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).

Differences in neurology residency training programmes across Europe - a survey among the Residents and Research Fellow Section of the European Academy of Neurology national representatives.

BACKGROUND AND PURPOSE: Neurology is rapidly evolving as a result of continuous diagnostic and therapeutic progress, which influences the daily work of neurologists. Therefore, updating residency training programmes is crucial for the future of neurology. Several countries are currently discussing and/or modifying the structure of their neurology residency training programme. A detailed and up-to-date overview of the available European residency training programmes will aid this process. METHODS: A questionnaire addressing numerous aspects of residency training programmes in neurology was distributed among 38 national representatives of the Resident and Research Fellow Section of the European Academy of Neurology. RESULTS: We obtained data from 32 European countries (response rate 84%). The median (range) duration of the residency training programmes was 60 (12-72) months. In the majority of countries, rotations to other medical disciplines were mandatory, mostly psychiatry (69%), internal medicine (66%) and neurosurgery (59%). However, the choice of medical fields and the duration of rotations varied substantially between countries. In 50% of countries, there were formal regulations regarding training in evidence-based medicine, teaching skills and/or leadership qualities. In many countries (75%), residents had to take an examination. CONCLUSIONS: We found substantial variation among European countries in the duration of residency training programmes, and especially in the choice of obligatory rotations to external medical disciplines. Despite a presumably similar spectrum of patients, neurology residency training programmes across Europe are not harmonized. The structure of the programme should be determined by its relevance for neurologists today and in the future.

[Anxiety, depression and sleep disorders in Parkinson's disease: a complex interaction between body and mind]. / Angst, depressie en slaapproblemen bij de ziekte van Parkinson: een complexe interactie tussen lichaam en geest.

BACKGROUND: Anxiety and depression in Parkinson's disease (PD) are often unrecognized, partially due to a complex relationship with sleep disorders and other PD-related symptoms.
AIM: To gain more insight in anxiety, depression and sleep disorders in PD, their reciprocal interaction and relationship with other (non)motor symptoms.
METHOD: With three epidemiological studies in this thesis article we describe: the symptom dimensions of anxiety, motor symptoms and autonomic failure; predictors of the course of anxiety; and the temporal relationship between anxiety, depression and insomnia in PD.
RESULTS: Anxiety in PD has one affective and various somatic symptom dimensions. There is a symptomatic overlap between anxiety and symptoms of motor and autonomic dysfunctions. Anxiety, depression and impulsive-compulsive behaviors in de novo PD show a parallel course. Cognitive dysfunctions and REM-sleep behaviour disorder are risk factors for anxiety in PD patients. The relationship between insomnia and anxiety and depression is bi-directional.
CONCLUSION: There is an overlap, co-morbidity and interaction between anxiety, depression, sleep disorders and (non)motor symptoms, which warrants a multi-disciplinary approach to PD. Sleep disorders and cognitive dysfunctions may provide starting points for treatment and preventions of anxiety in PD.

[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.

Early-onset cortico-cortical synchronization in the hemiparkinsonian rat model.

Changes in synchronized neuronal oscillatory activity are reported in both cortex and basal ganglia of Parkinson's disease patients. The origin of these changes, in particular their relationship with the progressive nigrostriatal dopaminergic denervation, is unknown. Therefore, in the present study we studied interregional neuronal synchronization in motor cortex and basal ganglia during the development of dopaminergic degeneration induced by a unilateral infusion of 6-hydroxydopamine (6-OHDA) into the rat medial forebrain bundle. We performed serial local field potential recordings bilaterally in the motor cortex and the subthalamic nucleus of the lesioned hemisphere prior to, during, and after development of the nigrostriatal dopaminergic cell loss. We obtained signal from freely moving rats in both resting and walking conditions, and we computed local spectral power, interregional synchronization (using phase lag index), and directionality (using Granger causality). After neurotoxin injection the first change in phase lag index was an increment in cortico-cortical synchronization. We observed increased bidirectional Granger causality in the beta frequency band between cortex and subthalamic nucleus within the lesioned hemisphere. In the walking condition, the 6-OHDA lesion-induced changes in synchronization resembled that of the resting state, whereas the changes in Granger causality were less pronounced after the lesion. Considering the relatively preserved connectivity pattern of the cortex contralateral to the lesioned side and the early emergence of increased cortico-cortical synchronization during development of the 6-OHDA lesion, we suggest a putative compensatory role of cortico-cortical coupling.

