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

Thunderclap headache is an uncommon type of headache, but recognition and diagnosis are important because of the possibility of a serious underlying brain disorder. In this chapter, primary thunderclap headache in relation to other primary headache disorders and secondary, symptomatic headache disorders are discussed. Most importantly, subarachnoid hemorrhage should be excluded. The first investigation is a computed tomography (CT) scan, and, if the CT scan is negative, investigation of the cerebrospinal fluid. Other symptomatic vascular causes are intracranial hemorrhage, cerebral venous sinus thrombosis, cervical artery dissection, or a reversible vasoconstriction syndrome. These and other serious underlying intracranial disorders should be detected by magnetic resonance imaging or the appropriate investigations. The remaining patients with thunderclap headache most likely represent a primary headache disorder, including migraine, primary cough headache, primary exertional headache, or primary headache associated with sexual activity. Within the group of primary headache disorders, primary thunderclap headache represents a distinct clinical entity; it is characterized by a sudden severe headache lasting from 1h up to 10 days and not attributed to another disorder. The pathogenesis of primary thunderclap headache is still not known, but the sympathetic nervous system may play an important role.
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PMID:Primary thunderclap headache. 2081 48

Migraine is an episodic brain disorder that is characterized by recurrent attacks of severe unilateral headache that are accompanied by various neurological symptoms. In addition, many patients have what is called an aura with visual and sensory disturbances. The majority of patients are female, suggesting that female hormones play an important role in the pathophysiology of the disorder. The molecular mechanisms, however, underlying this female preponderance are not well understood. It can be expected that the field of genetics that aims at identifying genetic factors that cause migraine by lowering the threshold for attacks will unravel some of these mechanisms. The 3 best known migraine genes encode ion transporters and were identified in families with familial hemiplegic migraine (FHM), a rare subtype of migraine with aura. FHM gene mutations cause alterations in mechanisms that control and modulate the neurotransmitter balance in the brain. Transgenic mice knock-in with human pathogenic mutations that were shown to exhibit some migraine-relevant features were very helpful in dissecting molecular mechanisms of migraine and pointed to a central role for cortical glutamate. In addition, transgenic mice that overexpress human RAMP1 exist and exhibit an increased sensitivity to calcitonin gene-related peptide. Findings from genetic and animal experiments on gender differences in migraine are discussed. Recently, a role for glutamate also came forward from a genome-wide association study in common migraine. By deciphering genetic and pathogenic migraine pathways, it can be expected that in the near future we will better understand mechanisms behind the female preponderance in migraine.
Headache 2011 Jun
PMID:Migraine genes and the relation to gender. 2163 74

Migraine affects about 15 percent of the population; it is ranked number 12 amongst women and 19 in the general population for the degree of handicap it causes, according to the World Health Organization. Migraine is a complex and often disabling brain disorder. It has internationally agreed diagnostic clinical criteria but they are somewhat subjective and arbitrary. Functional imaging studies have the potential to advance our understanding of the underlying migraine mechanism and that of other headache disorders. This article reviews the pivotal neuroimaging studies in migraine that have advanced the field.
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PMID:What has imaging taught us about migraine? 2180 73

Migraine is a chronic. disabling, biologically determined, inherited brain disorder rendering life much less tolerable. The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches, in a document called 'The International Classification of Headache Disorders, 2nd edition' (ICHD-2). Migraine affects 10-16% of the population world-wide. For the 20-30% of migraine sufferers who experience migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. There are three main aspects of treatment: trigger avoidance, acute symptomatic control, and pharmacological prevention. Acute medications are more effective if used earlier in an attack. The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraines, and to increase quality of life.
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PMID:[Migraine - diagnostic features, acute therapy and prophylactics]. 2188 46

Migraine is a common and complex brain disorder. Although it is clear that head pain is a key manifestation of the disorder for most patients, what drives the activation of neuronal pain pathways in susceptible patients is less obvious. There is growing evidence that migraine pathophysiology may, in part, include dysfunction of subcortical structures. These include diencephalic and brainstem nuclei that can modulate the perception of activation of the trigeminovascular system, which carries sensory information from the cranial vasculature to the brain. Dysfunction of these nuclei, and their connections to other key brain centres, may contribute to the cascade of events that results in other symptoms of migraine - such as light and sound sensitivity - thus providing a comprehensive explanation of the neurobiology of the disorder.
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PMID:Diencephalic and brainstem mechanisms in migraine. 2193 34

