Ultrastructural evidence for neurogenically mediated changes in blood vessels of the rat dura mater and tongue following antidromic trigeminal stimulation
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Trigeminal nerve stimulation triggers oral mast cell activation and vascular permeability
2014, Annals of Allergy, Asthma and ImmunologyPsilocybin dose-dependently causes delayed, transient headaches in healthy volunteers
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2010, Handbook of Clinical NeurologyCitation Excerpt :Susceptibility genes for primary headache syndromes is a challenging research area that is likely to help identify specific targets for novel treatment strategies and facilitate our understanding of the interplay between genetic and environmental factors. The trigeminovascular system plays a fundamental role in headache (Ray and Wolff, 1940; Mayberg et al., 1981, 1984) in regard to peripheral sensitization (Strassman et al., 1996) and neurogenic inflammation in the meninges (Dimitriadou et al., 1992; Johnson and Bolay, 2006), and is also a predominant site of action for pharmaceutical agents such as triptans, ergots, neuropeptide antagonists, and non-steroidal anti-inflammatory drugs (NSAIDs) (Buzzi et al., 1989, 1992; Kaube et al., 1993; Durham and Russo, 2002). Recent findings suggest that synaptic transmission between primary sensory trigeminal ganglia neurons and trigeminal nucleus caudalis (TNC) neurons within the brainstem is a primary target of triptans and calcitonin gene-related peptide (CGRP) antagonists (Levy et al., 2004, 2005).
Migraine: General aspects
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