Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-five patients with non-organic abdominal pain, were interviewed with the help of a questionnaire. Those who responded to a high fibre diet were excluded from the study. Twenty-seven patients had multiple pains and 58 described a single pain, which was intermittent in 39. A detailed analysis of the symptoms and family history of the latter group suggested that in 19 patients the symptoms might have been caused by abdominal migraine. Six of these 19 had typical migraine-associated symptoms during the attack, characteristic abdominal pain and a family or personal history of classical migraine. Abdominal migraine should be considered in patients with non-organic abdominal pain where symptoms are not typical of irritable bowel syndrome and when organic disease has been excluded.
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PMID:Abdominal migraine: a cause of abdominal pain in adults? 157 6

We studied the prevalence of migraine in low-tension glaucoma (LTG) and primary open-angle glaucoma (POAG). Seventy seven Japanese patients with LTG, 73 with POAG, and 75 normal subjects were randomly selected and tested with a headache questionnaire. The prevalence of headache with or without typical migrainous features (unilateral headache or ocular pain, nausea, vomiting, and visual disturbance before headache) was 51% in LTG, 42% in POAG, and 44% in normal patients. The prevalence of headache with two migrainous features or more (probable migraine) was 17% in LTG, 11% in POAG, and 12% in normal subjects. The prevalence of headache with three migrainous features (classical migraine) was 5% in LTG, 3% in POAG, and 3% in normal subjects. There was no statistically significant difference in the prevalence of any types of migraine between the three groups of patients (p greater than 0.05). These results suggest there is no significant relationship between migraine and LTG or POAG in Japanese patients.
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PMID:Prevalence of migraine in low-tension glaucoma and primary open-angle glaucoma in Japanese. 202 90

In an open multicentre study in Switzerland, the dihydroergotamine nasal spray was studied for its efficacy and tolerability in the treatment of acute migraine attacks (common and classical migraine--one attack each patient) in a total of 904 patients. In the global assessment, 76.8% of all the patients reported good efficacy (freedom from pain, less pain or shorter duration of pain). When the nasal spray was used already in the prodromal phase, good efficacy could be obtained by 90 (63%) of 143 patients. 18.1% of all the patients treated--more frequently those who obtained no beneficial effect and/or who took additional medication during the migraine attack--reported one or more--minor side-effects such as local nasal irritation (congestion, burning or stinging), nausea, dizziness and vomiting. 3.9% of the patients said they would not use the spray again because of the side effects.
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PMID:[Dihydroergotamine as a nasal spray in the therapy of migraine attacks. Efficacy and tolerance]. 220 27

The sensation of pain derived from intracranial and extracranial blood vessels is conveyed to the central nervous system chiefly by the trigeminal nerve, with first order neurones terminating in the nucleus caudalis of the spinal trigeminal tract and an area lateral to the dorsal horn of the spinal cord at the second cervical segment. The evoked discharge of second order neurons can be suppressed by activation of the endogenous pain control system or, in about one third of cases, by the local application of ergot derivatives or the serotonin (5HT1) agonist sumatriptan (GR43175). Stimulation of brainstem structures such as locus ceruleus, raphe nuclei and the trigeminal system induce changes in the cerebral and extracranial circulations of the experimental animal that mimic those of migraine with aura (classical migraine). Clinical and laboratory observations have led to a neural hypothesis for migraine in which changes in hypothalamic function (an 'internal clock') and reactions to stress or excessive afferent stimuli are thought to initiate brainstem activity, causing secondary vascular changes and release of inhibition of the trigeminal pain pathways to cause headache. Painful distension of cranial blood vessels may contribute the throbbing component to migraine headache. Migraine is associated with a lowered level of platelet serotonin that is thought to reflect monoamine depletion in brainstem nuclei. Migraine headache can be precipitated by reserpine, which releases serotonin from body stores, and relieved by the intravenous infusion of serotonin. The new 5HT1 agonist sumatriptan promises to have the beneficial effects of serotonin without the side-effects that limited its clinical use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Headache: classification, mechanism and principles of therapy, with particular reference to migraine. 251 13

