N P Quinn

UCL Eastman Dental Institute, Londinium, England, United Kingdom

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Publications (369)2494.09 Total impact

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    ABSTRACT: α-Synuclein (SNCA) locus duplications are associated with variable clinical features and reduced penetrance but the reasons underlying this variability are unknown.
    JAMA Neurology 07/2014; · 7.58 Impact Factor
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    ABSTRACT: IMPORTANCE Recent advances in stem cell technologies have rekindled an interest in the use of cell replacement strategies for patients with Parkinson disease. This study reports the very long-term clinical outcomes of fetal cell transplantation in 2 patients with Parkinson disease. Such long-term follow-up data can usefully inform on the potential efficacy of this approach, as well as the design of trials for its further evaluation. OBSERVATIONS Two patients received intrastriatal grafts of human fetal ventral mesencephalic tissue, rich in dopaminergic neuroblasts, as restorative treatment for their Parkinson disease. To evaluate the very long-term efficacy of the grafts, clinical assessments were performed 18 and 15 years posttransplantation. Motor improvements gained gradually over the first postoperative years were sustained up to 18 years posttransplantation, while both patients have discontinued, and remained free of any, pharmacological dopaminergic therapy. CONCLUSIONS AND RELEVANCE The results from these 2 cases indicate that dopaminergic cell transplantation can offer very long-term symptomatic relief in patients with Parkinson disease and provide proof-of-concept support for future clinical trials using fetal or stem cell therapies.
    JAMA neurology. 11/2013;
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    ABSTRACT: Mutations in the gene encoding parkin (PARK2) are the commonest cause of autosomal recessive juvenile and young onset parkinsonism. The few available detailed neuropathological reports suggest that homozygous and compound heterozygous parkin mutations are characterised by severe substantia nigra pars compacta neuronal loss. In this study we investigate whether parkin-linked parkinsonism is a different clinicopathological entity to Parkinson's disease (PD). We describe the clinical, genetic and neuropathological findings in five unrelated cases of parkin disease and compare them with pathologically confirmed PD and controls. Presenting signs in the parkin disease cases were hand or leg tremor often combined with dystonia. Mean age of onset was 34 years; all were compound heterozygous for mutations of parkin. Freezing of gait, postural deformity and motor fluctuations were common late features. No patients had any evidence of cognitive impairment or dementia. Neuronal counts in the substantia nigra pars compacta revealed that neuronal loss in the parkin cases was as severe as that seen in PD, but relative preservation of the dorsal tier was seen in comparison with PD (p=0.04). Mild neuronal loss was identified in the locus coeruleus and dorsal motor nucleus of the vagus, but not in the nucleus basalis of Meynert, raphe nucleus or other brain regions. Sparse Lewy bodies (LBs) were identified in 2 cases (brainstem and cortex). These findings support the notion that parkin disease is characterised by a more restricted morphological abnormality than is found in PD, with predominantly ventral nigral degeneration and absent or rare Lewy bodies.
    Journal of neurology, neurosurgery, and psychiatry 11/2013; 84(11):e2. · 4.87 Impact Factor
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    ABSTRACT: BACKGROUND: Multiple system atrophy (MSA) presents with fairly symmetrical, levodopa unresponsive parkinsonism and additional features like autonomic dysfunction, cerebellar and corticospinal tract involvement. Marked asymmetry in atypical parkinsonism suggests alternative diagnosis like Corticobasal syndrome (CBS). METHODS: We describe five unusual cases, who presented initially with markedly asymmetric parkinsonism, rigid dystonic abnormal limb posturing and subsequently developed clinical and/or radiological features consistent with probable MSA-P. RESULTS: Using the internationally accepted diagnostic criteria, the patients fulfilled the diagnostic criteria for probable MSA-P after 5 years from disease onset. Case 4 and 5 had characteristic MRI features and Case 2 was pathologically confirmed. CONCLUSIONS: We use these cases to highlight that MSA-P MSA-P can present rarely with very marked asymmetry, dystonic limb and myoclonic jerks leading to a diagnosis of CBS at onset.
    Parkinsonism & Related Disorders 06/2013; · 3.27 Impact Factor
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    ABSTRACT: Recently, a number of genetic parkinsonian conditions have been recognized that share some features with the clinical syndromes of progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and multiple system atrophy (MSA), the classic phenotypic templates of atypical parkinsonism. For example, patients with progranulin, dynactin, or ATP13A gene mutations may have vertical supranuclear gaze palsy. This has made differential diagnosis difficult for practitioners. In this review, our goal is to make clinicians aware of these genetic disorders and provide clinical clues and syndromic associations, as well as investigative features, that may help in diagnosing these disorders. The correct identification of these patients has important clinical, therapeutic, and research implications. © 2013 Movement Disorder Society.
