Sunday, 30 June 2013
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.
Radboud University Nijmegen Medical Centre, Nijmegen Centre for Evidence Based Practice, Department of Neurology (935), Nijmegen, Netherlands.
Our health care system faces major threats as the number of people with multiple chronic conditions rises dramatically.
To study the use of Online Health Communities (OHCs) as a tool to facilitate high-quality and affordable health care for future generations.
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.
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.
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.
Saturday, 29 June 2013
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.
Department of Neuroregeneration, Kitasato University School of Medicine, Sagamihara, Japan.
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.
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.
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.
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.
Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Montréal, Quebec, Canada.
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.
Friday, 28 June 2013
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.
Department of Psychology, Second University of Naples, Caserta, Italy; IDC Hermitage-Capodimonte, Naples, Italy.
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.
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.
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.
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.
1 Institut du Cerveau et de la Moelle épinière, Centre de Neuroimagerie de Recherche, Paris, France.
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.
Thursday, 27 June 2013
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
Neurology. 2013 Jun 21. [Epub ahead of print]
Broeders M, de Bie RM, Velseboer DC, Speelman JD, Muslimovic D, Schmand B.
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.
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.
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.
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.
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.
Wednesday, 26 June 2013
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.
1Departments of Neurology and Neurosurgery, Center for Movement Disorders and Neurorestoration, University of Florida , Gainesville, FL , USA.
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.
Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College, London, W12 0NN, UK.
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.
Tuesday, 25 June 2013
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.
John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
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.
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.
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.
(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.
Front Psychol. 2013 Jun 10;4:336. doi: 10.3389/fpsyg.2013.00336. Print 2013.
Sotgiu I, Rusconi ML.
Department of Human and Social Sciences, University of Bergamo Bergamo, Italy.
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.
Monday, 24 June 2013
Front Neurol. 2013 Jun 10;4:64. doi: 10.3389/fneur.2013.00064. Print 2013.
Sánchez-Ferro A, Benito-León J, Gómez-Esteban JC.
Department of Neurology, University Hospital "12 de Octubre," Madrid , Spain ; Department of Medicine, Faculty of Medicine, Complutense University , Madrid , Spain ; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas , Madrid , Spain ; Instituto de Salud Carlos III , Madrid , Spain.
Orthostatic hypotension (OH) is a common and disabling symptom affecting Parkinson's disease (PD) patients. We present the effect of the different therapies commonly used to manage PD on this clinical manifestation. For this purpose, we describe the relationship between OH and the current treatments employed in PD, such as L-DOPA, dopaminergic agonists, and continuous dopaminergic stimulation therapies. Additionally, we review the therapeutic measures that could be used to ameliorate OH. There are different approaches to deal with this manifestation, including pharmacological and non-pharmacological treatments, although none of them is specifically aimed for treating OH in PD.
J Neuropathol Exp Neurol. 2013 Jun 13. [Epub ahead of print]
Mu L, Sobotka S, Chen J, Su H, Sanders I, Nyirenda T, Adler CH, Shill HA, Caviness JN, Samanta JE, Sue LI, Beach TG; the Arizona Parkinson’s Disease Consortium.
Upper Airway Research Laboratory, Department of Research, Hackensack University Medical Center, Hackensack, New Jersey (LM, SS, JC, HS, TN); Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York (SS); Alice and David Jurist Institute for Biomedical Research, Hackensack University Medical Center, Hackensack, New Jersey (IS); Parkinson's Disease and Movement Disorders Center, Mayo Clinic Arizona, Scottsdale, Arizona (CHA, JNC); Cleo Roberts Center for Clinical Research, Banner Sun Health Research Institute, Sun City, Arizona (HAS); Banner Good Samaritan Medical Center, Phoenix, Arizona (JES); and Civin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona (LIS, TGB).
