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Approach to the patient with thunderclap headache

Todd J Schwedt, MD, MSCI
David W Dodick, MD
Section Editor
Jerry W Swanson, MD, MHPE
Deputy Editor
John F Dashe, MD, PhD


Thunderclap headache (TCH) refers to a severe headache of sudden onset. Its explosive and unexpected nature is likened to a "clap of thunder." Although TCH initially referred to pain associated with an unruptured intracranial aneurysm [1], multiple etiologies are now recognized [2] (table 1).

This topic will review the clinical presentation, etiologies, and diagnostic evaluation of TCH.


A thunderclap headache (TCH) is a very severe headache of abrupt onset that reaches its maximum intensity within one minute or less of onset. The key feature that differentiates TCH from other headaches is the rapidity with which it develops; extreme severity alone is insufficient [3]. Other severe headaches may be worrisome and compel a diagnostic evaluation, but would not qualify as TCH unless reaching maximum intensity quickly.


The underlying pathophysiology of primary thunderclap headache (TCH) and reversible cerebral vasoconstriction syndromes (RCVS) is unclear. Excessive sympathetic activity or an abnormal vascular response to circulating catecholamines may be involved. This would explain the occurrence of TCH during physical activity, in patients with pheochromocytoma, acute hypertensive crises, and in patients who take sympathomimetic drugs or tyramine containing foods concurrently with monoamine oxidase (MAO) inhibitors. In further support of this hypothesis, reversible cerebral vasoconstriction like that which can occur with some cases of TCH has been documented in pheochromocytoma, eclampsia, sympathomimetic drug intoxication, and autonomic dysreflexia [4-8].

Although vasoconstriction can be initiated by mechanical and biochemical stimuli, a neurogenic mechanism is implied when vasoconstriction is associated with the abrupt onset of headache. Sympathetic afferents that innervate the intracranial vasculature contain neuropeptide Y and noradrenaline, both vasoconstrictors [9,10]. Vascular caliber may be a reflection of sympathetic tone and sympathetic receptor sensitivity, and TCH may be a result of spontaneous and abnormal central sympathetic response. This theory is supported by models of vasospasm in subarachnoid hemorrhage as well as the clinical finding of multifocal vasospasm in patients with pheochromocytoma and sympathomimetic drug intoxication [4,6,7,11,12].

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Literature review current through: Nov 2017. | This topic last updated: Jul 26, 2017.
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