Cortical Spreading Depression—Better Understanding and More Questions . Focus on “Distinct Vascular Conduction With Cortical Spreading Depression”
2007; American Physiological Society; Volume: 97; Issue: 6 Linguagem: Inglês
10.1152/jn.00232.2007
ISSN1522-1598
Autores Tópico(s)Trigeminal Neuralgia and Treatments
ResumoEDITORIAL FOCUSCortical Spreading Depression—Better Understanding and More Questions. Focus on "Distinct Vascular Conduction With Cortical Spreading Depression"Peter J. GoadsbyPeter J. GoadsbyPublished Online:01 Jun 2007https://doi.org/10.1152/jn.00232.2007This is the final version - click for previous versionMoreSectionsPDF (32 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations In this issue of the Journal of Neurophysiology Brennan et al. (p. 4143–4151) present a provocative, carefully conducted series of studies that challenge a very tightly held belief about cortical spreading depression (CSD) showing propagation of the dilation of cortical surface arterioles at a greater velocity than the wave changes in cellular activity. How could this be? Do not changes in blood flow follow neuronal changes passively with flow-metabolism coupling? It seems the issue is not that simple.Cortical spreading depression (CSD) was first described by Leao (1944a,b), who observed a depression of electroencephalographic (EEG) activity that moved across the cortex at a rate of 3–6 mm/min. It has been observed in clinical practice that the migraine aura, a transient neurological disturbance (Headache Classification Committee of The International Headache Society 2004) that moves slowly across the visual field or over the limbs, has the same rate of progression at least for visual changes (Lashley 1941). The observation by Olesen and colleagues (1981) of a spreading reduction in cerebral blood flow, spreading oligemia, in patients with migraine aura triggered a revolution in thinking about migraine aura. For much of the 20th century, aura was considered a vascular process, i.e., primarily vasoconstriction as the initial event, with head pain as a consequence of a reactive vasodilation (Wolff 1948). The CSD hypothesis completely reversed this concept with the primary event being neural and brain blood flow changes being secondary to changes in neuronal activity (Lauritzen 1994). Indeed cerebral blood flow changes seen with single photon emission computerized tomography (Olesen et al. 1990) and perfusion-weighted magnetic resonance imaging (MRI) (Cutrer et al. 1998) lent support to this notion as a spreading oligemia was observed during aura, considered to be due to changes in neuronal activity, with different imaging modalities. Most recently functional MRI (fMRI) changes again consistent with CSD have been seen in migraine aura (Hadjikhani et al. 2001), so it is generally accepted that CSD is the animal experimental equivalent of migraine aura—thus its importance to human neurobiology.It has been shown with single modality blood flow, such as autoradiographic methods (Duckrow 1991, 1993) or laser Doppler flowmetry (Piper et al. 1991), that triggering CSD results in a wave of reduced cortical blood flow. Moreover, using dual modality methods, such as laser Doppler flowmetry and extracellular electrophysiology (Akerman and Goadsby 2005; Goadsby et al. 1992), changes in neuronal firing and cerebral blood flow could be seen to occur together. However, these methods have lacked the combination of parallel spatial and temporal resolution. Brennan and colleagues (2007) have overcome this by combining electrophysiological measurements with optic intrinsic signal imaging. They show vasomotor changes in cortex traveling at significantly greater velocity than the neuronal changes, a circuitous pathway and crucially dissociation of vasomotor and neuronal changes. Their data suggest a mechanism that requires the vasculature and not the neuronal component. These data demand a complete re-evaluation of flow-metabolism coupling, blood flow changes that accompanying changes in demand for energy substrates in the brain (Edvinsson and Krause 2002), as the single explanation for brain blood flow changes in migraine. Moreover, the authors challenge the cerebrovascular physiology community to consider this remarkable new mechanism. As is typical for more interesting studies, the work by Brennan and colleagues raises more questions than it answers.REFERENCESAkerman and Goadsby 2005 Akerman S, Goadsby PJ. Topiramate inhibits cortical spreading depression in rat and cat: impact in migraine aura. Neuroreport 16: 1383–1387, 2005.Crossref | PubMed | ISI | Google ScholarBrennan et al. 2007 Brennan KC, Beltran-Parrazal L, Lopez-Valdes HE, Theriot J, Toga AW, Charles AC. Distinct