    Movement Disorders 05/2013; · 5.63 Impact Factor
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    ABSTRACT: IMPORTANCE Mutations in the gene encoding parkin (PARK2) are the most common cause of autosomal recessive juvenile-onset and young-onset parkinsonism. The few available detailed neuropathologic reports suggest that homozygous and compound heterozygous parkin mutations are characterized by severe substantia nigra pars compacta neuronal loss. OBJECTIVE To investigate whether parkin -linked parkinsonism is a different clinicopathologic entity to Parkinson disease (PD). DESIGN, SETTING, AND PARTICIPANTS We describe the clinical, genetic, and neuropathologic findings of 5 unrelated cases of parkin disease and compare them with 5 pathologically confirmed PD cases and 4 control subjects. The PD control cases and normal control subjects were matched first for age at death then disease duration (PD only) for comparison. RESULTS Presenting signs in the parkin disease cases were hand or leg tremor often combined with dystonia. Mean age at onset was 34 years; all cases were compound heterozygous for mutations of parkin. Freezing of gait, postural deformity, and motor fluctuations were common late features. No patients had any evidence of cognitive impairment or dementia. Neuronal counts in the substantia nigra pars compacta revealed that neuronal loss in the parkin cases was as severe as that seen in PD, but relative preservation of the dorsal tier was seen in comparison with PD (P = .04). Mild neuronal loss was identified in the locus coeruleus and dorsal motor nucleus of the vagus, but not in the nucleus basalis of Meynert, raphe nucleus, or other brain regions. Sparse Lewy bodies were identified in 2 cases (brainstem and cortex). CONCLUSIONS AND RELEVANCE These findings support the notion that parkin disease is characterized by a more restricted morphologic abnormality than is found in PD, with predominantly ventral nigral degeneration and absent or rare Lewy bodies.
    JAMA neurology. 03/2013;
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    ABSTRACT: We report a British family with young-onset Parkinson's disease (PD) and a G51D SNCA mutation that segregates with the disease. Family history was consistent with autosomal dominant inheritance as both the father and sister of the proband developed levodopa-responsive parkinsonism with onset in their late thirties. Clinical features show similarity to those seen in families with SNCA triplication and to cases of A53T SNCA mutation. Post-mortem brain examination of the proband revealed atrophy affecting frontal and temporal lobes in addition to the caudate, putamen, globus pallidus and amygdala. There was severe loss of pigmentation in the substantia nigra and pallor of the locus coeruleus. Neuronal loss was most marked in frontal and temporal cortices, hippocampal CA2/3 subregions, substantia nigra, locus coeruleus and dorsal motor nucleus of the vagus. The cellular pathology included widespread and frequent neuronal α-synuclein immunoreactive inclusions of variable morphology and oligodendroglial inclusions similar to the glial cytoplasmic inclusions of multiple system atrophy (MSA). Both inclusion types were ubiquitin and p62 positive and were labelled with phosphorylation-dependent anti-α-synuclein antibodies In addition, TDP-43 immunoreactive inclusions were observed in limbic regions and in the striatum. Together the data show clinical and neuropathological similarities to both the A53T SNCA mutation and multiplication cases. The cellular neuropathological features of this case share some characteristics of both PD and MSA with additional unique striatal and neocortical pathology. Greater understanding of the disease mechanism underlying the G51D mutation could aid in understanding of α-synuclein biology and its impact on disease phenotype.
