Migraine: A lateralizing disorder with onset before aura/headache?
Vinod K.Gupta, Physician / Director, Migraine-Headache Institute, New Delhi, Indiadr_vkgupta@yahoo.com
Submitted September 19, 2017
Schulte et al. presented evidence from fMRI to suggest that the hypothalamus is a mediator of chronic migraine. [1] Neither aura nor headache mark the true onset of migraine attack; these symptoms are part of an evolving process and represent endpoints of a series of physiologic changes embedded in the prodromal and pre-prodromal phases -- the latter becoming evident in the significant delay of migraine onset after stress, exercise, alcohol consumption, ingestion of tyramine containing foods (up to 22 hours), cocaine abuse or abstinence, caffeine withdrawal, nitroglycerine challenge, exposure to m-chlorophenylpiperazine, and catastrophic trauma (physical or psychological). [2] The fMRI changes recorded by Schulte et al. [1] do not represent primary pathogenetic changes.
As a pathognomonically lateralizing (unilateral or side-locked) headache, migraine cannot be related to diffuse or bilateral hypothalamic activation. [2] Atenolol is as good a migraine preventive agent as propranolol, but atenolol does not cross the blood-brain barrier, making primary pathogenetic brain neuronal involvement highly unlikely. [2]
1. Schulte LH, Allers A, Arne May. Hypothalamus as a mediator of chronic migraine: Evidence from high-resolution fMRI. Neurology 2017;88:2011-2016.
2. Gupta VK. Adaptive Mechanisms in Migraine: A Comprehensive Synthesis in Evolution - Breaking the Migraine Code. New York: Nova Science Publishers, Inc; 2009.
For disclosures, please contact the editorial office at journal@neurology.org.
Schulte et al. presented evidence from fMRI to suggest that the hypothalamus is a mediator of chronic migraine. [1] Neither aura nor headache mark the true onset of migraine attack; these symptoms are part of an evolving process and represent endpoints of a series of physiologic changes embedded in the prodromal and pre-prodromal phases -- the latter becoming evident in the significant delay of migraine onset after stress, exercise, alcohol consumption, ingestion of tyramine containing foods (up to 22 hours), cocaine abuse or abstinence, caffeine withdrawal, nitroglycerine challenge, exposure to m-chlorophenylpiperazine, and catastrophic trauma (physical or psychological). [2] The fMRI changes recorded by Schulte et al. [1] do not represent primary pathogenetic changes.
As a pathognomonically lateralizing (unilateral or side-locked) headache, migraine cannot be related to diffuse or bilateral hypothalamic activation. [2] Atenolol is as good a migraine preventive agent as propranolol, but atenolol does not cross the blood-brain barrier, making primary pathogenetic brain neuronal involvement highly unlikely. [2]
1. Schulte LH, Allers A, Arne May. Hypothalamus as a mediator of chronic migraine: Evidence from high-resolution fMRI. Neurology 2017;88:2011-2016.
2. Gupta VK. Adaptive Mechanisms in Migraine: A Comprehensive Synthesis in Evolution - Breaking the Migraine Code. New York: Nova Science Publishers, Inc; 2009.
For disclosures, please contact the editorial office at journal@neurology.org.