vascular conduction with cortical spreading depression. J Neurophysiol 97: 4143–4151, 2007.Link | ISI | Google ScholarCutrer et al. 1998 Cutrer FM, Sorensen AG, Weisskoff RM, Ostergaard L, Sanchez del Rio M, Lee J, et al. Perfusion-weighted imaging defects during spontaneous migrainous aura. Ann Neurol 43: 25–31, 1998.Crossref | PubMed | ISI | Google ScholarDuckrow 1991 Duckrow RB. Regional cerebral blood flow during spreading cortical depression in conscious rats. J Cereb Blood Flow Metab 11: 150–154, 1991.Crossref | PubMed | ISI | Google ScholarDuckrow 1993 Duckrow RB. A brief hypoperfusion precedes spreading depression if nitric oxide synthesis is inhibited. Brain Res 618: 190–195, 1993.Crossref | PubMed | ISI | Google ScholarEdvinsson and Krause 2002 Edvinsson L, Krause DN. Cerebral Blood Flow and Metabolism. Philadelphia: Lippincott Williams and Wilkins, 2002.Google ScholarGoadsby et al. 1992 Goadsby PJ, Kaube H, Hoskin K. Nitric oxide synthesis couples cerebral blood flow and metabolism. Brain Res 595: 167–170, 1992.Crossref | PubMed | ISI | Google ScholarHadjikhani et al. 2001 Hadjikhani N, Sanchez del Rio M, Wu O, Schwartz D, Bakker D, Fischl B, et al. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci USA 98: 4687–4692, 2001.Crossref | PubMed | ISI | Google ScholarHeadache Classification Committee of The International Headache Society 2004 Headache Classification Committee of The International Headache Society. The International Classification of Headache Disorders (2nd ed.). Cephalalgia 24: 1–160, 2004.ISI | Google ScholarLashley 1941 Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psychiatry 46: 331–339, 1941.Crossref | Google ScholarLauritzen 1994 Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain 117: 199–210, 1994.Crossref | PubMed | ISI | Google ScholarLeao 1944a Leao AAP. Pial circulation and spreading activity in the cerebral cortex. J Neurophysiol 7: 391–396, 1944a.Link | Google ScholarLeao 1944b Leao AAP. Spreading depression of activity in cerebral cortex. J Neurophysiol 7: 359–390, 1944b.Link | Google ScholarOlesen et al. 1990 Olesen J, Friberg L, Skyhoj-Olsen T, Iversen HK, Lassen NA, Andersen AR, et al. Timing and topography of cerebral blood flow, aura, and headache during migraine attacks. Ann Neurol 28: 791–798, 1990.Crossref | PubMed | ISI | Google ScholarOlesen et al. 1981 Olesen J, Larsen B, Lauritzen M. Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol 9: 344–352, 1981.Crossref | PubMed | ISI | Google ScholarPiper et al. 1991 Piper RD, Lambert GA, Duckworth JW. Cortical blood flow changes during spreading depression in cats. Am J Physiol Heart Circ Physiol 261: H96–H102, 1991.Link | ISI | Google ScholarWolff 1948 Wolff HG. Headache and Other Head Pain. New York: Oxford, 1948.Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: (E-mail: [email protected]) Download PDF Back to Top Next FiguresReferencesRelatedInformation Cited ByEpidemiological association between migraine and lipoprotein(a): a systematic review30 April 2014 | Journal of Thrombosis and Thrombolysis, Vol. 39, No. 1Meta-analysis of factor V Leiden and prothrombin G20210A polymorphism in migraineBlood Coagulation & Fibrinolysis, Vol. 26, No. 1Migraine and erythrocyte biology: a review14 March 2014 | International Journal of Laboratory Hematology, Vol. 36, No. 6Homocysteine and migraine. A narrative reviewClinica Chimica Acta, Vol. 433No Evidence for an Association of Vitamin D Deficiency and Migraine: A Systematic Review of the LiteratureBioMed Research International, Vol. 2014A Young Man Presenting with Acute Encephalopathy, Hemiparesis, and HeadacheThe Journal of Emergency Medicine, Vol. 43, No. 2Potential mechanisms of prospective antimigraine drugs: A focus on vascular (side) effectsPharmacology & Therapeutics, Vol. 129, No. 3"Prolonged" migraine aura: New information on underlying mechanismsTranslational Neuroscience, Vol. 2, No. 2Migraine and stroke: current perspectives19 July 2013 | Neurological Research, Vol. 30, No. 8Mechanically-induced cortical spreading depression associated regional cerebral blood flow changes are blocked by Na+ ion channel blockadeBrain Research, Vol. 1229Posterior Cerebral Hypoperfusion in Migraine Without Aura1 August 2008 | Cephalalgia, Vol. 28, No. 8Examining the Essence of Migraine—Is it the Blood Vessel or the Brain? A DebateHeadache: The Journal of Head and Face Pain, Vol. 48, No. 4 More from this issue > Volume 97Issue 6June 2007Pages 3827-3827 Copyright & PermissionsCopyright © 2007 by the American Physiological Societyhttps://doi.org/10.1152/jn.00232.2007PubMed17409171History Received 4 March 2007 Accepted 2 April 2007 Published online 1 June 2007 Published in print 1 June 2007 Metrics
Referência(s)