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

Two unusual cases of vascular headache, one caused by jugular venous compression from a goiter and one triggered by flushing associated with a CGRP-producing renal tumour, are reported. Their histories are compared with those experiencing other headaches of vascular origin. Two patients with a primary neural irritative lesion, one with a sphenoid sinus carcinoma and one with Tolosa-Hunt syndrome, presented with headaches resembling migraine. These case-histories are used to illustrate the interaction of nervous system and vascular system in the production of headache which has implications for the pathophysiology of migraine and cluster headache.
Headache 1991 Jul
PMID:Solved and unsolved headache problems. 177 58

1. Human alpha calcitonin gene-related peptide (h alpha CGRP) is a potent vasodilator which in doses up to 1.5 micrograms min-1 i.v. produces little or no fall in blood pressure in normal volunteers, but does cause a substantial tachycardia. 2. We have explored the underlying mechanism of this effect by comparing h alpha CGRP infused so as to maintain heart rate 25-30% above baseline with glyceryl trinitrate (GTN) in a dose sufficient to maintain a throbbing headache. 3. Ten normal volunteers were studied. In addition to blood pressure and heart rate, blood velocity and pulsatility index (PI) were determined from Doppler signals recorded from the internal and external carotid, renal and femoral arteries. 4. Following h alpha CGRP blood pressure (mean +/- s.d., mm Hg) did not significantly change: 120 +/- 10/70 +/- 7 before compared with 121 +/- 12/67 +/- 7 during h alpha CGRP infusion. Heart rate (mean +/- s.d., beats min-1) increased from 62 +/- 8 to 86 +/- 10 (P less than 0.0001). In contrast the blood pressure fell following GTN: 124 +/- 12/74 +/- 8 before compared with 111 +/- 13/62 +/- 6 following treatment (P less than 0.02). Heart rate did not change following GTN: 64 +/- 9 compared with 69 +/- 10. 5. GTN significantly increased PI (mean +/- s.d.) in the common carotid artery from 2.8 +/- 0.5 to 3.4 +/- 0.5 (P less than 0.003) while h alpha CGRP increased PI in the internal carotid from 1.3 +/- 0.2 to 2.1 +/- 0.4 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the effects of human alpha calcitonin gene-related peptide and glyceryl trinitrate on regional blood velocity in man. 252 83

Hyperreflectory rhinopathy (HR) is a non-specific hyperreactivity of the nasal mucosa. It causes hypersecretion, decreased nasal patency, sneezing and sometimes headache by local reflexes, which are beyond voluntary control. The synonymous name "vasomotor rhinitis" or "vasomotor rhinopathy" is no longer adequate with regard to our present state of knowledge of the autonomous innervation of the human nasal mucosa. Recent pharmacological investigations show the great importance of peptidergic neurons. In our own studies, the presence and the topical effects of the neuropeptide substance-P in human nasal mucosa are examined. A new concept of the autonomous innervation of the human nasal mucosa is presented. Apart from adrenergic and cholinergic neurons, it also includes peptidergic neurons (SP, CGRP, NKA, VIP, PHI, APP, GRP). According to this model, a hypothesis on the pathogenesis of HR is developed. A key position is occupied by the so-called "axon reflex" which is mediated by substance-P immunoreactive nerve fibers. It is released by a chemical, thermal or mechanical irritation. This axon reflex mediates pain, vasodilation and plasma extravasation (neurogenic oedema), hypersecretion such as smooth muscle contraction, and sneezing reflex. Capsaicin (8-methyl-N-vanillyl-6-nonenamid) leads to a selective degeneration of substance-P immunoreactive nerve fibres and desensitisation of its receptors after repeated topical or systemic application, thus blocking the axon reflex. The risk-free application of capsaicin was shown in self-experiments and in volunteers. Our hypothesis was confirmed by the good results of the treatment of a group of volunteer patients who suffered from HR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[New aspects in the pathogenesis and therapy of hyperreflexive rhinopathy]. 305 Mar 40

