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Keisuke Suzuki,
Tomoyuki Miyamoto,
Masayuki Miyamoto,
Yuka Watanabe,
Shiho Suzuki,
Muneto Tatsumoto,
Masaoki Iwanami,
Tsubasa Sada, Taro Kadowaki,
Ayaka Numao,
Kenichi Hashimoto,
Hideki Sakuta,
Koichi Hirata
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ABSTRACT: BACKGROUND: Increasing evidence provides a clear association between rapid eye movement sleep behavior disorders (RBD) and Parkinson's disease (PD), but the clinical features that determine the co-morbidity of RBD and PD are not yet fully understood. METHODS: We evaluated the characteristics of nocturnal disturbances and other motor and non-motor features related to RBD in patients with PD and the impact of RBD on their quality of life. Probable RBD (pRBD) was evaluated using the Japanese version of the RBD screening questionnaire (RBDSQ-J). RESULTS: A significantly higher frequency of pRBD was observed in PD patients than in the controls (RBDSQ-J >= 5 or >= 6: 29.0% vs. 8.6%; 17.2% vs. 2.2%, respectively). After excluding restless legs syndrome and snorers in the PD patients, the pRBD group showed higher scores compared with the non-pRBD group on the Parkinson's disease sleep scale-2 (PDSS-2) total and three-domain scores. Early morning dystonia was more frequent in the pRBD group. The Parkinson's Disease Questionnaire (PDQ-39) summary index and the scores for the PDQ-39 cognition and emotional well-being were higher in the patients with pRBD than in the patients without pRBD. There were no differences between these two groups with respect to the clinical subtype, disease severity or motor function. When using a cut-off of RBDSQ-J = 6, a similar trend was observed for the PDSS-2 and PDQ-39 scores. Patients with PD and pRBD had frequent sleep onset insomnia, distressing dreams and hallucinations. The stepwise linear regression analysis showed that the PDSS-2 domain "motor symptoms at night", particularly the PDSS sub-item 6 "distressing dreams", was the only predictor of RBDSQ-J in PD. CONCLUSION: Our results indicate a significant impact of RBD co-morbidity on night-time disturbances and quality of life in PD, particularly on cognition and emotional well-being. RBDSQ may be a useful tool for not only screening RBD in PD patients but also predicting diffuse and complex clinical PD phenotypes associated with RBD, cognitive impairment and hallucinations.
BMC Neurology 02/2013; 13(1):18. · 2.17 Impact Factor
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Keisuke Suzuki,
Masayuki Miyamoto,
Tomoyuki Miyamoto,
Shiho Suzuki,
Yuka Watanabe,
Ayaka Numao,
Masaoki Iwanami,
Muneto Tatsumoto,
Tsubasa Sada, Taro Kadowaki,
Kenichi Hashimoto,
Hideki Sakuta,
Koichi Hirata
[show abstract]
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ABSTRACT: Objective There are conflicting results regarding the frequency and clinical significance of sleep related breathing disorders in patients with Parkinson's disease (PD). The aim of this study was to investigate the relationship between snoring and its clinical correlates in patients with PD. Methods A total of 93 PD patients and 93 controls were analyzed from a previously conducted cross-sectional study. Snoring was defined as a snoring frequency of ≥2 days/week (a score of 2 or higher on the PD Sleep Scale-2 subitem 15). Excessive daytime sleepiness (EDS) was defined as an Epworth Sleepiness Scale score of ≥10. Results Snoring was more prevalent in the patients with PD than in the controls (14.0% vs. 1.1%). The PD patients who snored exhibited greater disease severity, worse scores on the motor section of the Unified Parkinson's Disease Rating Scale (UPDRS) and the Parkinson fatigue scale and more impaired scores in several domains of the Parkinson's Disease Questionnaire, including the domains of mobility, activities of daily living, emotional well-being, communication and bodily discomfort, when compared to those who did not snore. No between-group differences were found in EDS. A higher proportion of the UPDRS motor scores for bradykinesia was seen in the PD patients who snored compared to that observed in the PD patients who did not snore. Conclusion We found that snoring was more frequent in PD patients than in controls. Furthermore, snoring in PD patients was associated with disease severity, an impaired motor function and a decreased quality of life, although it was not associated with EDS.
