Using online health communities to deliver patient-centered care to people with chronic conditions

J Med Internet Res. 2013 Jun 25;15(6):e115. doi: 10.2196/jmir.2476.

van der Eijk M, Faber MJ, Aarts JW, Kremer JA, Munneke M, Bloem BR.

Source

Radboud University Nijmegen Medical Centre, Nijmegen Centre for Evidence Based Practice, Department of Neurology (935), Nijmegen, Netherlands.

Abstract

BACKGROUND:

Our health care system faces major threats as the number of people with multiple chronic conditions rises dramatically.

OBJECTIVE:

To study the use of Online Health Communities (OHCs) as a tool to facilitate high-quality and affordable health care for future generations.

METHODS:

OHCs are Internet-based platforms that unite either a group of patients, a group of professionals, or a mixture of both. Members interact using modern communication technologies such as blogs, chats, forums, and wikis. We illustrate the use of OHCs for ParkinsonNet, a professional network for Parkinson disease whose participants-both patients and professionals-use various types of OHCs to deliver patient-centered care.

RESULTS:

We discuss several potential applications in clinical practice. First, due to rapid advances in medical knowledge, many health professionals lack sufficient expertise to address the complex health care needs of chronic patients. OHCs can be used to share experiences, exchange knowledge, and increase disease-specific expertise. Second, current health care delivery is fragmented, as many patients acquire relationships with multiple professionals and institutions. OHCs can bridge geographical distances and enable interdisciplinary collaboration across institutions and traditional echelons. Third, chronic patients lack adequate tools to self-manage their disease. OHCs can be used to actively engage and empower patients in their health care process and to tailor care to their individual needs. Personal health communities of individual patients offer unique opportunities to store all medical information in one central place, while allowing transparent communication across all members of each patient's health care team.

CONCLUSIONS:

OHCs are a powerful tool to address some of the challenges chronic care faces today. OHCs help to facilitate communication among professionals and patients and support coordination of care across traditional echelons, which does not happen spontaneously in busy practice.

Transdermal rotigotine in early stage Parkinson's disease: A randomized, double-blind, placebo-controlled trial

Mov Disord. 2013 Jun 25. doi: 10.1002/mds.25537. [Epub ahead of print]

Mizuno Y, Nomoto M, Kondo T, Hasegawa K, Murata M, Takeuchi M, Ikeda J, Tomida T, Hattori N; on behalf of the Rotigotine Trial Group.

Source

Department of Neuroregeneration, Kitasato University School of Medicine, Sagamihara, Japan.

Abstract

BACKGROUND:

We conducted a randomized, double-blind, placebo-controlled trial to determine the safety and efficacy of transdermal rotigotine at doses up to 16 mg/24 hours in patients with early stage Parkinson's disease (PD) in Japan.

METHODS:

Patients received once-daily rotigotine 2 to 16 mg/24 hours (mean dose, 12.8 mg/24 hours; n = 82) or placebo (n = 90) for 12 weeks. The primary endpoint was the change in Unified Parkinson's Disease Rating Scale (UPDRS) part II (activities of daily living) and part III (motor function) scores from baseline to the end of treatment.

RESULTS:

The mean (± standard deviation) changes in UPDRS part II and III scores were -8.4 ± 9.7 in the rotigotine group and -4.1 ± 8.2 in the placebo group and were significantly different (P = 0.002). More patients in the rotigotine group than in the placebo group had a ≥20% score reduction. No serious drug-related adverse events were reported.

CONCLUSIONS:

Rotigotine at doses up to 16 mg/24 hours was well tolerated and improved function in patients with early stage PD. © 2013 Movement Disorder Society.

Mild cognitive impairment in patients with Parkinson's disease is associated with increased cortical degeneration

Mov Disord. 2013 Jun 25. doi: 10.1002/mds.25541. [Epub ahead of print]

Hanganu A, Bedetti C, Jubault T, Gagnon JF, Mejia-Constain B, Degroot C, Lafontaine AL, Chouinard S, Monchi O.

Source

Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Montréal, Quebec, Canada.

