Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine preventive therapy, even in the absence of a headache, is given in an attempt to reduce the frequency, duration, or severity of attacks. Circumstances that might warrant preventive treatment include disabling migraine attacks, the overuse of acute medications or failure of or contraindication to acute medications, troublesome side effects from medication, hemiplegic migraine, or very frequent headaches (more than 2 a week). The major medication groups for preventive treatment include anticonvulsants, antidepressants, b-adrenergic blockers, calcium channel antagonists, serotonin antagonists, neurotoxins, nonsteroidal anti-inflammatory drugs, and others. If preventive medication is indicated, the agent preferentially should be chosen from one of the first-line categories, based on the drug's side-effect profile and the patient's coexistent and comorbid conditions.
 ...
PMID:Preventive treatment of migraine. 1662 94

Hemiplegic migraine is a rare subtype of migraine with aura associated with transient hemiplegia. The weakness is caused by motor aura. Hemiplegic migraine is the only headache syndrome associated with known genetic mutations and serves as a model for understanding more common varieties of migraine. Because the phenotype includes striking yet transient neurological signs and symptoms, it is imperative that clinicians know the differential diagnosis to rule out possible secondary etiologies when treating patients with hemiplegic spells. Hemiplegic migraine occurs with equal prevalence in either a sporadic or familial form differentiated only by family history. Thus far, treatment trials are anecdotal, although verapamil and acetazolamide have shown promise.
 ...
PMID:Sporadic and familial hemiplegic migraine: diagnosis and treatment. 1662 31

We report here an 1-year-old boy who was diagnosed as sporadic hemiplegic migraine demonstrated transient changes in electroencephalographic (EEG) background activity accompanied with migraine attacks. The attacks were associated with various neurological complications such as impairment of consciousness and hemiplegia and so on, which coincided with the changes of EEG findings. When his first headache developed with fever and impairment of consciousness, diffuse slow waves (1-2 Hz, 250-300 microV) appeared transiently. The slow wave gradually improved thereafter, and disappeared on the 24th day. On the 25th day, when he had the second attack with left hemiplegia and impairment of consciousness and sensation, slow waves, (2-3 Hz, 250-300 microV) appeared on right side of the brain. Constriction of the right middle cerebral artery was found on MR angiography at that time. The EEG change had improved to normal background activity 3 days after the episode. This unique case demonstrated that transient EEG changes seem to be correlated with the existence of unconsciousness and the laterality of the ischemic insult. We may assume that the changes of electroencephalographic findings may represent the cortical dysfunction caused by vascular constriction.
 ...
PMID:[Changes of electroencephalographic findings in a case of migraine with various neurological symptoms]. 1671 37

Migraine is the most frequent primary headache disorder. It is a neurovascular disorder in which the primary abnormality is thought to be a neuronal excitability underlined by a complex genetic susceptibility. Epidemiogenetic studies have shown that migraine without aura and migraine with aura are polygenic conditions. The three known migraine genes have been identified by the study of the unique monogenic variety of migraine, i.e. familial hemiplegic migraine. These genes all encode ion transporters: the P/Q type calcium channel, a calcium/potassium ATPase and a sodium channel. According to the latter hypothesis about the mechanisms of migraine attacks, poorly known triggers initiate a cortical wave of depolarisation that is responsible for the transient aura symptoms. This cortical spreading depression induces several biochemical changes which, by diffusion through the extracellular space, stimulate the trigeminovascular fibres. These fibres release vasoactive neuropeptides that initiate the neurogenic inflammation. Trigeminovascular fibres transmit nociceptive information centrally via the brainstem. The trigeminovascular fibres also activate the parasympathetic system that is responsible for the persistence of vasodilation in meningeal vessels.
 ...
PMID:[Mechanisms and genetics of migraine]. 1684 22

Biomarkers are physical signs or laboratory measurements that occur in association with a pathological process and have putative diagnostic and/or prognostic utility. In migraine, clinical, radiological, and biochemical biomarkers might be helpful to improve diagnosis, get insight in pathophysiology, and facilitate treatment choices. Genetic biomarkers are defined as genetic variations (mutations or polymorphisms) that can predict disease susceptibility, disease outcome, or treatment response. As yet, only a few genetic biomarkers for migraine are available. Mutations in 3 different genes responsible for familial hemiplegic migraine, a monogenetic subtype of migraine with aura, and the MTHFR C677T polymorphism in common forms of migraine are clear examples. Many positive findings from linkage studies and association studies in common forms of migraine have not been replicated, and are therefore of less clinical use. In this review, we will discuss genetic biomarkers in migraine.
Headache
PMID:Genetic biomarkers for migraine. 1686 10