Capsaicin, when repeatedly applied to the nasal mucosa of cluster headache patients, has been shown to prevent the occurrence of pain attacks. In order to investigate the mechanism of the drug's action, we evaluated the effect of repeated nasal application of capsaicin on the contents of sensory fibres immunoreactive to substance P and CGRP in the rat nasal mucosa. Further, considering the possible involvement of the cerebral circulation, we verified the effect of a single application of capsaicin on the blood flow velocity of the internal carotid and middle cerebral arteries (of both sides) and the basilar artery, in a group of healthy humans. The measurements were taken using Doppler devices. In order to verify the reproducibility of therapeutic effect of capsaicin, we carried out a 2-year follow-up study on patients affected by cluster headache (17 by episodic form, 8 by chronic form) who responded positively to the first treatment with capsaicin. During this period they were treated again with capsaicin in case of re-occurrence of symptoms. Capsaicin depletes the fibers immunoreactive to substance P and CGRP in the rat nasal mucosa. In the healthy controls, a single application induced vasodilation in the internal carotid, whereas middle cerebral arteries and basilar artery were narrowed. The results of the follow-up study, demonstrates that in 65% of the patients, the beneficial effect of capsaicin was again present when the treatment was repeated. In the chronic patients the therapeutic effect was always transitory (lasting, at maximum one month).(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1994 Mar
PMID:"Capsaicin-sensitive" sensory neurons in cluster headache: pathophysiological aspects and therapeutic indication. 751 83

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

Human nasal mucosa biopsy samples were studied by biochemical and histological methods to determine whether the concentration of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) as a marker of sensory nerves was dependent on the activity of neutral endopeptidase-like enzyme (NEP-LE). Mucosal samples from the middle turbinate were obtained from 32 patients undergoing functional endoscopic nasal surgery for non-allergic chronic rhinosinusitis. The degree of symptoms related to nasal obstruction, rhinorrhea and headaches was recorded. The number of inflammatory cells in each biopsy sample was evaluated by conventional histopathological examination. CGRP-LI was measured by radioimmunoassay. The activity of NEP-LE was evaluated in vitro using [3H] Leu5-enkephalin as substrate. A good correlation was observed between increased concentrations of CGRP, abundant inflammatory cells and the intensity of symptoms (R2 = 0.80). A low activity of NEP-LE was associated with a high concentration of both inflammatory cells and CGRP, suggesting that NEP-LE activity was reduced during inflammation. These observations further support the hypothesis that reduced degradation of sensory neuropeptides could be involved in the pathophysiological mechanisms of non-specific chronic rhinosinusitis.
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PMID:Neutral endopeptidase activity and concentration of sensory neuropeptide in the human nasal mucosa. 871 87

This study describes a novel intravital microscope technique for direct measurement of dural blood vessel diameter through a closed cranial window in anaesthetized rats. This technique avoids removal of the skull, which can lead to problems of altered vessel reactivity and brain swelling that are encountered with open cranial window techniques. Substance P and calcitonin gene-related (CGRP) evoked increases in dural vessel diameter, which were abolished by the NK1 receptor antagonist, RP67580 and the CGRP receptor antagonist, human-alpha CGRP(8-37) respectively. Neurokinin A produced increases in dural vessel diameter which were unaffected by the NK2 receptor antagonist SR 48968 but were blocked by RP67580, suggesting that neurokinin A can act through NK1 receptors to produce dural vasodilation in rats. The NK3 receptor agonist, senktide, had no effects on dural vessel diameter. All drugs were administered intravenously. In humans, vasodilation within the meningeal vasculature has been implicated in the pathogenesis of migraine, the present experiments indicate that substance P or neurokinin A (both acting through NK1 receptors) or CGRP may be responsible.
Cephalalgia 1997 Jun
PMID:Intravital microscope studies on the effects of neurokinin agonists and calcitonin gene-related peptide on dural vessel diameter in the anaesthetized rat. 920 73

