In Europa e in USA questa linea di ricerche ha avuto ampissima risonanza, specialmente per quanto riguarda le lesioni evidenziabili a livello della sostanza bianca nel cervello. In USA si sono aperti molti blog che sottolineavano come l’emicrania non fosse più a lungo da considerarsi mero dolore ma una malattia neurologica che compromette l’organicità cerebrale. Si arriva forse all’allarmismo certo è che tali lesioni son presenti. Posson esser riportati alla spreading depression e quindi alla successiva reperfusion injury. Di sicuro, al momento, ci indicano la necessità di curare l’emicrania come vera malattia.
Se nel settore delle lesioni cerebrali le nostre osservazioni sono in linea con quelle realizzate in Europa ed in USA, i problemi cardiovascolari ci sembrano legati a una diatesi disfunzionale vegetativo dolorosa che ha un largo ventaglio di espressioni a cominciare dalla cosiddetta angina X. Inoltre, non concordiamo sul fatto che i triptani possan provocare angor o infarto miocardico se non in soggetti predisposti. A quanto diciamo si può obiettare che i cefalalgici potrebbero in realtà essere , anche per quanto noi stessi abbiamo detto, dei soggetti predisposti
Dati e lavori personali degli afferenti alla Fondazione Sicuteri-Nicolodi
Sicuteri F, Nicolodi M. A human model of reperfusion injury-Relevance of the mechanism in plegic migraine. Abstract of Symposium “Cerebral Ischemia”, Wenner Gren Foundation, Stockholm, 25-27 October 1994
Nicolodi M, Sicuteri F. Il dolore anginoso in assenza di positività elettrocardiografica e coronarografica. Il ruolo della iperalgesia e del deficit dei sistemi sopraspinali di controllo del segnale sensitivo/algogeno viscerale. Atti del XCVI Congresso della Società Italiana di Medicina Interna, Roma 12-15 Ottobre, 1995
Nicolodi M. Chest pain and sumatriptan: a disagreeable sensation or a witness for prosecution? Cephalalgia 16 (5): 397, 1966
Nicolodi M. Gender and region difference in side-effects induced by sumatriptan. Cephalalgia 16 (5): 396, 1996
Nicolodi M, Pettinati G, Portone F, Sicuteri F. Systemic visceral hyperalgesia in the mechanism of chest pain-The interaction of homotopic and generalised visceral hyperalgesia in the worsening of chest pain and angina” 8th World Congress”The pain Clinic” May 6-10, 1998, Santa Cruz de Tenerife -Spain, plenary lecture
Nicolodi M, Pettinati G, Portone F, Sicuteri F. First demonstration of generalised visceral hyperalgesia in angina sufferers: its possible activity in the crescendo of the disease. In: J:A: De Vera, W. Parris, S.Erdine (Eds:), Management of pain : A world perspecive, Bologna: Internat Proc. Div. Monduzzi, pp 473-476, 1988
M. Nicolodi , Torrini A. Severe migraine, silent brain lesion, and dementia. Cephalalgia 26, 1316, 2006
Nicolodi M, Fanfani F, Torrini A. Cortical atrophy and memory deficits in 4 clusters of chronic migraine sufferers: a 6 years’ observation . Cephalalgia 7(6): 598, 2007
Dall’Estero
Migraine as a Risk Factor
for Subclinical Brain Lesions
Mark C. Kruit, MD
Mark A. van Buchem, MD, PhD
Paul A. M. Hofman, MD, PhD
Jacobus T. N. Bakkers, MD
Gisela M. Terwindt, MD, PhD
Michel D. Ferrari, MD, PhD
Lenore J. Launer, PhD
MIGRAINE IS A COMMON,
chronic, multifactorial
– neurovascular disorder
Is Migraine a Progressive Brain Disease?
1. Richard B. Lipton, MD;
2. Jullie Pan, MD, PhD
[+] Author Affiliations
1. Author Affiliation: Departments of Neurology, Epidemiology and Public Health (Dr Lipton) and Neuroscience (Dr Pan), Albert Einstein College of Medicine, Bronx, NY.
Since this article does not have an abstract, we have provided the first 150 words of the full text.
KEYWORDS:
• cerebral infarction,
• migraine.
In this issue of THE JOURNAL, Kruit and colleagues1 provide important new data on the prevalence of brain infarction and white matter lesions in persons with migraine. The authors systematically recruited individuals with migraine with aura and migraine without aura as well as group-matched controls without migraine from the general Dutch population.
Migraine and Ischaemic Heart Disease and Stroke: Potential Mechanisms and Treatment Implications
1. E Gretchen and
2. MD Tietjen
1. Gretchen E. Tietjen, 3120 Glendale Avenue, RHC 1450, Department of Neurology, The University of Toledo-Health Science Campus, Toledo, OH 43614, USA. Tel. +1 419 383 6187; fax +1 419 383 3093; e-mail gretchen.tietjen@utoledo.edu
Abstract
The migraine-ischemia relationship is best understood in the context of the pathophysiology of migraine. Potential mechanisms of migrainous infarction (stroke occurring during migraine) include vasospasm, hypercoagulability, and vascular changes related to cortical spreading depression. Stroke occurring remote for the migraine attack may be related to arterial dissection, cardioembolism, and endothelial dysfunction. Endothelial dysfunction, a process mediated by oxidative stress
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