    Acta Neuropathologica 02/2013; · 9.73 Impact Factor
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    ABSTRACT: BACKGROUND: Multiple system atrophy (MSA) is a fatal and still poorly understood degenerative movement disorder that is characterised by autonomic failure, cerebellar ataxia, and parkinsonism in various combinations. Here we present the final analysis of a prospective multicentre study by the European MSA Study Group to investigate the natural history of MSA. METHODS: Patients with a clinical diagnosis of MSA were recruited and followed up clinically for 2 years. Vital status was ascertained 2 years after study completion. Disease progression was assessed using the unified MSA rating scale (UMSARS), a disease-specific questionnaire that enables the semiquantitative rating of autonomic and motor impairment in patients with MSA. Additional rating methods were applied to grade global disease severity, autonomic symptoms, and quality of life. Survival was calculated using a Kaplan-Meier analysis and predictors were identified in a Cox regression model. Group differences were analysed by parametric tests and non-parametric tests as appropriate. Sample size estimates were calculated using a paired two-group t test. FINDINGS: 141 patients with moderately severe disease fulfilled the consensus criteria for MSA. Mean age at symptom onset was 56·2 (SD 8·4) years. Median survival from symptom onset as determined by Kaplan-Meier analysis was 9·8 years (95% CI 8·1-11·4). The parkinsonian variant of MSA (hazard ratio [HR] 2·08, 95% CI 1·09-3·97; p=0·026) and incomplete bladder emptying (HR 2·10, 1·02-4·30; p=0·044) predicted shorter survival. 24-month progression rates of UMSARS activities of daily living, motor examination, and total scores were 49% (9·4 [SD 5·9]), 74% (12·9 [8·5]), and 57% (21·9 [11·9]), respectively, relative to baseline scores. Autonomic symptom scores progressed throughout the follow-up. Shorter symptom duration at baseline (OR 0·68, 0·5-0·9; p=0·006) and absent levodopa response (OR 3·4, 1·1-10·2; p=0·03) predicted rapid UMSARS progression. Sample size estimation showed that an interventional trial with 258 patients (129 per group) would be able to detect a 30% effect size in 1-year UMSARS motor examination decline rates at 80% power. INTERPRETATION: Our prospective dataset provides new insights into the evolution of MSA based on a follow-up period that exceeds that of previous studies. It also represents a useful resource for patient counselling and planning of multicentre trials. FUNDING: Fifth Framework Programme of the European Union, the Oesterreichische Nationalbank, and the Austrian Science Fund.
    The Lancet Neurology 02/2013; · 23.92 Impact Factor
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    ABSTRACT: BACKGROUND: The Unified Multiple System Atrophy Rating Scale (UMSARS) was developed to provide a surrogate measure of disease progression in multiple system atrophy. In the present study, the intrarater agreement of the motor examination part of the UMSARS was determined. METHODS: All patients were first examined face to face, while being video-recorded, by two senior and two junior investigators. The patients' videotaped examinations were reevaluated after 3 months. Intrarater reliability for each item was analyzed by kappa statistics. RESULTS: Overall weighted kappa (κ) values were at least substantial or excellent for all UMSARS motor examination items, except for ocular motor dysfunction, which showed only moderate intrarater agreement. Intrarater reliability was comparable between senior and junior raters, with all κ differences being ≤ 0.22. CONCLUSIONS: The motor examination part of the UMSARS was found to have satisfactory intrarater reliability in the present cohort. © 2012 Movement Disorder Society.
    Movement Disorders 10/2012; · 5.63 Impact Factor
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    ABSTRACT: Cell therapy studies in patients with Parkinson's disease (PD) have been confined to intrastriatal transplantation of dopamine-rich fetal mesencephalic tissue in efforts to improve motor performance. Although some PD patients receiving the dopamine-rich grafts showed improvements in motor symptoms due to replacement of dopaminergic neurons, they still suffered from nonmotor symptoms including depression, fatigue, visual hallucinations, and sleep problems. Using functional imaging and clinical evaluation of motor and nonmotor symptoms in three PD patients transplanted with intrastriatal fetal grafts 13 to 16 years previously, we assessed whether reestablishment of dopaminergic neuronal networks is sufficient to improve a broad range of symptoms. At 13 to 16 years after transplantation, dopaminergic innervation was restored to normal levels in basal ganglia and preserved in a number of extrabasal ganglia areas. These changes were associated with long-lasting relief of motor symptoms. Then, we assessed the integrity of their serotonergic and norepinephrine neuronal systems using [¹¹C]DASB {[¹¹C]3-amino-4-(2-dimethylaminomethylphenylthio) benzonitrile} positron emission tomography (PET) and ¹⁸F-dopa PET, respectively. ¹⁸F-dopa uptake in the locus coeruleus was within the normal range. In contrast, [¹¹C]DASB uptake in the raphe nuclei and regions receiving serotonergic projections was markedly reduced. These results indicate ongoing degeneration of serotonergic raphe nuclei and their projections to regions involved in the regulation of sleep, arousal, feeding, satiety, mood, and emotion. Our findings indicate that future cell-based therapies using fetal tissue or stem cells in PD patients may require additional grafts of serotonergic neurons to relieve nonmotor symptoms by restoring serotonergic neurotransmission in specific cerebral targets.
