Term for a curtain dropping over vision

[melvindo]

You know how pts describe that they feel like a curtain is being lowered over their vision. We had a lady with temporal arteritis and my attending asked me to find the term that applies to the curatin dropping. any body know ?
thanks y'all

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[Andrew_Doan]

You know how pts describe that they feel like a curtain is being lowered over their vision. We had a lady with temporal arteritis and my attending asked me to find the term that applies to the curatin dropping. any body know ?
thanks y'all

"curtain" = altitudinal visual field defect

 

[DrMom]

Amaurosis fugax?

 

[Andrew_Doan]

He's probably looking for the term amaurosis fugax like DrMom stated. Amaurosis cases a "curtain" like effect and is associated with GCA. The vision loss is usually brief in amaurosis. Patients often describe a curtain being pulled over their vision.

Patients also complain of a "shade" or "curtain" if permanent visual loss develops in GCA. If damage has occured to the optic nerve head in GCA (arteritic ischemic optic neuropathy), then it will result in an altitudinal visual field defect due to distribution of the nerve fiber layer.

http://www.emedicine.com/OPH/topic254.htm

 

[mdkurt]

He's probably looking for the term amaurosis fugax like DrMom stated. Amaurosis cases a "curtain" like effect and is associated with GCA. The vision loss is usually brief in amaurosis. Patients often describe a curtain being pulled over their vision.

Patients also complain of a "shade" or "curtain" if permanent visual loss develops in GCA. If damage has occured to the optic nerve head in GCA (arteritic ischemic optic neuropathy), then it will result in an altitudinal visual field defect due to distribution of the nerve fiber layer.

http://www.emedicine.com/OPH/topic254.htm

Amaurosis fugax should be used only when the vision comes back. Unfortunately, your lady with GCA won't experience that, so it's plain old amaurosis.

 

[ituryu]

Amaurosis fugax should be used only when the vision comes back. Unfortunately, your lady with GCA won't experience that, so it's plain old amaurosis.

I totally agree , Amaurosis fugax is a transient loss of vision , and the V/Fields would probably not show any altitudinal field defect , it's mostly central field defects.

 

[Andrew_Doan]

I totally agree , Amaurosis fugax is a transient loss of vision , and the V/Fields would probably not show any altitudinal field defect , it's mostly central field defects.

You see both central and altitudinal VF defects in GCA:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7800356

Ophthalmology. 1994 Nov;101(11):1779-85.

Visual morbidity in giant cell arteritis. Clinical characteristics and prognosis for vision.

Liu GT, Glaser JS, Schatz NJ, Smith JL.

Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine.

PURPOSE: To characterize visual morbidity in giant cell arteritis and to assess prognosis with respect to treatment. METHODS: Record review of 185 patients with coded diagnosis of giant cell (cranial) arteritis examined at the Bascom Palmer Eye Institute from January 1, 1980, to January 31, 1993. RESULTS: Forty-five patients with biopsy-proven giant cell arteritis had visual symptoms, and 41 individuals (63 eyes) lost vision. The visual loss was unilateral in 19 patients (46%), sequential in 15 (37%), and simultaneous in 7 (17%). Anterior ischemic optic neuropathy developed in 88% of eyes, visual acuity was 20/200 or worse in 70%, 21% had no light perception, and the majority of field defects in testable eyes, aside from central scotomas associated with loss, showed altitudinal or arcuate patterns. Six patients lost vision during corticosteroid therapy for systemic symptoms of giant cell arteritis, whereas in 39 patients visual symptoms prompted steroid treatment. For visual symptoms, 25 patients received intravenous methylprednisolone, whereas 20 received oral prednisone alone. In the 41 patients with visual loss, vision was unchanged in 20 (49%), it worsened in 7 (17%), and it improved in 14 (34%). Subsequent fellow eye involvement was observed only with oral therapy, and a greater percentage of patients (9/23 [39%] versus 5/18 [28%]) improved after intravenous treatment. CONCLUSIONS: In the authors' series, patients with visual loss due to giant cell arteritis had a 34% chance for some improvement in visual function after corticosteroid treatment. Intravenous therapy may diminish the likelihood of fellow eye involvement and was associated with a slightly better prognosis for visual improvement.

 

[cpw]

I've seen one patient with confirmed GCA and one with suspected GCA in the last week... (the second was on his way to his blood draw on my way out of clinic this evening)

 

[sjkpark]

A question about GCA:

Does visual loss in GCA occur as the direct result of inflammation of ophthalmic artery?

 

[ituryu]

The inflamation result to an ischemia of the retinal arterioles that the ophthalmic artery supplies, and thus there would be a sequential atrophy of the affected regions of the retina which they nourish. The inflammation of the ophthalmic artery brings about an indirect effect of vision loss.

 

[Andrew_Doan]

The inflamation result to an ischemia of the retinal arterioles that the ophthalmic artery supplies, and thus there would be a sequential atrophy of the affected regions of the retina which they nourish. The inflammation of the ophthalmic artery brings about an indirect effect of vision loss.