Migraine is a primary headache disorder with an unknown pathophysiology. The growing evidence in recent years indicates migraine being a brain disorder, a sensory dysmodulation, and a system failure of normal sensory processing of the brainstem that involves the vascular tone and pain. At the moment, triptan family and NSAIDs are the first choice drugs for the treatment of acute migraine. There are several prophylactic drugs including the antiepileptic drugs (AEDs), betablockers, and Ca2+ channel blockers that are used for the treatment of migraine. Although many drugs including the triptans, NSAIDs, and others target the peripheral sites of activation, several novel drugs are being developed to target neural sites of action in the central nervous system (CNS). The first trigeminal synapses in the brain stem as well as the ascending and descending pathways and higher brain centers are involved in the transmission of pain and therefore be the main targets of several drugs some of which are in clinical trials. Central sensitization may also aggravate the headache and some drugs tend to alleviate pain by targeting neurotransmitters, receptors, or signalling molecules involved in this phenomenon. This article discusses the CNS acting novel drugs and those that are currently in use for the treatment of migraine.
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PMID:Central nervous system acting drugs in treatment of migraine headache. 2253 10

Migraine is a common disabling brain disorder whose key manifestations are recurrent attacks of unilateral headache and interictal hypersensitivity to sensory stimuli. Migraine arises from a primary brain dysfunction that leads to episodic activation and sensitization of the trigeminovascular pain pathway and as a consequence to headache. Major open issues concern the molecular and cellular mechanisms of the primary brain dysfunction(s) and of migraine pain. We review here our current understanding of these mechanisms, focusing on recent advances regarding migraine genetics, headache mechanisms, and the primary brain dysfunction(s) underlying migraine onset and susceptibility to cortical spreading depression, the neurophysiological correlate of migraine aura. We also discuss insights obtained from the functional analysis of familial hemiplegic migraine mouse models.
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PMID:Migraine: a disorder of brain excitatory-inhibitory balance? 2263 69

Migraine is a complex and often disabling brain disorder that affects about 15 % of the population. The diagnosis of migraine is based on clinical features as proposed by the International Headache Society criteria but they are somewhat subjective and arbitrary. Functional neuroimaging of patients with migraine has been recently employed to study the underlying pathophysiology of headache. These studies have suggested that migraine involves functional and structural plasticity of both central and peripheral nervous system. Insights into the fundamental physiology of migraine have been limited by the lack of methods available to detect the pathophysiological background of critical moment of migraine attack onset that is greatly different from the onset of pain or pain phase of a migraine attack. In order to overcome methodological caveats in detecting "migraine origin" or a "migraine generator", functional brain imaging has been lately dominated by experimental acute-pain research. Along this research line functional imaging using experimental pain stimulation have greatly improved our knowledge about physiological or dysfunctional neuronal activity pattern in patients with migraine, but at the same time, it is important to emphasize that experimental pain is different from spontaneous migraine pain.
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PMID:The pain in migraine beyond the pain of migraine. 2264 82

Fibromyalgia is a primary brain disorder or a result of peripheral dysfunctions inducing brain alterations, with underlying mechanisms that partially overlap with other painful conditions. Although there are methodologic variations, neuroimaging studies propose neural correlations to clinical findings of abnormal pain modulation in fibromyalgia. Growing evidences of specific differences of brain activations in resting states and pain-evoked conditions confirm clinical hyperalgesia and impaired inhibitory descending systems, and also demonstrate cognitive-affective influences on painful experiences, leading to augmented pain-processing. Functional data of neural activation abnormalities parallel structural findings of gray matter atrophy, alterations of intrinsic connectivity networks, and variations in metabolites levels along multiple pathways. Data from positron-emission tomography, single-photon-emission-computed tomography, blood-oxygen-level-dependent, voxel-based morphometry, diffusion tensor imaging, default mode network analysis, and spectroscopy enable the understanding of fibromyalgia pathophysiology, and favor the future establishment of more tailored treatments.
Curr Pain Headache Rep 2012 Oct
PMID:Brain imaging in fibromyalgia. 2271 98

Migraine is a prevalent and disabling brain disorder that costs billions of dollars annually in direct healthcare costs, and school and work absenteeism and presenteeism. The objective of acute treatment is a cost-effective, rapid restoration of functional ability, with minimal recurrence and adverse effects. The acute treatment of migraine includes specific drugs, which currently all have vasoconstrictive effects (dihydroergotamine and triptans), and nonspecific drugs that include paracetamol (acetaminophen), combination analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), dopamine antagonists, narcotics and corticosteroids. NSAIDs have both peripheral and central effects on reversing migraine, and so may represent the best alternative for patients who cannot use triptans and ergots due to vascular contraindications. Narcotics and habituating medications should be avoided in the acute treatment of migraine, as the risk for transformation to chronic daily headache is excessively high at a relatively infrequent rate of exposure.
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PMID:Acute treatment of migraines. 2282 82


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