2015
DOI: 10.1590/0004-282x20150094
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Abstract: Three different mechanisms -vascular, trigeminovascular and cortical hyperexcitability -have been proposed for the pathogenesis of migraine and have recently been the subject of extensive reviews 1,2,3,4 . In our own assessment 5 we presented the results of therapeutic transcranial magnetic stimulation (tTMS) as evidence that, in at least some patients, virtually all migraine symptoms during the headache phase are cortical in origin and that a neuroinflammatory mechanism could not be involved in the initiation… Show more

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Cited by 4 publications
(3 citation statements)
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References 54 publications
(61 reference statements)
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“…For several decades, it has been generally assumed that migraine's pathophysiology is based on a phenomenon called Cortical Spreading Depression (CSD), which is thought to be a wave of initial increase, followed by a sustained decrease in electrocortical activity that is associated with initial vasodilation and prolonged vasoconstriction. However, two recent studies have challenged the role of CSD in migraine [1,2]. The present paper provides additional arguments to re-examine the CSD hypothesis.…”
Section: Introductionmentioning
confidence: 59%
See 1 more Smart Citation
“…For several decades, it has been generally assumed that migraine's pathophysiology is based on a phenomenon called Cortical Spreading Depression (CSD), which is thought to be a wave of initial increase, followed by a sustained decrease in electrocortical activity that is associated with initial vasodilation and prolonged vasoconstriction. However, two recent studies have challenged the role of CSD in migraine [1,2]. The present paper provides additional arguments to re-examine the CSD hypothesis.…”
Section: Introductionmentioning
confidence: 59%
“…Only positive symptoms like flashing lights, castellations, scintillations, and pins and needles are described by a number of patients with aura, without negative symptoms, like scotoma, hemianopsia, or numbness and loss of sensibility as expected from neurosilencing by CSD [29]. In other patients, visual aura symptoms are superimposed on a normal visual image, or numbness and tingling exists without a loss of touch [2]. The preservation of function seems incompatible with a process such as CSD, during which electric activity in the somatosensory cortex is strongly depressed [48].…”
Section: Arguments Against a Role For Csd In Migraine Aura (See Table 1)mentioning
confidence: 99%
“…However, in recent years (2015–2022), even from researchers who have conducted significant studies in support of this theory, numerous contradictions have begun to highlight its inadequacy and plausibility and to suggest the need to clarify and modify some aspects [ 11 , 12 , 13 , 14 , 15 , 16 ], and also in the light of data that come from clinical practice [ 6 , 7 , 17 ]. In fact, in light of both experimental and clinical data, the theory of CSD was subjected to revision and criticism for its poor adaptation to the clinical presentation of the migraine aura, at least in a relevant percentage of “presentations with atypical clinical pictures” [ 2 , 11 , 12 , 13 , 14 , 15 , 16 ].…”
Section: Introductionmentioning
confidence: 99%