Hypothèse vasculaire des crises de migraines

Vascular hypothesis of migraine attacks

Nov 09, 2020

Many debates on the origin of headache: the vascular theory

The vascular theory of migraine attacks has been debated for a very long time. During the second century, Galen suggested that the throbbing, throbbing character of headache originated in blood vessels. In the Middle Ages, Ibn Sïnä (Avicenna) wrote his medical encyclopaedia Qanûn (Canon of Medicine) in which he suggested that headache could originate " from the bone of the skull, from the membrane below it, or of substances reaching the site of the headache through the blood vessels ” (Abokrysha 2009). It was not until 1672 that Thomas Willis proposed the first vascular theory of migraine and suggested that it was the consequence of a dilation of the blood vessels in the head (Borsook et al. 2012). In the second half of the 19th century, Du Bois-Reymond, a German electrophysiologist, attributed migraine headaches to an arterial spasm following sympathetic stimulation. It was a few years later that Peter Wallmark Latham attempted to combine the 2 hypotheses: " we first observe a contraction of the cerebral vessels, and therefore a reduction in blood flow, which is produced by the excited action of the sympathetic, then the exhaustion of the sympathetic caused by this excitation causes dilation of the vessels which triggers the headache ” (Foxhall 2019). Latham extended his vasomotor theory to all aspects of migraine, including scotomas and the various manifestations present during the aura phase. According to him, these phenomena are the consequence of cerebral vasoconstriction associated with local anemia (Sacks 1999). Edward Liveing, while admitting that the immediate cause of the headaches lies in the dilation of the extracranial arteries, refused to impute all the facets of migraine to this single theory.

In his view, this hypothesis did not account for the multiple, varied and often bilateral symptoms of the migraine aura, nor for the typical changes associated with the migraine attack (mood disorder, fatigue, hunger, etc.) (Foxhall 2019). The greatest scientists of the previous century had clearly spotted the weaknesses of Latham's vasomotor hypothesis. They had already understood that no such theory, however elaborate, could account for all the characteristics of migraine and its auras. Nevertheless, this theory made it possible to stimulate research in understanding the physiopathology of migraine, but divided the researchers into two groups: the provascular, but which did not make it possible to apprehend the migraine as a whole, and those at the search for more global hypotheses (Dalessio 1993). This is the case of Liveing ​​who formulated his own theory of “nerve storms” and described migraine as “ a neurosis due to the accumulation and irregular discharge of nervous forces ” (Weatherall 2012).

Observations by Harold G. Wolff

For his part, Harold G. Wolff, a physician and researcher in psychopathology, tried to understand the link between the nervous storm theory and the Latham vascular hypothesis (Akkermans 2015). Himself a migraine sufferer, he first succeeded in demonstrating that the intensity of the headache was strictly proportional to the dilation of the extra cranial arteries, and that this pain could be reduced either by manual compression of the dilated arteries, or by administration of adrenaline or ergotamine, or else by the centrifugal rotation of the whole body. His capital discovery was to understand that the dilation of these arteries was the cause of the exudation of a fluid rich in polypeptides, having the effect of causing localized pain, itself followed by an inflammatory reaction (Sacks 1999). Thus, Wolff's observations provided an almost definitive picture of the mechanism of migraine headaches. However, when he tried to use the same methods to study auras and in particular scotomas, by testing several vasoactive substances, the results were much less consistent and for many of them impossible to reproduce (Blau 2004). Wolff nevertheless proposed a hypothesis with many precautions, of the probable existence of a local cortical ischemia which could explain the scotomas, while admitting that this theory cannot, on its own, explain all the symptoms of migraine. But many scientists and doctors embraced this theory without considering its inconsistencies (Foxhall 2019).

Gradually, the vascular hypotheses became rigid in postulates, and for several years, the vasomotor theory of migraine prevailed in describing its pathophysiology (Graham 1952). Abokrysha, Noha. 2009. “Ibn Sina (Avicenna) on Pathogenesis of Migraine Compared With the Recent Theories.” Headache: The Journal of Head and Face Pain 49 (6): 923‑27. https://doi.org/10.1111/j.1526-4610.2009.01394.x. Akkermans, Rebecca. 2015. “Harold G. Wolff”. The Lancet Neurology 14 (10): 982-83. https://doi.org/10.1016/S1474-4422(15)00184-2. Blau, JN 2004. “Harold G Wolff: The Man and His Migraine”. 2004. https://journals.sagepub.com/doi/10.1111/j.1468-2982.2003.00642.x. Borsook, David, Peter J. Goadsby, and Richard Hargreaves. 2012. The Migraine Brain: Imaging Structure and Function . OOP USA. Dalessio, Donald J. 1993. Wolff's Headache and Other Head Pain . Oxford University Press. Foxhall, Katherine. 2019. Migraine: A History . JHU Press. Graham, JR 1952. “The Natural History of Migraine: Some Observations and a Hypothesis”. Transactions of the American Clinical and Climatological Association 64: 61-73; discussion, 73-74. Sacks, Oliver. 1999. Migraine . Edition of the Threshold. Paperback. New York: Vintage. Weatherall, MW 2012. “The Migraine Theories of Living and Latham: A Reappraisal”. Brain 135 (8): 2560‑68. https://doi.org/10.1093/brain/aws020.

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