonistic properties.3 Cerebrovascular lesions, which are suggested as a mechanism for VP,1 might cause not reduced presynaptic dopaminergic activity but dysregulated dopaminergic activity. Although the utility of aripiprazole in managing psychosis and parkinsonism in PD remains controversial,4,5 the present case suggests the potential utility of aripiprazole monotherapy in treating VP.