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.

Gray matter differences contribute to variation in cognitive performance in Parkinson's disease.

BACKGROUND AND PURPOSE: A substantial proportion of patients with Parkinson's disease (PD) suffer from cognitive deficits, although there is a large variability in the severity of these impairments. Whilst the cognitive deficits are often attributed to monoaminergic changes, there is evidence that alterations in structural brain volume also play a role. The aim of our study was to gain more insight into the variability of cognitive performance amongst PD patients by examining the relation between regional gray matter (GM) volume and cognitive performance. METHODS: Linear regression analyses were performed between task performance and GM volume for six neuropsychological tasks within a group of 93 PD patients; they were additionally compared at a group level with matched healthy controls, using voxel-based morphometry. RESULTS: Our most important findings were positive correlations between GM volume and cognitive performance for (i) parahippocampal gyrus and verbal memory, (ii) medial temporal lobe and putamen and visuospatial memory, and (iii) middle temporal gyrus and frontal lobe and verbal fluency. In addition, decreased GM volume was found in the frontal, parietal and temporal cortices of PD patients compared with matched healthy controls. CONCLUSIONS: It is argued that the large variability in cognitive function across PD patients is partly mediated by GM volume differences in the implicated areas. Volume differences in these brain regions do not discriminate between patients and controls but explain cognitive variation within the patient population.

Early-stage cognitive impairment in Parkinson's disease and the influence of dopamine replacement therapy.

BACKGROUND AND PURPOSE: The aim of this study was to establish the cognitive profile of newly diagnosed untreated (de novo) patients with Parkinson's disease (PD) and more advanced, treated patients, and to determine the effects of dopamine (DA) replacement therapy. METHODS: A cohort of 23 de novo patients, 55 mild to moderately advanced, medicated PD patients and 21 healthy controls participated. Cognitive tests included the Cambridge Examination for Mental Disorders and a battery of neuropsychological tests taken from the Cambridge Neuropsychological Test Automated Battery and the Vienna Test System. RESULTS: De novo patients with PD were more impaired in working memory strategy use than healthy controls and treated patients with PD. Furthermore, the generation of random motor behaviour was more impaired in both de novo and treated PD patients than in healthy controls. Correlation analysis revealed that in treated patients with PD, ascending doses of dopaminergic medication were associated with poorer performance on a pattern recognition task. CONCLUSION: Selective impairments in strategy use and the generation of random motor behaviour are a very early feature of PD and might be of predictive value in further frontal cognitive deterioration. Furthermore, DA replacement therapy seems to improve frontal lobe function (strategy use) and worsen temporal lobe function (visual memory).

[Impulse control disorders in Parkinson's disease]. / Impulscontrolestoornissen bij de ziekte van Parkinson en de relatie tot andere stoornissen binnen het impulsieve-compulsieve spectrum.

BACKGROUND: Parkinson's disease is characterised not only by the classic triad of bradykinesia, rigidity and tremor, but also by the frequent occurrence of various non-motor symptoms such as the impulse control disorders (pathological gambling, hypersexuality, compulsive buying, binge eating, punding and dopamine dependency). AIM: To increase insight into the clinical presentation, risk factors, treatment and the underlying pathophysiological mechanisms of impulse control disorders in Parkinson's disease. METHOD: Relevant literature was reviewed. RESULTS: Impulse control disorders belong to an important group of neuropsychiatric disorders that occur at some point in 5-10% of patients with Parkinson's disease. They generally occur in conjunction with dopaminergic medication and can have a marked social, relational and/ or financial impact. CONCLUSION: Early recognition of impulse control disorders in Parkinson's disease is important and a close collaboration between the neurologist and the psychiatrist is essential in order to ensure correct diagnosis and the best possible treatment. Impulse control disorders in Parkinson's disease show considerable phenomenological overlap with other repetitive behaviours within the impulsive-compulsive spectrum of disorders to which the obsessive-compulsive disorders and addiction disorders belong. The overlap can possibly be explained by a shared pathophysiological mechanism involving an imbalance between the direct and indirect pathways of the dorsal and ventral frontal-striatal circuits.

Structural network topology and microstructural alterations of the anterior insula associate with cognitive and affective impairment in Parkinson's disease.

