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

A case of Paget's disease in an elderly female who had a favourable evolution following ventriculoperitoneal (V-P) shunt is reported. On May 28, 1983, a 52-year-old female was transferred and admitted to us from the Dept. of Neurology because of headache in the occipital region and ataxic gait. On admission, neurological examinations revealed remarkably increased tendon reflexes, ataxic gait, and mild dementia. Headache was also observed, but urinary incontinence was not present. Skull X-ray showed "cotton wool appearance", which was characteristic of Paget's disease. On chemical analysis of blood and urine, serum Al-P and urinary OH-proline level were elevated, which established a diagnosis of Paget's disease. Triventricular dilatation was found on CT scan, and neck tomography showed basilar impression. After admission, the patient was treated with calcitonin, but it was interrupted because of side effects such as nausea and vomiting. Then she gradually took a turn for the worse, particularly dementia became severer. On July 25, 1983, V-P shunt was performed. After operation, "soft landing maneuver" was employed, namely the intraventricular pressure was checked and was gradually lowered with external CSF drainage system for 7 days. Thereafter the patient's head was elevated gradually from supine to sitting position through 7 days. Her hospital course after operation was that of gradual improvement. The purpose of this maneuver was to prevent sudden change of intraventricular pressure that causes aggravation of basilar impression and sudden respiratory arrest.
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PMID:[Hydrocephalus in Paget's disease--a case report]. 374 85

In eight patients carotid angiography was required for evaluation of transient neurological attacks. Cerebral blood flow results, angiography and clinical observations subsequently suggested the diagnosis of migraine. We measured plasma concentrations of substance P(SP), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) in repeated blood samples obtained from the carotid artery and the internal jugular vein in conjunction with cerebral angiography followed by 4 to 6 repeated recordings of regional cerebral blood flow (rCBF) with the intracarotid Xenon-133 injection technique. This technique is known to induce attacks of migraine with aura in many sufferers. Four patients developed aura symptoms. In three this was succeeded by throbbing headache. Typical, migraine-related, focal hypoperfusion occurred in conjunction with the aura symptoms. The remaining four patients had no symptoms or rCBF changes. There were no systematic or statistically significant changes over time in arterial-venous plasma concentrations or in the release rates of any of the peptides. All migraineurs had an overall elevated mean CGRP value compared to control values from the literature. The overall plasma levels of the potent vasoconstrictor NPY were higher (p < 0.10) in the group that developed symptoms and rCBF changes (136 pmol/l) than in the non-symptomatic group (97 pmol/l). The difference in NPY levels could perhaps be associated with the focal rCBF decrease seen in the attack group.
Cephalalgia 1994 Feb
PMID:Absence of vasoactive peptide release from brain to cerebral circulation during onset of migraine with aura. 751 29

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

In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated. Peptide variations after spontaneous or sumatriptan-induced remission were also assessed. Blood was collected from the external jugular vein homolateral to the pain side of 30 male cluster headache patients; 18 men were in an active and 12 in a remission one. Plasma levels of CGRP and SP were determined using sensitive radioimmunoassays for each peptide. CGRP-like immunoreactivity (CGRP-LI) was found to be augmented in patients in an active period and became elevated further at the peak of the provoked attack. A complete reversal occurred both after spontaneous and sumatriptan-induced remission. On the contrary, nitroglycerin neither provoked a cluster headache attack nor altered CGRP-LI in the patients in a remission period. The augmented levels of CGRP-LI measured before and after nitroglycerin administration, when the provoked attack reached the maximum intensity, suggest an activation of the trigeminovascular system during the active period of cluster headache. Moreover, the clinical and biochemical actions showed by sumatriptan stress the involvement of serotonin in cluster headache mechanisms.
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PMID:Increase in plasma calcitonin gene-related peptide from the extracerebral circulation during nitroglycerin-induced cluster headache attack. 754 Feb 79