    Science translational medicine 04/2012; 4(128):128ra41. · 10.76 Impact Factor
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    ABSTRACT: The reasons for the differences in emphasis on striatonigral or olivopontocerebellar involvement in multiple system atrophy (MSA) remain to be determined. Semi-quantitative pathological analyses carried out in the United Kingdom and Japan demonstrated that olivopontocerebellar-predominant pathology was more frequent in Japanese MSA than British MSA. This observation provides evidence for a difference in phenotype distribution between British and Japanese patients with definite MSA. Studies of the natural history and epidemiology of MSA carried out in various populations have revealed that the relative prevalences of clinical subtypes of MSA probably differ among populations; the majority of MSA patients diagnosed in Europe have predominant parkinsonism (MSA-P), while the majority of MSA patients diagnosed in Asia have predominant cerebellar ataxia (MSA-C). Although potential drawbacks to the published frequencies of clinical subtypes and pathological subtypes should be considered because of selection biases, the difference demonstrated in pathological subtype is also consistent with the differences in clinical subtype of MSA demonstrated between Europe and Asia. Modest alterations in susceptibility factors may contribute to the difference in MSA phenotype distribution between populations. Synergistic interactions between genetic risk variants and environmental toxins responsible for parkinsonism or cerebellar dysfunction should therefore be explored. Further investigations are needed to determine the environmental, genetic, and epigenetic factors that account for the differences in clinicopathological phenotype of MSA among different populations.
    Journal of Parkinson's disease. 01/2012; 2(1):7-18.
  • Journal of neurology, neurosurgery, and psychiatry 07/2011; 83(3):350-1. · 4.87 Impact Factor
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    ABSTRACT: Neuronal intermediate filament inclusion disease and atypical frontotemporal lobar degeneration are rare diseases characterized by ubiquitin-positive inclusions lacking transactive response DNA-binding protein-43 and tau. Recently, mutations in the fused in sarcoma gene have been shown to cause familial amyotrophic lateral sclerosis and fused in sarcoma-positive neuronal inclusions have subsequently been demonstrated in neuronal intermediate filament inclusion disease and atypical frontotemporal lobar degeneration with ubiquitinated inclusions. Here we provide clinical, imaging, morphological findings, as well as genetic and biochemical data in 14 fused in sarcoma proteinopathy cases. In this cohort, the age of onset was variable but included cases of young-onset disease. Patients with atypical frontotemporal lobar degeneration with ubiquitinated inclusions all presented with behavioural variant frontotemporal dementia, while the clinical presentation in neuronal intermediate filament inclusion disease was more heterogeneous, including cases with motor neuron disease and extrapyramidal syndromes. Neuroimaging revealed atrophy of the frontal and anterior temporal lobes as well as the caudate in the cases with atypical frontotemporal lobar degeneration with ubiquitinated inclusions, but was more heterogeneous in the cases with neuronal intermediate filament inclusion disease, often being normal to visual inspection early on in the disease. The distribution and severity of fused in sarcoma-positive neuronal cytoplasmic inclusions, neuronal intranuclear inclusions and neurites were recorded and fused in sarcoma was biochemically analysed in both subgroups. Fused in sarcoma-positive neuronal cytoplasmic and intranuclear inclusions were found in the hippocampal granule cell layer in variable numbers. Cortical fused in sarcoma-positive neuronal cytoplasmic inclusions were often 'Pick body-like' in neuronal intermediate filament inclusion disease, and annular and crescent-shaped inclusions were seen in both conditions. Motor neurons contained variable numbers of compact, granular or skein-like cytoplasmic inclusions in all fused in sarcoma-positive cases in which brainstem and spinal cord motor neurons were available for study (five and four cases, respectively). No fused in sarcoma mutations were found in any cases. Biochemically, two major fused in sarcoma species were found and shown to be more insoluble in the atypical frontotemporal lobar degeneration with ubiquitinated inclusions subgroup compared with neuronal intermediate filament inclusion disease. There is considerable overlap and also significant differences in fused in sarcoma-positive pathology between the two subgroups, suggesting they may represent a spectrum of the same disease. The co-existence of fused in sarcoma-positive inclusions in both motor neurons and extramotor cerebral structures is a characteristic finding in sporadic fused in sarcoma proteinopathies, indicating a multisystem disorder.
