Knowledge, Attitude and Practices Regarding Consumption of Carbonated Soft Drinks Among the Dental Students: A Cross-Sectional Study

Objective: To assess and evaluate the knowledge, attitude, and practices regarding the consumption of carbonated drinks among dental students. Carbonated drinks are pervaded by carbon dioxide and have more adverse effects since they are acidic in nature. Nowadays, these are consumed more widely globally, causing many systemic diseases; diabetes and obesity are common. Material and Methods: This study includes 204 individuals belonging to the age group of 18-26 years. A self-structured objective type cross-sectional questionnaire survey was conducted to assess the knowledge, attitude, and practice of dental students regarding carbonated drinks. The participants were instructed to mark the most appropriate correct answer from the given list of close-ended type questions. Results: Of 204 dental students, the study population includes 125 female and 79 male students. 98.5% of the students knew about carbonated drinks, while 1.5% were unaware. Conclusion:  Most participants preferred to have carbonated drinks even with their awareness about the ill effects of these drinks. Possible implications by the government authorities may probably increase awareness among the population

The real-life effect of catechol-O-methyltransferase inhibition on non-motor symptoms in levodopa-treated Parkinson's disease: opicapone versus entacapone

Objective: To evaluate the long-term, real-life effects on non-motor symptoms (NMS) of opicapone compared to entacapone in levodopa-treated people with Parkinson's disease (PwP). Methods: A retrospective data analysis, with pre- and post-opicapone initiation data of 17 PwP with motor fluctuations compared to a comparable group of 18 PwP introduced on entacapone. The primary outcome was changes in the NMS Scale (NMSS) total score after 1-year follow-up. Secondary outcomes included changes in the NMSS domains, and Parkinson's Disease Sleep Scale (PDSS) total and item scores after the same time span. Results: Groups were comparable for baseline demographics and Parkinson's-related features (p ≥ 0.314) as well as duration of follow-up (1.33 ± 0.66 years for PwP on opicapone and 1.23 ± 0.49 years for those on entacapone; p = 0.858). PwP who were introduced on opicapone showed no changes in NMSS and PDSS total scores after 1 year (p = 0.605 and p = 0.507, respectively), whereas PwP who were introduced on entacapone showed significant worsening of NMSS and PDSS total scores at follow-up (p = 0.005 and p = 0.001, respectively). In neither group changes in individual NMSS domains from baseline to follow-up were observed (p ≥ 0.288 for entacapone and p ≥ 0.816 for opicapone, respectively). In PwP on entacapone significant worsening was seen in the distressing dreams, hallucinations, and limb numbness items of the PDSS (p ≤ 0.05). Conclusions: Introduction of opicapone in real-life PwP with motor fluctuations seems to stabilise NMS burden and aspects of sleep dysfunction, in contrast to entacapone where there was a worsening of NMS burden and PDSS scores over 1 year follow-up.The views expressed are those of the authors and not necessarily those of the NHS, NIHR or Department of Health. The authors acknowledge the support of the International Parkinson and Movement Disorder Society Non-Motor Parkinson’s disease Study Group, the NIHR London South Clinical Research Network, the NIHR Biomedical Research Centre, and the clinical research team at the Parkinson’s Foundation centre of excellence at King’s College Hospital and King’s College London. This article represents independent collaborative research part funded by the NIHR Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London.S

A 12-month prospective real-life study of opicapone efficacy and tolerability in Emirati and non-White subjects with Parkinson's disease based in United Arab Emirates