This study used intravital microscopy to measure the diameter of dural arteries in anaesthetized rats. Electrical stimulation of the surface of a closed cranial window produced increases in dural vessel diameter which were blocked by the CGRP receptor antagonist human-alpha CGRP(8-37) but unaffected by the NK1 receptor antagonist RP67580. Sumatriptan (3 and 10 mg kg-1, i.v.) significantly reduced the response to electrical stimulation. In contrast, sumatriptan (3 mg kg-1) had no effects on the response to exogenously administered CGRP. These results indicate that neurokinins play no role in neurogenic vasodilation in this preparation and that neurogenic vasodilation in rat dural vessels is mediated predominantly by CGRP. Furthermore, the data indicate that sumatriptan attenuates neurogenic vasodilation, probably by inhibiting the release of CGRP from perivascular trigeminal nerve endings innervating the dura. These experimental data parallel the clinical findings that CGRP levels are elevated in migraine and normalized, concomitantly with headache relief, by sumatriptan.
Cephalalgia 1997 Jun
PMID:Sumatriptan inhibits neurogenic vasodilation of dural blood vessels in the anaesthetized rat--intravital microscope studies. 920 74

1. Migraine headache pain is thought to result from an abnormal distention of intracranial, extracerebral blood vessels and the consequent activation of the trigeminal nervous system. Migraine is also often accompanied by extracranial sensory disturbances from facial tissues. These experiments investigate whether meningeal dilation produces central sensitization of neurones that receive convergent input from the face. 2. Single unit extracellular activity was recorded from the trigeminal nucleus caudalis of anaesthetized rats in response to either noxious stimulation of the dura mater, innocuous stimulation of the vibrissae or to a transient dilation of the meningeal vascular bed. 3. Rat alpha-CGRP (calcitonin gene-related peptide; 1 microg kg(-1), i.v.) caused a dilation of the middle meningeal artery and facilitated vibrissal responses by 36+/-7%. 4. The 5-HT1B/1D agonist, L-741,604 (3 mg kg(-1), i.v.), inhibited responses to noxious stimulation of the dura mater (16+/-7% of control) and, in a separate group of animals, blocked the CGRP-evoked facilitation of vibrissal responses. 5. L-741,604 (3 mg kg(-1), i.v.) also inhibited responses to innocuous stimulation of the vibrissa (14+/-10% of control) with neurones that received convergent input from the face and from the dura mater, but not with cells that received input only from the face (70+/-12% of control). 6. These data show that dilation of meningeal blood vessels causes a sensitization of central trigeminal neurones and a facilitation of facial sensory processing which was blocked by activation of pre-synaptic 5-HT1B/1D receptors. 7. Sustained dural blood vessel dilation during migraine may cause a sensitization of trigeminal neurones. This may underlie some of the symptoms of migraine, such as the headache pain and the extracranial allodynia. Inhibition of this central sensitization may therefore offer a novel strategy for the development of acute and/or prophylactic anti-migraine therapies.
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PMID:Dural vasodilation causes a sensitization of rat caudal trigeminal neurones in vivo that is blocked by a 5-HT1B/1D agonist. 1021 43

The meninges of the brain are innervated by afferent nerve fibres containing SP and CGRP, two typical peptides found in sensory neurons. These fibres project to the trigeminal nuclear complex and the cervical dorsal horn. Discharge of the afferents may provide a physiological basis for some types of headaches. Considerable speculation surrounds the possible causes of meningeal afferent activation. Blood-borne substances released during subarachnoid haemorrhage are one possibility and there is a possibility that these also play a role in migraine. In the case of migraine, blood components, e.g. from platelets, cannot be excluded. To investigate the possible effects of platelets and plasma factors, the subarachnoid space of the rat was continuously perfused with artificial cerebrospinal fluid during extracellular recordings from single units of the caudal trigeminal nucleus. Washed and concentrated suspensions of adenosindiphosphate (ADP)--activated platelets and plasma, from which platelets had been removed--were introduced as a bolus into the continuous flow. Neurons in the caudal nucleus of the trigeminal complex receiving input from the meninges were stimulated. They did not respond to the activated platelet suspensions but showed intense responses to plasma. Plasma completely lost its ability to excite trigeminal neurons after heat inactivation (30 min, 56 degrees C). It is concluded that the complement system may be involved in the excitatory nociceptive effect of platelet-poor plasma.
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PMID:Nociceptive neurons in the rat caudal trigeminal nucleus respond to blood plasma perfusion of the subarachnoid space: the involvement of complement. 1043 15


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