Abstract

Mild cognitive impairment (MCI) can occur early in the course of Parkinson's disease (PD), and its presence increases the risk of developing dementia. Determining the cortical changes associated with MCI in PD, thus, may be useful in predicting the future development of dementia. To address this objective, 37 patients with PD, divided into 2 groups according to the presence or absence MCI (18 with and 19 without) and 16 matched controls, underwent anatomic magnetic resonance imaging. Corticometry analyses were performed to measure the changes in cortical thickness and surface area as well as their correlation with disease duration. Compared with healthy controls, the PD-MCI group exhibited increased atrophy and changes of local surface area in the bilateral occipital, left temporal, and frontal cortices; whereas the PD non-MCI group exhibited only unilateral thinning and decreased surface area in the occipital lobe and in the frontal cortex. In addition, a comparison between the PD-MCI and PD non-MCI groups revealed increased local surface area in the occipital lobe, temporal lobe, and postcentral gyrus for the cognitively impaired patients. It is noteworthy that, in the PD-MCI group, cortical thickness had a significant negative correlation with disease duration in the precentral, supramarginal, occipital, and superior temporal cortices; whereas, in the PD non-MCI group, such a correlation was absent. The findings from this study reveal that, at the same stage of PD evolution, the presence of MCI is associated with a higher level of cortical changes, suggesting that cortical degeneration is increased in patients with PD because of the presence of MCI. © 2013 Movement Disorder Society.

Subthreshold depression and subjective cognitive complaints in Parkinson's disease

Eur J Neurol. 2013 Jun 21. doi: 10.1111/ene.12219. [Epub ahead of print]

Santangelo G, Vitale C, Trojano L, Angrisano MG, Picillo M, Errico D, Agosti V, Grossi D, Barone P.

Source

Department of Psychology, Second University of Naples, Caserta, Italy; IDC Hermitage-Capodimonte, Naples, Italy.

Abstract

BACKGROUND AND PURPOSE:

Subthreshold depression (SubD) is characterized by clinically relevant depressive symptoms not meeting criteria for major depression. The possible association of SubD with subjective cognitive complaints and/or objective cognitive impairments was investigated in a sample of consecutive, non-demented Parkinson's disease (PD) outpatients.

METHODS:

Amongst 115 patients, SubD was identified in 30 patients, major depression in 33; 36 patients were classified as non-depressed. Enrolled patients were administered tests and questionnaires validated in PD for assessing objective and subjective cognitive dysfunctions.

RESULTS:

On objective cognitive measures SubD patients did not differ from non-depressed patients, whereas depressed patients achieved significantly lower scores than the other two groups. SubD and depressed patients reported more cognitive complaints than non-depressed patients.

CONCLUSIONS:

SubD is a non-motor aspect of PD that is not related to objective cognitive deficits but is associated with subjective cognitive complaints, thus impacting on patients' well-being.

The coeruleus/subcoeruleus complex in rapid eye movement sleep behaviour disorders in Parkinson's disease

Brain. 2013 Jul;136(Pt 7):2120-2129.

García-Lorenzo D, Longo-Dos Santos C, Ewenczyk C, Leu-Semenescu S, Gallea C, Quattrocchi G, Pita Lobo P, Poupon C, Benali H, Arnulf I, Vidailhet M, Lehericy S.

Source

1 Institut du Cerveau et de la Moelle épinière, Centre de Neuroimagerie de Recherche, Paris, France.

Abstract

In Parkinson's disease, rapid eye movement sleep behaviour disorder is an early non-dopaminergic syndrome with nocturnal violence and increased muscle tone during rapid eye movement sleep that can precede Parkinsonism by several years. The neuronal origin of rapid eye movement sleep behaviour disorder in Parkinson's disease is not precisely known; however, the locus subcoeruleus in the brainstem has been implicated as this structure blocks muscle tone during normal rapid eye movement sleep in animal models and can be damaged in Parkinson's disease. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex in patients with Parkinson's disease using combined neuromelanin-sensitive, structural and diffusion magnetic resonance imaging approaches. We compared 24 patients with Parkinson's disease and rapid eye movement sleep behaviour disorder, 12 patients without rapid eye movement sleep behaviour disorder and 19 age- and gender-matched healthy volunteers. All subjects underwent clinical examination and characterization of rapid eye movement sleep using video-polysomnography and multimodal imaging at 3 T. Using neuromelanin-sensitive imaging, reduced signal intensity was evident in the locus coeruleus/subcoeruleus area in patients with Parkinson's disease that was more marked in patients with than those without rapid eye movement sleep behaviour disorder. Reduced signal intensity correlated with the percentage of abnormally increased muscle tone during rapid eye movement sleep. The results confirmed that this complex is affected in Parkinson's disease and showed a gradual relationship between damage to this structure, presumably the locus subcoeruleus, and abnormal muscle tone during rapid eye movement sleep, which is the cardinal marker of rapid eye movement sleep behaviour disorder. In longitudinal studies, the technique may also provide early markers of non-dopaminergic Parkinson's disease pathology to predict the occurrence of Parkinson's disease.