Prolonged hemiparetic migraine aura can cause diagnostic confusion and be mistaken for ischaemic stroke occurring during the course of a migraine--'migrainous infarction'. We report a case of prolonged hemiparesis occurring during the course of a migraine attack. Though initially confused with migrainous infarction, we suggest with sequential magnetic resonance imaging, magnetic resonance angiography, diffusion, perfusion images and magnetic resonance spectroscopy that the hemiplegia was not of vascular origin and that the patient had sporadic hemiplegic migraine. We hypothesize that the mechanisms of sporadic hemiplegic migraine probably lie at a cellular level, similiar to familial hemiplegic migraine.
Cephalalgia 2006 Aug
PMID:Imaging abnormalities in sporadic hemiplegic migraine on conventional MRI, diffusion and perfusion MRI and MRS. 1688 37

When a patient with migraine has a stroke, all other causes of stroke should be ruled out before the stroke is attributed to migraine. Migraine mimics that present with headaches and stroke, including arteriovenous malformation and cervical carotid artery dissection, should be considered. Patent foramen ovale is a risk factor for both migraine and stroke and should be ruled out with transesophageal echocardiography. A patient with migraine with aura with persistent focal neurologic deficits in the distribution of the typical aura can be diagnosed with migrainous stroke. Patients with migraine with aura with persistent focal neurologic deficits can be treated pharmacologically with intravenous verapamil or magnesium sulfate to relieve the symptoms in familial hemiplegic migraine and sporadic hemiplegic migraine. Prophylactic treatment should be administered to patients with frequent attacks of migraine with aura to prevent recurrence. Oral verapamil is recommended for patients with familial hemiplegic migraine and may be effective in patients with sporadic hemiplegic migraine. Endovascular closure of patent foramen ovale has been reported to prevent recurrence of migraine with aura. The role of patent foramen ovale closure remains controversial pending completion of controlled randomized trials.
 ...
PMID:Interactions between migraine and stroke. 1703 72

It is well recognized that headache, and especially migraine, runs in families. Recent studies into the heritability of primary headache subtypes, migraine, cluster and tension headache, and conditions in which headache is a prominent feature, such as the mitochondrial disease, mitochondrial encephalopathy, lactic acidosis, and strokelike episodes, and the arteriopathy, cerebral autosomal-dominant arteriopathy with subcortical infarctions and leukoencephalopathy, are improving our understanding of the genetic contribution to headache. Studies of the rare familial hemiplegic migraine are leading to advances in understanding the pathophysiological mechanisms of the more common migraine types. Current knowledge of hereditary and genetic features of headache subtypes is reviewed and the implications for understanding the pathophysiology of migraine are discussed.
 ...
PMID:Heredity, genes, and headache. 1704 52

Migraine is a complex, disabling disorder of the brain that manifests itself as attacks of often severe, throbbing head pain with sensory sensitivity to light, sound and head movement. There is a clear familial tendency to migraine, which has been well defined in a rare autosomal dominant form of familial hemiplegic migraine (FHM). FHM mutations so far identified include those in CACNA1A (P/Q voltage-gated Ca(2+) channel), ATP1A2 (N(+)-K(+)-ATPase) and SCN1A (Na(+) channel) genes. Physiological studies in humans and studies of the experimental correlate--cortical spreading depression (CSD)--provide understanding of aura, and have explored in recent years the effect of migraine preventives in CSD. Therapeutic developments in migraine have come by targeting the trigeminovascular system, with the most-recent being the proof-of-principle study of calcitonin gene-related peptide (CGRP) receptor antagonists in acute migraine. To understand the basic pathophysiology of migraine, brain imaging studies have firmly established reproducible changes in the brainstem in regions that include areas that are involved in sensory modulation. These data lead to the view that migraine is a form of sensory dysmodulatio--a system failure of normal sensory processing.
 ...
PMID:Recent advances in understanding migraine mechanisms, molecules and therapeutics. 1714 70

Alternating hemiplegia of childhood (AHC) is a severe brain disorder, mainly characterised by episodes of hemiplegia, progressive mental retardation, and other severe paroxysmal and permanent neurological symptoms. Clinically and genetically, there is some overlap with sporadic (SHM) and familial (FHM) hemiplegic migraine, a severe monogenic subtype of migraine. Although no mutations were detected in the FHM1 CACNA1A and FHM2 ATP1A2 genes in sporadic AHC patients, a mutation was found in the FHM2 ATP1A2 gene in a family with AHC. Recently, a missense mutation was found in the SLC1A3 gene that encodes the glutamate transporter EAAT1, in a patient with alternating hemiplegia, episodic ataxia, seizures, and headache. Because of the remarkable clinical similarities and the potential role of glutamate in AHC, we analysed six sporadic patients with AHC for mutations in the SLC1A3 gene. No mutations were found. The SLC1A3 EAAT1 glutamate transporter gene does not seem to be involved in the pathogenesis of AHC.
 ...
PMID:Alternating hemiplegia of childhood: no mutations in the glutamate transporter EAAT1. 1723 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>