Can association between transient global amnesia and migraine tell us something about the pathophysiology of transient global amnesia?
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Transient global amnesia
Cortical Spreading Depression
Pathophysiology
Transient (computer programming)
Depression
Association (psychology)
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Acute confusional migraine (ACM) is a rare migraine variant, affecting children and adolescents, as well as adults. Between 0.45 and 7.8% of children with migraine present with ACM, but the disorder may well be underdiagnosed. ACM is an exclusion diagnosis and some dangerous causes of confusion (e.g., epilepsy, ischemia, hemorrhagia, neoplasm, intoxication and encephalitis) should be ruled out. The confusional state often manifests with a wide diversity of cortical dysfunctions, such as speech difficulties, increased alertness, agitation and amnesia. Exact history taking, clinical examination, and laboratory, radiological and electroencephalographical findings lead the practitioner towards the diagnosis. Approximately half of the cases may be triggered by mild head trauma. Transient global amnesia is an important differential diagnosis, possibly caused by similar pathophysiological mechanisms. The exact pathomechanism remains unclear, with the common hypothesis comprising of the confusional state as a complex aura phenomenon, in which the cortical spreading depression wave reaches not only the occipital, but also the temporal, parietal and frontal cortex, as well as the brainstem and the hippocampi, leading to transient hypoperfusion and dysfunction of these brain areas.
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Familial hemiplegic migraine type 1 (FMH-1) is a rare form of migraine with aura, which is characterized by transient hemiparesis, sensory loss and visual disturbances. This monogenic disease shares many common features with classic migraine, suggesting a similar molecular pathophysiology. Migraine is triggered by activation and sensitization of the trigeminovascular system, specifically the trigeminal nociceptive afferents innervating the meninges. Aura migraine is associated with cortical spreading depression (CSD), which is a short-lasting intense wave of neuronal and glial cell depolarization that slowly progresses over the cortex and is followed by long-lasting neuronal activity depression.
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Transient global amnesia
Cortical Spreading Depression
Retrograde amnesia
Neurological examination
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Transient global amnesia
Cortical Spreading Depression
Pathophysiology
Transient (computer programming)
Depression
Association (psychology)
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Spreading depression (SD) is a slowly propagating wave of near-complete depolarization of neurons and glial cells across the cortex. SD is thought to contribute to the underlying pathophysiology of migraine aura, and possibly also an intrinsic brain activity causing migraine headache. Experimental models of SD have recapitulated multiple migraine-related phenomena and are considered highly translational. In this review, we summarize conventional and novel methods to trigger SD, with specific focus on optogenetic methods. We outline physiological triggers that might affect SD susceptibility, review a multitude of physiological, biochemical, and behavioral consequences of SD, and elaborate their relevance to migraine pathophysiology. The possibility of constructing a recurrent episodic or chronic migraine model using SD is also discussed.
Cortical Spreading Depression
Depression
Pathophysiology
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Transient global amnesia is described in two patients suffering from classical and common migraine, respectively. These cases are peculiar in that the amnesic attack was part of the aura in one patient, while it behaved like an accompanying symptom in the other. The close temporal relation between the attacks of transient global amnesia and migraine strengthens the hypothesis of an etiologic role of migraine. The nature of this mechanism could be the cerebral blood flow changes or the neural perturbation which characterize migraine attacks.
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Transitory global amnesia and migraine without aura are diseases with unclear pathophysiologic mechanisms, but with evidence of comorbidity. We describe twin monozygotic brothers, both presenting episodes of transitory global amnesia occurring only during attacks of migraine without aura. This report supports the hypothesis of a common underlying pathogenetic mechanism, possibly related to the cortical spreading depression. Furthermore, a common genetic trait in both the diseases or more probably in a particular subgroup of patients could be hypothesized.
Transient global amnesia
Cortical Spreading Depression
Pathophysiology
Depression
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Migraine is a most common neurological disease that affects nearly 10% of the general population. Although the pathophysiology of migraine is obscure, cortical spreading depression (CSD) is believed to be a phenomenon underlying migraine auras. On the other hand, the activation of the trigemino-vascular system is considered to be related to headaches. Furthermore, satellite ganglion cells located around the neurons in the trigeminal ganglion may contribute to migraine headaches. Besides, CSD has also been reported to activate the trigemino-vascular system, which subsequently causes migraine headaches. The present review discusses the recent findings of migraine pathophysiology, and mentions some newly developed calcitonin gene-related peptide (CGRP) receptor antagonists, which have revealed the efficaciousness for acute migraine attacks.
Cortical Spreading Depression
Pathophysiology
Trigeminal ganglion
Depression
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Migraine is a collection of perplexing neurological conditions in which the brain and its associated tissues have been implicated as major players during an attack. Once considered exclusively a disorder of blood vessels, compelling evidence has led to the realization that migraine represents a highly choreographed interaction between major inputs from both the peripheral and central nervous systems, with the trigeminovascular system and the cerebral cortex among the main players. Advances in in vivo and in vitro technologies have informed us about the significance to migraine of events such as cortical spreading depression and activation of the trigeminovascular system and its constituent neuropeptides, as well as about the importance of neuronal and glial ion channels and transporters that contribute to the putative cortical excitatory/inhibitory imbalance that renders migraineurs susceptible to an attack. This review focuses on emerging concepts that drive the science of migraine in both a mechanistic direction and a therapeutic direction.
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In comparison with 27 similar cases, sampled from literature, 4 observations of amnesic episodes in migraine are presented and discussed. These disturbances known as so-called "Migranedammerattacken" seem to be identical with transient global amnesia in all respects. In most of cases, they occur as migraine-precursors or - equivalents. Headache, vegetative und neurological symptoms are frequent but not necessary companions. It is proposed to look for migraine disposition in all cases of transient global amnesia. Perhaps, this approach might be of some use to understand their enigmatic pathogenesis.
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