The spreading depression phenomenon may explain clinical as well experimental findings in migraine. Its propagation velocity mirrors what is found in clinical aura, it may activate the spinal trigeminal nucleus and may induce CGRP and NO release. Circulatory changes detected with various imaging procedures during migraine also support the pathophysiological role of spreading depression. Three abnormal loci chromosomes 1 and 19 have been recently found in familial hemiplegic migraine.
|Published (Last):||28 December 2007|
|PDF File Size:||4.14 Mb|
|ePub File Size:||2.85 Mb|
|Price:||Free* [*Free Regsitration Required]|
The spreading depression phenomenon may explain clinical as well experimental findings in migraine. Its propagation velocity mirrors what is found in clinical aura, it may activate the spinal trigeminal nucleus and may induce CGRP and NO release. Circulatory changes detected with various imaging procedures during migraine also support the pathophysiological role of spreading depression.
Three abnormal loci chromosomes 1 and 19 have been recently found in familial hemiplegic migraine. It is possible that a channelopathy underlies the pathophysiology of migraine, as in other paroxysmal neurological disorders secondary to membrane hyperexcitability.
Em , Olesen e cols. Moskowitz e col. O mesmo ocorreu com o bosentan RO, mg EV , um antagonista da endotelina Existem muitos receptores para 5-HT, separados em grupos numerados de 1 a 7. Sua nomenclatura tem sido confusa e frequentemente modificada O sumatriptan comporta-se como um agonista 5-HT 1-like. Feniuk e col. Um medicamento com afinidade predominante para o receptor 5-HT 1D teoricamente pode ter algum efeito anti-enxaquecoso sem ser vasoconstrictor.
A CP Este foi o primeiro modelo no qual o sumatriptan mostrou qualquer efeito sobre a DA. Um dos estudos mais interessantes em enxaquecas foi publicado por Woods et al. O estudo de Woods et al. Usando magnetoencefalografia MEG , Barckley et al. Pacientes com MELAS m itochondrial myopathy, e ncephalopathy, l actic a cidosis and s troke-like episodes , uma encafalopatia mitocondrial geneticamente determinada, sofrem quase na sua totalidade de crises enxaquecosas.
Logo verificou-se novos loci no cromossoma 1q 59 e 1q31 Mechanism of migraine headache and action of ergotamine tartrate. Arch Neurol Psychiatry ; Focal Hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Ann Neurol ; Spreading depression of activity in cerebral cortex. J Neurophysiol ; Migraine Pain associated with middle cerebral artery dilatation: reversal by sumatriptan.
Lancet ; Sumatriptan relaxes isolated porcine ophthalmic artery, but inhibits VIP-induced relaxation. Cephalalgia ; Occurence of vasoactive intestinal polypeptide VIP -like immunoreactivity in certain cholinergic neurons of the cat: evidence from combined immunohistochemistry and acetylcholinesterase staining.
Neuroscience ; Uddman R, Edvinsson L. Neuropeptides in the cerebral circulation. Cerebrovasc Brain Metab Rev ; Lundberg JM. Pharmacology of cotransmission in the autonomic nervous system: integrative aspects on amines, neuropeptides, adenosine triphosphate, aminoacids and nitric oxide. Pharmacol Rev ; Substance P augments the rate of vasodilation induced by calcitonin gene-related peptide in porcine ophthalmic artery in vitro.
Neuropeptides ; Calcitonin gene related peptide is a potent inhibitor of substance P degradation. Eur J Pharmacol ; Molecular characterization of endothelin receptors.
Trends Pharmacol Sci ; Endothelin-1 in migraine and tension-type headache. Acta Neurol Scand ; Increased plasma level of endothelin-1 in cluster headache. In: Olesen J, Edvinsson L eds. Frontiers in headache research, Vol 7. Headache pathogenesis: monoamines, neuropeptides, purines, and nitric oxide. Philadelphia: Lippincott-Raven ; Characterization of endothelin receptors in the cerebral vasculature and their lack of effect on spreading depression.
J Cer Blood Flow Metab ; The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature ; Nitric oxide: physiology, pathophysiology and pharmacology. The nitric oxide hypothesis of migraine and other vascular headaches. Nitric oxide synthase inhibition: a new principle in the treatment of migraine attacks.
