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Cristina Tassorelli

Bio: Cristina Tassorelli is an academic researcher from University of Pavia. The author has contributed to research in topics: Migraine & Medicine. The author has an hindex of 50, co-authored 346 publications receiving 15732 citations. Previous affiliations of Cristina Tassorelli include University of Rochester Medical Center & UniFi.


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Jes Olesen, André Bes, Robert S. Kunkel, James W. Lance, Giuseppe Nappi, V Pfaffenrath, Frank Clifford Rose, Bruce S. Schoenberg, D. Soyka, Peer Tfelt-Hansen, K. Michael A. Welch, Marica Wilkinson, Marie-Germaine Bousser, Hans-Christoph Diener, David W. Dodick, Michael First, Peter J. Goadsby, Hartmut Göbel, Miguel J. A. Láinez, Richard B. Lipton, Fumihiko Sakai, Jean Schoenen, Stephen D. Silberstein, Timothy J. Steiner, Lars Bendtsen, Anne Ducros, Stefan Evers, Andrew D. Hershey, Zaza Katsarava, Morris Levin, Julio Pascual, Michael Bjørn Russell, Todd J. Schwedt, Cristina Tassorelli, Gisela M. Terwindt, Maurice Vincent, Shuu Jiun Wang, Andrew Charles, R. Lipton, Hayrunnisa Bolay, Michel Lantéri-Minet, E. A. Macgregor, T. Takeshima, Henrik Winther Schytz, S. Ashina, M. T. Goicochea, K. Hirata, Kenneth A. Holroyd, Christian Lampl, Dimos-Dimitrios Mitsikostas, P. Goadsby, C. Boes, C. Bordini, E. Cittadini, Andrew I. Cohen, M. Leone, A. May, L. Newman, J. Pareja, J. W. Park, T. Rozen, E. Waldenlind, Jong Ling Fuh, Aynur Özge, J. A. Pareja, Mario Fernando Prieto Peres, William B. Young, S. Y. Yu, Ishaq Abu-Arafeh, J. Gladstone, S. J. Huang, Rigmor Jensen, J.M. Láinez, D. Obelieniene, Peter S. Sandor, A. I. Scher, Marcel Arnold, Martin Dichgans, E. Houdart, José M. Ferro, Elizabeth Leroux, Y. S. Li, Aneesh B. Singhal, Gretchen E. Tietjen, Deborah I. Friedman, S. Kirby, B. Mokri, A. Purdy, K. Ravishankar, W. Schievink, R. Stark, F. Taylor, A. V. Krymchantowski, A. Tugrul, N. J. Wiendels, E. Marchioni, V. V. Osipova, Lidia Savi, J. R. Berger, Marcelo E. Bigal, J. González Menacho, Federico Mainardi, J. Pereira-Monteiro, M. Serrano-Dueñas, Roger Cady, C. Fernandez de las Peñas, Vincenzo Guidetti, J. Lance, Peter Svensson, Elizabeth Loder, A. E. Lake, Françoise Radat, J. I. Escobar, R. Benoliel, Claudia Sommer, A. Woda, Joanna M Zakrzewska, V. Aggarwal, L. Bonamico, Dominik A Ettlin, S. Graff-Radford, Jean-Paul Goulet, S. Jääskeläinen, Volker Limmroth, Ambra Michelotti, Donald R. Nixdorf, Mark Obermann, Richard Ohrbach, Paul Pionchon, Tara Renton, S. De Siqueira, Çiçek Wöber-Bingöl 
TL;DR: The International Classification of Headache Disorders, 3 edition (beta version), may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals as mentioned in this paper. But the authors require the permission of the International Headache Society.
Abstract: The International Classification of Headache Disorders, 3 edition (beta version), may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals. Otherwise, copyright belongs exclusively to the International Headache Society. Reproduction of any part or parts in any manner for commercial uses requires the Society’s permission, which will be granted on payment of a fee. Please contact the publisher at the address below. International Headache Society 2013. Applications for copyright permissions should be submitted to Sage Publications Ltd, 1 Oliver’s Yard, 55 City Road, London EC1Y 1SP, United Kingdom (tel: þ44 (0) 20 7324 8500; fax: þ44 (0) 207 324 8600) (www.sagepub.co.uk). Translations

6,519 citations

Journal ArticleDOI
TL;DR: The identification of the role of the subthalamic nucleus and, more in general, of the glutamatergic mechanisms in the pathophysiology of Parkinson's disease might lead to a new approach in the pharmacological treatment of the disease.