Dysphagia is very common in patients with Parkinson disease (PD) and often leads to aspiration pneumonia, the most common cause of death in PD. Current therapies are largely ineffective for dysphagia. Because pharyngeal sensation normally triggers the swallowing reflex, we examined pharyngeal sensory nerves in PD patients for Lewy pathology.Sensory nerves supplying the pharynx were excised from autopsied pharynges obtained from patients with clinically diagnosed and neuropathologically confirmed PD (n = 10) and healthy age-matched controls (n = 4). We examined the glossopharyngeal nerve (cranial nerve IX), the pharyngeal sensory branch of the vagus nerve (PSB-X), and the internal superior laryngeal nerve (ISLN) innervating the laryngopharynx. Immunohistochemistry for phosphorylated α-synuclein was used to detect Lewy pathology. Axonal α-synuclein aggregates in the pharyngeal sensory nerves were identified in all of the PD subjects but not in the controls. The density of α-synuclein-positive lesions was greater in PD patients with dysphagia versus those without dysphagia. In addition, α-synuclein-immunoreactive nerve fibers in the ISLN were much more abundant than those in cranial nerve IX and PSB-X. These findings suggest that pharyngeal sensory nerves are directly affected by pathologic processes in PD. These abnormalities may decrease pharyngeal sensation, thereby impairing swallowing and airway protective reflexes and contributing to dysphagia and aspiration.
Sunday, 23 June 2013
J Neurol. 2013 Jun 16. [Epub ahead of print]
Rosenblum S, Samuel M, Zlotnik S, Erikh I, Schlesinger I.
Department of Occupational Therapy, Faculty of Social Welfare and Health Sciences, University of Haifa, 31905, Haifa, Israel
To date, clinical assessment remains the gold standard in the diagnosis of Parkinson's disease (PD). We sought to identify simple characteristics of handwriting which could accurately differentiate PD patients from healthy controls. Twenty PD patients and 20 matched controls wrote their name and copied an address on a paper affixed to a digitizer. Mean pressure and mean velocity was measured for the entire task and the spatial and temporal characteristics were measured for each stroke. Results of the MANOVAs for the temporal, spatial, and pressure measures (stroke length, width, and height; mean pressure; mean time per stroke; mean velocity), for both the name writing and address copying tasks, showed significant group effects (F(6,32) = 6.72, p < 0.001; F(6,31) = 14.77, p < 0.001, respectively). A discriminant analysis was performed for the two tasks. One discriminant function was found for the group classification of all participants (Wilks' Lambda = 0.305, p < 0.001). Based on this function, 97.5 % of participants were correctly classified (100 % of the controls and 95 % of PD patients). A Kappa value of 0.947 (p < 0.001) was calculated, demonstrating that the group classification did not occur by chance. In this pilot study we identified two simple short and routine writing tasks which differentiate PD patients from healthy controls. These writing tasks have future potential as cost-effective, fast and reliable biomarkers for PD.
Mov Disord. 2013 Jun 17. doi: 10.1002/mds.25543. [Epub ahead of print]
Lee JY, Kim JM, Ahn J, Kim HJ, Jeon BS, Kim TW.
Department of Neurology, Seoul National University-Seoul Metropolitan Government Boramae Medical Center, Seoul, Republic of Korea; Department of Neurology, Seoul National University College of Medicine, Seoul, Republic of Korea; Parkinson Disease Study Group, Movement Disorders Center, Seoul National University Hospital, Seoul, Republic of Korea.
Defective visual information processing from both central and peripheral pathways is one of the suggested mechanisms of visual hallucination in Parkinson's disease (PD). To investigate the role of retinal thinning for visual hallucination in PD, we conducted a case-control study using spectral domain optical coherence tomography. We examined a representative sample of 61 patients with PD and 30 healthy controls who had no history of ophthalmic diseases. General ophthalmologic examinations and optical coherence tomography scans were performed in each participant. Total macular thickness and the thickness of each retinal layer on horizontal scans through the fovea were compared between the groups. In a comparison between patients with PD and healthy controls, there was significant parafoveal inner nuclear layer thinning, whereas other retinal layers, including the retinal nerve fiber layer, as well as total macular thicknesses were not different. In terms of visual hallucinations among the PD subgroups, only retinal nerve fiber layer thickness differed significantly, whereas total macular thickness and the thickness of other retinal layers did not differ. The retinal nerve fiber layer was thinnest in the group that had hallucinations without dementia, followed by the group that had hallucinations with dementia, and the group that had no hallucinations and no dementia. General ophthalmologic examinations did not reveal any significant correlation with hallucinations. There were no significant correlations between retinal thicknesses and duration or severity of PD and medication dosages. The results indicate that retinal nerve fiber layer thinning may be related to visual hallucination in nondemented patients with PD. Replication studies as well as further studies to elucidate the mechanism of thinning are warranted. © 2013 Movement Disorder Society.
