Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic treatment with beta-blockers was interrupted abruptly in six patients with arterial hypertension. Three patients, who had experienced symptoms during a previous withdrawal, again complained of transient palpitations, tremor, sweating, headache and general malaise. A significant increase in standing blood pressure (BP) and heart rate (HR) was noted after 24 h. The standing HR reached a maximum after 48 h and had decreased significantly on the 7th day (p less than 0.005). There was a strong tendency to greater increase in standing BP and HR in the patients who experienced symptoms than in those who did not. Plasma concentrations of noradrenaline, adrenaline and prolactin did not change significantly. Thus, beta-blocker withdrawal symptoms are reproducible and are indicative of a transient sympathetic hyperresponse. The increased activity is not likely to be caused by increased production of circulating catecholamines, but rather by increased sensitivity of the beta-receptor.
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PMID:Abrupt withdrawal of beta-blocking agents in patients with arterial hypertension. Effect on blood pressure, heart rate and plasma catecholamines and prolactin. 3 93

Treatment was interrupted abruptly in 6 hypertensive patients receiving clonidine 0-45-5-4 mg daily. Blood-pressure rose to pretreatment levels within 24-48 h of withdrawal and was accompanied by insomnia, headache, flushing, sweating, and apprehension. These symptoms began 18-20 h after the last dose of clonidine. Plasma-noradrenaline levels and urinary catecholamine excretion increased 24-72 h after withdrawal of clonidine. The subjective symptoms were most prominent in patients on higher doses (greater than 1 mg/day) and in those who had previously been receiving treatment with other antihypertensive drugs. One patient on a very low daily dose (0-15 mg) of clonidine had no symptoms and no significant changes in blood-pressure or catecholamine production after drug withdrawal.
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PMID:Clonidine withdrawal in hypertension. Changes in blood-pressure and plasma and urinary noradrenaline. 6 74

In idiopathic headache (IH) sufferers, phenylephrine and fenfluramine induce a pupillary dilatation respectively greater and lesser than in controls. The difference may be due to a supersensitivity of the iris alpha adrenoceptors caused by a deficiency of noradrenaline in the iris adrenergic nerve terminal of the IH sufferer. These findings seem to support the hypothesis of a brain receptorial, monoamine supersensitivity in IH.
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PMID:Adrenergic supersensitivity of the pupil in idiopathic headache. 19 97

Central panalgesia is a syndrome which includes systemic pains of a central nature, usually classified as hysteria, fibrositis and masked depression. Exploration of the peripheral neuromuscular junctions (in the iris by pupillometry, and in veins by computerized venotest) indicates an increased monoamine receptor sensitivity. 5-HT vein sensitivity is particularly impressive (up to 1,000 times). In the vein there appears to be a decentralization supersensitivity, as it is extended to different monoamines (5-HT, dopamine, noradrenaline, tyramine). This type of supersensitivity is compatible with the theory of a deficiency of neurotransmitters at the level of the anti-nociceptive and integrated systems, with subsequent central and peripheral supersensitivity. A similar condition limited to the rostral section of the anti-nociceptive system is valid for the mechanism of idiopathic headache including migraine: central and peripheral supersensitivity to monoamines and opiates is also episodically observed in headache sufferers.
Res Clin Stud Headache 1978
PMID:Decentralization supersensitivity in headache and central panalgesia. 72 53

The hypothesis that pro-inflammatory spasmogens may be generated locally in the vessels of the head by neurohumoral stimuli has been tested using an isolated extracranial vascular bed from the rabbit. No spasmogen release was detected after adenosine triphosphate, histamine, acetylcholine or noradrenaline and was seen rarely after tyramine and 5-hydroxytryptamine. Both sympathetic nerve stimulation and periods of vascular stasis released spasmogen, probably an E-type prostaglandin. The local generation of pro-inflammatory substances by excess sympathetic stimulation and/or vascular stasis might contribute to the development and maintenance of the acute migraine attack.
Res Clin Stud Headache 1978
PMID:Spasmogen release from an extracranial vascular bed evoked by neurohumoral stimuli and periods of vascular stasis. 72 55