MDS 17 Annual Video Challenge in Sydney Australia

This year's MDS Video Challenge saw 5 experts on the panel pit their wits against rare diagnoses presented by Movement Disorders teams from around the world. The cases were as follows:

Case 1 – Episodic occulogyria – AADC

Case 2 – Dystonia and mineralization of the basal ganglia – NCL

Case 3 – Primary progressive aphasia and extra-pyramidal disorder – CSF1R

Case 4  – Exercise induced ataxia with areflexia – Leukoencephalopathy of brainstem and spinal cord involvement and increased lactate (DARS2 mutation)

Case 5 – Progressive hyperkinetic movement disorder & chorioretinitis – SSPE

Case 6 – Progressive dystonia & cognitive impairment, strong FHx – GSS disease

Case 7 – Myoclonus and dystonia – Klinefelter’s syndrome

Case 8 – Generalised myoclonus (Ramsay Hunt picture) & ataxia – mutations in SCA6 and MRE11 (Ataxia telangiectasia like syndrome)

Case 9 – Progressive pyramidal dysfunction, strong FHx – SPAX1 mutation

Case 10 – Acute alien limb in hypertensive patient – intracerebral haemorrhage

Case 11 – Parkinsonism, dysmorphic facies – 22q11.2 deletion syndrome

Case 12 – Acute haemolysis, movement disorder and X-linked inheritance – phosphoglycerate kinase deficiency

Evolution of mild cognitive impairment in Parkinson disease

Neurology. 2013 Jun 21. [Epub ahead of print]

Broeders M, de Bie RM, Velseboer DC, Speelman JD, Muslimovic D, Schmand B.

Source

From the Department of Brain and Cognition (M.B., B.S.), University of Amsterdam, Amsterdam; Department of Neurology (M.B., R.M.A.d.B., D.C.V., J.D.S., B.S.), Amsterdam Medical Center, Amsterdam; and Department of Medical Psychology and Psychiatry (D.M.), Groene Hart Hospital, Gouda, the Netherlands.

Abstract

OBJECTIVE:

We examined the development of Parkinson disease (PD)-mild cognitive impairment (MCI) in patients with newly diagnosed PD over 5 years using recently proposed consensus criteria, and we assessed the reliability of the criteria.

METHODS:

Patients with PD (n = 123) underwent extensive neuropsychological testing at baseline and after 3 (n = 93) and 5 years (n = 59). Two neuropsychologists independently applied the PD-MCI criteria to examine the interrater and intrarater reliability.

RESULTS:

At baseline, 35% of patients had PD-MCI. Three years later, 53% of the patients had PD-MCI. At 5-year follow-up, 20 patients who had PD-MCI at an earlier assessment had converted to PD dementia and 50% of the remaining patients without dementia had MCI. The interrater reliability (kappa) was 0.91. The intrarater reliabilities were 0.85 and 0.96.

CONCLUSION:

Approximately one-third of patients with newly diagnosed PD fulfill the consensus criteria for PD-MCI; after 5 years, this proportion is approximately 50% of patients without dementia. The criteria have good interrater and intrarater reliability.

Variability in Clinical Phenotypes of Heterozygous and Homozygous Cases of Parkin-related Parkinson's Disease

Int J Neurosci. 2013 Jun 17. [Epub ahead of print]

Thompson AJ, Scholz SW, Singleton AB, Hardwick A, McFarland N, Okun MS.

Source

1Departments of Neurology and Neurosurgery, Center for Movement Disorders and Neurorestoration, University of Florida , Gainesville, FL , USA.

Abstract

Abstract Parkin mutations are a common cause of early-onset Parkinson's disease. To study the clinical features and treatment responses of patients with homozygous or heterozygous Parkin mutations, we performed a retrospective chart review in six early-onset parkinsonism patients with pathogenic Parkin mutations. The clinical phenotypes observed in this cohort, all drawn from different families, were variable. All patients had a slowly progressive form of parkinsonism that responded well to dopaminergic therapy with the exception of one advanced case. Homozygous patients had an earlier age at disease onset than heterozygous patients. Two of our patients underwent bilateral deep brain stimulation (DBS) of the subthalamic nucleus or globus pallidus leading to a sustained positive response. Our observations support an earlier age of onset for homozygous cases and possible beneficial effects of DBS in Parkin-related parkinsonism.

Parkinson's disease is associated with altered expression of CaV1 channels and calcium-binding proteins

Brain. 2013 Jun 14. [Epub ahead of print]

Hurley MJ, Brandon B, Gentleman SM, Dexter DT.

Source

Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College, London, W12 0NN, UK.

