Specific Music Therapy Techniques in the Treatment of Primary Headache Disorders in Adolescents: A Randomized Attention-Placebo-Controlled Trial

2013 ◽  
Vol 14 (10) ◽  
pp. 1196-1207 ◽  
Author(s):  
Julian Koenig ◽  
Rieke Oelkers-Ax ◽  
Michael Kaess ◽  
Peter Parzer ◽  
Christoph Lenzen ◽  
...  
2019 ◽  
Vol 9 (3) ◽  
pp. 233-240 ◽  
Author(s):  
Peter J. Goadsby

Purpose of reviewTo review 5 new areas in primary headache disorders, especially migraine and cluster headache.Recent findingsCalcitonin gene-related peptide (CGRP) receptor antagonists (gepants—rimegepant and ubrogepant) and serotonin 5-HT1F receptor agonists (ditans—lasmiditan) have completed phase 3 clinical trials and will soon offer novel, effective, well-tolerated nonvasoconstrictor options to treat acute migraine. CGRP preventive treatment is being revolutionized after the licensing of 3 monoclonal antibodies (MABs), erenumab, fremanezumab, and galcanezumab, with eptinezumab to follow, especially designed for migraine; they are effective and well tolerated. For patients seeking a nondrug therapy, neuromodulation approaches, single-pulse transcranial magnetic stimulation, noninvasive vagus nerve stimulation (nVNS), and external trigeminal nerve stimulation, represent licensed, well-tolerated approaches to migraine treatment. For the acute treatment of episodic cluster headache, nVNS is effective, well tolerated, and licensed; nVNS is effective and well tolerated in preventive treatment of cluster headache. The CGRP MAB galcanezumab was effective and well tolerated in a placebo-controlled trial in the preventive treatment of episodic cluster headache. Sphenopalatine ganglion stimulation has been shown to be effective and well tolerated in 2 randomized sham-controlled studies on chronic cluster headache. Understanding the premonitory (prodromal) phase of migraine during which patients experience symptoms such as yawning, tiredness, cognitive dysfunction, and food cravings may help explain apparent migraine triggers in some patients, thus offering better self-management.SummaryHeadache medicine has made remarkable strides, particularly in understanding migraine and cluster headache in the past 5 years. For the most common reason to visit a neurologist, therapeutic advances offer patients reduced disability and neurologists a rewarding, key role in improving the lives of those with migraine and cluster headache.


2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Jasem Y. Al-Hashel ◽  
Samar Farouk Ahmed ◽  
Fatemah J Alshawaf ◽  
Raed Alroughani

Cephalalgia ◽  
2012 ◽  
Vol 32 (7) ◽  
pp. 583-584 ◽  
Author(s):  
Geneviève Demarquay ◽  
Christelle Créac’h ◽  
Roland Peyron

Author(s):  
Christopher Mares ◽  
Jehane H. Dagher ◽  
Mona Harissi-Dagher

AbstractThe most common symptom of post-concussive syndrome (PCS) is post-traumatic headache (PTH) accompanied by photophobia. Post-traumatic headache is currently categorized as a secondary headache disorder with a clinical phenotype described by its main features and resembling one of the primary headache disorders: tension, migraine, migraine-like cluster. Although PTH is often treated with medication used for primary headache disorders, the underlying mechanism for PTH has yet to be elucidated. The goal of this narrative literature review is to determine the current level of knowledge of these PTHs and photophobia in mild traumatic brain injury (mTBI) in order to guide further research and attempt to discover the underlying mechanism to both symptoms. The ultimate purpose is to better understand the pathophysiology of these symptoms in order to provide better and more targeted care to afflicted patients. A review of the literature was conducted using the databases CINAHL, EMBASE, PubMed. All papers were screened for sections on pathophysiology of PTH or photophobia in mTBI patients. Our paper summarizes current hypotheses. Although the exact pathophysiology of PTH and photophobia in mTBI remains to be determined, we highlight several interesting findings and avenues for future research, including central and peripheral explanations for PTH, neuroinflammation, cortical spreading depolarization and the role of glutamate excitotoxicity. We discuss the possible neuroanatomical pathways for photophobia and hypothesize a possible common pathophysiological basis between PTH and photophobia.


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