#Migraine after effects skin#
25 Skin flare of 6 hours following CGRP injection suggests either slow tissue clearance or prolonged receptor activation.
It has a serum half-life of 7–10 minutes, however the tissue half-life is unknown. 13 It is a blood-brain barrier impermeant neuropeptide that is expressed throughout the nervous system, and in high concentrations in the striatum, amygdala, thalamus, pineal gland, colliculi, trigeminal ganglion, trigeminal nucleus caudalis, cerebellum and cerebral cortex, 24 as well as peripherally in nociceptors and the enteric nervous system. 23ĬGRP is a 37 amino acid peptide with two isoforms (α-CGRP and β-CGRP) which differ by only three amino acids and are encoded by two distinct genes-CALC1 and CALC2 on chromosome 11. 20–22 Its release is triggered by activation of transient receptor potential cation channel subfamily V member 1 and transient receptor potential ankyrin 1 channels, in response to a variety of agonists, as well as by angiotensin and norepinephrine. 6ĬGRP is increased during migraine, dilates blood vessels and is involved in nociceptor signalling. 17 18 Finally, there is wider activation of diencephalic nuclei within the hypothalamus, thalamus and cortex which is thought to contribute to the autonomic, endocrine, cognitive and affective symptoms experienced throughout migraine episodes.
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6 The TCC then has a complex network of ascending connections within the brainstem with other medullary pontine nuclei, midbrain nuclei, the ventrolateral periaqueductal grey and the cuneiform nucleus, leading to activation and subsequent sensitisation of second and third order nociceptive trigeminovascular neurons. 16 The TCC itself has reflex connection with the superior salivatory nucleus, which is stimulated either directly from the brainstem or the dura. Nociceptive signalling from cranio-vascular structures is relayed via the TCC, which has been shown on functional imaging to activate ascending connections to other areas of the brain. 11–14 Furthermore, the lack of a blood brain barrier makes it a potential therapeutic target. 5-hydroxytryptamine (serotonin) receptors are abundant in its neurons and it has higher CGRP-containing fibres and CGRP mRNA than other regions. The trigeminal ganglion, which is involved in pain signalling and vascular dilatation, appears to be a pivotal structure. Disruption of these networks may play a direct role in TCC activation. The second inhibitory network runs from the primary sensory cortex and projects into TCC lamina III and IV. The first arises from the insula and projects to lamina I and II neurons in the TCC and regulates trigeminovascular nociceptive tone. Furthermore, two distinct functional networks that connect the cortex and the trigeminocervical complex (TCC) have been shown with tract tracing. These terminals that innervate the dura contain vasoactive neuropeptides including CGRP, substance P, neurokinin A and pituitary adenylate cyclase-activating peptide (PACAP) which are thought to be released when activated. In patients with aura, cortical spreading depression can act peripherally, activating Panx1 channels which results in sensitisation of afferent trigeminovascular fibres.
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