    Brain 07/2011; 134(Pt 9):2548-64. · 9.92 Impact Factor
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    ABSTRACT: Graft-induced dyskinesias are a serious complication after neural transplantation in Parkinson's disease. One patient with Parkinson's disease, treated with fetal grafts 14 years ago and deep brain stimulation 6 years ago, showed marked improvement of motor symptoms but continued to suffer from OFF-medication graft-induced dyskinesias. The patient received a series of clinical and imaging assessments. Positron emission tomography and single-photon emission computed tomography 14 years posttransplantation revealed an elevated serotonin/dopamine transporter ratio in the grafted striatum compatible with serotonergic hyperinnervation. Inhibition of serotonin neuron activity by systemic administration of a 5-HT(1A) agonist suppressed graft-induced dyskinesias. Our data provide further evidence that serotonergic neurons mediate graft-induced dyskinesias in Parkinson's disease. Achieving a normal striatal serotonin/dopamine transporter ratio following transplantation of fetal tissue or stem cells should be necessary to avoid the development of graft-induced dyskinesias.
    Movement Disorders 05/2011; 26(11):1997-2003. · 5.63 Impact Factor
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    Parkinsonism & Related Disorders 05/2011; 17(7):575-6. · 3.27 Impact Factor
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    ABSTRACT: Deep brain stimulation to the internal globus pallidus is an effective treatment for primary dystonia. The optimal clinical effect often occurs only weeks to months after starting stimulation. To better understand the underlying electrophysiological changes in this period, we assessed longitudinally 2 pathophysiological markers of dystonia in patients prior to and in the early treatment period (1, 3, 6 months) after deep brain stimulation surgery. Transcranial magnetic stimulation was used to track changes in short-latency intracortical inhibition, a measure of excitability of GABA(A) -ergic corticocortical connections and long-term potentiation-like synaptic plasticity (as a response to paired associative stimulation). Deep brain stimulation remained on for the duration of the study. Prior to surgery, inhibition was reduced and plasticity increased in patients compared with healthy controls. Following surgery and commencement of deep brain stimulation, short-latency intracortical inhibition increased toward normal levels over the following months with the same monotonic time course as the patients' clinical benefit. In contrast, synaptic plasticity changed rapidly, following a nonmonotonic time course: it was absent early (1 month) after surgery, and then over the following months increased toward levels observed in healthy individuals. We postulate that before surgery preexisting high levels of plasticity form strong memories of dystonic movement patterns. When deep brain stimulation is turned on, it disrupts abnormal basal ganglia signals, resulting in the absent response to paired associative stimulation at 1 month. Clinical benefit is delayed because engrams of abnormal movement persist and take time to normalize. Our observations suggest that plasticity may be a driver of long-term therapeutic effects of deep brain stimulation in dystonia.
    Movement Disorders 05/2011; 26(10):1913-21. · 5.63 Impact Factor
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    ABSTRACT: Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post-mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.
    European Journal of Neurology 01/2011; 2(5):435 - 444. · 4.16 Impact Factor
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    ABSTRACT: The commonest cause of pathological tremor is essential tremor (ET). However, it has proved difficult to identify genetic mutations causing ET, particularly because other causes of tremor continue to be misdiagnosed as ET. Whether subjects with dystonia or Parkinson's disease (PD) carry an increased genetic risk of developing ET, or vice versa, is controversial. In addition, the notion of a separate disorder of benign tremulous parkinsonism (BTP) has been debated. This article gives a selective viewpoint on some areas of uncertainty and controversy in tremor.
    Movement Disorders 01/2011; 26(1):18-23. · 5.63 Impact Factor
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    ABSTRACT: In the elderly, fear of falling (FoF) can lead to activity restriction and affect quality of life (QoL). Our aim was to identify the characteristics of FoF in Parkinson's disease and assess its impact on QoL. We assessed FoF in 130 patients with Parkinson's disease (PD) on scales measuring perceived self-efficacy in performing a range of activities (FES), perceived consequences of falling (CoF), and activity avoidance (SAFFE). A significant difference was found in FoF between PD patients who had previously fallen and those who had not and between frequent and infrequent fallers. Patient-rated disability significantly influenced FoF. Difficulty in rising from a chair, difficulty turning, start hesitation, festination, loss of balance, and shuffling were the specific mobility problems which were associated with greater FoF in PD. Disability was the main predictor of FoF, additionally depression predicted perceived consequences of falling, while anxiety predicted activity avoidance. The FoF measures explained 65% of the variance of QoL in PD, highlighting the clinical importance of FoF. These results have implications for the clinical management of FoF in PD.