535 citations

Journal ArticleDOI
TL;DR: This is the first comprehensive estimation of how economic resources are lost to headache in Europe, and it is hoped that this will help clarify the financial costs of headaches in Europe.
Abstract: Background and purpose: Headache disorders are very common, but their monetary costs in Europe are unknown. We performed the first comprehensive estimation of how economic resources are lost to headache in Europe. Methods: From November 2008 to August 2009, a cross-sectional survey was conducted in eight countries representing 55% of the adult EU population. Participation rates varied between 11% and 59%. In total, 8412 questionnaires contributed to this analysis. Using bottom-up methodology, we estimated direct (medications, outpatient health care, hospitalization and investigations) and indirect (work absenteeism and reduced productivity at work) annual per-person costs. Prevalence data, simultaneously collected and, for migraine, also derived from a systematic review, were used to impute national costs. Results: Mean per-person annual costs were €1222 for migraine (95% CI 1055–1389; indirect costs 93%), €303 for tension-type headache (TTH, 95% CI 230–376; indirect costs 92%), €3561 for medication-overuse headache (MOH, 95% CI 2487–4635; indirect costs 92%), and €253 for other headaches (95% CI 99–407; indirect costs 82%). In the EU, the total annual cost of headache amongst adults aged 18–65 years was calculated, according to our prevalence estimates, at €173 billion, apportioned to migraine (€111 billion; 64%), TTH (€21 billion; 12%), MOH (€37 billion; 21%) and other headaches (€3 billion; 2%). Using the 15% systematic review prevalence of migraine, calculated costs were somewhat lower (migraine €50 billion, all headache €112 billion annually). Conclusions: Headache disorders are prominent health-related drivers of immense economic losses for the EU. This has immediate implications for healthcare policy. Health care for headache can be both improved and cost saving.

521 citations

Journal ArticleDOI
TL;DR: It is confirmed that ATP13A2 homozygous mutations are associated with human parkinsonism, and the associated genotypic and clinical spectrum is expanded, by describing a homozygOUS missense mutation in this gene in a patient with a phenotype milder than that initially associated with ATP 13A2 mutations (Kufor-Rakeb syndrome).
Abstract: Objective: To assess the prevalence, nature, and associated phenotypes of ATP13A2 gene mutations among patients with juvenile parkinsonism (onset Methods: We studied 46 patients, mostly from Italy or Brazil, including 11 with juvenile parkinsonism and 35 with YOPD. Thirty-three cases were sporadic and 13 had positive family history compatible with autosomal recessive inheritance. Forty-two had only parkinsonian signs, while four (all juvenile-onset) had multisystemic involvement. The whole ATP13A2 coding region (29 exons) and exon-intron boundaries were sequenced from genomic DNA. Results: A novel homozygous missense mutation (Gly504Arg) was identified in one sporadic case from Brazil with juvenile parkinsonism. This patient had symptoms onset at age 12, levodopa-responsive severe akinetic-rigid parkinsonism, levodopa-induced motor fluctuations and dyskinesias, severe visual hallucinations, and supranuclear vertical gaze paresis, but no pyramidal deficit nor dementia. Brain CT scan showed moderate diffuse atrophy. Furthermore, two Italian cases with YOPD without atypical features carried a novel missense mutation (Thr12Met, Gly533Arg) in single heterozygous state. Conclusions: We confirm that ATP13A2 homozygous mutations are associated with human parkinsonism, and expand the associated genotypic and clinical spectrum, by describing a homozygous missense mutation in this gene in a patient with a phenotype milder than that initially associated with ATP13A2 mutations (Kufor-Rakeb syndrome). Our data also suggest that ATP13A2 single heterozygous mutations might be etiologically relevant for patients with YOPD and further studies of this gene in Parkinson disease are warranted.

