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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Ann+Indian+Acad+Neurol
2018 ; 21
(Suppl 1
): S45-S50
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Classification of Trigeminal Autonomic Cephalalgia: What has Changed in
International Classification of Headache Disorders-3 Beta?
#MMPMID29720818
Ravishankar K
Ann Indian Acad Neurol
2018[Apr]; 21
(Suppl 1
): S45-S50
PMID29720818
show ga
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, 2(nd) edition (ICHD-2) published in 2004.[3] The beta version of the
3(rd) 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.[45] 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.