The above is incorrect. GCA is a disease process affecting small to medium size arteries. It does NOT affect the retinal arterioles. The main arteries affected are the posterior ciliary arteries, ophthalmic arteries, and sometimes the central retinal artery. The affected regions of the retina is in the distribution of the posterior ciliary arteries or the distribution of the nerve fiber layer in the case of AION (see below), NOT the retinal arterioles. In addition, the most common manifestation of GCA is Ischemic Optic Neuropathy (ION). This is why it is very important to distinguish between arteritic ION (i.e. GCA) vs non-arteritic ION. If the patient has AION, then the vision loss is the result of infarction of the optic nerve head due to the occlusion of the posterior ciliary artery (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7556490&dopt=Abstract). Because of all the different areas of infarction in GCA, we can see central visual loss, amaurosis fugax, altitudinal visual field loss, and arcuate pattern visual field loss.

http://webeye.ophth.uiowa.edu/dept/GCA/04-ocular.htm

OCULAR MANIFESTATIONS OF GCA

As mentioned above, visual loss is the most feared and irreversible complication of GCA. Therefore, ophthalmologists are likely to be the first physicians consulted by GCA patients with visual loss, especially those with occult GCA3 who have no associated systemic symptoms at all.

Of a total of 170 GCA patients in our study, 50% presented in our clinic with ocular symptoms.2 Of the 85 patients with ocular symptoms, both eyes were involved in 45% of the patients.

Ocular symptoms: These were amaurosis fugax in 26%, visual loss of varying severity in 92%, diplopia in 7% and eye pain in 7%. These occurred in various combinations. Amaurosis fugax was the only presenting visual symptom in 10%. That indicates that amaurosis fugax in persons aged >50 years is a red flag for GCA.
Visual acuity: It was 20/40 or better in 21%, 20/50 - 20/100 in 17%, 20/200 - 20/400 in 8%, count fingers in 15%, hand motion in 10%, light perception in 13% and no light perception in 15% (see Table below).

Ocular ischemic lesions: These were AION in 76.4%, central retinal artery occlusion in 13%, cilioretinal artery occlusion in 25%, posterior ischemic optic neuropathy in 6% and ocular ischemia in 1%. Cotton-wool spots were seen in one third of the eyes. Peripheral triangular chorioretinal ischemic lesions were seen in 10 eyes. The various ocular ischemic lesions were seen in a variety of combinations.

Fluorescein fundus angiography: This is an extremely helpful test in diagnosis of GCA during the early stages of visual loss (see below) and also as a source of information about the cause of visual loss. In almost every patient with GCA in our series, it revealed occlusion of one or more of the posterior ciliary arteries.2,11-14 (see Figure 1-b) When central retinal artery occlusion was present, there was almost always associated posterior ciliary artery occlusion as well; this is because the central retinal artery and posterior ciliary artery often arise by a common trunk from the ophthalmic artery,2,13 and when that common trunk is involved by GCA, the eye presents with evidence of occlusion of both central retinal and posterior ciliary arteries.

The above angiogram was from a patient with GCA in Dr. Hayreh's study. Notice that the retinal arterioles still profuse the retina (white); however, because of the occlusion of the medial posterior ciliary artery and cilioretinal artery, the choroidal circulation under the retina is absent. Even though the retinal arterioles are profusing the retina, this patient had severe visual loss due to defects in the choroidal circulation.

 

[ituryu]

The above is incorrect. GCA is a disease process affecting small to medium size arteries. It does NOT affect the retinal arterioles. The main arteries affected are the posterior ciliary arteries, ophthalmic arteries, and sometimes the central retinal artery. The affected regions of the retina is in the distribution of the posterior ciliary arteries or the distribution of the nerve fiber layer in the case of AION (see below), NOT the retinal arterioles. In addition, the most common manifestation of GCA is Ischemic Optic Neuropathy (ION). This is why it is very important to distinguish between arteritic ION (i.e. GCA) vs non-arteritic ION. If the patient has AION, then the vision loss is the result of infarction of the optic nerve head due to the occlusion of the posterior ciliary artery (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7556490&dopt=Abstract). Because of all the different areas of infarction in GCA, we can see central visual loss, amaurosis fugax, altitudinal visual field loss, and arcuate pattern visual field loss.

http://webeye.ophth.uiowa.edu/dept/GCA/04-ocular.htm

The above angiogram was from a patient with GCA in Dr. Hayreh's study. Notice that the retinal arterioles still profuse the retina (white); however, because of the occlusion of the medial posterior ciliary artery and cilioretinal artery, the choroidal circulation under the retina is absent. Even though the retinal arterioles are profusing the retina, this patient had severe visual loss due to defects in the choroidal circulation.

O.k I agree, but doesn't the CRAO translates it's effect to the arterioles of the retina? Basically there is a sequela!

 

[Andrew_Doan]

O.k I agree, but doesn't the CRAO translates it's effect to the arterioles of the retina? Basically there is a sequela!

Yes, you're correct. According to Dr. Hayreh's studies, CRAO occurs in 13% of GCA. In the setting of a CRAO, there is hypoperfusion of the retinal arterioles.

I wanted to emphasize that the majority of visual problems in GCA arise due to defects in the posterior ciliary arteries and posterior circulation supplying the optic nerve.

 

[ituryu]

Yes, you're correct. According to Dr. Hayreh's studies, CRAO occurs in 13% of GCA. In the setting of a CRAO, there is hypoperfusion of the retinal arterioles.

I wanted to emphasize that the majority of visual problems in GCA arise due to defects in the posterior ciliary arteries and posterior circulation supplying the optic nerve.

True to the fact, this means that definitely the photoreceptors are affected as you say, the posterior ciliary arteries and posterior circulation supplying the optic nerve; also supply the photoreceptor layer of the retina and this really should be the pathophysiological pathway for the altitudinal visula field defect.