324 citations

Journal ArticleDOI
TL;DR: PINK1 homozygous mutations are a relevant cause of disease among Italian sporadic patients with early-onset parkinsonism, and this study suggests that, at least in some patients, these mutations are disease causing, in combination with additional, still unknown factors.
Abstract: Objective: To assess the prevalence, nature, and associated phenotypes of PINK1 gene mutations in a large series of patients with early-onset ( Methods: The authors studied 134 patients (116 sporadic and 18 familial; 77% Italian) and 90 Italian controls. The whole PINK1 coding region was sequenced from genomic DNA; cDNA was analyzed in selected cases. Results: Homozygous pathogenic mutations were identified in 4 of 90 Italian sporadic cases, including the novel Gln456Stop mutation; single heterozygous truncating or missense mutations were found in another 4 Italian sporadic cases, including two novel mutations, Pro196Leu and Gln456Stop. Pathogenic mutations were not identified in the familial cases. Novel (Gln115Leu) and known polymorphisms were identified with similar frequency in cases and controls. In cases carrying single heterozygous mutation, cDNA analysis detected no additional mutations, and revealed a major pathogenic effect at mRNA level for the mutant C1366T/Gln456Stop allele. All patients with homozygous mutations had very early disease onset, slow progression, and excellent response to l-dopa, including, in some, symmetric onset, dystonia at onset, and sleep benefit, resembling parkin-related disease. Phenotype in patients with single heterozygous mutation was similar, but onset was later. Conclusions: PINK1 homozygous mutations are a relevant cause of disease among Italian sporadic patients with early-onset parkinsonism. The role of mutations found in single heterozygous state is difficult to interpret. Our study suggests that, at least in some patients, these mutations are disease causing, in combination with additional, still unknown factors.

309 citations


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TL;DR: Clinical diagnostic criteria for probable and possible PD‐D are proposed, characterized by impairment in attention, memory, executive and visuo‐spatial functions, behavioral symptoms such as affective changes, hallucinations, and apathy are frequent.
Abstract: Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. Specific criteria for the clinical diagnosis of dementia associated with PD (PD-D), however, have been lacking. A Task Force, organized by the Movement Disorder Study, was charged with the development of clinical diagnostic criteria for PD-D. The Task Force members were assigned to sub-committees and performed a systematic review of the literature, based on pre-defined selection criteria, in order to identify the epidemiological, clinical, auxillary, and pathological features of PD-D. Clinical diagnostic criteria were then developed based on these findings and group consensus. The incidence of dementia in PD is increased up to six times, point-prevelance is close to 30%, older age and akinetic-rigid form are associated with higher risk. PD-D is characterized by impairment in attention, memory, executive and visuo-spatial functions, behavioral symptoms such as affective changes, hallucinations, and apathy are frequent. There are no specific ancillary investigations for the diagnosis; the main pathological correlate is Lewy body-type degeneration in cerebral cortex and limbic structures. Based on the characteristic features associated with this condition, clinical diagnostic criteria for probable and possible PD-D are proposed.