Parkinson's disease (PD) is the second most common neurodegenerative disorder, and the condition is complicated by the emergence of wearing off/motor fluctuations with levodopa treatment after a variable period. COMT inhibitors when used as adjunct therapy to levodopa tend to smoothen out these wearing off fluctuations by enhancing delivery of levodopa and increasing its bioavailability to the brain. The study was conducted to investigate the motor and nonmotor effect, safety and tolerability of the third generation once-daily COMT inhibitor (opicapone), as add-on, adjuvant therapy to levodopa and at 6 and 12 months follow-up in a real-life cohort of consecutive Emirati and non-White PD patients. A real-life observational analysis using tolerability parameters as used previously by Rizos et al. and Shulman et al. based on clinical database of cases rat Kings College Hospital Dubai Parkinson care database. This was a prospective, single-arm follow-up clinical evaluation study that evaluated the effectiveness of opicapone 50 mg once-daily regime in 50 patients diagnosed with idiopathic neurodegenerative disorder. All patients were assessed with scales used in clinical pathway and include motor Unified Parkinson's Disease Rating Scale (UPDRS), nonmotor symptom scale (NMSS), quality of life (PDQ8) Parkinson's fatigue scale (PFS16) and King's Parkinson's Pain Scale (KIPS). Out of 50 patients treated with opicapone (72% male, mean age 66.9 years (SD 9.9, range 41-82 years) and mean duration of disease 5.7 years (SD 2.5 range (2-11), there was significant statistical improvements shown in motor function-UPDRS part 3: baseline 40.64 ± 2.7, at 6 months 32.12 ± 3.14 and after 12 months 33.72 ± 3.76. Nonmotor burden NMSS: 107.00 ± 21.86, at 6 months 100.78 ± 17.28 and 12 months 96.88 ± 16.11. Reduction in dyskinesias (UPDRS part 4): baseline 8.78 ± 1.07, at 6 months 7.4 ± 0.81 and 12 months 6.82 ± 0.75. Opicapone provides beneficial motor and nonmotor effects in Emirati and other non-White Parkinson's patients, resident in UAE, proving its efficacy across different racial groups as COMT activity may vary between races.S

Chaudhuri’s Dashboard of Vitals in Parkinson’s syndrome: an unmet need underpinned by real life clinical tests

We have recently published the notion of the “vitals” of Parkinson’s, a conglomeration of signs and symptoms, largely nonmotor, that must not be missed and yet often not considered in neurological consultations, with considerable societal and personal detrimental consequences. This “dashboard,” termed the Chaudhuri’s vitals of Parkinson’s, are summarized as 5 key vital symptoms or signs and comprise of (a) motor, (b) nonmotor, (c) visual, gut, and oral health, (d) bone health and falls, and finally (e) comorbidities, comedication, and dopamine agonist side effects, such as impulse control disorders. Additionally, not addressing the vitals also may reflect inadequate management strategies, leading to worsening quality of life and diminished wellness, a new concept for people with Parkinson’s. In this paper, we discuss possible, simple to use, and clinically relevant tests that can be used to monitor the status of these vitals, so that these can be incorporated into clinical practice. We also use the term Parkinson’s syndrome to describe Parkinson’s disease, as the term “disease” is now abandoned in many countries, such as the U.K., reflecting the heterogeneity of Parkinson’s, which is now considered by many as a syndrome

Exploring hyperhidrosis and related thermoregulatory symptoms as a possible clinical identifier for the dysautonomic subtype of Parkinson’s disease

ObjectiveTo identify associated (non-)motor profiles of Parkinson’s disease (PD) patients with hyperhidrosis as a dominant problem.MethodsThis is a cross-sectional, exploratory, analysis of participants enrolled in the Non-motor Longitudinal International Study (NILS; UKCRN No: 10084) at the Parkinson’s Centre at King’s College Hospital (London, UK). Hyperhidrosis scores (yes/no) on question 28 of the Non-Motor Symptom Questionnaire were used to classify patients with normal sweat function (n = 172) and excessive sweating (n = 56) (Analysis 1; n = 228). NMS scale (NMSS) question 30 scores were used to stratify participants based on hyperhidrosis severity (Analysis 2; n = 352) using an arbitrary severity grading: absent score 0 (n = 267), mild 1–4 (n = 49), moderate 5–8 (n = 17), and severe 9–12 (n = 19). NMS burden, as well as PD sleep scale (PDSS) scores were then analysed along with other correlates.ResultsNo differences were observed in baseline demographics between groups in either analysis. Patients with hyperhidrosis exhibited significantly higher total NMSS burden compared to those without (p p p ConclusionsChronic hyperhidrosis appears to be associated with a dysautonomia dominant subtype in PD patients, which is also associated with sleep disorders and a higher rate of dyskinesia (fluctuation-related hyperhidrosis). These data should prompt the concept of hyperhidrosis being used as a simple clinical screening tool to identify PD patients with autonomic symptoms.</div

A Clinical and Imaging Study Investigating Pathophysiology of Fatigue in Parkinson's Disease.