Excretion of the vaso-active amines tyramine, serotonin, noradrenaline, adrenaline and histamine and blood levels of serotonin, noradrenaline, adrenaline and histamine, were estimated in 10 patients before, during and after an attack of migraine. During the headache process there was a statistically significant fall in the excretion of tyramine and a similarly significant rise in the excretion of serotonin. Excretion of the other 3 amines showed no significant fluctuation during the various phases of the migraine attack. Blood levels of serotonin were significantly lower during headache than during freedom from headach. whilst whole blood histamine was significantly higher only during the postheadach phase. The meaning of the latter observation is not obvious. The above results are discussed in the light of recent reports that tyramine is the substance responsible for headache attacks in patients who have a history of dietary migraine. Reasons are offered as to why this is unlikely to be the case.
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PMID:Amine turnover in migraine. 121 95

Of 27 patients with phaeochromocytoma, 20 were subject to headaches as a part of their symptom complex and 7 were not, in spite of the fact that 4 of the latter had experienced other forms of headache at other times. There was no correlation between the proportion of noradrenaline to adrenaline produced by the tumour and the presence or absence of headache or the nature of the headache. Liability to headache appeared to be linked with the rate of change in blood pressure and was not related to absolute values of blood pressure. Two patients experienced a "funny turn" typical of catecholamine release during a spontaneous migraine headache. The migraine headache became pulsatile and severe in one patient but was unaltered in the other. The variable duration and intensity of the headache in different patients can be explained by the pressor and cranial vasoconstrictor effects of the secreted amines which respectively enhance and diminish vascular headache.
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PMID:The headaches of phaeochromocytoma. 121 96

A 40-year-old woman was admitted with complaints of headache, palpitation and diaphoresis. She had undergone right hemithyroidectomy 12 years previously. Histological reexamination of the operative specimen revealed a medullary thyroid carcinoma. Abdominal ultrasonography, CT scan and angiography showed bilateral adrenal tumors. Serum catecholamine levels in both adrenal veins were high. Based on these data, bilateral adrenalectomy was performed. Histological examination confirmed the diagnosis of pheochromocytomas. After operation, serum calcitonin and urinary noradrenaline levels were still high. Further examination by 131I-metaiodobenzylguanidine (MIBG) scintigraphy is planned.
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PMID:Multiple endocrine neoplasia type 2A. 135 24

The vasoreactivity of the intracranial segment of the internal carotid artery to transmitters, present in the perivascular sympathetic, parasympathetic and sensory nerves, as well as to other vasoactive agents of relevance for headache, was tested in man and monkey. The total arterial segment from both species is equipped with contractile receptors for noradrenaline, serotonin, prostaglandin F2 alpha, ergotamine and sumatriptan. Further, the total arterial segment dilated upon exposure to calcitonin gene-related peptide in both species. Other vascoactive transmitters, acetylcholine, substance P and neurokinin A, caused only weak dilatation, restricted to the proximal extracavernous segment in the monkey. The findings are discussed in relation to the pathogenesis and treatment of cluster headache.
Cephalalgia 1992 Oct
PMID:Vasoreactivity of the intracranial internal carotid artery. 135 56

Autonomic nervous system functions were studied in 13 females with migraine without aura during headache-free intervals, using physiological, pharmacological and biochemical methods. Heart-rate in the resting condition and blood pressure rises in the cold-face and isometric handgrip tests were higher than in controls. Normal cardiovascular responses to the Valsalva manoeuvre and to noradrenaline infusion suggest that the baroreflex arc is intact. Normal heart rate responses to the Valsalva manoeuvre, to the cold-face test and to deep breathing confirmed a normal cardiac parasympathetic function. Clonidine infusion showed a sedative and depressor effect and an inhibition of plasma NA similar to those occurring in controls, suggesting a normal central sympathetic tone. As a whole, the physiological, pharmacological and biochemical tests were consistent with a non-specific sympathetic hyperactivity, but do not confirm any impairment of the autonomic control of the cardiovascular system in migraine patients in headache-free intervals.
Headache 1991 Jul
PMID:Autonomic nervous system function in migraine without aura. 177 61


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