Internal Medicine 01/2013; 52(8):863-9. · 0.94 Impact Factor
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Keisuke Suzuki,
Masayuki Miyamoto,
Tomoyuki Miyamoto,
Muneto Tatsumoto,
Yuka Watanabe,
Shiho Suzuki,
Masaoki Iwanami,
Tsubasa Sada, Taro Kadowaki,
Ayaka Numao,
Claudia Trenkwalder,
Koichi Hirata
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ABSTRACT: The aim of this study was to assess the validity and the reliability of the Japanese version of the Parkinson's disease sleep scale (PDSS)-2 and to use this scale to identify nocturnal symptoms and their impact on patient's quality of life.
A cross-sectional, case-controlled study was conducted consisting of 93 patients with Parkinson's disease (PD) and 93 age- and gender-matched control subjects. The Japanese version of the PDSS-2 was used for the evaluation of nocturnal disturbances. The patient's quality of life was evaluated with the Parkinson's Disease Quality of Life questionnaire (PDQ-39) and their depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II), respectively. In addition, the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS) and Parkinson Fatigue Scale (PFS) were administered.
As assessed using the PDSS-2, PD patients had significantly impaired scores compared with control subjects (15.0±9.7 vs. 9.1±6.6, p<0.001). The ESS, BDI-II and PFS scores were significantly impaired in PD patients compared with controls. A satisfactory internal consistency and test-retest reliability score were obtained for the PDSS-2 total score (Cronbach's alpha=0.86). The PDSS-2 was correlated with the PSQI, ESS, BDI-II, PFS, PDQ-39 summary index, all of the PDQ-39 domains and Unified Parkinson's Disease Rating Scale part III. The frequency of restless legs syndrome (RLS) was not significantly different between PD patients and controls (5.5% vs. 2.2%), but nocturnal restlessness was significantly more frequent in PD patients than controls. Stepwise linear regression analyses revealed the PDQ-39 summary index and the PSQI global score as significant predictors for the PDSS-2 total score.
Our study confirmed the usefulness of the Japanese version of the PDSS-2 that enables the comprehensive assessment of nocturnal disturbances in PD. The association between RLS and nocturnal restlessness in PD requires further study.
Journal of the neurological sciences 04/2012; 318(1-2):76-81. · 2.32 Impact Factor
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Movement Disorders 03/2011; 26(8):1561-2. · 4.51 Impact Factor
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Parkinsonism & Related Disorders 11/2010; 17(2):133-4. · 3.80 Impact Factor
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ABSTRACT: ABSTRACT Environmental enrichment (EE) facilitates recovery from behavioral abnormalities and spatial memory disabilities in several neurological disease models. Exposure to EE improves spatial memory acquisition and enhances the survival of newly generated cells in the dentate gyri of adult rodents. However, the effects of EE on spatial learning and neurogenesis in the methylazoxymethanol acetate-induced microencephalic rat have not been investigated. Depletion of serotonin in the rat hippocampus is known to influence spatial memory and adult neurogenesis, suggesting a role for serotonin in these processes. To confirm this hypothesis, male methylazoxymethanol acetate-induced microencephalic rats were exposed to EE or conventional housing after weaning; half of these rats further received intracisternal 5,7-dihydroxytryptamine on postnatal day 3, to induce long-lasting depletion of serotonin. As adults, these microencephalic rats were observed using the Morris water maze test and examined for hippocampal neurogenesis. EE alleviated the impairment of spatial memory acquisition and enhanced neurogenesis in the dentate gyri of adult microencephalic rats. Injection of 5,7-dihydroxytryptamine during the neonatal period caused pronounced reductions in hippocampal serotonin levels in these rats. Long-lasting depletion of serotonin eliminated the EE-induced alleviation of spatial memory acquisition and neurogenesis impairment in microencephalic rats. The present results suggest that EE alleviates spatial memory performance deficits in microencephalic rats and further indicate that serotonin might be involved in the underlying mechanisms through increased hippocampal neurogenesis. These data provide new insights into therapeutic interventions for individuals with human migration disorders associated with learning disabilities.
