I had an eye stroke, AION [anterior ischemic optic neuropathy], caused by GCA nov 2017. It caused loss of upper half of vision in left eye. My sister had CRAO [central retinal arteric occlusion] in one eye in 2010 losing most of vision in that eye. She recently had BRVO [branch retinal vein occlusion] in the good eye with some temporary vision loss now back to normal. Link:
"Sudden vision loss without pain is the most common symptom of a stroke involving your eye. An eye stroke, or anterior ischemic optic neuropathy (AION), is a condition in which blood flow either becomes blocked or reduced to the tissues of the front part of the optic nerve............................
Depending on the area of the eye where blood flow becomes blocked or reduced, the following occlusions may occur.
Central retinal artery occlusion (CRAO): This occlusion usually occurs with sudden, profound vision loss in one eye, with no pain. It occurs in the retina.
Central retinal vein occlusion (CRVO): Usually causing sudden, painless vision loss that can be mild or severe, this blockage occurs in the central retinal vein where it enters the eye.
Branch retinal artery occlusion (BRAO): This blockage is usually painless and occurs suddenly. The patient usually loses peripheral vision, and sometimes central vision as well. Underlying causes include narrowing of the carotid artery, high blood pressure, cholesterol disorders, and/or cardiac disease.
Branch retinal vein occlusion (BRVO): This type of blockage causes bleeding and clotting along the retinal vein It may result in decreased vision, peripheral vision loss, distorted vision, or blind spots. This type involves one eye and may be caused by high blood pressure or diabetes.
A dangerous form of AION known as arteritic AION is caused by a condition known as giant cell arteritis (GCA)." Another link:
Visual Manifestations in Giant Cell Arteritis: Trend over Five Decades in a Population-based Cohort
Abha G. Singh, MBBS,1 Tanaz A. Kermani, MD MS,2 Cynthia S. Crowson, MS,1 Cornelia M. Weyand, MD, PhD,3 Eric L. Matteson, MD MPH,1 and Kenneth J. Warrington, MD1
"Among the 47 patients with visual manifestations, the most common visual symptoms were blurred vision (31 patients, 66%) and diplopia (11 patients, 23%) (Table 2). Other visual manifestations included amaurosis fugax (7 patients, 15%) and partial visual field loss (9 patients, 19%). Nine patients (19%) had complete loss of vision, which was unilateral in 7 patients and bilateral in 2 patients. Ischemic optic neuropathy (ION) was the predominant ophthalmologic diagnosis (17 patients, 36%). Other diagnoses included central retinal artery occlusion (2 patients, 4%) and non-specific ophthalmologic findings such as venous congestion and retinal hemorrhages (Table 3)."
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"GCA can disrupt vision by causing ischaemia of either the afferent or the efferent visual pathways [1]. The former produces visual loss, whereas the latter produces double vision. All acute ophthalmic manifestations of GCA are emergencies, given the risk for progressive and permanent damage. Arteritic anterior ischaemic optic neuropathy (AAION), which often is severe and irreversible, is the most common cause of GCA-associated blindness [2]."
Giant cell arteritis: early diagnosis is key excerpts:
"PMR and GCA are closely associated, with ~50% of
patients with PMR having biopsy-proven GCA.5,18........................................
The most concerning symptom for GCA is vision loss,
with 50% of patients complaining of ocular involvement ranging from eye pain to amaurosis fugax.19 ................
Visual loss of varying severity was
present in 98% of patients with a positive TAB, while 31% complained of amaurosis fugax, 6% complained of diplopia, and 8.2% complained of eye pain.19........................
The most common ocular ischemic lesion in GCA is
A-AION (81.2%).19 Acute pallid edema (pale and swollen optic disc) is a red flag for GCA (as opposed to typical NAION) and PION (retrobulbar optic neuropathy) (7.1%) in an elderly patient is especially concerning for GCA.19 In addition, other ocular ischemic events including nonembolic
CRAO (14.1%), cilioretinal artery occlusion (21.8%), or ophthalmic artery occlusion can occur in GCA.19 The main blood supply for the optic nerve head are the posterior ciliary arteries, whose occlusion produces A-AION.1
Fluorescein
angiography in A-AION, CRAO, cilioretinal artery occlusion,
or PION may confirm choroidal perfusion loss consistent
Based on information on the blood supply of the optic nerve,
I divided ischemic optic neuropathy into two types: [8, 9]
1. Anterior ischemic optic neuropathy (AION) involving the
anterior part of the optic nerve (optic nerve head) is of two
types:
a. Arteritic AION: This is due to giant cell arteritis (GCA).
b. Non-arteritic AION (NA-AION): This is due to other
causes, and is much more common.
2. Posterior ischemic optic neuropathy (PION) involving the
posterior part of the optic nerve, is of 3 types:
a. Arteritic PION: This is due to GCA.
b. Non-arteritic PION: This is due to other causes, and
is the most common type.
c. Surgical PION: This is associated with various extraocular surgical procedures. This has also been called
postoperative or perioperative PION. I have used the
term “surgical PION” because it is more inclusive.
"................................
" Management of arteritic AION
Arteritic AION is due to GCA, which is an ocular emergency;
it requires early diagnosis and management to prevent visual
loss. These issues are discussed at length elsewhere [5,
36]. It is well-established that high-dose systemic corticosteroid therapy is the treatment of choice. Corticosteroid therapy in GCA is discussed at length elsewhere
[5, 36].
When a patient aged 50 years or older is seen with AION,
the first essential is to determine whether it is due to GCA or
not, by immediately doing erythrocyte sedimentation rate
(ESR) and C-reactive protein (CRP) estimations; other findings suggesting GCA are the presence of systemic symptoms
of GCA and arteritic AION. Conventionally, diagnosis of
GCA is based on systemic symptoms of GCA and elevated
ESR. However, both these parameters may be misleading in
some patients. It is well-established that normal ESR does
not always rule out GCA [36, 37]. For example, I have seen
temporal artery biopsy-confirmed GCA patients with
Westergren ESR as low as 4 or 5 mm/h [36, 37]. Similarly,
there is the clinical entity of occult GCA [37], in which
patients have no systemic symptoms of GCA at all; in my
study [38], 21 % of patients who lost vision due to GCA had
incipient GCA. Thus, the presence of normal ESR and absence of systemic symptoms does not rule out GCA; elevated
I have GCA, nearly 1 year now and have lost the sight in my left eye, it will never recover and that’s very sad, but the worst part now is that I have chronic pain 24/7 and my consultant has told me , it’s due to nerve pain , which they can do nothing about. Very sad, some days I think I am going to go insane as I have many side effects from the illness and my steriods. But I am a wee proud lady and I need to keep going, if I don’t then my life will be over. Is there anyone else out there feeling like this? I am happy to talk.
Hi meg1933, that is a terrible thing to have to deal with. I am sure if you can cut and paste this message into a new post, more people will see it. I "only" have PMR but I also have chronic pain , fibromyalgia and neuropathy from diabetes. Nerve pain is not easy at all but there are meds and procedures that may help. Like I say make a new post and hopefully you will get more responses. My best wishes. 🌻
Top right of the page there should be a blue box saying Write and a picture of a pen. Click on that and you should get a box come up to write your message in. Then lots of people will see it.
I have GCA, 1 year now and sadly it has taken away the sight in my left eye. I struggle every day, with my illness and the side effects of my steriods. I also have 24/7 chronic pain from a botched hip replacement nearly 4 years ago. And I now suffer nerve pain from damage to my sciatic nerve and I gave a drop foot. I am a wee proud lady who has lost her life but soldiers on. If you want to talk I am here.
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