Giant cell arteritis

Cho, Hyeon Jeong; Bloomberg, Justin D.; Nichols, Jeffrey

doi:10.1016/j.disamonth.2016.10.006

Cited by 13 publications

(13 citation statements)

References 12 publications

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“…Our patient met all the five features established by the American College of Rheumatology as diagnostic criteria for GCA: age ≥ 50 years, recent onset headache, tenderness and lack of pulse in the temporal artery, ESR > 50 mm/h, abnormal TAB [6,15]. Additionally, he had jaw claudication which is an alternative diagnostic criteria for GCA [3].…”

Section: Discussionmentioning

confidence: 66%

“…Ophthalmological manifestations appear in 30% of all cases, the most frequent cause of vision loss being AOIN, due to the involvement of ciliary posterior arteries which supply the optic nerve [3,7]. The risk factors for GCA are age ≥ 50 years, Caucasian race and 60-70% of cases are women [3,6,8,9,11]. However, ophthalmological manifestations are more severe and more frequent in men [12].…”

Section: Discussionmentioning

confidence: 99%

“…Giant cell arteritis (GCA) was first described by Hutchinson in 1890 [1,2], but the first histological evidence was presented by Horton in 1932 [2][3][4]. GCA touches typically the branches of the extracranial carotid artery: ophthalmic, posterior ciliary and superficial temporal [5,6]. Anterior optic ischemic neuropathy (AOIN) is the most frequent cause of visual loss in GCA [7].…”

Section: Introductionmentioning

confidence: 99%

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Bilateral irreversible visual loss due to arteritic anterior optic ischemic neuropathy

Damian¹

2022

Case Rep Int

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Introduction:Anterior optic ischemic neuropathy (AOIN) is the most frequent cause of visual loss in giant cell arteritis (GCA). As blindness is rarely reversible, the main therapeutic goal is to prevent bilateral disease by immediate initiation of high-dose intravenous steroids. Approximately, one third of patients present with bilateral visual impairment. Case Report: A 77-year-old patient, came to the Ophthalmology Emergency Room for sudden loss of vision in the left eye (OS) to no light perception (NLP) with two days duration and significant narrowing of the visual field in the right eye (OD) with 10 hours duration. Fundus examination revealed swelling and pallor of the optic disc in both eyes (OU). Laboratory examination showed elevated ESR (56 mm/h) and CRP (5.24 mg/dl). Temporal artery biopsy (TAB) proved granulomas and fibrosis within the vessel wall. Immediate Methylprednisolon 1 gm was administered intravenously for five days, followed by oral Prednisone 1mg/kg for four weeks with tapering of 10 mg per month. The patient was put on diabetic and low sodium regimen. During the 3rd day of treatment, vision OD dropped to NLP. Despite continuing systemic steroid therapy, vision remained

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bilateral irreversible visual loss due to arteritic anterior optic ischemic neuropathy

Damian¹

2022

Case Rep Int

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“…It is histologically characterised by granulomatous inflammation of medium-sized to large-sized vessels 10. According to ACR criteria, a positive histology is no prerequisite to verify diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Hypertrophic pachymeningoencephalitis associated with temporal giant cell arteritis

et al. 2018

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We report the rare case of an 80-year-old male patient with hypertrophic pachymeningoencephalitis that may be associated with temporal arteritis. The patient presented to our neurological department with a 2-week history of latent paresis and ataxia affecting his right hand. He had been diagnosed with temporal arteritis 12 years earlier. Brain MRI showed an enhancement of the left-sided frontoparietal meninges with oedema of the adjacent tissue of the precentral and postcentral cortex. A leptomeningeal biopsy was performed. An autoimmune-mediated immunoglobulin G4-associated hypertrophic pachymeningoencephalitis was diagnosed. The patient received a high-dose corticosteroid therapy and his symptoms gradually improved. Our results suggest that hypertrophic pachymeningoencephalitis may occur as a complication of giant cell arteritis and may cause central neurological deficits by cerebral perifocal oedema.

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“…The superior temporal artery is almost always involved. 13 The patient may deny headache and may call the symptom "head pain" instead.…”

Section: Supraorbital Neuralgiamentioning

confidence: 99%

Craniofacial neuralgias

Katta-Charles

2020

NRE

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While non-headache, non-oral craniofacial neuralgia is relatively rare in incidence and prevalence, it can result in debilitating pain. Understanding the relevant anatomy of peripheral branches of nerves, natural history, clinical presentation, and management strategies will help the clinician better diagnose and treat craniofacial neuralgias. This article will review the nerves responsible for neuropathic pain in periorbital, periauricular, and occipital regions, distinct from idiopathic trigeminal neuralgia. The infratrochlear, supratrochlear, supraorbital, lacrimal, and infraorbital nerves mediate periorbital neuralgia. Periauricular neuralgia may involve the auriculotemporal nerve, the great auricular nerve, and the nervus intermedius. The greater occipital nerve, lesser occipital nerve, and third occipital nerve transmit occipital neuralgias. A wide range of treatment options exist, from modalities to surgery, and the evidence behind each is reviewed.

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Giant cell arteritis

Cited by 13 publications

References 12 publications

Bilateral irreversible visual loss due to arteritic anterior optic ischemic neuropathy

Bilateral irreversible visual loss due to arteritic anterior optic ischemic neuropathy

Hypertrophic pachymeningoencephalitis associated with temporal giant cell arteritis

Craniofacial neuralgias

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