Annals of Indian Academy of Neurology
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Year : 2018  |  Volume : 21  |  Issue : 5  |  Page : 45-50

Classification of trigeminal autonomic cephalalgia: What has changed in international classification of headache Disorders-3 beta?

The Headache and Migraine Clinic, Jaslok Hospital and Research Centre, Lilavati Hospital and Research Centre, Mumbai, Maharashtra, India

Correspondence Address:
Dr. K Ravishankar
A-64, Kalpataru Residency, Sion, Mumbai - 400 022, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_350_17

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The term “Trigeminal Autonomic Cephalalgia (TAC)” was first coined by Goadsby and Lipton[1] to include a group of relatively rare primary headache disorders characterized by moderate to severe, short-lived head pain in the trigeminal distribution with unilateral cranial parasympathetic autonomic features, such as lacrimation, rhinorrhea, conjunctival injection, eyelid edema, and ptosis. In the current International Classification of Headache Disorders (ICHD-3 beta),[2] the TAC group includes cluster headache (CH), paroxysmal hemicrania (PH), short-lasting unilateral neuralgiform headache attacks (SUNHAs) and their 2 subforms - SUNHAs with conjunctival injection and tearing (SUNCT), SUNHAs with cranial autonomic symptoms (SUNA). Hemicrania Continua (HC) is also now included in the TAC group. Although the entities included under TACs seem broadly similar, they differ in attack duration, frequency and their response to different treatments. At one end of the spectrum lies CH, the prototypic TAC where the duration of attacks is the longest and at the other end is the SUNCT syndrome where the duration is shortest. There is some overlap across the entities; they are not difficult to recognize and subclassify. The umbrella term “TAC” for the short-lasting headaches with autonomic features was for the first time introduced in The ICHD, 2nd edition (ICHD-2) published in 2004.[3] The beta version of the 3rd edition of The ICHD[2] was published in 2013. Headache classification being an evolving process, there have been some changes within the TAC group between ICHD-2 and ICHD-3 beta.[4],[5] Diagnostic criteria have been revised to reflect pathophysiological and clinical observations. Neuroimaging has provided insights into the pathophysiology of TACs. Functional neuroimaging has helped to elucidate key structures activated during attacks of TACs. Correct diagnosis remains the key to correct management of the TACs because treatment options vary. The aim of this article will be to highlight the changes in ICHD-3 beta to this group and to emphasize the clinical implications of these changes. Description of individual entities included under TACs are included elsewhere and will therefore not be detailed here.

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