Saturday, 22 June 2013
Abstracts of the Seventeenth International Congress of Parkinson's Disease and Movement Disorders. June 17, 2013
Mov Disord. 2013 Jun;28 Suppl 1:S1-511. doi: 10.1002/mds.25605.
Click the link to access the abstracts from this year's Congress via the MDS website
Curr Aging Sci. 2013 Jun 14. [Epub ahead of print]
Caslake R, Summers F, McConachie D, Ferris C, Gordon J, Harris C, Caie L, Counsell C.
Dept of Old Age Medicine Institute of Applied Medicine University of Aberdeen Polwarth Building Foresterhill Aberdeen AB25 2ZD, Scotland.
Introduction Cognitive decline is common in Parkinson's disease (PD) but may not be adequately identified by the mini-mental state examination (MMSE), which is better suited to Alzheimer's disease. The mini-mental Parkinson (MMP) examination is a cognitive screening tool designed in French specifically for PD. We aimed to establish the validity and reliability of the English language version of the MMP compared with the MMSE. Methods People with various stages of PD underwent testing with the MMP and MMSE, which was then compared with a reference standard battery of neuropsychological tests to identify those with significant cognitive impairment. Results Forty-nine patients were recruited. Both the MMP and MMSE were significantly correlated with scores on all the neuropsychological tests in the validation battery. The median MMP score was proportionally lower (80% of maximum) than the MMSE (90% of maximum) in PD patients with cognitive impairment and those with prior neuropsychiatric complications but there was no difference between the MMP and MMSE in areas under the curves (0.84) for detecting cognitive impairment. Test-retest reliability of the MMP was good (intra-class correlation coefficient 0.793). An MMP of 28 or lower out of 32 detected cognitive impairment with 87% sensitivity and 76% specificity. Discussion The English language version of the MMP has now been validated. It detects more cognitive deficits in PD patients than the MMSE and identifies significant cognitive impairment in those with PD at least as well as the MMSE.
Dopamine Agonists Rather than Deep Brain Stimulation Cause Reflection Impulsivity in Parkinson's Disease
Journal of Parkinson's Disease
Volume 3, Number 2 / 2013, 139-144
Atbin Djamshidian1, Sean S. O'Sullivan1, Thomas Foltynie2, Iciar Aviles-Olmos2, Patricia Limousin2, Alastair Noyce1, Ludvic Zrinzo2, Andrew J. Lees1, Bruno B. Averbeck2, 3
1Department of Molecular Neuroscience and Reta Lila Weston Institute for Neurological Studies, University of London, London, UK
2Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, London, UK
3Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
Background: Dopamine agonist therapy is the main risk factor for impulse control disorders in Parkinson's disease (PD). However, it is unclear whether bilateral deep brain stimulation of the subthalamic nucleus also causes impairment in decision making. Objectives: To assess the role of dopamine agonist therapy and deep brain stimulation on reflection impulsivity in non-demented patients with PD. Methods: We recruited 61 PD patients, 20 treated with L-dopa in combination with a dopamine agonist, 14 taking L-dopa monotherapy, a further 16 PD patients with bilateral subthalamic nucleus deep brain stimulation treated with L-dopa in combination with a dopamine agonist, and 11 PD patients with bilateral subthalamic nucleus deep brain stimulation taking L-dopa but not a dopamine agonist. Results were compared with 18 healthy controls. Patients who had evidence of impulsive compulsive behaviour were excluded. Reflection impulsivity was assessed with the beads task, which is a validated information sampling task. Results: All patients treated with a dopamine agonist gathered significantly less information and made more irrational decisions than all other groups regardless of whether they had surgical treatment. Conclusions: Our results imply that dopamine agonist therapy but not deep brain stimulation leads to “reflection impulsivity” in PD.
