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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nerve fibres containing noradrenaline, acetylcholinesterase, vasoactive intestinal polypeptide and substance P were demonstrated in the dura mater of guinea-pigs using histochemical and immunohistochemical methods. These fibres accompanied blood vessels of all size, indicating a vasomotor role. In addition, some nerve fibres were observed without any obvious relation to the blood vessels. The rich supply of nerve fibres to the various parts of the dura mater may possibly be of importance in the pathogenesis of some types of headache.
Cephalalgia 1981 Dec
PMID:Adrenergic, cholinergic and peptidergic nerve fibres in dura mater--involvement in headache? 618 93

Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. In this study patients with episodic cluster headache fulfilling the criteria of the International Headache Society were examined during an acute spontaneous attack of headache to determine the local cranial release of neuropeptides. Blood was sampled from the external jugular vein ipsilateral to the pain before and after treatment of the attack. Samples were assayed for calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), substance P and neuropeptide Y. Attacks were treated with either oxygen inhalation, sumatriptan or an opiate. Thirteen patients were studied of whom 10 were male and three female. All had well-established typical attacks of cluster headache when blood was sampled. During the attacks external jugular vein blood levels of CGRP and VIP were raised while there was no change in neuropeptide Y or substance P. Calcitonin gene-related peptide levels rose to 110 +/- 7 pmol/l (normal: < 40) while VIP levels rose to 20 +/- 3 pmol/l (normal: < 7). Treatment with both oxygen and subcutaneous sumatriptan reduced the CGRP level to normal, while opiate administration did not alter the peptide levels. These data demonstrate for the first time in vivo human evidence for activation of the trigeminovascular system and the cranial parasympathetic nervous system in an acute attack of cluster headache. Furthermore, it is shown that both oxygen and sumatriptan abort the attacks and terminate activity in the trigeminovascular system.
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PMID:Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies. 751 21

Capsaicin was applied unilaterally to the nostril mucosa of 18 episodic cluster headache sufferers in remission. Plasma and saliva levels of substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay. Increase of salivary SP-LI and CGRP-LI as well as of plasma CGRP-LI occurred after capsaicin stimulation. Capsaicin-induced neurochemical changes in saliva and in plasma were compared to the changes observed during cluster headache attacks measured in a separate study. The comparative changes in SP, CGRP and VIP characterizing these two conditions suggest that trigeminal capsaicin-sensitive sensory neurones are unlikely to play any fundamental role in the mechanics of cluster headache.
Cephalalgia 1994 Apr
PMID:Nostril capsaicin application as a model of trigeminal primary sensory neuronal activation. 752 Mar 65

A rich supply of nerve fibers containing neuropeptide Y-like (NPY-LI) and tyrosine hydroxylase-like immunoreactivity was seen in human cerebral arteries, arterioles and veins. Only a sparse supply of vasoactive intestinal polypeptide (VIP-LI), substance P (SP-LI), and calcitonin gene-related peptide (CGRP-LI) was demonstrated in the walls of human cerebral vessels. In isolated ring segments of human cerebral arteries, NPY and noradrenaline caused vasoconstriction but did not potentiate each other. VIP, peptide histidine methionine, SP, neurokinin A, and CGRP relaxed arteries precontracted by prostaglandin F2 alpha. The degree of innervation and the vasomotor responses are discussed in relation to migraine pathophysiology.
Cephalalgia 1994 Apr
PMID:Demonstration of neuropeptide containing nerves and vasomotor responses to perivascular peptides in human cerebral arteries. 752 Mar 66

An unusual pheochromocytoma was incidentally discovered in a 48-year-old woman. The patient had a 3-year history of myasthenia gravis. At the time of examination in our hospital, the right adrenal tumor was incidentally discovered by ultrasonography of the abdomen. She had no history of headache, perspiration, palpitation or hypertension. Although blood catecholamine levels were within the normal limits, urinary secretion of catecholamine was elevated. Histologically, the tumor was diagnosed to be mixed ganglioneuroma/pheochromocytoma and histochemically confirmed to produce vasoactive intestinal polypeptide. Such a tumor is quite rare.
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PMID:Silent mixed ganglioneuroma/pheochromocytoma which produces a vasoactive intestinal polypeptide. 849 50

Chronic paroxysmal hemicrania (CPH) is a rare headache syndrome of short-lasting attacks of pain, characterized clinically by trigemino-parasympathetic activation. The features of the headache are severe attacks of pain that generally last no more than minutes in association with autonomic activation, such as lacrimation or rhinorrhea. We report a patient fulfilling International Headache Society guidelines for the diagnosis of CPH in whom levels of calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were elevated in the cranial circulation during attacks. Moreover, successful treatment of the problem with indomethacin leads to normalization of the levels of both CGRP and VIP. Given that similar neuropeptide changes are seen in cluster headache the data suggest a shared underlying pathophysiology between CPH and cluster headache.
Cephalalgia 1996 Oct
PMID:Neuropeptide changes in a case of chronic paroxysmal hemicrania--evidence for trigemino-parasympathetic activation. 890 56