    Behavioural neurology 01/2011; 24(3):219-28. · 1.25 Impact Factor
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    ABSTRACT: Progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) are progressive disabling neurological conditions usually fatal within 10 years of onset. Little is known about the economic costs of these conditions. This paper reports service use and costs from France, Germany and the UK and identifies patient characteristics that are associated with cost. 767 patients were recruited, and 760 included in the study, from 44 centres as part of the NNIPPS trial. Service use during the previous six months was measured at entry to the study and costs calculated. Mean six-month costs were calculated for 742 patients. Data on patient sociodemographic and clinical characteristics were recorded and used in regression models to identify predictors of service costs and unpaid care costs (i.e., care from family and friends). The mean six-month service costs of PSP were €24,491 in France, €30,643 in Germany and €25,655 in the UK. The costs for MSA were €28,924, €25,645 and €19,103 respectively. Unpaid care accounted for 68-76%. Formal and unpaid costs were significantly higher the more severe the illness, as indicated by the Parkinson's Plus Symptom scale. There was a significant inverse relationship between service and unpaid care costs.
    PLoS ONE 01/2011; 6(9):e24369. · 3.73 Impact Factor

Publication Stats

18k Citations
2,494.09 Total Impact Points


  • 2008–2014
    • UCL Eastman Dental Institute
      Londinium, England, United Kingdom
    • Radboud University Medical Centre (Radboudumc)
      Nymegen, Gelderland, Netherlands
    • Cardiff University
      • School of Medicine
      Cardiff, WLS, United Kingdom
    • Università degli Studi di Messina
      • Dipartimento di Scienze Pediatriche, Ginecologiche, Microbiologiche e Biomediche
      Messina, Sicily, Italy
  • 2013
    • Philipps-Universität Marburg
      • Klinik für Neurologie (Marburg)
      Marburg, Hesse, Germany
  • 2000–2013
    • Medizinische Universität Innsbruck
      • Univ.-Klinik für Neurologie
      Innsbruck, Tyrol, Austria
  • 1998–2013
    • University College London
      • • Sobell Department of Motor Neuroscience and Movement Disorders
      • • Institute of Neurology
      • • Royal Free Hospital
      Londinium, England, United Kingdom
  • 2003–2012
    • Imperial College London
      • • Division of Experimental Medicine
      • • Faculty of Medicine
      London, ENG, United Kingdom
    • University of Vienna
      • Institute of Neurophysiology
      Vienna, Vienna, Austria
    • Mayo Foundation for Medical Education and Research
      • Department of Neurology
      Scottsdale, AZ, United States
    • University of Louisville
      • Division of Movement Disorders
      Louisville, KY, United States
  • 2010
    • Harvard University
      • Department of Health Policy and Management
      Boston, MA, United States
  • 1989–2010
    • SAE Institute, London
      Oxford, England, United Kingdom
  • 2007
    • The Peninsula College of Medicine and Dentistry
      Plymouth, England, United Kingdom
  • 2005
    • WWF United Kingdom
      Londinium, England, United Kingdom
    • Hospital Universitario Virgen del Rocío
      • Servicio de Neurología
      Hispalis, Andalusia, Spain
  • 2002
    • Centre Hospitalier Universitaire de Bordeaux
      Burdeos, Aquitaine, France
  • 1982–2002
    • University of London
      • The School of Pharmacy
      Londinium, England, United Kingdom
  • 1999–2000
    • Lund University
      • Division of Neurology
      Lund, Skane, Sweden
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
    • University of Michigan
      • Department of Neurology
      Ann Arbor, MI, United States
  • 1995–2000
    • Medical Research Council (UK)
      Londinium, England, United Kingdom
  • 1997
    • University of Bristol
      Bristol, England, United Kingdom
  • 1996
    • University of Illinois at Chicago
      Chicago, Illinois, United States
  • 1986–1996
    • King's College London
      • • MRC Centre for Neurodegeneration Research
      • • School of Biomedical Sciences
      London, ENG, United Kingdom
    • McMaster University
      Hamilton, Ontario, Canada
  • 1994
    • Sapienza University of Rome
      • Department of Anatomical, Histological, Forensic Medicine and Orthopedic Science
      Roma, Latium, Italy
  • 1992–1993
    • University of Cambridge
      • Department of Psychology
      Cambridge, ENG, United Kingdom