Monday, 17 June 2013
Parkinsonism Relat Disord. 2013 Jun 10. pii: S1353-8020(13)00195-8. doi: 10.1016/j.parkreldis.2013.05.008. [Epub ahead of print]
Tijero B, Gómez Esteban JC, Somme J, Llorens V, Lezcano E, Martinez A, Rodríguez T, Berganzo K, Zarranz JJ.
Movement Disorders and Autonomic Unit, Neurology Service, Cruces University Hospital, Basque Health Service (Osakidetza), Department of Neurosciences, University of the Basque Country, Spain.
The aim of this study was to compare autonomic function in PD symptomatic carriers of the LRRK2 mutations and idiopathic Parkinson's disease (iPD) patients.
MATERIAL AND METHODS:
We studied 25 PD patients: 12 with the LRRK2 mutation (6 G2019S and 6 R1441G), and 13 with iPD. All patients underwent blood pressure and heart rate monitoring during head up tilt, Valsalva maneuver and deep breathing, along with recording of sympathetic skin response (SSR) and cardiac MIBG scintigraphy.
Three of the patients with iPD and one of the LRRK2 carriers had orthostatic hypotension. Arterial pressure "overshoot" during phase IV of Valsalva maneuver was less pronounced in patients with iPD. During passive tilt, LRRK2 carries had higher increase of blood pressure than iPD patients MIBG late myocardial/mediastinal uptake ratios were higher in LRRK2 mutation carriers (1.51 ± 0.28 vs 1.32 ± 0.25; p < 0.05).
Carriers of the LRRK2 mutation had less autonomic impairment than those with iPD as shown by higher cardiac MIBG uptake and a tendency to less impairment of autonomic non-invasive tests. It is important to carry out larger studies comparing the clinical, functional and pathological characteristics of these patients.
Sunday, 16 June 2013
Short- and long-term efficacy of intensive rehabilitation treatment on balance and gait in parkinsonian patients: a preliminary study with a 1-year followup
Parkinsons Dis. 2013;2013:583278. doi: 10.1155/2013/583278. Epub 2013 May 26.
Frazzitta G, Bertotti G, Uccellini D, Boveri N, Rovescala R, Pezzoli G, Maestri R.
Department of Parkinson Disease Rehabilitation, "Moriggia-Pelascini" Hospital, Via Pelascini 3, 22015 Gravedona ed Uniti (CO), Italy ; Fondazione Europea Ricerca Biomedica FERB, "S.Isidoro" Hospital, Via Ospedale 34, 24069 Trescore Balneario, Italy.
Parkinson's disease (PD) is a neurodegenerative disease in which gait and balance disturbances are relevant symptoms that respond poorly to pharmacological treatment. The aim of this study was to investigate whether a 4-week inpatient multidisciplinary intensive rehabilitation treatment (MIRT) is effective in improving balance and gait and whether improvements persist at a one-year followup. We studied 20 PD inpatients (stage 3 Hoehn-Yahr) who underwent a MIRT. Outcome measures were UPDRS items for balance (30), falls (13), and walk (29), Berg Balance Scale, six-minute walking test, Timed Up and Go Test, and Comfortable-Fast gait speeds. Patients were evaluated at admission, at the end of the 4-week treatment, and at a 1-year followup. Pharmacological therapy was unchanged during MIRT and follow-up. All outcome measures improved significantly at the end of treatment. At 1-year follow-up control, UPDRS walk and Comfortable-Fast gait speeds still maintained better values with respect to admission (P = 0.009, P = 0.03, and P = 0.02, resp.), while the remaining scales did not differ significantly. Our results demonstrate that the MIRT was effective in improving balance and gait and that the improvement in gait performances was partially maintained also after 1 year.
Wednesday, 12 June 2013
Dement Geriatr Cogn Dis Extra. 2013 May 18;3(1):168-78. doi: 10.1159/000351421. Print 2013 Jan.
Hanna-Pladdy B, Jones K, Cabanban R, Pahwa R, Lyons KE.
Division of Neuropsychology, Department of Neurology, Emory University School of Medicine, Atlanta, Ga. ; Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Ga.
The aim of this study was to identify mild cognitive deficits in Parkinson's disease (PD) prior to extensive neurodegeneration and to evaluate the extent to which dopamine depletion and other disease-related predictors can explain cognitive profiles.
