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)

The root and stem decoctions of Sinomenium acutum Rehd. et Wils. (formerly Sinomenium diversifolius Diels, one type of Fang-chi (Chinese)) have been used as a folk remedy for neuralgia and rheumatoid arthritis in many areas of the Far East. In Japan and China various viny plants have been identified as Fang-chi (Boi in Japanese) since antiquity. This uncertain nomenclature has made it difficult to evaluate the efficacy of the Fang-chi described in the classic literature. Among traditional Fang-chi plants only Sinomeniumacutum has been demonstrated to contain the alkaloid sinomenine, which is now known to be effective in neuralgia and rheumatic diseases. Sinomenine is a unique plant alkaloid, as it potently releases histamine in association with degranulation of tissue mast cells in mammalian tissues. This action occurs preferentially in the skin and joint capsules. The released histamine is responsible for the dominant pharmacological actions of sinomenine, such as vasodilatation, increased vascular permeability, acceleration of the thoracic and peripheral lymph flow, contraction of plain muscles, increased peristalsis of the intestines, and stimulation of gastric acid secretion. At toxic doses of sinomenine, convulsive central excitation was observed in most laboratory animals. Clinical side effects encountered with high doses of injected sinomenine or of decocted Sinomenium acutum were: injection site flare, pruritus in the head and upper part of the body, edema around the lips and eyelids, and temporary cephalalgia. Most of these side effects were reduced by classical antihistamines (H1-receptor antagonists). Daily subcutaneous injections of sinomenine for more than one week produced an analgesic effect in mice. Granulation tissue growth and adjuvant arthritis induced in rats were both inhibited by daily injections of a small dose of sinomenine hydrochloride or histamine dihydrochloride. These inhibitory effects were mediated through histamine H2-receptors probably on fibroblasts (for granulation tissue growth) and on T-cells (for adjuvant arthritis), since these effects were clearly inhibited by the H2-antagonist burimamide but not by the H1-antagonist mepyramine. The anti-rheumatic effect on Sinomenium acutum are probably genuine and can probably be attributed to the histamine-releasing properties of sinomenine.
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PMID:Pharmacology of sinomenine, an anti-rheumatic alkaloid from Sinomenium acutum. 6 10

35 children (16 girls and 19 boys) at the age of 1 11/12 to 16 11/12 with acute leukaemia were injected intrathecally with 198Au-radiogold colloids (HOECHST-BEHRING) for "prophylaxis of meningosis". The colloid size of the isotope amounted to 5 or 30 nm, the applied activity lay between 1.4 and 3.12 mCi. According to a dosage estimation made with the help of LOEWINGERS formula 1 mCi of radiogold corresponds to approximately 1200 rad. Clinical observations, such as headaches, vomiting or fever up to 39 degrees C, could only be found in 6 children (17.1%) during the first 24 hours. All symptoms subsided quickly and without any sequels. Even retarded complications could not be detected. An electroencephalogram was made from all children before and after applying radiogold (1-8 d afterwards). After the injection of radiogold the majority of children had no change of findings in the electroencephalogram, 11 children even showed a tendency towards an improvement up to normalisation. Only 4 children had a deterioration of findings with unspecific disorders or appearances suspected of peak potential discharges. Simultaneously an accumulation of clinical complaints could be found. Judging from the clinical and electroencephalographic behaviour of our patients no absolute neurotoxity of radiogold could be ensured.
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PMID:[The cerebral sensitivity to "meningosis-prophylaxis" with 198Au radiogold according to EEG findings]. 6 10

Autoradiographic investigations with 3H-thymidine were performed on cerebrospinal fluid (CSF) cells from a case of meningeal carcinomatosis following carcinoma of the breast. The cells were found to be anaplastic histologically. Within a period of 12 days 3 X 25 mg methotrexate were injected into the subarachnoid space by lumbar (2 X) or cisternal (1 X) puncture. The CSF cells were reduced from 283/3 to 19/3, while the proportion of tumour cells fell from 90 to 2%. The labelling index before onset of therapy was 33%; it increased to 70% after the first intrathecal administration of cytostatic and finally fell to 23%. The mitotic index, which was generally less reliable, behaved in a parallel way; the initial value of 1.5% increased to 3% and then declined to values less than 0.5%. Despite detailed histological investigation, carcinomatous cells could not be found anywhere on the surfaces of the central nervous system or meninges. Clinically, the patient had never shown significant neuropathological or psychopathological findings. However, the headache which had been very severe during the meningeal carcinomatosis vanished completely after the second application of methotrexate.
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PMID:Intrathecal cytostatic therapy of meningeal carcinomatosis. Autoradiographic investigations of the CSF cells. 6 30

