O estimulador

do gânglio esfenopalatino é aprovado na Europa para uso em cefaleia em salvas crônica. Estudos sobre estimulação não invasiva do nervo vago, uso do estimulador do gânglio esfenopalatino e estimulação do nervo occipital serão realizados nos EUA em 2014. Até o momento nenhum desses dispositivos para neuromodulação foi aprovação pelo FDA para uso nos EUA. Para encontrar mais recursos visite The American Obeticholic Acid Migraine Foundation (http://kaywa.me/ir2eb) “
“The practice of headache medicine is challenging, and excluding secondary causes of headaches is essential for proper diagnosis and treatment. The evaluation of secondary headaches often leads to investigations involving organ systems other than the nervous system. As such, headache, which is typically thought to be neurologic in origin, can be a manifestation of cardiac pathology in the form of cardiac cephalalgia. Conversely, chest pain, which is typically thought compound screening assay to be cardiac in origin, could be a manifestation of a neurologic disease process in the form of atypical migraine aura. In the presented cases, we demonstrate headaches that involve cardiac and neurologic pathology with atypical presentations. “
“Though thyroid growths are considered to be a frequent cause of Horner’s

syndrome, concurrent headache attacks are not commonly seen. A 63-year-old woman presented with severe, daily occurring, unilateral headache attacks with ipsilateral Horner’s

syndrome. Magnetic resonance imaging arteriography showed a multinodular goiter displacing the left common carotid artery. This case exemplifies the combination of headache attacks and Horner’s syndrome due to mechanical pressure of an enlarged thyroid, mimicking the symptoms both of carotid dissection as well as trigeminal autonomic cephalgias like paroxysmal hemicrania. “
“The International Classification of Headache Terminal deoxynucleotidyl transferase Disorders, 3rd Edition (ICHD-3) beta version defines migrainous infarction as 1 or more otherwise typical aura symptoms that persist beyond 1 hour with neuroimaging confirmation of an ischemic infarction in the affected territory.[1] Here we describe a woman with migraine with brainstem aura, who experienced acute-onset left sensorimotor deficits in addition to her typical aura symptoms in the midst of a prolonged, but otherwise typical attack. Magnetic resonance imaging (MRI) of the brain revealed a pontine lesion consistent with an ischemic stroke. Our case illustrates potential limitations of the ICHD-3 beta definition of migrainous infarction. Our patient developed episodic headaches that fulfilled ICHD-3 beta criteria for episodic migraine without aura in her adolescence.[1] At the age of 30, she began to experience episodes of transient neurological symptoms antecedent to her typical headache attacks.