An hypothesis that migraine is the experience of a protective vascular response to cerebral information overload has been explored to a limited extent by examining the association between laterality of the attack and verbal and spatial performances under standard symptom-free conditions. The study was restricted to individuals with unilateral symptoms always presenting on the same side. It emerged that those with classical migraine do not always have prodromata referable to the same side as the pain. Indeed, in the present study, prodromata were almost exclusively referable to the left (dominant) cerebral hemisphere. A subgroup of those with speech disturbances as a feature of the prodromal symptoms was also found to have relatively impaired language abilities on routine testing. It is this finding that lends some support to the hypothesis. The findings also invite the refining proposition that information overload, as defined in the hypothesis, is almost always borne by the dominant (verbal) hemisphere in our species. Such overload might concurrently or sequentially also overtax a suggested limited right hemisphere language capacity, in terms of the hypothesis, accounting for the right-sided pain sometimes presenting in these cases. Otherwise, pain appears to be predominantly left-sided or midline. Perhaps the frequency of this particular syndrome is an indictment of the limitations of language as a basis for communication, as well as reflecting the possibility that most of our stressful transactions and their cerebral processing use a verbal substrate. The results also reveal the need for agreement on rules for classification of laterality in migraine.
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PMID:Cerebral hemisphere function and migraine. 263 18

Classical migraine is associated with two distinct phases; an initial vasoconstriction followed by vasodilatation. The "purinergic" hypothesis for migraine was originally put forward in 1981 as a basis for the reactive hyperaemia and pain during the headache phase. It was suggested that adenosine 5'-triphosphate (ATP) and its breakdown products adenosine 5'-monophosphate and adenosine were strong contenders for mediating the vasodilatation following the initial vasospasm and subsequent hypoxia. ATP was also implicated in the pathogenesis of pain during migraine via stimulation of primary afferent nerve terminals located in the cerebral vasculature. Recent studies have shown that the ATP-induced cerebral vasodilation is endothelium-dependent via activation of P2Y-purinoceptors on the endothelial cell surface and subsequent release of endothelium-derived relaxing factor (EDRF); and that the endothelial cells are the main local source of the ATP involved, although adenosine 5'-diphosphate and ATP released from aggregating platelets may also contribute to this vasodilatation. These findings have extended the "purinergic" hypothesis for migraine in two ways. Firstly, they have clarified the mechanism of purinergic vasodilatation during the headache phase of migraine. Secondly, they suggest that a purinergic mechanism may also be involved in the initial local vasospasm, via P2X-purinoceptors on smooth muscle cells occupied by ATP released either as a cotransmitter with noradrenaline from perivascular sympathetic nerves or from damaged endothelial cells.
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PMID:The role of adenosine triphosphate in migraine. 270 Dec 87

The evaluation of central opiate activity could be of clinical value in the diagnosis and treatment of pain syndromes. The current approach via direct measurement of endogenous opioid peptides in cerebrospinal fluid (CSF) is not devoid of side effects and cannot be used in every-day practice. As an alternative to this method, we have studied the neuroendocrine response of plasma LH to an i.v. naloxone injection in 39 headache sufferers from different diagnostic subgroups, and in 12 age- and sex-matched healthy volunteers. Patients (19 females and 20 males) were affected by common migraine (CM, 11 cases), migraine with interparoxysmal headache (MIH, 9), classical migraine (CIM, 9), and chronic cluster headache (CH, 10). Headache lasted 3-36 years. Prior to naloxone challenge (4 mg i.v.), LH pulsatility was evaluated for 1 h. The next morning, the pituitary response to LH-RH (10 micrograms i.v.) was tested in 20 patients. Plasma LH was measured by RIA in every sample. The response to the tests was evaluated as secretion area of plasma LH minus the mean basal value. Controls (497.5 +/- 85.5 mIU/ml x 120 min), ClM (357.8 +/- 78.9) and CH (450.5 +/- 70.4) patients showed similar results, while in cases of CM (155.3 +/- 71.7, P less than 0.05) and MIH (104.1 +/- 53.7, P less than 0.01) the LH secretion after naloxone injection was significantly blunted. On the contrary, the response of LH to LH-RH was similar in controls and patient groups, thus excluding pituitary dysfunctions in this response.(ABSTRACT TRUNCATED AT 250 WORDS)
Pain 1988 Jul
PMID:Neuroendocrine evaluation of central opiate activity in primary headache disorders. 304 18

