Article

The neurobiology of migraine.

Handbook of Clinical Neurology 01/2010; 97:99-108. DOI: 10.1016/S0072-9752(10)97007-3
Source: PubMed

ABSTRACT The understanding of migraine has moved well beyond its traditional characterization as a "vascular headache." In considering the basic neurobiology of migraine, it is important to begin with the concept of migraine as not merely a headache, but rather a heterogeneous array of episodic symptoms. Among the array of phenomena experienced by migraine patients are visual disturbances, nausea, cognitive dysfunction, fatigue, and sensitivity to light, sound, smell, and touch. These symptoms may occur independently or in any combination, and in some patients occur even in the absence of headache. The diversity and variability of symptoms experienced by migraine patients belies a complex neurobiology, involving multiple cellular, neurochemical, and neurophysiological processes occurring at multiple neuroanatomical sites. Migraine is a multifaceted neurobiological phenomenon that involves activation of diverse neurochemical and cellular signaling pathways in multiple regions of the brain. Propagated waves of cellular activity in the cortex, possibly involving distinct glial and vascular signaling mechanisms, can occur along with activation of brainstem centers and nociceptive pathways. Whether different brain regions become involved in a linear sequence, or as parallel processes, is uncertain. The modulation of brain signaling by genetic factors, and by sex and sex hormones, provides important clues regarding the fundamental mechanisms by which migraine is initiated and sustained. Each of these mechanisms may represent distinct therapeutic targets for this complex and commonly disabling disorder.

1 Follower
 · 
75 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Migraine is characterised by debilitating pain, which affects the quality of life in affected patients in both the western and the eastern worlds. The purpose of this article is to give a detailed outline of the pathophysiology of migraine pain, which is one of the most confounding pathologies among pain disorders in clinical conditions. We critically evaluate the scientific basis of various theories concerning migraine pathophysiology, and draw insights from brain imaging approaches that have unraveled the prevalence of cortical spreading depression (CSD) in migraine. The findings supporting the role of CSD as a physiological substrate in clinical pain are discussed. We also give an exhaustive overview of brain imaging approaches that have been employed to solve the genesis of migraine pain, and its possible links to the brainstem, the neocortex, genetic endophenotypes, and pathogenetic factors (such as dopaminergic hypersensitivity). Furthermore, a roadmap is proposed to provide a better understanding of pain pathophysiology in migraine, to enable the development of strategies using leads from brain imaging studies for the identification of early biomarkers, efficient prognosis, and treatment planning, which eventually may help in alleviating some of the devastating impact of pain morbidity in patients afflicted with migraine.
    European Journal of Neuroscience 09/2013; DOI:10.1111/ejn.12368 · 3.67 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Migraine symptoms often include auditory discomfort. Nitroglycerin (NTG)-triggered central sensitization (CS) provides a rodent model of migraine, but auditory brainstem pathways have not yet been studied in this example. Our objective was to examine brainstem auditory evoked potentials (BAEPs) in rat CS as a measure of possible auditory abnormalities. We used four subdermal electrodes to record horizontal (h) and vertical (v) dipole channel BAEPs before and after injection of NTG or saline. We measured the peak latencies (PLs), interpeak latencies (IPLs), and amplitudes for detectable waveforms evoked by 8, 16, or 32 KHz auditory stimulation. At 8 KHz stimulation, vertical channel positive PLs of waves 4, 5, and 6 (vP4, vP5, and vP6), and related IPLs from earlier negative or positive peaks (vN1-vP4, vN1-vP5, vN1-vP6; vP3-vP4, vP3-vP6) increased significantly 2 hours after NTG injection compared to the saline group. However, BAEP peak amplitudes at all frequencies, PLs and IPLs from the horizontal channel at all frequencies, and the vertical channel stimulated at 16 and 32 KHz showed no significant/consistent change. For the first time in the rat CS model, we show that BAEP PLs and IPLs ranging from putative bilateral medial superior olivary nuclei (P4) to the more rostral structures such as the medial geniculate body (P6) were prolonged 2 hours after NTG administration. These BAEP alterations could reflect changes in neurotransmitters and/or hypoperfusion in the midbrain. The similarity of our results with previous human studies further validates the rodent CS model for future migraine research.
    Brain research 05/2014; DOI:10.1016/j.brainres.2014.03.033 · 2.83 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study was designed to compare the efficacy of the transpalpebral versus endoscopic approach to decompression of the supraorbital and supratrochlear nerves in patients with frontal migraine headaches. The medical charts of 253 patients who underwent surgery for frontal migraine headaches were reviewed. These patients underwent either transpalpebral nerve decompression (n = 62) or endoscopic nerve decompression (n = 191). Preoperative and 12-month or greater postoperative migraine frequency, duration, and intensity were analyzed to determine the success of the surgeries. Forty-nine of 62 patients (79 percent) in the transpalpebral nerve decompression group and 170 of 191 patients (89 percent) who underwent endoscopic nerve decompression experienced a successful outcome (at least a 50 percent decrease in migraine frequency, duration, or intensity) after 1 year from surgery. Endoscopic nerve decompression had a significantly higher success rate than transpalpebral nerve decompression (p < 0.05). Thirty-two patients (52 percent) in the transpalpebral nerve decompression group and 128 patients (67 percent) who underwent endoscopic nerve decompression observed elimination of migraine headaches. The elimination rate was significantly higher in the endoscopic nerve decompression group than in the transpalpebral nerve decompression group (p < 0.03). Endoscopic nerve decompression was found to be more successful at reducing or eliminating frontal migraine headaches than transpalpebral nerve decompression and should be selected as the first choice whenever it is anatomically feasible. Therapeutic, III.
    Plastic and Reconstructive Surgery 05/2012; 129(5):1113-9. DOI:10.1097/PRS.0b013e31824a2c31 · 3.33 Impact Factor