The alteration of extracranial blood flow in conjunction with clinical signs of autonomic nervous system dysfunction have led to various explanations concerning the pathophysiology of migraine headache. Reflex sympathetic dystrophy, a painful disorder of the sympathetic nervous system, can be treated by blocking the sympathetic nerves located in the stellate ganglion, resulting in vasodilation, ptosis, miosis, and anhydrosis. In theory, these changes could trigger a migraine headache attack secondary to autonomic dysfunction reflecting an imbalance between sympathetic and parasympathetic nervous systems. This may be especially true in a patient with a previous history of meningitis that may have resulted in a disorder of cerebrovascular regulation. We report a 56-year-old man with no previous history of migraine who developed migraine with aura after a stellate ganglion block. These episodic headaches occurred with decreasing frequency and severity for over 6 months, with eventual complete resolution. This interesting phenomenon has not been reported in the English literature and may help to better understand the pathophysiology of migraine.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1046/j.1526-4610.1996.3605335.x | DOI Listing |
Brain
January 2025
Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
The neurobiological mechanisms driving the ictal-interictal fluctuations and the chronification of migraine remain elusive. We aimed to construct a composite genetic-microRNA model that could reflect the dynamic perturbations of the disease course and inform the pathogenesis of migraine. We prospectively recruited four groups of participants, including interictal episodic migraine (i.
View Article and Find Full Text PDFHeadache
January 2025
Section of Clinical Pharmacology and Oncology, Department of Health Sciences, University of Florence, Florence, Italy.
Antibodies targeting either the calcitonin gene-related peptide (CGRP), such as galcanezumab, fremanezumab, and eptinezumab, or the receptor (erenumab) have been approved for the prevention of episodic and chronic migraine. Although widely used and generally effective, a proportion of patients discontinue treatment due to lack of efficacy. In both randomized controlled trials and observational studies, all anti-CGRP monoclonal antibodies (mAbs) have consistently demonstrated comparable efficacy and tolerability, suggesting a pharmacological class effect.
View Article and Find Full Text PDFJ Headache Pain
January 2025
Department of Neurology, The David Geffen School of Medicine at UCLA, Los Angeles, USA.
Background: Migraine progression, particularly from episodic to chronic migraine (CM), increases disease burden and healthcare costs. Understanding the new concept of "Medication Underuse Headache" should encourage the health care provider to consider early intervention with calcitonin gene-related peptide (CGRP) monoclonal antibodies. Galcanezumab given early in the course of the disease, may prevent migraine chronification and have a robust response, moreso than when initiated in later stages of migraine.
View Article and Find Full Text PDFJ Clin Neurosci
January 2025
Family and Community Medicine Department, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Background: Migraine is a common primary headache disorder that significantly affects academic life and is often associated with stress, depression, anxiety, and irregular sleep patterns among university students. This study aimed to assess the prevalence of migraine among King Khalid University (KKU) students, identify its determinants, and evaluate the impact of migraine and other headaches on academic life and performance.
Methods: An analytical cross-sectional study was conducted among 732 students from Colleges of Medicine, Pharmacy, Engineering, and Computer science.
Brain
January 2025
Institute of Neurological Sciences and Psychiatry, Hacettepe University, 06100, Ankara, Turkey.
Cortical spreading depolarization (CSD), the neurophysiological event believed to underlie aura, may trigger migraine headaches through inflammatory signaling that originates in neurons and spreads to the meninges via astrocytes. Increasing evidence from studies on rodents and migraine patients supports this hypothesis. The transition from pro-inflammatory to anti-inflammatory mechanisms is crucial for resolving inflammation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!