The aim of the current study was to assess the structural centrality and microstructural integrity of the cortical hubs of the salience network, the anterior insular cortex (AIC) subregions and anterior cingulate cortex (ACC), and their relationship to cognitive and affective impairment in PD. MRI of 53 PD patients and 15 age-matched controls included 3D-T1 for anatomical registration, and diffusion tensor imaging for probabilistic tractography. Network topological measures of eigenvector and betweenness centrality were calculated for ventral (vAI) and dorsal (dAI) AIC. Microstructural tract integrity between vAI, dAI and the ACC was quantified with fractional anisotrophy (FA) and mean diffusivity (MD). Structural integrity and connectivity were related to cognitive and affective scores. The dAI had significantly higher eigenvector centrality in PD than controls (p < 0.01), associated with higher depression scores (left dAI only, rs = 0.28, p < 0.05). Tracts between dAI and ACC showed lower FA and higher MD in PD (p < 0.05), and associated with lower semantic fluency, working memory and executive functioning, and higher anxiety scores (range 0.002 < p < 0.05). This study provides evidence for clinically relevant structural damage to the cortical hubs of the salience network in PD, possibly due to extensive local neuropathology and loss of interconnecting AIC-ACC tracts.

Graph theoretical analysis of magnetoencephalographic functional connectivity in Alzheimer's disease.

In this study we examined changes in the large-scale structure of resting-state brain networks in patients with Alzheimer's disease compared with non-demented controls, using concepts from graph theory. Magneto-encephalograms (MEG) were recorded in 18 Alzheimer's disease patients and 18 non-demented control subjects in a no-task, eyes-closed condition. For the main frequency bands, synchronization between all pairs of MEG channels was assessed using a phase lag index (PLI, a synchronization measure insensitive to volume conduction). PLI-weighted connectivity networks were calculated, and characterized by a mean clustering coefficient and path length. Alzheimer's disease patients showed a decrease of mean PLI in the lower alpha and beta band. In the lower alpha band, the clustering coefficient and path length were both decreased in Alzheimer's disease patients. Network changes in the lower alpha band were better explained by a 'Targeted Attack' model than by a 'Random Failure' model. Thus, Alzheimer's disease patients display a loss of resting-state functional connectivity in lower alpha and beta bands even when a measure insensitive to volume conduction effects is used. Moreover, the large-scale structure of lower alpha band functional networks in Alzheimer's disease is more random. The modelling results suggest that highly connected neural network 'hubs' may be especially at risk in Alzheimer's disease.

Visual hallucinations in Parkinson's disease are associated with thinning of the inner retina.

Visual hallucinations (VH) are common in patients with Parkinson's disease (PD), yet the underlying pathophysiological mechanisms are still unclear. We aimed to explore the association of the presence of VH with inner retinal thinning and, secondarily, with visual acuity. To this end, we included 40 PD patients in this exploratory study, of whom 14 had VH, and 22 age- and sex-matched healthy controls. All participants were interviewed for the presence of VH by a neurologist specialized in movement disorders and underwent a thorough ophthalmologic examination, including measurement of the best-corrected visual acuity (BCVA) and optical coherence tomography to obtain macular scans of the combined ganglion cell layer and inner plexiform layer (GCL-IPL). Patients with VH had a thinner GCL-IPL than patients without VH, which persisted after correction for age, disease stage, levodopa equivalent daily dose (LED) and cognitive function. Furthermore, BCVA was lower in the PD group with VH than in the PD group without VH, although only a trend remained after correction for age, disease stage, LED and cognitive function. Taken together, in patients with PD, visual hallucinations appear to be associated with a thinning of the inner retinal layers and, possibly, with reduced visual acuity. Further research using a longitudinal design is necessary to confirm these findings and to establish the causality of these relationships.

Neuropathological correlates of parkinsonian disorders in a large Dutch autopsy series.