Abstract

In Parkinson's disease oxidative stress and calcium-induced excitotoxicity have been considered important mechanisms leading to cell death for decades, but the factors that make some neurons vulnerable to neurodegeneration while others remain resistant are not fully understood. Studies of the disorder in animal models suggest that the voltage-gated calcium channel subtype CaV1.3 has a role in making neurons susceptible to neurodegeneration and support earlier work in post-mortem human brain that suggested loss of calcium buffering capacity in neurons correlated with areas of neuronal loss in the substantia nigra of parkinsonian brain. This study examined expression of CaV1 subtypes and the calcium-binding proteins calbindin, calmodulin and calreticulin in areas vulnerable and resistant to neurodegeneration in Parkinson's disease, in brain from neurologically normal individuals and patients with Parkinson's disease. In control brain the expression of a specific CaV1 subtype or distribution of each calcium-binding protein did not associate with those regions prone to neurodegeneration in Parkinson's disease. Whereas, alterations in the amount of both CaV1 subtypes and the calcium-binding proteins were found throughout the brain in Parkinson's disease. Some changes reflected the cell loss seen in Parkinson's disease, whereas others represented altered levels of cellular expression, which as they occurred in the absence of cell loss could not be explained as solely compensatory to the neurodegeneration. The finding of increased CaV1.3 subtype expression in the cerebral cortex of early stage Parkinson's disease, before the appearance of pathological changes, supports the view that disturbed calcium homeostasis is an early feature of Parkinson's disease and not just a compensatory consequence to the neurodegenerative process. This interpretation is supported further by the finding that the ratio of CaV1 subtypes differed throughout the brain in patients with Parkinson's disease compared with control subjects, in favour of an increased use of CaV1.3, which would add to the metabolic burden for cells that rely on this CaV1 subtype for electrical activity and could therefore render specific neuronal populations more vulnerable to neurodegeneration.

The CamPaIGN study of Parkinson's disease: 10-year outlook in an incident population-based cohort

J Neurol Neurosurg Psychiatry. 2013 Jun 18. [Epub ahead of print]

Williams-Gray CH, Mason SL, Evans JR, Foltynie T, Brayne C, Robbins TW, Barker RA.

Source

John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

Abstract

BACKGROUND:

Prognosis in Parkinson's disease (PD) remains poorly understood due to a lack of unbiased data on the natural history of treated PD. The CamPaIGN study has been the first to prospectively track disease evolution from diagnosis in an unselected population-representative incident cohort. We now report the 10-year follow-up data, focusing on three key irreversible milestones: postural instability (Hoehn and Yahr 3), dementia and death.

METHODS:

The cohort was collected between December 2000 and 2002. Those meeting diagnostic criteria (n=142) were followed-up until 1 January 2012. Clinical, neuropsychological and genetic testing were performed. Progression to key milestones was evaluated using Kaplan-Meier and Cox regression survival analyses.

RESULTS:

At 10 years, 55% had died, 68% of survivors had postural instability and 46% dementia. 23% had a good outcome at 10 years (surviving free of dementia/postural instability). Death rate was comparable with the UK population (standardised mortality ratio 1.29 (0.97-1.61)). Death certificates indicated PD was a substantial contributor in only 20%, with pneumonia being the commonest cause of death. Age, non-tremor-dominant motor phenotype and comorbidity predicted earlier postural instability. Baseline predictors of dementia were age, motor impairment, 'posterior-cortical' cognitive deficits and MAPT genotype.

CONCLUSIONS:

(1) outlook in PD is heterogeneous, with most dying or developing dementia or postural instability by 10 years from diagnosis, but a quarter still doing well, with preserved mobility and intact cognition; (2) death is not directly related to PD in the majority; (3) baseline clinical and genetic variables are predictive of outcome and may be helpful in selecting patients for clinical trials.

Investigating emotions in Parkinson's disease: what we know and what we still don't know

Front Psychol. 2013 Jun 10;4:336. doi: 10.3389/fpsyg.2013.00336. Print 2013.

Sotgiu I, Rusconi ML.

Source

Department of Human and Social Sciences, University of Bergamo Bergamo, Italy.

Abstract

Over the last decade, there has been an increasing attention to the role played by emotional processes in Parkinson's disease (PD). However, most of what is known in this area is based on research conducted in laboratory or clinical settings. In this article, the authors underline the need to expand our current knowledge of the psychological correlates of PD by investigating patients' everyday emotions in natural contexts. Specifically, the authors illustrate new research avenues based on the implementation of experience sampling methods. It is argued that these methods could permit future researchers to ecologically assess the frequency and intensity with which parkinsonian patients experience specific emotions (either negative or positive) during their everyday life, providing at the same time precious information on what are the most typical situations in which these emotions occur and on how patients behave in these circumstances. Potential practical implications associated with investigating these issues are discussed.