Background: Non motor symptoms (NMS) have emerged as one of the key determinants of quality of life in people with Parkinson’s and fatigue is a common specific and distinctive NMS in PD but is often under diagnosed.Aims: In this body of work, I have attempted to explore firstly, the clinical correlates of fatigue, which may confound the characterisation of fatigue. Thereafter, the work has attempted to explore possible patho-physiological basis of fatigue in PD, addressing peripheral mechanisms such as cardiac sympathetic dysfunction within the spectrum of dysautonomia or centrally mediated mechanisms via striatal and limbic dopaminergic or serotoninergic pathways.Methods: In the first study, 135 non-depressed PD patients with an age range of 50-75 years and a clinical diagnosis of idiopathic Parkinson’s disease were studied using clinically validated scales and specifically the fatigue visual analogue scale initially to identify patients with central fatigue and those without. Collateral assessment of other confounders of fatigue chiefly depression and excessive daytime sleepiness were assessed by Non motor assessment sale (NMSS), Parkinson’s Disease Sleep Scale (PDSS), Epworth Sleepiness Scale (ESS) and Hospital anxiety and Depression Scale (HADS) In the following study, 20 patients from the above cohort with significant fatigue were further corroborated using the Parkinson fatigue Scale (PFS-16). Then 10 patients with high fatigue scores, fatigue +v patients (PFS 16 score-> 8) and 10 patients with no fatigue , fatigue -ve cases ( PFS-16 8) and 20 fatigue -ve cases (PFS-16 < 8)) Patients were matched for motor severity of PD and cases with significant depression or excessive daytime sleepiness were excluded. PET imaging was performed with 18Fluoro-dopa (dopaminergic) and C-amino-4-(2-dimethylaminomethylphenylsulfanyl) benzonitrile (11)C-DASB) (serotoninergic) ligands.Results: In the first study, fatigue correlated with disease severity as measured by Hoehn and Yahr (HY) staging which stratified the condition into three categories (HY 1-2.5=Mild; HY 3=Moderate; HY 4+5 = Severe; Kruskal-Wallis test, p=0.004). There were no differences in fatigue levels between different subtypes of PD while anxiety, depression and sleepiness emerged as key clinical associations of fatigue. In the second study, a pilot exploratory work, MIBG data from 20 non-depressed PD patients (53% male, mean age (mean&#xa0;± SD) of 68.75&#xa0;± 9.7 years (range: 41-88 years), mean disease duration 7 65&#xa0;± 5.5 years (range: 1-35 years) were analysed based on fatigue positive and negative cases (10 in each group) after a total assessment of 30 patients where scan was only possible in 20. The majority (51%) was at HY stage 2. Cardiac MIBG uptake was expressed as mediastinum to heart ratios at 15 min and 3 hrs (R1 and R2) and showed no difference between the fatigue versus non fatigue cases (Mean R1 of Fatigue Positive (1.6&#xa0;± 0.53) vs Mean R1 of Fatigue -ves (1.5&#xa0;± 1.37) and mean R2 of Fatigue Positives (1.58&#xa0;± 0.48 ) vs Mean R2 of Fatigue-ves (1.48&#xa0;± 0.23 )). In the third stage PET data was analysed and Fatigue + cases showed, a significantly depressed uptake of 11C-DASB binding in comparison to PD-Fatigue - cases, in caudate, putamen, ventral striatum and thalamus (p<0.001, p<0.05, p<0.01, p<0.01; Mann-Whitney-Test) and fatigue severity was inversely correlated with 11C-DASB binding. This is a novel finding never reported before. 18F-dopa uptake in the same structures was similar in the two groups using a region of interest approach, however, voxel-based statistical parametric mapping detected relatively reduced 18F-dopa uptake in caudate, thalamus and the insula in the PD-F group (p<0.001).Conclusions: Our preliminary data suggest, fatigue in PD is associated with anxiety, depression and sleepiness and appears to increase with disease severity although also evident in early-untreated phase of PD. The underlying mechanism is likely to be independent of peripheral sympathetic dysfunction as judged by cardiac sympathetic function but is associated with a severe loss of serotoninergic and dopaminergic innervation in the basal ganglia and limbic system (ventral striatum and thalamus) while sparing the raphe serotoninergic innervations. This suggests a dominant role of central serotonergic and in part, dopaminergic dysfunction in the origin of fatigue in PD

A clinical and imaging study investigating pathophysiology of fatigue in Parkinson's disease