Neuropsychological performances of 40 nondemented early-stage PD patients and 42 healthy controls were compared across on or off dopaminergic medications. Stepwise regression evaluated cognitive predictors of early-stage PD and disease-related predictors of PD cognition (levodopa dose, disease duration, Unified Parkinson's Disease Rating Scale score, sleep, quality of life, and mood) across on and off states.
Neuropsychological performance was lower in PD patients across cognitive domains with significant memory, naming, visuomotor, and complex attention/executive deficits, but with intact visuospatial, simple attention, and phonemic fluency functions. However, medication effects were absent except for simple attention. Regression analyses revealed age, working memory, and memory recall to be the best cognitive predictors of PD, while age, quality of life, disease duration, and anxiety predicted PD cognition in the off state.
Nondemented early-stage PD patients presented with extensive mild cognitive deficits including prominent memory impairment. The profile was inconsistent with expected isolated frontostriatal dysfunction previously attributed to dopamine depletion and this highlights the need to further characterize extranigral sources of mild cognitive impairment in PD.
Sunday, 2 June 2013
Parkinsonism Relat Disord. 2013 May 21. pii: S1353-8020(13)00171-5. doi: 10.1016/j.parkreldis.2013.04.024. [Epub ahead of print]
Luca CC, Singer C.
Department of Neurology, Movement Disorders Division, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Gait dysfunction and postural instability represent a major therapeutic challenge in Parkinson's disease (PD). Gait disability in PD has been historically attributed to striato-nigral degeneration, however there is emerging evidence that multiple neurotransmitter deficits contribute to mobility impairment in PD. 4-aminopyridine (4-AP), a potent neurotransmitter modulator, has a wide range of favorable effects on gait in patients with neurological conditions including multiple sclerosis, spinal cord injury and cerebellar ataxia. In this Review we identify the neurobiological pathways involved in gait dysfunction in PD and discuss the mechanisms of action of 4-AP and its effect on gait related neuronal networks. The proposed mechanisms that may facilitate 4-AP favorable effect on gait in Parkinson's disease include 1) neurotransmitter release (dopamine, glutamate, acetylcholine and noradrenaline) 2) modulation of neuronal network oscillations and 3) increased cortical excitation. Recent clinical trials of 4-AP in neurological conditions associated with gait disorders will be highlighted and the importance of studying non-dopaminergic medications such as 4-AP in PD patients with gait impairment will be emphasized.
Saturday, 1 June 2013
Mov Disord. 2013 May 27. doi: 10.1002/mds.25507. [Epub ahead of print]
González-Aramburu I, Sánchez-Juan P, Jesús S, Gorostidi A, Fernández-Juan E, Carrillo F, Sierra M, Gómez-Garre P, Cáceres-Redondo MT, Berciano J, Ruiz-Martínez J, Combarros O, Mir P, Infante J.
Service of Neurology, Universitary Hospital Marqués de Valdecilla (IFIMAV), University of Cantabria (UC), Santander, Spain.
Low serum uric acid (UA) levels have been associated with increased Parkinson's disease (PD) risk and accelerated disease progression. We analyzed the effect of polymorphisms in 9 genes influencing serum UA concentration on the risk of PD.
We genotyped SLC2A9 rs734553, ABCG2 rs2231142, SLC17A1 rs1183201, SLC22A11 rs17300741, SLC22A12 rs505802, GCKR rs780094, PDZK1 rs12129861, LRRC16A+SCGN rs742132, and SLC16A9 rs12356193 in 1061 PD patients and 754 controls. For each subject we calculated a cumulative genetic risk score (GRS), defined as the total number of PD-risk alleles (range, 2-15) associated to lower serum UA levels. Serum UA levels were measured in a subgroup of 365 PD cases and 132 controls.
Serum UA levels were significantly lower in men with PD than in controls. Subjects (both men and women) carrying more than 9 risk alleles (third GRS tertile) had a 1.5 higher risk of developing PD than subjects with less than 8 risk alleles (first GRS tertile). An inverse correlation was observed between higher GRS and lower serum UA concentration in both men and women.
Genetic variability influencing serum UA levels might modify susceptibility to PD. © 2013 Movement Disorder Society.
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