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Patients with Parkinson’s disease (PD) experience significantly reduced quality of life when PD is complicated with Pisa syndrome (PS). PS is a postural abnormality associated with a lateral bending of the trunk, causing the patient to lean to one side. Microsaccades during fixation are transmitted to the visual cortex, and this gaze movement may be impaired in PD. We aimed to detect presymptomatic signs of PS. We enrolled 50 patients with PD without dementia and investigated the visual systems in patients with concurrent PD and PS based on a Romberg ratio of

Objective. It is difficult to distinguish patients with schizophrenia with neuroleptic-induced parkinsonism (NIP) from those with existing idiopathic Parkinson’s disease when their striatal dopamine transporter uptake is reduced. There is a possibility of misdiagnosis of Parkinson’s disease in patients with schizophrenia as schizophrenia with NIP, which leads to inappropriate treatment. This prospective study aimed at determining the underlying pathophysiology using detailed clinical and psychological assessments. Methods. We enrolled six patients with schizophrenia who had parkinsonism and were diagnosed with Parkinson’s disease according to the Movement Disorder Society Clinical Diagnostic Criteria, except for the fifth absolute exclusion criteria. Results. Five patients had been treated with neuroleptics for 20 years. One patient refused treatment for schizophrenia. All patients had impaired cognitive function at enrolment, olfactory dysfunction, and constipation. All patients were treated with dopaminergic therapy, and their parkinsonism substantially improved; one woman in her 40s experienced a wearing-off effect and dyskinesia. The uptake of dopamine transporter in the striatum decreased by 13%/year during the study period. Conclusion. Some patients with schizophrenia and parkinsonism benefit from dopaminergic therapy. Some of these patients may also exhibit Lewy pathology.

We previously assessed the prevalence and risks of motor/nonmotor symptoms in a large sample of Japanese patients with Parkinson’s disease. In the present study, we longitudinally assessed the prevalence and risk of motor/nonmotor symptoms, changes in treatment, disease progression, and death in patients with Parkinson’s disease. We enrolled 1,227 patients diagnosed and treated at our hospital in Tokyo at first evaluation. We were able to follow-up 445 patients until the second evaluation, 7.4 years later. Using Kaplan–Meier survival curves and the Cox proportional-hazards model in 1,227 patients, motor/nonmotor symptoms were analyzed in association with the following events: pain, wearing-off, camptocormia, psychosis, orthostatic hypotension, pneumonia, tube feeding, modified Hoehn and Yahr stages (H–Y) 3 and 4 of the on state, and death. The mean age (standard deviation) at the first evaluation was 67.2 (9.9) years, while the mean ages at onset and disease duration were 57.8 (11.7) years and 9.3 (6.6) years, respectively. The mean H–Y of the on state was 2.7 (1.1) at the first evaluation. Age at onset and duration of levodopa use decreased the hazard ratios (HRs) (0.968 and 0.910, respectively) for wearing-off. Female sex increased the HRs (1.414) for wearing-off and decreased the HRs for orthostatic hypotension (0.540) and pneumonia (0.510). Older age at onset increased the HR for psychosis (1.035), orthostatic hypotension (1.033), H–Y 3 (1.048) and 4 (1.071), pneumonia (1.123), tube feeding (1.140), and death (1.095). Early onset of orthostatic hypotension itself increased the HR for numerous events, especially for death (0.893). Our results indicated that age, sex, and some nonmotor symptoms may predict many Parkinson’s disease-related events. In addition, these data may provide a useful reference for the clinical course of Parkinson’s disease.

Decreased 123I-meta-iodobenzylguanidine (MIBG) uptake in MIBG myocardial scintigraphy, olfactory dysfunction, and rapid eye movement (REM) sleep behavior disorder (RBD) are considered useful early indicators of Parkinson disease. We investigated whether patients with PARK2 mutations exhibited myocardial sympathetic abnormalities using MIBG scintigraphy, olfactory dysfunction using the Sniffin’ Sticks olfactory test, and RBD using polysomnography. None of the examined patients had RBD, and all except 1 patient exhibited an increase in the olfactory threshold. Moreover, one of the oldest patients exhibited impairment in identification and discrimination. Of 12 patients with PARK2 mutations, 4 patients, who were older than patients without abnormal uptake, exhibited decreased MIBG uptake. The results obtained in this study suggest that some patients with PARK2 mutations have increased thresholds of olfactory function and myocardial sympathetic dysfunction as nonmotor symptoms.