Non motor symptoms (NMS) have emerged as one of the key determinants of quality of life in people with Parkinson's and fatigue is a common specific and distinctive NMS in PD but is often under diagnosed. Aims: In this body of work, I have attempted to explore firstly, the clinical correlates of fatigue, which may confound the characterisation of fatigue. Thereafter, the work has attempted to explore possible patho-physiological basis of fatigue in PD, addressing peripheral mechanisms such as cardiac sympathetic dysfunction within the spectrum of dysautonomia or centrally mediated mechanisms via striatal and limbic dopaminergic or serotoninergic pathways. Methods: In the first study, 135 non-depressed PD patients with an age range of 50-75 years and a clinical diagnosis of idiopathic Parkinson's disease were studied using clinically validated scales and specifically the fatigue visual analogue scale initially to identify patients with central fatigue and those without. Collateral assessment of other confounders of fatigue chiefly depression and excessive daytime sleepiness were assessed by Non motor assessment sale (NMSS), Parkinson's Disease Sleep Scale (PDSS), Epworth Sleepiness Scale (ESS) and Hospital anxiety and Depression Scale (HADS) In the following study, 20 patients from the above cohort with significant fatigue were further corroborated using the Parkinson fatigue Scale (PFS-16). Then 10 patients with high fatigue scores, fatigue +v patients (PFS 16 score-> 8) and 10 patients with no fatigue, fatigue -ve cases ( PFS-16 8) and 20 fatigue - ve cases (PFS-16 < 8)) Patients were matched for motor severity ofPD and cases with significant depression or excessive daytime sleepiness were excluded. PET imaging was performed with l8Fluoro-dopa (dopaminergic) and C-amino-4-(2-dimethylaminomethylphenylsulfanyl) benzonitrile (11 )C-DASB) (serotoninergic) ligands. Results: In the first study, fatigue correlated with disease severity as measured by Hoehn and Yahr (HY) staging which stratified the condition into three categories (HY l-2.5=Mild; HY 3=Moderate; HY 4+5 = Severe; Kruskal-Wallis test, p=0.004). There were no differences in fatigue levels between different subtypes of PD while anxiety, depression and sleepiness emerged as key clinical associations of fatigue. In the second study, a pilot exploratory work, MIBG data from 20 non-depressed PD patients (53% male, mean age (mean ± SD) of 68.75 ± 9.7 years (range: 41-88 years), mean disease duration 7.65 ± 5.5 years (range: 1-35 years) were analysed based on fatigue positive and negative cases (10 in each group) after a total assessment of 30 patients where scan was only possible in 20. The majority (51 %) was at BY stage 2. Cardiac MIBG uptake was expressed as mediastinum to heart ratios at 15 min and 3 hrs (RI and R2) and showed no difference between the fatigue versus non fatigue cases (Mean RI of Fatigue Positive (1.6 ± 0.53) vs Mean RI of Fatigue -ves (1.5 ± 1.37) and mean R2 of Fatigue Positives ( 1.58 ± 0.48 ) vs Mean R2 of Fatigue -ves ( 1.48 ± 0.23 )). In the third stage PET data was analysed and Fatigue + cases showed, a significantly depressed uptake of lIC-DASB binding in comparison to PD-Fatigue - cases, in caudate, putamen, ventral striatum and thalamus (p<0.001, p<0.05, p<O.OI, p<O.OI; Mann-Whitney-Test) and fatigue severity was inversely correlated with lIC-DASB binding. This is a novel finding never reported before. 18F -dopa uptake in the same structures was similar in the two groups using a region of interest approach, however, voxel-based statistical parametric mapping detected relatively reduced 18F-dopa uptake in caudate, thalamus and the insula in the PD-F group (p<0.001). Conclusions: Our preliminary data suggest, fatigue in PD is associated with anxiety, depression and sleepiness and appears to increase with disease severity although also evident in early-untreated phase of PD. The underlying mechanism is likely to be independent of peripheral sympathetic dysfunction as judged by cardiac sympathetic function but is associated with a severe loss of serotoninergic and dopaminergic innervation in the basal ganglia and limbic system (ventral striatum and thalamus) while sparing the raphe serotoninergic innervations. This suggests a dominant role of central serotonergic and in part, dopaminergic dysfunction in the origin of fatigue in PD.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Personalised Advanced Therapies in Parkinson's Disease: The Role of Non-Motor Symptoms Profile

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