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Headache Disorders
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
The trigeminal autonomic cephalalgias (TACs) are a group of headache disorders marked by trigeminal-based head pain and prominent cranial autonomic-associated symptoms of both cranial parasympathetic activation (conjunctival injection, lacrimation, nasal congestion and/or rhinorrhea, eyelid edema) and sympathetic dysfunction (ptosis, miosis—partial or full Horner’s syndrome).1 This subgroup of headache syndromes is also marked by their severity (many times off the pain scale), repetitive attacks per day of typically short duration, and seasonal and diurnal predilection indicating a possible hypothalamic/circadian influence over the syndromes. Currently recognized TACs include cluster headache (CH), paroxysmal hemicrania, SUNCT syndrome, and hemicrania continua.
Diagnosis and Management of Facial Pain
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Rajiv K. Bhalla, Timothy J. Woolford
The trigeminal autonomic cephalalgias are a group of primary headache disorders that include cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing/cranial autonomic features (SUNCT/SUNA).25 Trigeminal autonomic cephalalgias are generally characterized by relatively short-lasting attacks of severe pain and lateralized associated features including pain, cranial autonomic symptoms and where present, migrainous symptoms, such as photophobia. Key for the otolaryngologist when diagnosing a trigeminal autonomic cephalalgia is the consideration of underlying pituitary or pituitary-region pathology, since the posterior hypothalamus is crucial in the pathophysiology of these headaches.26 Although the syndromes share much in their pathophysiology and investigation paths, their treatment is distinct, so that accurate differentiation is important for optimal management. Due to the associated autonomic symptoms, there is a great propensity for the presentation to be confused with sinus pathology, causing misdiagnosis and subsequent mismanagement. It is of great value if such patients are managed in conjunction with a neurologist and/or colleague with a special interest in pain management.
The Governor Vessel (GV)
Published in Narda G. Robinson, Interactive Medical Acupuncture Anatomy, 2016
Stimulation of the supraorbital and supratrochlear nerves can aid patients with otherwise intractable trigeminal autonomic cephalalgias (TAC).7 While implanted stimulators may work, why not try for relief with noninvasive neuromodulation first?
Updated review on the link between cortical spreading depression and headache disorders
Published in Expert Review of Neurotherapeutics, 2021
Doga Vuralli, Hulya Karatas, Muge Yemisci, Hayrunnisa Bolay
As pain is transmitted through the trigeminal nerve, and the brain parenchyma is devoid of trigeminal innervation, demonstration of trigeminal activation by CSD constitutes an important causal link between CSD and headache [11]. CSD waves were shown to cause long-lasting blood flow increase in the overlying dural middle meningeal artery (MMA) and plasma protein extravasation, which were dependent on trigeminal nerve activation. The peak increase in the ipsilateral MMA blood flow was 20 min after CSD coinciding with the oligemia phase [11]. CSD waves were shown to induce mast cell degranulation in the dura mater [11,36]. These CSD-induced peripheral changes in the dura mater were associated with the activation of ipsilateral second order pain neurons in the brainstem trigeminal nuclei. Transection of trigeminal nerve or sumatriptan administration blocked the CSD-triggered activation in the brainstem trigeminal nucleus. Additionally, CSD waves were shown to evoke a brainstem reflex involving trigeminal afferents and parasympathetic efferents to cephalic vascular structures which further increased rCBF. The latter can explain autonomic symptoms seen in migraine as well as trigeminal autonomic cephalalgias.
Drug profile: galcanezumab for prevention of cluster headache
Published in Expert Review of Neurotherapeutics, 2021
Dharani Mudugal, Teshamae S. Monteith
CH belongs to the class of trigeminal autonomic cephalalgias [TAC]. According to the International Classification of Headache Disorders-3rd edition, it is characterized by severe, unilateral pain lasting 15–180 minutes and associated with ipsilateral cranial autonomic symptoms such as lacrimation, drooping of the eye, rhinorrhea, and agitation [Table 1] [3]. The attacks are maximally located in the orbital and supraorbital regions and may occur every other day up to 8 times per day. Approximately 10%–15% may have CCH with attacks occurring without remission for at least 1 year or with remissions lasting less than 3 months.
Insights into real-world treatment of cluster headache through a large Italian database: prevalence, prescription patterns, and costs
Published in Expert Review of Clinical Pharmacology, 2021
Carlo Piccinni, Sabina Cevoli, Giulia Ronconi, Letizia Dondi, Silvia Calabria, Antonella Pedrini, Aldo P. Maggioni, Immacolata Esposito, Alice Addesi, Valentina Favoni, Giulia Pierangeli, Pietro Cortelli, Nello Martini
Cluster headache (CH) is the most common of the trigeminal autonomic cephalalgias. It is characterized by intense unilateral pain at the cranial level, accompanied variably by symptoms mediated by the autonomic nervous system, such as ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis and/or eyelid edema, and by restlessness or agitation [1]. This condition is defined by the 3rd version of the International Classification of Headache Disorders (ICHD-3) as a strictly unilateral headache characterized by attacks lasting from 15 to 180 minutes and commonly localized within or above the orbit [2].