RESUMEN
Cluster headache is a primary headache disorder affecting up to 0.1% of the population. Patients suffer from cluster headache attacks lasting from 15 to 180 min up to 8 times a day. The attacks are characterized by the severe unilateral pain mainly in the first division of the trigeminal nerve, with associated prominent unilateral cranial autonomic symptoms and a sense of agitation and restlessness during the attacks. The male-to-female ratio is approximately 2.5:1. Experimental, clinical, and neuroimaging studies have advanced our understanding of the pathogenesis of cluster headache. The pathophysiology involves activation of the trigeminovascular complex and the trigeminal-autonomic reflex and accounts for the unilateral severe headache, the prominent ipsilateral cranial autonomic symptoms. In addition, the circadian and circannual rhythmicity unique to this condition is postulated to involve the hypothalamus and suprachiasmatic nucleus. Although the clinical features are distinct, it may be misdiagnosed, with patients often presenting to the otolaryngologist or dentist with symptoms. The prognosis of cluster headache remains difficult to predict. Patients with episodic cluster headache can shift to chronic cluster headache and vice versa. Longitudinally, cluster headache tends to remit with age with less frequent bouts and more prolonged periods of remission in between bouts.
RESUMEN
The term trigeminal autonomic cephalalgias (TACs) encompasses four primary headache disorders - cluster headache, paroxysmal hemicrania (PH), hemicrania continua (HC), short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)/short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA). All of these except HC are characterized by short-lasting headaches. HC is characterized by a continuous unilateral headache that waxes and wanes in its intensity without complete resolution. It is included in the TACs group given the overlap in the activation of the posterior hypothalamic grey, and the shared clinical feature of unilateral head pain with ipsilateral cranial autonomic symptoms. The present review gives an overview of the nosologic evolution, diagnosis, and management of TACs.
RESUMEN
Migraine is a common and disabling neurological disorder, with a significant socioeconomic burden. Its pathophysiology involves abnormalities in complex neuronal networks, interacting at different levels of the central and peripheral nervous system, resulting in the constellation of symptoms characteristic of a migraine attack. Management of migraine is individualised and often necessitates the commencement of preventive medication. Recent advancements in the understanding of the neurobiology of migraine have begun to account for some parts of the symptomatology, which has led to the development of novel target-based therapies that may revolutionise how migraine is treated in the future. This review will explore recent advances in the understanding of migraine pathophysiology, and pharmacotherapeutic developments for migraine prevention, with particular emphasis on novel treatments targeted at the calcitonin gene-related peptide (CGRP) pathway.