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Headache
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Oral sumatriptan is more effective than conventional treatment with aspirin and metoclopramide or oral ergotamine plus caffeine, particularly in the second and third attacks, suggesting greater consistency for sumatriptan. Recurrence of headache occurs within 24–48 hours in about one-third of responders to sumatriptan (and any other acute antimigraine drug). Repeated drug administration is usually effective, but the headache may recur again. Recurrence can be reduced by about one-third by the coadministration of naproxen 500 mg.26
Medications
Published in R. Andrew Chambers, The 2 × 4 Model, 2017
Topiramate is an anticonvulsant/antimigraine drug that in parallel to bupropion, may also represent a bonafide, PDDA, given the reasonably strong evidence that it has efficacy as both a mood stabilizer and an anti-addiction medication. However, the drug still lacks FDA indications for psychiatric or addiction indications. The mechanism of action of the drug is quite complex and incompletely understood but seems to modulate both glutamatergic and GABAergic neurotransmission with activities involving calcium channels (transmitter release) and sodium channels (action potential propagation). The anti-addiction properties of the drug may extend to alcohol and psychostimulant addiction, and possibly behavioral addictions such as compulsive eating, where it does have FDA approved efficacy, as a component of weight loss medication.
Other Central Nervous System Diseases and Disorders
Published in Divya Vohora, The Third Histamine Receptor, 2008
Paul L. Chazot, Fiona C. Shenton
Current drug treatment for migraine headaches includes nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen, the ergot dihydroergotamine (DHE) and the 5-HT1D agonist, sumatriptan. NSAIDs inhibit prostaglandin synthesis and attenuate neurogenic inflammation in the trigeminovascular system. However, NSAIDs are ineffective for many migraine patients and are associated with the risk of dyspepsia and gastrointestinal hemorrhage. DHE is associated with nausea, vomiting, abdominal pain, diarrhea, and cerebral vasoconstriction. Side effects associated with sumatriptan are coronary vasospasm and chest heaviness (reviewed in Ref. 40). Furthermore, both DHE and sumatriptan are significantly less active in humans after oral administration. Newer 5-HT1D agonists are available (e.g., Eletriptan and Almotriptan). These drugs are orally active and are more potent than sumatriptan; however, the pharmacology of these second-generation sumatriptanlike drugs does not exclude potential cardiovascular effects. In light of these therapeutic limitations, an antimigraine drug that demonstrates oral efficacy without the cardiovascular liability of current therapies is still required.
A critical review of the neurovascular nature of migraine and the main mechanisms of action of prophylactic antimigraine medications
Published in Expert Review of Neurotherapeutics, 2021
Bruno A. Marichal-Cancino, Abimael González-Hernández, Raquel Guerrero-Alba, Roberto Medina-Santillán, Carlos M. Villalón
Based on these seminal findings, other lines of evidence suggest that acute antimigraine drugs, such as sumatriptan, dihydroergotamine and rizatriptan can inhibit the cranial NV produced by trigeminal release of CGRP [123–127]. Likewise, and most importantly within the context of the present review, the prophylactic antimigraine drug BOTOX decreases interictal CGRP plasma levels in patients with chronic migraine [128]. In keeping with these findings, other lines of clinical and preclinical research have shown that BOTOX: (i) decreases plasma levels of CGRP in patients with trigeminal neuralgia [129] or chronic migraine [128]; (ii) inhibits mechanical allodynia, inflammatory cell infiltration and the increase in CGRP levels in cranial dura (an indicator of trigeminal activation) in a rat model of trigeminal pain [130]; (iii) cleaves SNAP-25 (which colocalizes with CGRP), resulting in inhibition of CGRP release [130]; and (iv) is transported axonally (when injected peripherally) to the trigeminal ganglion and, by transcytosis, reaches the CGRP-containing dural nerve endings [130]. Hence, inhibition of cranial NV is also a plausible mechanism of action of prophylactic antimigraine medications.
Pharmacological strategies to treat attacks of episodic migraine in adults
Published in Expert Opinion on Pharmacotherapy, 2021
The Atlas of Headache Disorders, prepared by WHO in collaboration with Lifting The Burden: the Global Campaign against Headache, presents data collected in a questionnaire from a survey in 101 countries [6]. ‘For treatment of acute episodic migraine, other NSAID s (than aspirin) are, as a class, the most widely preferred drugs (86% of countries that responded). Paracetamol (69%) and aspirin (52%) follow.’ [6] ‘Globally, the equally-preferred specific anti-migraine drugs are ergotamine (34% of countries that responded) and sumatriptan (33%).’ [6] Ergotamine was preferred in all regions but Europe and the Western Pacific, where sumatriptan leads (with four-fold preference in Europe) [6]. Even in region in which sumatriptan is the preferred specific antimigraine drug triptans are only used by a minority of patients with episodic migraine. In the United States, it is 18% of these patients who actually use a triptan [7], and in 10 European countries, 3% to 11% of migraine patients actually use a triptan (an outlier is Spain with 22% of patients using a triptan) [8].
Almotriptan: a review of 20 years’ clinical experience
Published in Expert Review of Neurotherapeutics, 2019
The genetic determinants of drug response in migraine are complex; however, several polymorphisms associated with antimigraine drug metabolizing enzymes have been identified [94]. It is possible that in the future, pharmacogenetic considerations could help guide the selection of triptans for a number of individual patients. The variety of pathways involved in the metabolism of ALT may make it less susceptible to genomic variations between patients [95].