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)

Using the biometeorologic system proposed by Brezowsky, the chronological distribution of migraine attacks was analysed in 4 patients over a 5-year period. A correlation of complaints with physical indices (atmospheric pressure, temperature, humidity and ionisation) could not be established. However, a significantly high incidence of headache symptoms was shown in the biometeorologic phase 6Z (although other investigators have reported such an increase in weather phases 3 and 4). The important common denominator of these weather phases seems to be a disturbed circadian rhythm which interferes with endogenous biorhythms and triggers attacks of headache.
Res Clin Stud Headache 1978
PMID:Headache determination by meteorotropic influences. 72 46

In 1976, 310 patients attended the Princess Margaret Clinic for treatment of an acute headache. 90% were either symptom-free or had only slight residual headache after 4 h. The treatment given was metaclopramide and an effervescent analgesic. 69% of patients had some form of sedation and 10% ergotamine tartrate. Those patients who had treatment between 6 and 12 h following the onset of an attack had significantly fewer attacks in the next 7 days. Patients who slept during an attack, with a sedative where indicated, recovered more quickly than those who did not sleep. The depth of sleep did not affect the rate of recovery. A higher percentage of patients with migraine compared with those with tension headache were either symptom-free or had only slight residual headache on leaving.
Res Clin Stud Headache 1978
PMID:Observations on the treatment of an acute attack of migraine. 72 49

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

CBF was studied in 15 cases of vascular headache by the 135Xe intra-arterial injection method. The mean CBF was found to be increased during the headache phase of the migraine attacks in half the cases, mainly due to an increase in the rapid component (CBFg). After the attack there could be an increase or a decrease of the slow component (CBFw). Reactivity to anaesthetic depression was studied in 8 migraine cases and on the whole it was found not to be much altered in most cases. Finally, no modifications of CBF were found in any of 3 cases of cluster headache who were studied during attacks of severe pain.
Res Clin Stud Headache 1978
PMID:Cerebral blood flow in migraine and cluster headache. Compartmental analysis and reactivity to anaesthetic depression. 72 60

On the basis of reports of reduced MAO activity in migraine and cluster headaches and on a report that lithium carbonate activates MAO, the authors administered lithium carbonate to two patients whose cluster headaches had brought them to the point of contemplating suicide. Both patients responded quite dramatically. Case 1 has now been virtually free of headaches for over two years and Case 2 has been in remission for over twelve months.
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PMID:Lithium treatment of chronic cluster headaches. 73 93

Total plasma free fatty acids (FFAs), platelet serotonin content and plasma stearic, palmitic, oleic and linoleic acids were estimated in 10 migrainous patients before, during and after a migraine attack. Total and individual plasma FFA levels rose and platelet serotonin fell in most patients. Comparison of the pre-headache and headache mean values showed that of the FFAs linoleic acid rises most during headache. 10 non-migrainous controls had platelet serotonin content estimated before and after the ingestion of 20g linoleic acid. All showed a significant fall in platelet serotonin in the post-ingestion period. It is shown that linoleic acid releases platelet serotonin in vitro, and this study suggests that it has the same action in vivo. Further, it is the precursor of all prostaglandins in the body and its marked elevation during migraine may serve as a source of increased prostaglandin E1 (PGE1) synthesis. It is suggested that linoleic acid plays an important role in the biochemical process of the migraine attack, acting both as a serotonin releasing factor and a source of PGF1, the vasodilating action of which can aggravate the clinical symptoms of migraine.
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PMID:Individual free fatty acids and migraine. 75 14