Animal and human studies have shown that substance P (SP), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) are involved in the pathophysiology of acute and chronic pain conditions. The primary aim of the present study was to compare plasma levels of SP, NPY and VIP in external jugular vein between patients with chronic tension-type headache and healthy controls. The secondary aim was to examine plasma levels of these neuropeptides in relation to headache state. In addition, we wanted to study the relation between cranial circulation (jugular vein) and peripheral circulation (antecubital vein). Blood from the external jugular and antecubital vein was drawn from 20 patients with chronic tension-type headache and 20 healthy controls. Plasma SP in patients, 2.0 (1.4-2.2) pmol/l, did not differ significantly from plasma SP in controls, 1.7 (1.1-2.1) pmol/l, (P=0.44). No significant differences were found between SP levels on days with headache, 1.5 (0.3-1.7) pmol/l, and SP levels on days without headache, 1.7 (1.1-1. 9) pmol/l, (P=0.06). Plasma NPY in patients, 118+/-3 pmol/l, did not differ significantly from plasma NPY in controls, 113+/-5 pmol/l, (P=0.40). There was no difference between NPY levels on days with headache, 120+/-3 pmol/l, and on days without headache, 118+/-3 pmol/l, (P=0.73). VIP levels in patients, 6 (4-7) pmol/l, did not differ significantly from VIP levels in controls, 5 (5-7) pmol/l, (P=0.50). No significant differences were found between VIP levels measured on days with headache, 5 (4-6) pmol/l, and VIP levels measured on days without headache, 6 (4-7) pmol/l, (P=0.81). Plasma levels of SP, NPY and VIP did not significantly differ between the peripheral and the cranial circulation neither in patients nor in controls (0.05). In summary, the present study indicates that plasma levels of SP, NPY and VIP are normal in chronic tension-type headache patients and largely unrelated to headache state.
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PMID:Plasma levels of substance P, neuropeptide Y and vasoactive intestinal polypeptide in patients with chronic tension-type headache. 1056 63

Evidence from animals and humans suggests that brainstem nuclei such as the raphe nuclei, the locus coeruleus (LC) and the periaqueductal grey matter (PAG), are involved in the pathophysiology of migraine. In order to understand possible neurotransmitters involved we have, by means of indirect immunocytochemistry, analysed these regions for the occurrence and distribution of calcitonin gene-related peptide (CGRP), substance P (SP), pituitary adenylate-cyclase activating peptide (PACAP) and vasoactive intestinal polypeptide (VIP). CGRP-immunoreactive (-ir) cell bodies, but no fibres, were found to occur in high numbers, constituting 80% of all nerve cell bodies in the LC. A smaller number of these nerve cell bodies (40%) in the LC proved to be PACAP-ir. The LC neurones also stored the vesicular monoamine transporter (VMAT)- and the C-terminal flanking peptide of neuropeptide Y (C-PON)-ir, illustrating their adrenergic nature. Double immunostaining revealed that all VMAT-and C-PON-containing neurones, in addition, stored CGRP. Immunoreactive cell bodies were not seen in the nucleus raphe magnus (NRM) or PAG. Numerous SP-ir nerve fibres were observed in the NRM, the LC and the PAG. Few PACAP-ir nerve fibres were detected in the PAG and few VIP-ir nerve fibres were seen in the NRM and the PAG.
Cephalalgia 2001 Mar
PMID:Neuropeptide localization in the "migraine generator" region of the human brainstem. 1142 90

Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0.01-1 mm) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre-administration of hexamethonium chloride (20 mg/kg). The evoked increases in dural blood flow were also abolished by topical pre-administration of atropine (1 mm) and [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (0.1 mm), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino-parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.
Cephalalgia 2004 Mar
PMID:Noxious chemical stimulation of rat facial mucosa increases intracranial blood flow through a trigemino-parasympathetic reflex--an experimental model for vascular dysfunctions in cluster headache. 1500 14

Lacrimation and nasal secretion during attacks of cluster headache appear to be due to massive trigeminal-parasympathetic discharge. In addition, the presence of oculo-sympathetic deficit and loss of thermoregulatory sweating and flushing on the symptomatic side of the forehead indicate that the cervical sympathetic pathway to the face is injured in a subgroup of cluster headache patients. In this review, it is argued that a peripheral rather than a central lesion produces signs of cervical sympathetic deficit, probably resulting from compression of the sympathetic plexus around the internal carotid artery. Although trigeminal-parasympathetic discharge appears to be the main trigger for vasodilation during attacks, supersensitivity to neurotransmitters such as vasoactive intestinal polypeptide, together with release of sympathetic vasoconstrictor tone, may boost facial blood flow in patients with cervical sympathetic deficit. In addition, parasympathetic neural discharge may provoke aberrant facial sweating during attacks in patients with cervical sympathetic deficit. Although neither trigeminal-parasympathetic discharge nor cervical sympathetic deficit appears to be the primary trigger for attacks of cluster headache, these autonomic disturbances could contribute to the rapid escalation of pain once the attack begins. For example, a pericarotid inflammatory process that excites trigeminal nociceptors might initiate neurogenic inflammation and trigeminal-parasympathetic vasodilation. To complete the loop, neurogenic inflammation and trigeminal-parasympathetic vasodilation could provoke the release of mast cell products, which aggravate inflammation and intensify trigeminal discharge.
Cephalalgia 2006 Jun
PMID:Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache. 1668 2


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