Cluster headache is a rare headache entity that predominantly occurs in younger males. The clinical features are characterized by sudden attacks of unilateral excruciating pain localized periorbitally, associated with ipsilateral autonomic symptoms. The attacks occur in periods: clusters. The pathophysiology is still unknown. Such vasodilating substances as histamine, nitroglycerin and alcohol may provoke attacks. These substances may be used as diagnostic tests, but the interpretation of a negative result must be careful, as the attacks can not be induced in a refractory period after spontaneous occurrence, or at the beginning and end of cluster periods. As symptomatic treatment, ergotamine is the drug of first choice. High attack frequency may lead to overconsumption with ergotisme and further increased frequency. In such cases and for nocturnal attacks, oxygen inhalations represent an alternative. As prophylactic treatment ergotamine, methysergide, lithium and prednisone have proved efficacious. Most patients benefit from such treatment and may become virtually free from attacks. It is, therefore, important to differentiate this headache entity from classical migraine, common migraine and trigeminal neuralgia.
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PMID:Cluster headache: a review. 353 83

A clinically similar entity to classical migraine is seen in certain dental patients suffering from temporomandibular joint (TMJ) pain dysfunction syndrome. Patients selected for study gave symptoms of classical migraine on waking. Facial pain on waking is typical of some cases of TMJ dysfunction syndrome and the hypothesis was tested that some patients with symptoms of classical migraine were at the extreme end of the spectrum of dysfunction syndrome. However, rather than experience muscle or temporomandibular joint pain these patients had symptoms on waking which were typical of classical migraine. Nineteen patients with migraine symptoms were provided with acrylic occlusal splints for nocturnal wear. A good clinical response with considerable reduction in frequency and severity of pain attacks was achieved.
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PMID:Clinical effectiveness of occlusal splint therapy in patients with classical migraine. 356 68

New knowledge of intrinsic serotonergic and noradrenergic pathways, projecting from brainstem rostrally to cerebral cortex and caudally to spinal cord, makes a neurogenic hypothesis for migraine more plausible than the previously held humoral theory. Low frequency stimulation of locus ceruleus in the monkey increases cerebral vascular resistance, thus diminishing blood flow, while high frequency stimulation increases external carotid arterial flow by connections with the greater superficial petrosal component of the facial nerve. The latter connection also serves the 'trigeminovascular reflex' whereby stimulation of the trigeminal nerve causes vasodilatation in the external carotid circulation in cat and man. Vascular changes evoked from the locus ceruleus are predominantly unilateral and stimulate those recorded in classical migraine, suggesting that excessive discharge of ascending monoaminergic pathways may initiate these phenomena in man. Since descending monoaminergic pathways play an important part in the endogenous pain control system, a phase of monoamine depletion could open the pain gate and give rise to headache. The referral of ice-cream headache and ice-pick pains to the habitual site of migraine headache in some patients, even in the period between attacks, suggest a dormant neural excitability which becomes active periodically to induce a migrainous episode. The symptomatology and phenomena of clinical migraine can now be explained in terms of instability of central monoaminergic pathways, a hypothesis that can be tested experimentally and which should lead to more precise pharmacological management of migraine in the future.
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PMID:The pathophysiology of migraine. 400 26


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