2,454 citations

Journal ArticleDOI
TL;DR: The newly recommended evidence-based new DC/TMD protocol is appropriate for use in both clinical and research settings and includes both a valid screener for detecting any pain-related TMD as well as valid diagnostic criteria for differentiating the most common pain- related TMD.
Abstract: Temporomandibular disorders (TMD) are a significant public health problem affecting approximately 5% to 12% of the population.1 TMD is the second most common musculoskeletal condition (after chronic low back pain) resulting in pain and disability.1 Pain-related TMD can impact the individual's daily activities, psychosocial functioning, and quality of life. Overall, the annual TMD management cost in the USA, not including imaging, has doubled in the last decade to $4 billion.1 Patients often seek consultation with dentists for their TMD, especially for pain-related TMD. Diagnostic criteria for TMD with simple, clear, reliable, and valid operational definitions for the history, examination, and imaging procedures are needed to render physical diagnoses in both clinical and research settings. In addition, biobehavioral assessment of pain-related behavior and psychosocial functioning—an essential part of the diagnostic process—is required and provides the minimal information whereby one can determine whether the patient's pain disorder, especially when chronic, warrants further multidisciplinary assessment. Taken together, a new dual-axis Diagnostic Criteria for TMD (DC/TMD) will provide evidence-based criteria for the clinician to use when assessing patients, and will facilitate communication regarding consultations, referrals, and prognosis.2 The research community benefits from the ability to use well-defined and clinically relevant characteristics associated with the phenotype in order to facilitate more generalizable research. When clinicians and researchers use the same criteria, taxonomy, and nomenclature, then clinical questions and experience can be more easily transferred into relevant research questions, and research findings are more accessible to clinicians to better diagnose and manage their patients. The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) have been the most widely employed diagnostic protocol for TMD research since its publication in 1992.3 This classification system was based on the biopsychosocial model of pain4 that included an Axis I physical assessment, using reliable and well-operationalized diagnostic criteria, and an Axis II assessment of psychosocial status and pain-related disability. The intent was to simultaneously provide a physical diagnosis and identify other relevant characteristics of the patient that could influence the expression and thus management of their TMD. Indeed, the longer the pain persists, the greater the potential for emergence and amplification of cognitive, psychosocial, and behavioral risk factors, with resultant enhanced pain sensitivity, greater likelihood of additional pain persistence, and reduced probability of success from standard treatments.5 The RDC/TMD (1992) was intended to be only a first step toward improved TMD classification, and the authors stated the need for future investigation of the accuracy of the Axis I diagnostic algorithms in terms of reliability and criterion validity—the latter involving the use of credible reference standard diagnoses. Also recommended was further assessment of the clinical utility of the Axis II instruments. The original RDC/TMD Axis I physical diagnoses have content validity based on the critical review by experts of the published diagnostic approach in use at that time and were tested using population-based epidemiologic data.6 Subsequently, a multicenter study showed that, for the most common TMD, the original RDC/TMD diagnoses exhibited sufficient reliability for clinical use.7 While the validity of the individual RDC/TMD diagnoses has been extensively investigated, assessment of the criterion validity for the complete spectrum of RDC/TMD diagnoses had been absent until recently.8 For the original RDC/TMD Axis II instruments, good evidence for their reliability and validity for measuring psychosocial status and pain-related disability already existed when the classification system was published.9–13 Subsequently, a variety of studies have demonstrated the significance and utility of the original RDC/TMD biobehavioral measures in such areas as predicting outcomes of clinical trials, escalation from acute to chronic pain, and experimental laboratory settings.14–20 Other studies have shown that the original RDC/TMD biobehavioral measures are incomplete in terms of prediction of disease course.21–23 The overall utility of the biobehavioral measures in routine clinical settings has, however, yet to be demonstrated, in part because most studies have to date focused on Axis I diagnoses rather than Axis II biobehavioral factors.24 The aims of this article are to present the evidence-based new Axis I and Axis II DC/TMD to be used in both clinical and research settings, as well as present the processes related to their development.

2,283 citations

Journal ArticleDOI
TL;DR: Current human findings regarding sex differences in experimental pain indicate greater pain sensitivity among females compared with males for most pain modalities, including more recently implemented clinically relevant pain models such as temporal summation of pain and intramuscular injection of algesic substances.

2,178 citations

01 Jan 1998
TL;DR: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders as mentioned in this paper, who discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states.
Abstract: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders. Individuals discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states. Self-medication factors occur in a context of self-regulation vulnerabilities--primarily difficulties in regulating affects, self-esteem, relationships, and self-care. Persons with substance use disorders suffer in the extreme with their feelings, either being overwhelmed with painful affects or seeming not to feel their emotions at all. Substances of abuse help such individuals to relieve painful affects or to experience or control emotions when they are absent or confusing. Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders. The cause-consequence controversy involving psychopathology and substance use/abuse is reviewed and critiqued. In contrast, clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances. Subjective states of distress and suffering involved in motives to self-medicate with substances of abuse are considered with respect to nicotine dependence and to schizophrenia and posttraumatic stress disorder comorbid with a substance use disorder.

1,907 citations

Journal ArticleDOI
01 Jun 2016-Stroke
TL;DR: This guideline provides a synopsis of best clinical practices in the rehabilitative care of adults recovering from stroke to reduce the risk of downstream medical morbidity resulting from immobility, depression, loss of autonomy, and reduced functional independence.
Abstract: Purpose—The aim of this guideline is to provide a synopsis of best clinical practices in the rehabilitative care of adults recovering from stroke. Methods—Writing group members were nominated by th...

1,679 citations