2008
DOI: 10.1016/j.emc.2007.10.001
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The Painful Eye

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Cited by 35 publications
(19 citation statements)
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“…Increased hydrostatic pressure in the cystic lesions, where glands cannot excrete their fluid to the uterine cavity, as they normally do, is presumably involved in the mechanical hyperalgesia observed at these time points. Painful symptoms associated with such an increased pressure are also observed in abscesses (Kessler et al, 2012), dental pulpitis (Heyeraas and Berggreen, 1999), acute glaucoma (Dargin and Lowenstein, 2008) or benign intracranial hypertension (Galgano and Deshaies, 2013), which are also readily responsive to appropriate drainage interventions. Importantly, pro-algesic inflammatory mediators are known to be present in the fluid in endometriotic cysts (Darai et al, 2003; Zhang et al, 2008), suggesting that the effect of drainage is due to the decompression of a structure innervated by sensitized nociceptors.…”
Section: Discussionmentioning
confidence: 99%
“…Increased hydrostatic pressure in the cystic lesions, where glands cannot excrete their fluid to the uterine cavity, as they normally do, is presumably involved in the mechanical hyperalgesia observed at these time points. Painful symptoms associated with such an increased pressure are also observed in abscesses (Kessler et al, 2012), dental pulpitis (Heyeraas and Berggreen, 1999), acute glaucoma (Dargin and Lowenstein, 2008) or benign intracranial hypertension (Galgano and Deshaies, 2013), which are also readily responsive to appropriate drainage interventions. Importantly, pro-algesic inflammatory mediators are known to be present in the fluid in endometriotic cysts (Darai et al, 2003; Zhang et al, 2008), suggesting that the effect of drainage is due to the decompression of a structure innervated by sensitized nociceptors.…”
Section: Discussionmentioning
confidence: 99%
“…Previous recording studies, based mainly on response properties in naïve rats (Hirata et al, 1999; Hirata et al, 2000; Hirata et al, 2004; Meng et al, 1997; Meng et al, 1998), have led to the proposal that neurons at the Vi/Vc transition and in the superficial laminae at the Vc/C1 region serve different aspects of trigeminal function in ocular pain (Bereiter et al, 2000). Although ocular inflammation is a common clinical problem that causes pain and can develop from a variety of conditions such as refractive surgery, infection or trauma (Dargin and Lowenstein, 2008; Leibowitz, 2000), most animal models of ocular pain have been relied on approaches that involve direct nerve damage (see Belmonte et al, 2004; Wenk and Honda, 2003). Recently we reported that endotoxin-induced uveitis (EIU), an animal model that mimics some of the early signs of anterior uveitis in humans, produced time-dependent changes in responsiveness of neurons in the caudal trigeminal sensory brainstem complex (Bereiter et al, 2005).…”
mentioning
confidence: 99%
“…Optic neuritis is another cause of painful monocular visual loss but without a red eye 14. Occasionally, acute close angle glaucoma might present without pain 15…”
Section: Discussionmentioning
confidence: 99%