The Sphenopalatine Ganglion Block was first utilized in 1908 by Greenfield Sluder to treat Sluder's Neuralgia which is now thought to be Cluster Headaches or Combination of Autonomic Cephalgia and TMD particularly the Myofascial Pain and Dysfunction. In 1929 Hyram Byrd and his brother published a study on 10,000 SPG Blocks in 2000 patients for a wide rannger of disorders with great success and NO NEGATIVE SIDE EFFECTS.
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Dr. Ira Shapira, a neuromuscular dentist in Highland Park, Illinois, is known for teaching patients how to self-administer Sphenopalatine Ganglion (SPG) blocks. He trains both patients and dentists in this technique. Dr. Shapira's website, I Hate Headaches, and his practice, Think Better Life, are resources for learning more about SPG blocks and self-administration.
Galcanezumab reduces trigeminal nociception and is effective in preclinical models of migraine and trigeminal autonomic cephalalgia
Abstract
Objectives/background: This study was undertaken to assess the therapeutic efficacy of galcanezumab in preclinical models of migraine and cluster headache and to determine potential shared trigeminovascular mechanisms of action. Galcanezumab is a humanized monoclonal antibody that binds to the neuropeptide calcitonin gene-related peptide, preventing its biological activity. It has been approved as a preventive treatment for both episodic and chronic migraine and episodic cluster headache, the most common trigeminal autonomic cephalalgia.
Methods: Trigeminovascular and trigeminal-autonomic reflex activation was evoked via electrical stimulation of the dura mater or superior salivatory nucleus (SSN), respectively. Evoked responses were recorded in the spinal trigeminal nucleus along with ongoing spontaneous neuronal and cutaneous noxious-evoked and non-noxious-evoked neuronal activity. Rats received either galcanezumab or human control IgG, and responses were compared between groups.
Results: Galcanezumab robustly reduced spontaneous (maximum decrease in dural-evoked: 73% [±3.5] at 4 h 30 min [p = 0.002]; in SSN-evoked: 67% [±10.7] at 4 h [p = 0.01]) and cutaneous non-noxious-evoked (maximum decrease in dural-evoked: 50% [±5.7], p = 0.004; in SSN-evoked: 47% [±10.5], p = 0.005, at the last recording time point) neuronal activation in the trigeminocervical complex, highlighting a general inhibition of trigeminal sensory processing. Furthermore, it significantly inhibited cutaneous noxious-evoked (maximum decrease in dural-evoked: 38% [±5.2], p = 0.005; in SSN-evoked: 34% [±7.6], p = 0.005, at the last recording time point), durovascular-evoked (maximum decrease 48% [±6] at the last recording time point, p = 0.001), and SSN-evoked responses (maximum decrease: 32% [±2.6] at 4 h, p < 0.001), demonstrating a clear reduction of trigeminal nociception, independent of the mode of activation. Galcanezumab did not have any effect on the mean arterial blood pressure.
Conclusion: Galcanezumab likely acts via a shared trigeminovascular mechanism to dampen noxious and nonnoxious sensory stimuli in preclinical models of migraine and trigeminal autonomic cephalalgias. This further supports the clinical efficacy of galcanezumab for migraine and cluster headache, while demonstrating general inhibition that may be of relevance to other facial pain conditions.
Keywords: cluster headache; galcanezumab; migraine; trigeminal nociceptive processing; trigeminovascular system.
© 2025 The Author(s). Headache: The Journal of Head and Face Pain published by Wiley Periodicals LLC on behalf of American Headache Society.