Comprehensive Review of Headache Medicine

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Structural insights into RAMP modification of secretin family G protein-coupled receptors: implications for drug development. Trends Pharmacol Sci. Edvinsson L. Regulation of signal transduction by calcitonin gene-related peptide receptors. Ann Clin Transl Neurol.

Walker C, Hay D. Br J Pharmocol. Calcitonin gene-related peptide: functional role in cerebrovascular regulation. Vasoactive peptide release in the extracerebral circulation of humans during migraine headache. Ann Neurol. Goadsby P, Edvinsson L. The trigeminovascular system and migraine: studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats. CGRP may play a causative role in migraine. J Comp Neurol. A potential preclinical migraine model: CGRP-sensitized mice. Mol Cell Pharmocol.

BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain. Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X3 receptors. Functional bases for a central serotonergic involvement in classic migraine: a speculative view.

CAQ Certification - National Headache Foundation

Elevated saliva calcitonin gene-related peptide levels during acute migraine predict therapeutic response to rizatriptan. A controlled trial of erenumab for episodic migraine. Br J Clin Pharmacol.


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In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK J Pharmacol Exp Ther. Spotlight on anti-CGRP monoclonal antibodies in migraine: the clinical evidence to date.

Clin Pharmacol Drug Dev. Estimating the clinical effectiveness and value-based price range of erenumab for the prevention of migraine in patients with prior treatment failures: a US societal perspective. J Med Econ. Informa UK Ltd. Pharmacokinetic-pharmacodynamic relationship of erenumab AMG and capsaicin-induced dermal blood flow in healthy and migraine subjects.

Pharm Res Pharm Res. PubMed Google Scholar. Phase I, randomized, double-blind, placebo-controlled, single-dose, and multiple-dose studies of erenumab in healthy subjects and patients with migraine. Clin Pharmacol Ther. Calcitonin gene-related peptide receptor as a novel target for the management of people with episodic migraine: current evidence and safety profile of erenumab.

J Pain Res. ARISE: the phase 2 randomized trial of erenumab for episodic migraine. A randomized, double-blind, placebo-controlled study to evaluate the effect of erenumab on exercise time during a treadmill test in patients with stable angina. Phase I, randomized, parallel-group, double-blind, placebo-controlled trial to evaluate the effects of erenumab AMG and concomitant sumatriptan on blood pressure in healthy volunteers. Markham A. Pegvaliase: first global approval. Reinke T.

Synopsis About this title A broad review of headache pathophysiology, diagnosis and treatment, this book is divded into four parts.

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Review Its breadth of coverage will make it a useful tool for general practitioners and headache specialists alike. A thoughtful review of anatomy precedes comprehensive chapters discussing diagnosis, treatment, and the care and management of special populations This is one of the first books The contributing authors are among the most influential and knowledgeable experts in the world, and they discuss the latest in evidence-based diagnosis and treatment while inserting thoughtful personal views and pearls.

Buy New Learn more about this copy. About AbeBooks. Customers who bought this item also bought. Stock Image. New Quantity Available: 4. Seller Rating:. New Quantity Available: 2. Majestic Books London, ,, United Kingdom. Comrehensive Review Headche Medicine Levin.

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  6. It is widely appreciated to be perhaps the most severe pain condition known to humans. The pain is typically boring, periorbital or otherwise localized to the dermatome of the ophthalmic division of the trigeminal nerve, and without variation in location from attack to attack.

    It occurs in relatively brief episodes mean less than 1 hour, but between 15 and minutes often with highly predictable timing. In particular individuals, attacks will occur daily or nearly daily, for up to eight attacks per day, often occurring at the same times each day and typically during sleep. These daily attacks will also occur during periods lasting from weeks to a few months, and these periods will often recur on an annual or biannual basis during the same seasons, which are often perisolsticial.

    Attacks are associated with restlessness or agitation. As with the clinical features of migraine, any comprehensive theory of cluster headache pathogenesis will need to account for these cardinal features. Genetics Cluster headache has a population prevalence of 0. First-degree relatives of patients with cluster headache have approximately a fold higher risk of also having the disorder.

    Association studies from Italy and Germany have found increased odds ratios of 6. This association was not observed in a third large cohort from northern Europe. Brain Mechanisms The understanding of the pathophysiology of cluster headache was dramatically advanced over the past decade by the imaging studies of Goadsby and colleagues.

    PET imaging studies demonstrated focal activation during cluster attacks of a small region ipsilateral to the headache pain within the posteromedial inferior diencephalon that has been typically interpreted as being a hypothalamic structure but may actually lie within the thalamus. On the basis of this anatomic localization, Leone and colleagues have applied deep brain stimulation to this region in patients with intractable chronic cluster headache, often resulting in dramatic amelioration of symptoms.

    The nature of this diencephalic structure has been the focus of much speculation.

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    One very attractive candidate for this diencephalic structure in cluster headache is the group of neurons in the perifornical region of the hypothalamus that contain orexins as neurotransmitters. Orexins are two peptides derived from a common preprohormone, hypocretin. Orexin A is 34 amino acids and orexin B is 28 amino acids. Two g protein-coupled receptors bind the orexins: orexin-1 receptor binds orexin A, and orexin-2 receptor binds orexin A and orexin B.

    Orexinergic neurons project to a wide variety of neural structures previously implicated in mechanisms of migraine, including locus ceruleus, raphe nuclei, cerebral cortex, and autonomic structures such as the nucleus tractus solitarius and the intermediolateral cell column of the spinal cord. Moreover, orexinergic neurons are lost in narcolepsy, a disorder characterized by symptoms of loss of coordinated circadian brain state boundaries, including sleep and waking. They are also markedly diminished in multiple system atrophy, a condition of autonomic failure. Orexin B applied to rat hypothalamus potentiates trigeminal responses to dural stimulation or noxious facial stimulation, whereas orexin A has the opposite effect.

    Activation of the orexin-1 receptor produces analgesic effects in the rat formalin test. Could cluster headache, a condition characterized by extreme pain, autonomic hyperactivity, and motor restlessness and governed by strict timing, be a condition of transient orexinergic hyperactivity? Measurements of CSF orexins during cluster headache attacks and pathologic examination of the brains of cluster headache patients should answer this question.