Neurotransmitters and neuropeptides in headache. Curr Opin Neurol ; Nitric oxide synthase is induced in cerebral endothelial cells by spreading depression Abstract. Cephalalgia ;13[Suppl 13] Moskowitz MA. The neurobiology of vascular head pain. Vasoactive peptide release in the circulation of humans during migraine headaches. Release of vasoactive peptides in the external circulation of humans and the cat during activation of the trigeminovascular system.
Endothelin antagonist bosentan blocks neurogenic inflamation, but is not effective in aborting migraine attacks. Pain ; On serotonin and migraine: a clinical and pharmacological review. Effect of serotonin in migraine patients.
Neurology ; International union of pharmacology classification of receptors for 5-hydroxytryptamine serotonin. Sumatriptan is a potent vasoconstrictor of human dural arteries via a 5-HT 1 -like receptor. Rationale for the use of 5-HT1-like agonists in the treatment of migraine. J Neurol ; Suppl 1 :SS The antimigraine drug, sumatriptan GR , selectively blocks neurogenic plasma extravasation from blood vessels in dura mater.
Br J Pharmacol ; Neurogenic versus vascular mechanisms of sumatriptan and ergot alkaloids in migraine. The pre- and postjunctional activity of CP,, a conformationally restricted analogue of sumatriptan.
Molec Pharmacol ; Autoradiographic distribution of [ 3 H]Sumatriptan-binding sites in post-mortem human brain. Clifford Rose F. Sumatriptan arrests migraine aura. Headache ; Sumatriptan blocks spreading depression in isolated chick retina. Lashley KS. Patterns of cerebral integration indicated by the scotomas of migraine. Propagation of spreading cortical depression. Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms.
J Neurosci ; Possible mechanism of c-fos expression in trigeminal nucleus caudalis following cortical spreading depression. Involvement of calcitonin gene-related peptide CGRP and nitric oxide NO in the pial artery dilatation elicited by cortical spreading depression. Brain Res ; Cortical spreading depression does not result in the release of calcitonin gene-related peptide into the external jugular vein of the cat: relevance to human migraine.
Cortical spreading depression recorded from the human brain using a multiparametric monitoring system. Bilateral spreading cerebral hypoperfusion during spontaneous migraine headache. N Engl J Med ; Brain stem activation in human migraine attacks.
Nature Med ;
UMA PERSPETIVA MULTIDIMENSIONAL DO TRATAMENTO DA ENXAQUECA
Nathalia Guerra flag Denunciar. James MF et al. Weiller C et al. Nat Med. The first human study to show activation in the brain stem used positron emission tomography PET performed in subjects during spontaneous migraine. Because PET lacks sufficient resolution for exact anatomical localization, the activation was hypothesized to be in the regions of dorsal raphe nuclei DRN , periaqueductal gray PAG and locus ceruleus LC 1 1.
Sociedade Portuguesa de Neurologia. Primary headaches: a convergence hypothesis. Dodick D e Gragus J. Mecanismos que deflagram a enxaqueca. Duetto Scientific American. Focal Hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine. Striessnig J.
Its economic impact in the productivity and leisure is significant, and the headache attacks may incapacitate the patients for the usual activities. With a complex and still unknown pathophysiology, migraine may present with intermittent and peculiar episodes of intense headache. The most efficient approach for the treatment includes the avoidance of the trigger factors, preventive treatment, rescue treatment for the moments of pain and the accessory or non drug treatment. For the preventive treatment, scope of this update, various classes of substances are used and include the beta blockers, triciclic antidepressants and recently the selective serotonin reuptake inhibitors , calcium antagonists, serotonin antagonists, anticonvulsants and others. Even though its mechanisms of action in the treatment of migraine are unknown, it seems that all of the drugs influence the central serotonergic, noradrenergic and gabaergic functions. New proposals for the mechanisms of action of some of these drugs, also include the inhibition of the synthesis of nitric oxide and the modulation of the neuronal cationic channels. When individualized and correctly used, these preventive medications have been held responsible for important reductions in the frequency and intensity of migraine episodes, decreasing this way, the marathon of suffering and doubtful approaches, that these patients are usually submitted.