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

Criteria for the diagnosis of migraine have evolved from generalized descriptions to specific rules designed to ensure the selection of homogenous groups of patients for research studies. For clinical practice, the former are insufficiently specific and the latter are too complex. For care of headache patients by primary care physicians, we propose that the diagnosis of migraine without aura (common migraine) is warranted if any two of the following symptoms are present: unilateral site, throbbing quality, nausea, photophobia or phonophobia. These criteria are derived from a study comparing the features of 100 patients with migraine without aura and 100 patients with chronic daily headache. The proposed criteria for the diagnosis of migraine without aura were highly sensitive and adequately specific in discriminating groups. These simple criteria should facilitate the diagnosis of migraine by primary care physicians.
Headache 1991 Jun
PMID:Criteria for the diagnosis of migraine in clinical practice. 188 79

Platelet hyperactivity, one of the commonest findings associated with migraine, has been related to increased release of biologically active substances such as catecholamines and arachidonic acid metabolites, which seem to play a role in the pathogenesis of migraine. In this study, in vitro platelet aggregation tests were performed on samples from patients with different types of headache. The presence of platelet hyperactivity was clearly demonstrated in 11 patients with classical migraine between attacks, but not in 4 patients between attacks of common migraine. Nevertheless, the presence of a marked platelet hyporesponsivity was found during the attack phase of both classical and common migraine. No difference in platelet aggregability was found between attack and post-attack phases in 5 patients with cluster headache. Blood leukotrienes were analyzed in 8 patients with classical migraine and in the 5 patients with cluster headache. During the attack phase of classical migraine both LTC4 and LTB4 were present in the peripheral blood, while the post-attack phase was characterized by the disappearance of LTC4 and the presence of LTB4 and its transisomer delta 6-trans-LTB4. Blood leukotrienes were constantly absent during both phases of cluster headache. Incubation of normal platelets with LTC4 or delta 6-trans-LTB4 was followed by inhibition of platelet response to epinephrine. delta 6-trans-LTB4, at higher concentrations, induced the opposite effect. A possible role of blood leukotrienes in the changes occurring in platelet aggregability during the different phases of classical migraine, is discussed.
Headache 1991 Jun
PMID:Blood leukotrienes in headache: correlation with platelet activity. 188 85

According to widely accepted theory, migraine is a self-limited neurogenic sterile inflammation characterized by initial cerebral vasoconstriction, subsequent extracranial and intracranial vasodilation, sterile inflammation, and secondary muscle contraction. It is characterized by recurrent attacks of headache, usually unilateral and accompanied by nausea, vomiting, and, often, other symptoms. Frequency, duration, and intensity of attacks are widely variable. Migraine affects more women than men, and is often related to menses. Patients with classic migraine experience visual or neurologic prodromes, but vague "premonitions" occur in both classic and common migraine. Precipitating factors include foods, alcohol, medications, visual stimuli, changes in routine, and stress. The first-line agent for abortive therapy is ergotamine; corticosteroids are indicated for prolonged headache. Propranolol is recommended for daily prophylactic therapy, and alternatives include calcium channel blockers, nonsteroidal anti-inflammatory agents, and tricyclic antidepressants.
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PMID:Strategies for migraine management. 189 57

Cerebrovascular reactivity to CO2 inhalation was studied by transcranial Doppler sonography in 30 patients with classic or common migraine and 39 healthy controls without clinical or ultrasonic signs of arteriosclerosis. Systolic and diastolic Doppler frequencies of the middle cerebral artery were plotted against end-tidal CO2 partial pressure; the reactivity index (I x R) was defined as relative frequency change during a PCO2 increase of 5 mmHg. In the normal subjects, I x R was 20.0 +/- 6.3 for systolic velocities, and 26.0 +/- 8.2 for diastolic values. Migraineurs during their headache-free interval had significantly higher I x R values on the affected side (mean: 41.6 systolic, 61.2 diastolic), compared with either controls (P less than 0.01) or the contralateral side (mean: 28.3 systolic, 30.8 diastolic; P less than 0.01). During the headache attack, CO2 reactivity was significantly lower than normal only for systolic velocities (mean: 8.3; P less than 0.05). Increased CO2 reactivity is thought to be one phenomenon of migraine. Transcranial Doppler CO2 testing of cerebrovascular reactivity is a reliable method that may be of interest for the diagnostic evaluation and management of migraine patients.
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PMID:Cerebrovascular CO2 reactivity in migraine: assessment by transcranial Doppler ultrasound. 190 49

Common migraine and cervicogenic headache have many traits in common, so many that they may be mixed up. Both are unilateral headaches with a female preponderance. However, as for a number of variables, they differ. This first and foremost has to do with factors concerning the neck. In cervicogenic headache, the following symptoms and signs are present: a reduced range of motion in the neck; mechanical precipitation of attack, either by neck movements or by external pressure over the greater occipital nerve of the C2 root; ipsilateral shoulder/arm pain; unilaterality without side-shift. Similar findings are usually not made in common migraine. Typical migraine symptoms, such as nausea, vomiting, photophobia, and phonophobia also occur in cervicogenic headache, but less frequently and to a lesser degree. Operative procedures directed to occipital/nuchal structures may afford decisive differentiation between the two disorders. In our estimation, cervicogenic headache and common migraine are two distinct disorders, with their own clinical patterns, pathogenesis, treatment - and, in all probability, also prognosis.
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PMID:Cervicogenic headache. The differentiation from common migraine. An overview. 191 61