The clinical diagnosis in patients with parkinsonian disorders can be challenging, and a definite diagnosis requires neuropathological confirmation. The aim of this study was to examine whether a clinical diagnosis of Parkinson's disease (PD) and atypical parkinsonian disorders predict the presence of Lewy pathology (LP) and concomitant neuropathological lesions.We included 293 donors with a history of parkinsonism without dementia at disease onset, collected by the Netherlands Brain Bank (NBB) from 1989 to 2015. We retrospectively categorized donors according the International Parkinson and Movement Disorder Society clinical diagnostic criteria for PD (MDS-PD criteria) as 'not PD', 'probable PD' or 'established PD'. We compared the final clinical diagnosis to presence of neuropathological lesions as defined by BrainNet Europe and National Institute on Aging - Alzheimer's Association guidelines.LP was present in 150 out of 176 donors (85%) with a clinical diagnosis of PD, in 8 out of 101 donors (8%) with atypical parkinsonian disorders and in 4 out of 16 donors (25%) without a definite clinical diagnosis. Independent from age at death, stages of amyloid-ß, but not neurofibrillary tau or neuritic plaques, were higher in donors with LP compared to other types of pathology (p = 0.009). The MDS-PD criteria at a certainty level of 'probable PD' predicted presence of LP with a diagnostic accuracy of 89.3%. Among donors with LP, 'established PD' donors showed similar Braak α-synuclein stages and stages of amyloid-ß, neurofibrillary tau and neuritic plaques compared to 'not PD' or 'probable PD' donors.In conclusion, both a clinical diagnosis of PD as well as MDS-PD criteria accurately predicted presence of LP in NBB donors. LP was associated with more widespread amyloid-ß pathology, suggesting a link between amyloid-ß accumulation and LP formation.

Odor recognition memory is not independently impaired in Parkinson's disease.

The results of previous studies in small groups of Parkinson's disease (PD) patients are inconclusive with regard to the presence of an odor recognition memory impairment in PD. The aim of the present study was to investigate odor recognition memory in PD in a larger group of patients. Odor recognition memory and detection thresholds were assessed using components of the "Sniffin' Sticks" test battery in 55 non-demented PD patients (Hoehn and Yahr stages I-III) and 50 control subjects of comparable age and sex. PD patients performed slightly but significantly worse than control subjects on the odor recognition memory task. After correction for odor detection scores, however, the difference in odor recognition memory performance between PD patients and controls was no longer statistically significant. These data indicate that odor recognition memory is not independently impaired in PD patients.

The Association of Olfactory Function with BMI, Appetite, and Prospective Weight Change in Dutch Community-Dwelling Older Adults.

OBJECTIVES: The olfactory decline that often accompanies aging is thought to contribute to undernutrition in older adults. It is believed to negatively affect eating pleasure, appetite, food intake and subsequently nutritional status. We have evaluated the associations of olfactory function with BMI, appetite and prospective weight change in a cohort of Dutch community-dwelling older adults. DESIGN: Cross-sectional cohort study. PARTICIPANTS: Dutch community-dwelling older adults from the ongoing Longitudinal Aging Study Amsterdam (LASA). Measurements and setting: In 2012-2013, the 40-item University of Pennsylvania Smell Identification Test (UPSIT) was administered to 824 LASA participants to evaluate their olfactory function. Body weight, height, appetite, comorbidity, cognitive status and socio-demographic factors were also assessed. Follow-up weight was measured after three years. RESULTS: 673 participants (aged 55-65 years) were included in the regression analyses. Median UPSIT-score was 33. When adjusted for potential confounders, lower UPSIT-score (indicative of poorer olfactory function) was not associated with poor appetite (OR = 1.062, p = 0.137) or prospective weight change (B = -0.027, p = 0.548). It was, however, associated with lower BMI in smokers (B = 0.178, p = 0.032), but not in non-smokers (B = -0.015, p = 0.732). CONCLUSION: Lower olfactory function scores were associated with lower BMI in community-dwelling older adults who smoke, but not with appetite or prospective weight change. Therefore, smoking older adults with olfactory impairments may pose as a vulnerable group with respect to developing undernutrition.

Slowing of oscillatory brain activity is a stable characteristic of Parkinson's disease without dementia.