Using a 12-hour infusion of salmon synthetic calcitonin (S-CT), distinct and sustained inhibition of gastric acid and pepsin secretion has been demonstrated in 4 normal subjects, 3 patients with peptic ulcer disease and 3 high risk patients. In 3 patients with Zollinger-Ellison syndrome, treated in the same way, elevated serum gastrin was reduced by about 50% and acid secretion by more than 90%. In healthy volunteers oral administration of human synthetic CT (H-CT) led to reduction in basal and pentagastrin-stimulated acid and pepsin secretion by about 50%, lasting for more than 2 hours after the instillation of CT. In 4 subjects receiving CT intravenously, slight nausea and headache were registered, while there were no side effects after the oral route. Serum calcium did not change after i.v. or oral administration of CT. Wheras therapeutical applications of CT, given by i.v. route, seem to be restricted to selected cases, i.e. acute gastric ulcerations with imminent or existent bleeding, the eventual benefit or orally administered CT in peptic ulcer disease should be evaluated in controlled long-term trials.
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PMID:Long-term effects of calcitonin on gastric secretion in normals, peptic ulcer and high risk patients. 6 56

Forty patients attending the Prince Henry Hospital migraine clinic have been investigated for evidence of complement activation related to migraine. These patients had a history of clinically similar migraine attacks. Levels of serum complement components were determined in nine patients, both in and out of migraine. Comparison of these levels showed significant reductions in C4 and C5 during headache. In a further 31 patients C3 breakdown products were sought when these patients were headache-free. They were detected in the plasma of three patients who proceeded to a migraine attack but not in the plasma of the remaining twenty-eight who did not. These findings suggest the presence of complement activation, which could explain many of the previously reported phenomena associated with migraine.
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PMID:Complement activation in migraine. 6 74

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

A 35-year-old man ingested food contaminated with lindane, an insecticide containing almost pure gamma hexachlorocyclohexane. Grand mal seizures and severe acidemia developed rapidly. The seizures recurred for nearly 2 hours, then ceased. In addition, the patient had muscle weakness and pain, headaches, episodic hypertension, myoglobinuria, acute renal failure and anemia. Pancreatitis developed 13 days after the ingestion of lindane. A muscle biopsy on the 15th day of illness demonstrated widespread necrosis and regeneration of muscle fibres. The patient's condition improved and he was discharged 24 days after the onset of his illness. During the year following the poisoning the patient noted difficulty with recent memory, loss of libido and easy fatigability. One year after lindane ingestion the results of physical examination, including those for muscle power and bulk, were normal.
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PMID:Acute lindane poisoning with development of muscle necrosis. 7 42

Various parameters of histamine metabolism were studied in patients with migraine, cluster headache and chronic paroxysmal hemicrania. These included urinary excretion of radioactivity and of 14C histamine and its metabolites, exhaled 14CO2 and fecal radioactivity after oral as well as subcutaneous administration of radioactive histamine. No marked deviation from the normal was found except in one patient with the cluster headache variant, chronic paroxysmal hemicrania, in whom an aberration in 14C histamine degradation seemed to be present. Only minute quantities of the 14C histamine metabolite C14 imidazoleacetic acid riboside seemed to be formed during a period with severe paroxysms. During a symptom-free period no deviation from normal was observed. The most likely explanation for this finding seems to be a defect in the conversion of imidazoleacetic acid to its riboside. This defect may possibly explain the increased urinary excretion of histamine in this particular patient. The relationship of this metabolic aberration to the production of headache still remains dubious for various reasons.
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PMID:Histamine metabolism in cluster headache and migraine. Catabolism of 14C histamine. 7

Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The excretion was significantly higher on attack days than on attack free days. With migraine, increased excretion was found in 5 of 31 patients on days of an attack, whereas the corresponding figure for headache free days was 7 of 24 patients. Three patients showed increased histamine excretion during, as well as between, attacks. The excretion on attack days was not significantly different from that on attack free days. In cluster headache patients, L-histdine administration on attack days did not indicate that an increased histamine formation took place under such circumstances. The underlying mechanism behind the increased histamine output with cluster headache may be increased formation or liberation or altered catabolism. Histamine is more likely to be a consequence than the cause of an attack of cluster headache.
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PMID:Urinary histamine excretion in migraine and cluster headache. Further observations. 7 5

Among 296 patients with thrombocytopenia, 14 had frequent migraine-like headaches, 6 of them having definite migraine. Only 1 of the 6 patients had had migraine before the onset of the blood disorder, and all 6 had migraine attacks during periods of bruising tendency and low platelet count. Control of thrombocytopenia with splenectomy or steroids was accompanied by dramatic improvement in migraine. It is suggested that migraine attacks are caused by abnormal platelet activity and abnormal serotonin metabolism. It is suggested that the immediate factor producing the abnormal platelet activity in our patients was immunological and that other cases of migraine may have an immunological cause.
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PMID:Migraine thrombocytopenia, and serotonin metabolism. 7 65


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