Congenital Anomalies 03/2010; 50(1):58-63.
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ABSTRACT: In order to elucidate the regeneration properties of serotonergic fibers in the hippocampus of methylazoxymethanol acetate (MAM)-induced micrencephalic rats (MAM rats), we examined serotonergic regeneration in the hippocampus following neonatal intracisternal 5,7-dihydroxytryptamine (5,7-DHT) injection. Prenatal exposure to MAM resulted in the formation of hippocampal heterotopia in the dorsal hippocampus. Immunohistochemical and neurochemical analyses revealed hyperinnervation of serotonergic fibers in the hippocampus of MAM rats. After neonatal 5,7-DHT injection, most serotonergic fibers in the hippocampus of 2-week-old MAM rats had degenerated, while a small number of serotonergic fibers in the stratum lacunosum-moleculare (SLM) of the hippocampus and in the hilus adjacent to the granular cell layer of the dentate gyrus (DG) had not. Regenerating serotonergic fibers from the SLM first extended terminals into the hippocampal heterotopia, then fibers from the hilus reinnervated the DG and some fibers extended to the heterotopia. These findings suggest that the hippocampal heterotopia exerts trophic target effects for regenerating serotonergic fibers in the developmental period in micrencephalic rats.
Anatomical science international. 08/2009; 85(1):38-45.
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ABSTRACT: The effects of chronic treatment with the antioxidant hormone melatonin on degeneration of serotonergic fibers were studied in the striatum and olfactory tubercle of the zitter rat, which shows a loss-of-function mutation of the glycosylated transmembrane protein attractin. In these animals, serotonergic fibers in the striatum and olfactory tubercle undergo spontaneous and progressive degeneration as a result of abnormal metabolism of reactive oxygen species. Homozygous zitter (zi/zi) rats were provided ad libitum access to drinking water containing melatonin for 9 months (M) after weaning. High-performance liquid chromatography analysis revealed that melatonin treatment significantly increased serotonin in the caudate-putamen, (CPU), nucleus accumbens (NA) and olfactory tubercle (OT). Immunohistochemical staining for serotonin was consistent with the neurochemical data and further demonstrated substantially increased numbers of serotonergic nerve terminals in these areas. Aberrant serotonergic fibers characterized by swollen varicosities (>1 microm in diameter) were observed in the CPU and NA of 10 M zi/zi rats. The number of these fibers decreased after melatonin treatment ended. Furthermore, hyperinnervation of serotonergic fibers was observed in the OT of melatonin-treated zi/zi rats. These results suggest that melatonin protects serotonergic fibers and terminals in zitter rats and/or promotes their neuroplasticity.
Neuroscience Letters 12/2008; 448(2):212-6. · 2.11 Impact Factor
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ABSTRACT: Microglial activation has been associated with the pathogenesis of neurodegenerative disease. To characterize microglial responses in the zitter mutant rat, which shows progressive spongy degeneration, the development of microglial cells was investigated using ionized calcium-binding adaptor molecule (Iba1) antibody as a specific marker of microglial cells. Neurochemical analysis showed transiently increased Iba1 protein levels in the brains of developing Sprague-Dawley (SD) rats. However, high Iba1 protein readings continued in aged zitter rats. Immunohistochemical analysis revealed time-course differences in the transformation of microglia between SD and zitter rats and prolonged activation of microglial cells in the zitter rat. In the zitter rat, activated microglial cells characterized by swollen cell bodies and shorter, thicker processes were distributed throughout the brain from 2-weeks- to 2-months-old. After 2-months-old, numbers of activated microglial cells gradually decreased. However, these cells were not observed in SD rats. Iba1-immunoreactive cell-clusters organized by at least five activated microglial cells were also prominent in the zitter brain. These differences reflect the neuropathology of this mutant rat triggered by deletion of the attractin gene. The present data may thus suggest that microglial cells directly or indirectly contribute to progressive spongy degeneration in zitter mutant rats.
Neuroscience Letters 02/2007; 411(1):26-31. · 2.11 Impact Factor