Modern sleep research studies have provided the practicing physician with considerable new information concerning the basic psychophysiology of sleep, the effects of medical conditions on sleep and the role of maturational and emotional factors in producing certain sleep disorders. Medical and psychiatric disorders, sleep disorders and drug-induced sleep stage alterations are studied in the sleep laboratory using the same techniques developed to analyze sleep patterns in normal subjects. After initial sleep laboratory adaptation, a profile of the sleep characteristics of various clinical conditions is obtained. This profile can be compared to sleep profiles of normal subjects as well as to the effects on sleep of subsequent experimental or therapeutic procedures. Various studies have shown that coronary artery, duodenal ulcer and nocturnal headache patients experience angina, increased gastric acid secretion and migraine or cluster headaches, respectively during REM sleep. Adult nocturnal asthamtic episodes occur out of all sleep stages while attacks of dyspnea in asthmatic children occur in all stages except stage 4 sleep. Hypothyroid patients show decreases in stages 3 and 4 sleep, while in hyperthyroid patients the percentage of time spent in stages 3 and 4 sleep is markedly increased. Enuretic episodes occur predominantly in non-rapid eye movement (NREM) sleep. Sleepwalking and night terror episodes occur exclusively out of NREM sleep, particularly from stages 3 and 4 sleep. Most child somnambulists and children with night terrors "outgrow" this disorder, suggesting a delayed maturation of the central nervous system. Stimulant drugs are effective in the treatment of the sleep attacks of narcolepsy and in treating certain cases of hypersomnia, while imipramine is an effective treatment for the auxillary symptoms of narcolepsy. Psychological disturbances are frequent in adult somnambulism and night terrors as well as in hypersomnia and insomnia. Proper pharmacologic treatment to provide symptomatic relief for insomnia is recommended to enhance the psychotherapeutic process.
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PMID:Nocturnal psychophysiological correlates of somatic conditions and sleep disorders. 77 62

It is suggested that damage by mild trauma, viruses or bone disease to the otic capsule or to the membranes between the cochlea and the middle ear is common, and involved in many syndromes of obscure etiology. The clinical perilymph fistula (PF) syndrome can consist of any combination of the following: tinnitus, deafness, phonophobia, vertigo, ataxia, otalgia, facial palsy, headache, diplopia, blackouts, psychological distress. The following testable hypotheses are proposed: otitis media is due to perilymph in the middle ear, with secondary changes resulting from infection or inflammation: otosclerosis results from a slow leak in the presence of enzymes promoting bone growth: Meniere's syndrome follows reduced perilymph support for the endolymphatic system: Bell's palsy results from a perilymph provoked oedema in the bony facial nerve canal: PFs may be responsible for progressive rubella deafness, and for some cases of migraine, epilepsy, anxiety neurosis and hysteria: psychiatric sequelae of the PF syndrome predominate in the post-concussional syndrome and infantile autism: organisms can pass from the throat into the spinal fluid, causing meningitis or encephalitis. The tinnitus and vertigo are caused by random labyrinthine fluid movements, the headache and diplopia by reduced spinal fluid pressure.
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PMID:Perilymph fistula: a cause of auditory, vestibular, neurological and psychiatric disorder. 78 62

A brief survey of the literature on the side effects of oral contraceptives is given. Of the many influences on laboratory results those related to (reversible) cholestasis or to a change in protein synthesis are the most important ones. A decrease of the tolerance for glucose is sometimes observed. Few of the clinical side effects attributed to oral contraceptives can be directly correlated with the pharmaceutical action of these drugs. Many so-called side effects of the pill are due to other factors such as altered psychosociological or sexual behavior, etc. However, among users of oral contraceptives there is a significant decrease in the number of benign tumors, particularly of the breast, the uterus and the ovaries. It is still an open question if this also signifies protection against cancer. Anemias due to iron deficiency are less frequent among users of the pill. According to recent studies arterial hypertension and cholecystopathies are probably directly related to oral contraceptives, but a causal relation has not been proven for migraine, headaches, depression etc. An elevated risk for vascular complications seems to be well established: there is a 4-6-fold increase of the estimated risk for venous thrombo-embolism and a 4-9-fold increase for cerebrovascular accidents among users of oral contraceptives when compared with nonpregnant women of the same age not using the pill. Oral contraceptives act as a supplementary factor of risk which may cumulate with other similar factors, such as arterial hypertension, hyperlipidemia, overweight, smoking etc. Mortality due to oral contraceptives is very much 10-50 x) inferior to the one caused by delivery and the post partum state. Since the number of failures in prevention of pregnancies is less for oral contraceptives than for any other method of contraception, the overall risk of death under oral contraceptives in this age group of women is least.
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PMID:[Real and seeming side-effects of oral contraceptives with an emphasis on medical and haematological problems. Review of literature (author's transl)]. 79 Mar 74


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