Is dopaminergic medication dose associated with self-reported bruxism in Parkinson's disease? A cross-sectional, questionnaire-based study.

OBJECTIVES: It is not clear whether dopaminergic medication influences bruxism behaviour in patients with Parkinson's disease (PD). Therefore, the aims are to investigate (i) the prevalence of possible (i.e., self-reported) bruxism (sleep and awake) in PD patients, and (ii) whether the use of dopaminergic medication and other factors (viz., demographic characteristics, PD-related factors, and possible consequences of bruxism) are associated with possible bruxism (sleep or awake). MATERIALS AND METHODS: This study concerns a secondary analysis of an earlier published study. Three hundred ninety-five PD patients (67.9 ± 8.6 years of age; 58.7% males) were included. The levodopa equivalent daily dosage (LEDD) was used as a measure of the dopaminergic medication level. Subsequently, a logistic regression analysis was performed for the dependent variables 'awake bruxism' and 'sleep bruxism', with the following predictors: gender, age, LEDD, time since PD diagnosis, temporomandibular disorder (TMD) pain, jaw locks, and tooth wear. RESULTS: The prevalence of possible awake and sleep bruxism was 46.0% and 24.3%, respectively. Awake bruxism was associated with sleep bruxism (OR = 8.52; 95% CI 3.56-20.40), TMD pain (OR = 4.51; 95% CI 2.31-8.79), and tooth wear (OR = 1.87; 95% CI 1.02-3.43). Sleep bruxism was associated with tooth wear (OR = 12.49; 95% CI 4.97-31.38) and awake bruxism (OR = 9.48; 95% CI 4.24-21.19). Dopaminergic medication dose was not associated with awake bruxism (OR = 1.0; 95% CI 0.99-1.00) or sleep bruxism (OR = 1.0; 95% CI 0.99-1.00). CONCLUSION: Bruxism is a common condition in PD patients, but is not associated with the dopaminergic medication dose. CLINICAL RELEVANCE: (Oral) health care providers should be alerted about the possibility of sleep and awake bruxism activity in PD patients, along with this activity's possible negative health outcomes (viz., TMD pain, tooth wear).

[Early oral symptoms of Parkinson's disease]. / Vroege orale symptomen van de ziekte van Parkinson.

A family dentist established that the oral self-care of a 58-year-old man was suddenly inadequate. The dental hygienist who had been recruited subsequently noticed that the dexterity of the man was inadequate. The man's general medical practitioner referred him to a neurologist, who diagnosed Parkinson's disease. Due to this problematic situation, the man was off the family dentist's radar for approximately 1 year. Thereafter, a course of intensive support for his oral health behaviour was initiated. Given the progressivity of Parkinson's disease, it makes sense to aim at an oral health plan resistant to the patient's life course. The family dentist should be aware of his continuing responsibility to provide care and supervision until such time when informal and professional domiciliary care are no longer satisfactory or achievable and admission to a care facility is unavoidable. Only then can the family dentist hand over his responsibility to the geriatric dentist allied to that specific care facility.

[Possible treatment options for Parkinson's disease]. / Behandelingsmogelijkheden voor de ziekte van Parkinson.

Possible treatment options for Parkinson's disease consist of medications for motor symptoms as well as non-motor symptoms, such as cognitive decline, depression, hallucinations and delusions, constipation, and drooling. A number of these medications are in the experimental stage. In addition, physical activity and exercise can favourably influence the motor as well as the non-motor symptoms. Speech and dysphagia therapy are available, whereas cognitive behavioural therapy can control depressionand anxiety. Deep brain stimulation is the only surgical treatment currently used. Potential future surgical treatments are gene therapy, (stem) cell therapy, and the application of growth factors. Worldwide, research projects are being carried out in order to be able to control the disease. Once in a while surprising discoveries are made. Whether cure and/or prevention are possible remains to be seen.

[Parkinson's disease: pathogenesis, aetiology, symptoms, diagnostics, and its course]. / Ziekte van Parkinson: pathogenese, etiologie, symptomen, diagnostiek en beloop.

Parkinson's disease is a slowly progressive neurodegenerative disorder characterised by motor symptoms, which are accompanied or often even preceded by non-motor symptoms. Pathologically, the disease is characterised by neural degeneration in specific brain regions, including the dopaminergic neurons of the pars compacta of the substantia nigra. At the molecular level, mitochondrial dysfunction, oxidative stress, altered protein handling, and reactive microgliosis contribute to the neural degeneration. Advanced age is a significant risk factor. Men are more often affected by the disease than women. Environmental, life-style and genetic factors are potential aetiological factors. The disease is primarily diagnosed on the basis of clinical features. In clinically uncertain cases, magnetic resonance imaging and dopamine transporter single-photon emission computer tomography can provide additional information. Patients usually die due to comorbidity. Parkinson's disease has also several negative influences on the orofacial system.

Reduced α-synuclein levels in cerebrospinal fluid in Parkinson's disease are unrelated to clinical and imaging measures of disease severity.

BACKGROUND AND PURPOSE: The cerebrospinal fluid (CSF) concentration of α-synuclein may reflect the aggregation of α-synuclein in brain tissue that neuropathologically characterizes Parkinson's disease (PD). Although most studies in large cohorts report reduced CSF α-synuclein levels in PD, the available data to date are not consistent due to variation in group sizes, pre-analytical confounding factors and assay characteristics. Furthermore, it remains unclear whether CSF α-synuclein concentrations correlate with measures of disease severity. Acknowledging the methodological issues that emerged from previous studies, we evaluated whether CSF α-synuclein levels differ between patients with PD and controls, and relate to disease duration or severity. METHODS: α-Synuclein levels were measured in CSF samples of 53 well-characterized patients with PD and 50 healthy controls employing a recently developed time-resolved Förster's resonance energy transfer assay. In addition, we studied the relationship of CSF α-synuclein levels with disease duration, clinical measures of disease severity and the striatal dopaminergic deficit as measured by dopamine transporter binding and single photon emission computed tomography. RESULTS: In patients with PD, we observed a decrease in mean CSF α-synuclein levels that was unrelated to disease duration or measures of disease severity. Using total protein normalized α-synuclein, a sensitivity and specificity of 70% and 74% could be reached for distinguishing between patients with PD and controls. CONCLUSION: CSF α-synuclein levels are reduced in patients with PD compared with healthy controls. However, sensitivity and specificity indicate that α-synuclein will not suffice as a single biomarker. CSF α-synuclein levels do not correlate with measures of disease severity, including striatal dopaminergic deficit.