Headache and the eye

Dafer, Rima M.; Jay, Walter M.

doi:10.1097/icu.0b013e328331270d

Cited by 9 publications

(6 citation statements)

References 41 publications

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“…It is generally assumed that headaches involve the activation of intracranial afferents of the trigeminal nerve and/or the second order neurons in the spinal trigeminal nucleus, where these afferents are projecting to (Levy, Labastida-Ramirez, & MaassenVanDenBrink, 2018;Olesen, Burstein, Ashina, & Tfelt-Hansen, 2009;Schueler, Messlinger, Dux, Neuhuber, & Col, 2013). Headache and ocular pain are frequently associated (Dafer & Jay, 2009), and there is a close association between nasal/paranasal lesions and headaches (Pinto, Rossi, McQuone, & Sollecito, 2001;Silberstein, 2004). The effectivity of intranasal application of drugs for the treatment of headaches is supportive for this view (Rapoport, Bigal, Tepper, & Sheftell, 2004).…”

Section: Discussionmentioning

confidence: 99%

High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

Dux

Babeș

Manchen

et al. 2019

European Journal of Pain

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Background The α1‐adrenoceptor agonist, phenylephrine, is used at high concentrations as a mydriatic agent and for the treatment of nasal congestion. Among its adverse side‐effects transient burning sensations are reported indicating activation of the trigeminal nociceptive system. Methods Neuropeptide release, calcium imaging and meningeal blood flow recordings were applied in rodent models of meningeal nociception to clarify possible receptor mechanisms underlying these pain phenomena. Results Phenylephrine above 10 mM dose‐dependently released calcitonin gene‐related peptide (CGRP) from the dura mater and isolated trigeminal ganglia, whereas hyperosmotic mannitol at 90 mM was ineffective. The phenylephrine‐evoked release was blocked by the transient receptor potential vanilloid 1 (TRPV1) antagonist BCTC and did not occur in trigeminal ganglia of TRPV1‐deficient mice. Phenylephrine at 30 mM caused calcium transients in cultured trigeminal ganglion neurons responding to the TRPV1 agonist capsaicin and in HEK293T cells expressing human TRPV1. Local application of phenylephrine at micromolar concentrations to the exposed rat dura mater reduced meningeal blood flow, whereas concentrations above 10 mM caused increased meningeal blood flow. The flow increase was abolished by pre‐application of the CGRP receptor antagonist CGRP8‐37 or the TRPV1 antagonist BCTC. Conclusions Phenylephrine at high millimolar concentrations activates TRPV1 receptor channels of perivascular afferents and, upon calcium inflow, releases CGRP, which increases meningeal blood flow. Activation of TRPV1 receptors may underlie trigeminal nociception leading to cranial pain such as local burning sensations or headaches caused by administration of high doses of phenylephrine. Significance Phenylephrine is used at high concentrations as a mydriaticum and for treating nasal congestion. As adverse side‐effects burning sensations and headaches have been described. Phenylephrine at high concentrations causes calcium transients in trigeminal afferents, CGRP release and increased meningeal blood flow upon activation of TRPV1 receptor channels, which is likely underlying the reported pain phenomena.

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Section: Discussionmentioning

confidence: 99%

High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

Dux

Babeș

Manchen

et al. 2019

European Journal of Pain

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“…This may have been due to pituitary apoplexy, characterised by: sudden onset, severe headache; vomiting; visual impairment; ophthalmoplegia; meningism; altered level of consciousness; and endocrine dysfunction. This occurs as a result of sudden haemorrhage or infarction of the pituitary gland, usually within an adenoma 5 …”

Section: Discussionmentioning

confidence: 99%

Rapidly progressing giant invasive prolactinoma

Care

Sunkaraneni

Theaker³

et al. 2012

J. Laryngol. Otol.

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“…The headache can be chronic, diffuse, and nonspecific in character or localized to one or both eyes. Many patients describe it as worse in the morning, and exacerbated by Valsalva [22]. Patients with IIH often are young women of childbearing age with a body mass index of greater than 30 kg/m 2 .…”

Section: Idiopathic Intracranial Hypertensionmentioning

confidence: 98%

Ocular and Orbital Pain for the Headache Specialist

Ringeisen

Harrison

Lee

2010

Curr Neurol Neurosci Rep

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Ocular pain is most commonly associated with redness and inflammation; however, eye pain can also occur in the absence of grossly visible pathology. Pain in the quiet eye can be the first sign of a number of threatening conditions. Many of these conditions such as intermittent angle closure glaucoma, carotid artery dissection, idiopathic intracranial hypertension, and giant cell arteritis can lead to permanent vision loss or blindness. In this review, ocular history and examination techniques are summarized. The article also reviews pertinent ocular, orbital, referred, and other causes of eye pain in the quiet eye. The neurologist and headache specialist should recognize when consultation with an ophthalmologist is necessary.

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Headache and the eye

Cited by 9 publications

References 41 publications

High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

High‐dose phenylephrine increases meningeal blood flow through TRPV1 receptor activation and release of calcitonin gene‐related peptide

Rapidly progressing giant invasive prolactinoma

Ocular and Orbital Pain for the Headache Specialist

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