The article briefly describe the innervation of the human cerebral circulation by nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP). The neuropeptides in human cerebral arteries were characterized by radioimmunoassay in combination with HPLC. These neuropeptides mediate contraction (NPY) and dilation (VIP, SP, CGRP). In conjunction with spontaneous attacks of migraine or cluster headache, release of CGRP is seen. With the associated symptoms of nasal congestion and rhinorrhea, VIP is released. Successful treatment may abort the peptide release in parallel with disappearance of headache.
Cephalalgia 1995
PMID:Neuropeptides in the cerebral circulation: relevance to headache. 758 22

Two mechanisms have been proposed to explain the primary mode of action of sumatriptan: vasoconstriction, and trigeminal nerve terminal inhibition. Sumatriptan is a potent vasoconstrictor of intracranial arteries. It has been shown to increase blood flow velocity in large intracranial arteries in man in a dose-dependent fashion both during and between migraine attacks. Since the vasoconstrictor response of sumatriptan is reproducible outside the migraine attack, this action appears to be a direct vascular effect and not indirectly mediated via neural mechanisms. Sumatriptan also causes rapid constriction of dural and meningeal vessels in vivo. It does not modify cerebral blood flow but does constrict arterio-venous anastamoses that may be dilated during a migraine attack. This evidence suggests that sumatriptan has a direct, dose-related, vasoconstrictor action on certain intracranial blood vessels that correlates with its antimigraine activity. Alternatively, sumatriptan may act directly on the trigeminal sensory nerve terminals within the cranial blood vessel, inhibiting the release of sensory neuropeptides. Experimental data from animal studies have shown that following electrical stimulation of the trigeminal ganglion there is a neurogenic inflammatory response with plasma protein extravasation from dural blood vessels. This response can be significantly reduced by sumatriptan at a dose level similar to that used in clinical treatment. This finding is further supported by the clinical observation that sumatriptan reduces the plasma levels of calcitonin gene-related peptide which are raised during a migraine attack.
Cephalalgia 1994 Dec
PMID:The mode of action of sumatriptan is vascular? A debate. 769 99

Superficial temporal arteries (STAs) are abnormally dilated in the painful side during cluster headache (CH) attacks. We have assessed the possible dysfunction of these arteries by comparing in vitro the reactivity of STAs removed from the painful side of CH patients during a cluster of attacks with that of STAs from patients free of CH. The responses to KCl and norepinephrine (NE) of both types of arteries were similar. Serotonin (5HT) induced a classical dose-dependent constriction in arteries from non-CH patients, but systematically triggered rhythmic contractions in arteries from episodic CH patients. Arteries from chronic CH patients also showed spontaneous rhythmic contractions. In both cases, this activity was stopped by calcitonin gene-related peptide (CGRP) but, even in the presence of CGRP, it could be restored by low concentrations of 5HT. Thus, 5HT, unlike NA, can trigger rythmic activity in STAs of CH patients and may play a major role in CH through abnormal smooth muscle cell reactivity.
Cephalalgia 1994 Dec
PMID:Spontaneous and 5HT-induced cyclic contractions in superficial temporal arteries from chronic and episodic cluster headache patients. 769 3

We document a case of a patient who had been treated for a medullary cell carcinoma of the thyroid three years previously and who presented with a three month history of ataxia, weakness and headache. A CT scan showed contrast enhancing lesions in the posterior fossa. An MIBG uptake scan showed that there was some uptake in the cerebellar lesions; however, it was not sufficient to rely on this alone for treatment. The larger of these lesions was therefore surgically resected. Immunocytochemistry, using CAM 5.2, CEA and chromogranin, demonstrated a positive reaction which strongly favoured a diagnosis of metastases from a medullary cell carcinoma of the thyroid. However, absolute confirmation of the diagnosis was obtained using immunocytochemistry with calcitonin. Medullary cell carcinomas of the thyroid usually spread locally and metastasis to the brain has never before been reported.
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PMID:Medullary cell carcinoma of the thyroid: metastases to the central nervous system. 778 10


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