Ann Indian Acad Neur
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Primary trigeminal autonomic cephalalgias (TACs) are uncommon group of headache disorders. These are defined and diagnosed by the criteria given by the International Classification of Headache Disorders 3β version. ⋯ Many structural and other pathologies have been found in these patients that can be causally related to the headaches. This review attempts to critically analyze the existing literature including the new cases published during 2015-2017.
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Short-lasting unilateral neuralgiform headache attacks (SUNHA) is characterized by strictly unilateral trigeminal distribution pain that occurs in association with ipsilateral cranial autonomic features. There are two subtypes: short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) and short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA). These disorders are rare but highly disabling. ⋯ There is a considerable clinical, therapeutic, and radiological overlap between SUNCT, SUNA, and trigeminal neuralgia (TN). Despite being considered distinct conditions, the emerging evidence suggests a broader nosological concept of SUNCT, SUNA, and TN; these conditions may constitute a continuum of the same disorder, rather than separate clinical entities. Consideration needs to be given to classifying SUNHA with TN as a cranial neuralgia rather than as a trigeminal autonomic cephalalgia.
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Ann Indian Acad Neur · Apr 2018
ReviewOverview of Trigeminal Autonomic Cephalalgias: Nosologic Evolution, Diagnosis, and Management.
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. ⋯ 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.
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Ann Indian Acad Neur · Apr 2016
ReviewUnderstanding migraine: Potential role of neurogenic inflammation.
Neurogenic inflammation, a well-defined pathophysiologial process is characterized by the release of potent vasoactive neuropeptides, predominantly calcitonin gene-related peptide (CGRP), substance P (SP), and neurokinin A from activated peripheral nociceptive sensory nerve terminals (usually C and A delta-fibers). These peptides lead to a cascade of inflammatory tissue responses including arteriolar vasodilation, plasma protein extravasation, and degranulation of mast cells in their peripheral target tissue. Neurogenic inflammatory processes have long been implicated as a possible mechanism involved in the pathophysiology of various human diseases of the nervous system, respiratory system, gastrointestinal tract, urogenital tract, and skin. ⋯ Improved understanding of the molecular biology, pharmacology, and pathophysiology of neurogenic inflammation may provide the practitioner the context-specific feedback to identify the novel and most effective therapeutic approach to treatment. With this objective, the present review summarizes the evidence supporting the involvement of neurogenic inflammation and neuropeptides in the pathophysiology and pharmacology of migraine headache as well as its potential significance in better tailoring therapeutic interventions in migraine or other neurological disorders. In addition, we have briefly highlighted the pathophysiological role of neurogenic inflammation in various other neurological disorders.