Extensive changes in resting-state oscillatory brain activity have recently been demonstrated using magnetoencephalography (MEG) in moderately advanced, non-demented Parkinson's disease patients relative to age-matched controls. The aim of the present study was to determine the onset and evolution of these changes over the disease course and their relationship with clinical parameters. In addition, we evaluated the effects of dopaminomimetics on resting-state oscillatory brain activity in levodopa-treated patients. MEG background oscillatory activity was studied in a group of 70 Parkinson's disease patients with varying disease duration and severity (including 18 de novo patients) as well as in 21 controls that were age-matched to the de novo patients. Whole head 151-channel MEG recordings were obtained in an eyes-closed resting-state condition. Levodopa-treated patients (N = 37) were examined both in a practically defined 'OFF' as well as in the 'ON' state. Relative spectral power was calculated for delta, theta, low alpha, high alpha, beta and gamma frequency bands and averaged for 10 cortical regions of interest (ROIs). Additionally, extensive clinical and neuropsychological testing was performed in all subjects. De novo Parkinson's disease patients showed widespread slowing of background MEG activity relative to controls. Changes included a widespread increase in theta and low alpha power, as well as a loss of beta power over all but the frontal ROIs and a loss of gamma power over all but the right occipital ROI. Neuropsychological assessment revealed abnormal perseveration in de novo patients, which was associated with increased low alpha power in centroparietal ROIs. In the whole group of Parkinson's disease patients, longer disease duration was associated with reduced low alpha power in the right temporal and right occipital ROI, but not with any other spectral power measure. No association was found between spectral power and disease stage, disease severity or dose of dopaminomimetics. In patients on levodopa therapy, a change from the 'OFF' to the 'ON' state was associated with decreases in right frontal theta, left occipital beta and left temporal gamma power and an increase in right parietal gamma power. Widespread slowing of oscillatory brain activity is a characteristic of non-demented Parkinson's disease patients from the earliest clinical stages onwards that is (largely) independent of disease duration, stage and severity and hardly influenced by dopaminomimetic treatment. Some early cognitive deficits in Parkinson's disease appear to be associated with increased low alpha power. We postulate a role for hypofunctional non-dopaminergic ascending neurotransmitter systems in spectral power changes in non-demented Parkinson's disease patients.

Method to measure autonomic control of cardiac function using time interval parameters from impedance cardiography.

The time difference between the electrocardiogram and impedance cardiogram can be considered as a measure for the time delay between the electrical and mechanical activities of the heart. This time interval, characterized by the pre-ejection period (PEP), is related to the sympathetic autonomous nervous control of cardiac activity. PEP, however, is difficult to measure in practice. Therefore, a novel parameter, the initial systolic time interval (ISTI), is introduced to provide a more practical measure. The use of ISTI instead of PEP was evaluated in three groups: young healthy subjects, patients with Parkinson's disease, and a group of elderly, healthy subjects of comparable age. PEP and ISTI were studied under two conditions: at rest and after an exercise stimulus. Under both conditions, PEP and ISTI behaved largely similarly in the three groups and were significantly correlated. It is concluded that ISTI can be used as a substitute for PEP and, therefore, to evaluate autonomic neuropathy both in clinical and extramural settings. Measurement of ISTI can also be used to non-invasively monitor the electromechanical cardiac time interval, and the associated autonomic activity, under physiological circumstances.

Odour identification and discrimination in Dutch adults over 45 years.

OBJECTIVES: The aim of the study was to establish normative values for the two culture dependent components (odour identification and odour discrimination) of the "Sniffin' Sticks" test battery in the Dutch population over 45 years of age, and to assess the influence of age and sex on olfactory function in this population. METHODS: This study was performed in 150 healthy Dutch subjects (87 male and 63 female, mean age 59.2 years, range 45-78 years). Olfactory performance was assessed using the odour identification and discrimination parts of the "Sniffin' Sticks" test battery. RESULTS: In women, odour discrimination scores declined significantly with age, whereas there was no effect of age on odour discrimination performance in men. For odour identification, there were no effects of age or sex in this population. A moderate correlation was found between identification and discrimination test scores. CONCLUSION: Provisional population-specific normative data for olfactory testing using the identification and discrimination parts of the "Sniffin' Sticks" olfactory test battery have been established for the Dutch population over 45 years of age. The current data are applicable to the clinical evaluation of patients with olfactory disorders.

Observations on the cortical silent period in Parkinson's disease.

Transcranial magnetic stimulation is a tool in the neurosciences to study motor functions and nervous disorders, amongst others. Single pulses of TMS applied over the primary motor cortex lead to a so-called cortical silent period in the recording from the corresponding muscle, i.e. a period of approximately 100ms with no muscle activity. We here show that in Parkinson's disease (PD), this cortical silent period in some cases is interrupted by short bursts of EMG activity. We describe in detail these interruptions in two patients with PD. These interruptions may number up to 3 per cortical silent period and show a consistent frequency across trials and hemispheres within a given patient; the two patients described here do differ, however, in the time-delay of the interruptions and hence the induced frequency. For one patient, the frequency of the interruptions proved to be around 13 Hz, the other patient showed a frequency of around 17 Hz. The results corroborate earlier findings of cortical oscillations elicited by pulses of TMS and may be related to abnormal oscillatory activity found in the cortical-subcortical motor system in PD.