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

Since the time of Liveing and Gowers in the nineteenth century, migraine has been thought to be inherited, although family history has been widely studied, nearly all the reports are not scientifically based and studies on twins have never shown 100% concordance in monozygotic (MZ) pairs, indicating that migraine cannot be inherited by a single gene. Furthermore, the criteria for a polygenic trait are not fulfilled by migraine patients. The only two syndromes with a strong genetic basis of inheritance are familial hemiplegic migraine and migraine occurring in Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like episodes (MELAS). It is the predisposition to headache that is likely to be inherited; this is supported by the induction of migraine-like headaches with either m-chlorophenyl-piperazine (m-CPP) or nitroglycerin in normal subjects with a positive family history for migraine.
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PMID:Migraine and heredity. 149 12

There are many theories and hypotheses concerning with the pathogenesis of migraine. The clinical effectiveness of vasoactive drugs and many investigations on the cerebral blood flow in patients with migraine strongly support a vascular theory. In present paper we report a case of 26-year-old Japanese male, who suffered from hemiplegic migraine and coincidental coronary vasospasm, and discussed the pathogenesis of migraine. In October 1986, the patient developed the first attack of throbbing headache in the left temporal area with nausea and vomiting, following typical visual aura. One week later, he developed the second migrainous attack and then he felt his right extremities paralyzed and numb. Although the headache and weakness resolved within one hour, similar migrainous attack with transient hemiparesis repeated two or three times a month. Although the longest period required for resolving weakness was three days, the MRI, the CT and the electroencephalogram revealed no significant abnormality. In January 1987, during his stereotyped attack of hemiplegic migraine, he also developed oppressive feeling on his anterior chest and these symptoms resolved within fifteen minutes. Because the results of Holter electrocardiogram and ultrasound echocardiogram indicated angina pectoris, a coronary angiography was performed in February 1987. During the angiographical procedures, he began to complain of the oppressive feeling on his anterior chest, and the coronary angiography revealed the definite vasospasm in the anterior descending branch of the left coronary artery. Sublingual nitroglycerin administration resolved the vasospasm, but thereafter the patient developed his stereotyped hemiplegic migrainous attack.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemiplegic migraine complicated with coronary vasospasm]. 162 39

A patient affected by familial hemiplegic migraine underwent Transcranial Doppler Sonography twice: the first during a spontaneous attack with right hemiparesis and aphasia, the second during a headache-free period. During the attack the following haemodynamic changes were seen: (a) bilateral increase in the middle cerebral artery and anterior cerebral artery blood flow velocities (this increase was more pronounced on the left side), (b) decreased systo-diastolic ratio and pulsatility index on the right side, (c) increased systo-diastolic ratio and pulsatility index on the left side. Our results indicate that during the attack in this familial hemiplegic migraine patient a diffuse vasoconstriction of the basal cerebral arteries developed. Moreover, Transcranial Doppler Sonography data suggest that a prolonged vasoconstriction of the peripheral arterioles could play a role in determining the neurological symptoms in this syndrome.
Cephalalgia 1991 Feb
PMID:Transcranial Doppler sonography in familial hemiplegic migraine. 203 67

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

Idiopathic hemifacial atrophy (Parry-Romberg Syndrome) is characterised by progressive wasting or loss of subcutaneous tissue in half of the face, starting usually in childhood, and often associated with skin changes. Two adult onset cases are described. They did not demonstrate skin changes but one had complicated hemiplegic migraine with headaches always ipsilateral to the facial wasting.
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PMID:Progressive hemifacial atrophy--a report of 2 cases. 225 53

99mTC HM-PAO SPECT brain imaging was performed during the headache-free period in 19 young migraineurs, affected by common migraine (CM, 10 cases), classic migraine (CLM, 6 cases) and hemiplegic migraine (HM, 3 cases). SPECT findings were negative in all 10 patients with CM, in 3 cases of CLM and in 2 cases of HM. Positive findings in the remaining 4 patients (3 cases of CLM and 1 of HM) showed a decreased tracer distribution in the temporo-occipital regions (2 cases) and parietal regions (2 cases): the two with decreased temporo-occipital perfusion reported prodromal symptoms exclusively contralateral to the areas of hypoperfusion. An impaired regional cerebral vascular autoregulation may exist even during headache-free intervals in patients suffering from classic and hemiplegic migraine.
Headache 1990 Oct
PMID:99mTc HM-PAO SPECT in pediatric migraine. 227 14

