Major reviewCurrent concepts in giant cell (temporal) arteritis
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Cited by (81)
Ischemic ocular manifestations of giant cell arteritis: A Canadian case series
2022, Journal of the Neurological SciencesCharacterization of serological markers of healed/healing arteritis and giant cell arteritis
2018, Canadian Journal of OphthalmologyCitation Excerpt :Therefore, HH injury on TAB may represent active GCA, an inactive disease state that may not need to be aggressively treated, or a disease state that requires no treatment. Given this diagnostic equipoise, this TAB finding in case of high clinical suspicion is often treated with high-dose oral steroids in light of the potentially devastating consequences of delayed intervention, including blindness, aortitis, and stroke.1,8 Given that seromarker elevations in HH represent an intermediate state between GCA positive and GCA negative, this TAB finding likely represents a point on the continuum of the vasculitic process, from active to healed.
Visual Loss: Optic Neuropathies
2018, Liu, Volpe, and Galetta's Neuro-Ophthalmology: Diagnosis and ManagementNew developments in giant cell arteritis
2016, Survey of OphthalmologyGiant cell arteritis
2009, Journal of Clinical NeuroscienceCitation Excerpt :Ischemia of extraocular muscles, ocular motor nerves or the brainstem may be responsible for diplopia and ocular motor imbalance, transient or constant, in 2% to 15% of GCA patients. The occulomotor (III) nerve is thought to be most commonly involved, often sparing the pupil; however, involvement of the trochlear (IV) and abducens (VI) nerves has been reported.30,45 While the exact etiology of GCA is unknown, a variety of infectious agents have been suggested as potential immune triggers for the disease, including herpes virus, parainfluenza virus, cytomegalovirus, parvovirus B19, chlamydia and mycoplasma.46–49
Suspected giant cell arteritis: A study of referrals for temporal artery biopsy
2008, Canadian Journal of Ophthalmology