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Correspondence |

Brainstem Activity in Migraine: Primary or Secondary?

Vinod Kumar Gupta, MBBS, MD
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Copyright 2006 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

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Arch Neurol. 2006;63(9):1347-1347. doi:10.1001/archneur.63.9.1347-a
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Afridi et al1 concluded that activation of the dorsal pons in migraine supports a subcortical site of origin of the disorder. It is simplistic to assume that demonstration of cortical or brainstem activation in patients with migraine through positron emission tomography indicates the primary pathogenetic source.2 More than 5 decades ago, Leão’s3 experiments showed that retinal stimulation can also elicit spreading cortical silence and depression. Second, neuroimaging, however sophisticated, does not record early physiological events in migraine that occur in the prodromal or “preprodromal” periods; although the preprodromal phase is completely subclinical, the prodromal phase is characterized by subtle and protean clinical phenomena.4 Fundamentally, alterations of cerebral circulation or brain activation after onset of migraine aura or headache cannot be construed to reflect primary pathogenetic alterations. Third, inclusion of migraine patients with attacks as frequent as 4 per month1 assumes that cessation of pain indicates return to the basal physiological state by 72 hours; this assumption is erroneous.4 Fourth, Afridi et al1 offer no logical explanation why nonlateralizing ictal brainstem activation should manifest on the right side with brainstem deactivation on the left side regardless of the side of the headache. Fifth, the pathophysiological emphasis on the locus coeruleus1 is debatable; the locus caeruleus (and the dorsal raphe nucleus) does not directly innervate meningeal tissues and its involvement in migraine remains uncertain.5

To unravel the biology of migraine, the limitations of laboratory medicine, including neuroimaging, must be squarely acknowledged. Neuropharmacologically, a large body of available evidence does not support brain or brainstem neuronal origin for migraine.2 ,4 The study of Afridi et al1 clearly demonstrates secondary brainstem stimulation in migraine. There is, however, a wide conceptual gap between ictal brainstem activation/deactivation and primary pathogenetic aberrations in migraine. The obvious disconnect between basic sciences and primary headache research cannot go unaddressed.

AUTHOR INFORMATION

Correspondence: Dr Gupta, Dubai Police Medical Services, PO Box 12005, Dubai, United Arab Emirates (dr_vkgupta@yahoo.com).

REFERENCES

Afridi  SK, Giffin  NJ, Kaube  H.  et al.  A positron emission tomographic study in spontaneous migraine. Arch Neurol 2005;621270- 1275
PubMed
Gupta  VK. Glyceryl trinitrate and migraine: nitric oxide donor precipitating and aborting migrainous aura. J Neurol Neurosurg Psychiatry 2005.;http://jnnp.bmjjournals.com/cgi/eletters/76/8/1158. Accessed on July 17, 2006
Leão  AAP. Spreading depression of activity in the cerebral cortex. J Neurophysiol 1944;7359- 390
Gupta  VK. Migraine, cortical excitability and evoked potentials: a clinico-pharmacological perspective. Brain 2005;128E36
PubMed
Mathiau  P, Escurat  M, Aubineau  P. Immunohistochemical evidence for the absence of central neuron projection to pial blood vessels and dura mater. Neuroscience 1993;52667- 676
PubMed

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Afridi  SK, Giffin  NJ, Kaube  H.  et al.  A positron emission tomographic study in spontaneous migraine. Arch Neurol 2005;621270- 1275
PubMed
Gupta  VK. Glyceryl trinitrate and migraine: nitric oxide donor precipitating and aborting migrainous aura. J Neurol Neurosurg Psychiatry 2005.;http://jnnp.bmjjournals.com/cgi/eletters/76/8/1158. Accessed on July 17, 2006
Leão  AAP. Spreading depression of activity in the cerebral cortex. J Neurophysiol 1944;7359- 390
Gupta  VK. Migraine, cortical excitability and evoked potentials: a clinico-pharmacological perspective. Brain 2005;128E36
PubMed
Mathiau  P, Escurat  M, Aubineau  P. Immunohistochemical evidence for the absence of central neuron projection to pial blood vessels and dura mater. Neuroscience 1993;52667- 676
PubMed

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