Eight patients with hemiplegic migraine are described. Majority were in their second decade and suffered two or more episodes of dense hemiplegia outlasting the headache. Complete recovery was the rule.
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PMID:Hemiplegic migraine. 239 3

Despite ongoing dispute over the pathophysiologic basis of migraine, the vasospastic theory of pathogenesis has brought to the forefront a promising class of new antimigraine agents, the Ca2+ channel antagonists. Voltage-dependent Ca2+ channels, integral membrane proteins that permit extracellular Ca2+ to enter cells down their electrical and concentration gradients, have a universal role in stimulus-response coupling in excitable cells. Thus, they participate in translating electrical excitation into secretory and contractile events. Ca2+ channel antagonists, a structurally diverse group of organic compounds, inhibit ion flux through voltage-dependent Ca2+ channels by binding to specific, channel-associated drug receptor sites and thereby reduce the frequency of channel opening in response to membrane depolarization. Ca2+ channels in cardiac muscle, smooth muscle, and neurons all exhibit high affinity for Ca2+ channel antagonists, although neurons also contain a population of drug-resistant channels. Extensive clinical experience in the use of Ca2+ channel antagonists has accumulated from their application to nonneurologic, especially cardiovascular, disorders. Three such drugs, nifedipine, verapamil, and diltiazem, are currently available in the United States, although none are specifically approved for use in migraine. Other agents, such as nimodipine, are likely to be released in the near future. A large number of clinical studies have now addressed the efficacy of Ca2+ channel antagonists in the prophylaxis of migraine headache. Dihydropyridines (nifedipine and nimodipine), phenylalkylamines (verapamil), diphenylalkylamines (flunarizine), and benzothiazepines (diltiazem) have all been examined, and a beneficial effect has been noted in each case. The limited directly comparative data currently available and the difficulties involved in comparing the results of different studies do not presently support claims of superiority for any single agent. This is an issue that will require attention as these drugs achieve more widespread use in migraine. Existing evidence suggests that flunarizine, verapamil, nifedipine, and nimodipine are effective prophylactic agents in both common and classic migraine. Nifedipine and nimodipine also appear to be valuable for the treatment of cluster headache. Two case reports describing favorable responses to flunarizine in childhood hemiplegic migraine are the only available data concerning the utility of these drugs in "complicated" migraine syndromes. The role of Ca2+ channel antagonists in treating "muscle contraction" or "tension" headache has not been addressed in any detail.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists and the treatment of migraine. 242 60

We reviewed the medical records of 283 cocaine users consecutively admitted to a municipal hospital and identified 37 patients (13.1%) complaining of headaches. These patients were divided into three groups. Three patients had migraine-like headaches and transient hemiparesis associated with cocaine use. Five patients had headaches associated with cocaine withdrawal. In 29 patients headaches were not clearly associated with cocaine. Twenty-two of the 29 had chronic daily headaches; nine of these patients were depressed. Three had focal brain lesions with chronic daily headache or acute onset global headache. The four remaining patients had other headaches. Based on these findings, we conclude that: (1) Headache is a common complaint in hospitalized cocaine users; (2) Cocaine may occasionally trigger a syndrome which resembles hemiplegic migraine. The potential mechanisms of this syndrome will be discussed; (3) Hospitalized cocaine users who present with headaches most frequently have depression with suicidal ideation, often associated with cocaine withdrawal; and (4) Structural brain disease in these patients may result from a variety of causes.
Headache 1989 Apr
PMID:Headaches in hospitalized cocaine users. 271 72

There is some suggestion in the literature that patients with migraine may be at an increased risk for developing complications as a result of cerebral angiography. To assess this risk, we reviewed the charts of 142 patients with migraine. A total of 149 angiograms were performed for acute headache (55), new focal symptoms (40), exertional (including coital) headaches (nine), hemiplegic migraine (three), ophthalmoplegic migraine (five), vertebrobasilar migraine (six), migraine accompaniments (three), and other causes (14). Transient events were seen in six patients and these were transient amnesia (one), hemisensory changes (two), hemiparesis (one), global confusion (one), and angina (one). One patient with a history of severe ischemic heart disease developed a myocardial infarction two hours after angiography. Focal cerebral events occurred in 2.6% of cases. This compares with a rate of complications of 2.8% caused by angiography in a prospective study of 1002 patients from our center. According to our findings, it appears that a history of migraine does not increase the risk of complications caused by angiography. Angiography during episodes of acute headaches would also appear to be a safe procedure. Transient focal neurologic symptoms, however, are not infrequent, especially in cases of classic migraine.
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PMID:Migraine and the risks from angiography. 339 65


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