Electroencephalographic (EEG) changes occurring in patients with migraine have received much attention. However, almost equal number of reports indicate the predominance of normal and abnormal findings. We studied the EEG in symptom-free, otherwise healthy, unmedicated 18-28 year-old patients: 22 with common migraine, 20 with classic migraine, and 20 age-matched controls. The routine EEG findings in the three groups revealed mild non-specific slowing in 2 (9%), 3 (15%) and 2 (10%), respectively. Simultaneously, topographic EEG mapping and frequency analysis were performed in 13 consecutive patients with common migraine, 10 patients with classic migraine and 11 age-matched controls. EEG mapping showed minimal regional differences with lower power in the alpha range in patients with eyes closed. The peak alpha power, as well as its reactivity, were lower among patients than controls. This difference reached statistical significance only for patients with classic migraine versus controls in the left occipital region. Patients also had slightly faster peak alpha frequency. No frank right-left asymmetry was observed in the peak alpha power, neither among the controls, nor the patients. All the findings were rather minor. They may suggest some difference in the posterior background activity in the EEG in migraine patients as compared to the controls, but are not useful in differentiating migraine from non-migraine patients.
Headache 1991 Apr
PMID:EEG and topographic frequency analysis in common and classic migraine. 205 May 17

EEG abnormalities in migraine have been reported by a number of authors during the last 50 years. Prevalences vary considerably in the older literature. A number of unspecific rhythms related to drowsiness or hyperventilation have probably been counted as "abnormal", and the reported numbers of definitely abnormal EEG rhythms have been consistently low. In a few controlled and blinded studies, however, slight excess of various EEG rhythms has been found in migraine patients. Similar prevalences of interictal EEG abnormalities have generally been found in patients with classic and common migraine, but the diagnostic classification may not have been precise enough in some studies. During visual aura, either slow waves, depression of background activity amplitude or normal EEG have been reported. The most definitely abnormal EEGs with unilateral or bilateral delta activity have been recorded during attacks of hemiplegic migraine, and during attacks of migraine with disturbed consciousness. The relationship between migraine and epilepsy has still not been adequately clarified. The connection seems to exist in several small entities (e.g. migraine-like headache as an epileptic manifestation, epileptic seizures triggered by epileptic attacks, and possibly in epilepsies with occipital spike waves), but it is seemingly not "fundamental". Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in one topographic brain mapping study. Magnetoencephalographic studies of migraine patients have demonstrated slow wave-shifts (similar to those observed in animals with spreading depression). The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation and migraine. The study of such relationship may shed new light on migraine pathophysiology.
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PMID:EEG in migraine: a review of the literature. 205 54

A 30-year-old woman with a history of common migraine developed a permanent left homonymous hemianopia during a typical headache. CT scan demonstrated a right posterior cerebral infarction and angiography showed irregular narrowing of the ipsilateral posterior cerebral artery, suggestive of vasospasm. In the case no risk factors for atherosclerotic stroke were present except for smoking, and no other causes of stroke could be found.
Headache 1990 Nov
PMID:Angiographic changes suggestive of vasospasm in migraine complicated by stroke. 207 66

The CBF studies performed so far during attacks of migraine, may be interpreted as favouring "the vascular theory." This applies to migraine with aura as well as to migraine without aura. Migraine without aura may be due to mild focal CBF reduction--too mild to be detected by the available CBF techniques (i.e. 20% or less) and too mild to produce ischemia and aura phenomena. Migraine with aura may be due to focal CBF reduction severe enough to produce ischemia (i.e. 50% or more) and therefore also aura phenomena. The phenomenon termed "spreading oligemia" typically seen in CBF studies during migraine with aura, may be an artifact reflecting a gradual decrease of CBF in an area of constant size. The typical "march" of the aura symptoms may reflect differences in the ischemic threshold of various neurones leading to dysfunction of more and more neurones as the blood flow gradually decreases. It is concluded that migraine with and without aura may be due to the same disease process--the only difference being the intensity of vasospasm and CBF reduction.
Headache 1990 Apr
PMID:Migraine with and without aura: the same disease due to cerebral vasospasm of different intensity. A hypothesis based on CBF studies during migraine. 209 26

Transcranial Doppler (TCD) examinations were performed in 13 patients with common and 5 patients with classic migraine during attacks and compared to TCD findings during the headache-free period. Two distinct patterns of flow changes were detected to distinguish common from classic migraine on the basis of TCD findings. During attacks, patients with common migraine exhibited reduction of flow velocities associated with an increase of pulse wave amplitudes. Vascular bruits that were heard during the headache-free interval often disappeared. Opposite changes were found in attacks of classic migraine during the headache phase with increase of flow velocities, decrease of pulsatility and more prominent or newly appearing bruits. These findings were often diffuse and did not appear to correlate with side of headache or side of neurological aura. Uniform changes occurred in the cervical internal carotid artery and the basal cerebral arteries in either form of migraine. We propose that these changes represent caliber fluctuations of the large arteries, suggesting vasodilatation during attacks of common migraine and vasoconstriction during attacks of classic migraine. We do not intend to imply a casual role of these preliminary findings in migraine pathogenesis, but we suggest that TCD be used in combination with other methods to study vascular changes in migrainous disorders.
Headache 1990 Mar
PMID:Transcranial Doppler evaluation of common and classic migraine. Part II. Ultrasonic features during attacks. 218 16


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