see also the following behavioral neurology post http://behavioralneurologynotes.blogspot.com/2008/05/hallucinations-and-related-conditions.html
Consider: noninschemic
1. opthalmic surface disorders
a. tear film abnormalities-- visual blurring occurs many times a week often at the end of the day and under one environmental circumstance. Blinking and lubricating eye helps. Patients with blepharitis may be worse in the morning due to accumulated meibomian gland secretion overnight. With dry eyes causing epithelial breakdown, there may be foreign body sensation, pain or redness with a positive Schirmer's test. Patients with rosacea frequently have opthalmic involvement. Also PD.
2. Other ocular causes-- narrow angle glaucoma causes transient blurring with halos. Recurrent spontaneous anterior chamber hemorrhages is such patients needs to be differentiated from those occurring in juvenile xanthogranuloma, malpositioned lens with iris contact, and iris neovascularization.
Patients with corneal dysfunction have episodes of blurred vision that last for hours especially in the mornings, must examine during an episode. Episodes in patients with diabetes due to hyper or hypoglycemia occur.
Ischemic Causes
Causes-- 60 % are due to carotid stenosis/occlusion. Also called TMB, amaurosis fugax, or retinal tia. In usual cases , emboli from carotid are common but low flow also occurs when collaterals from the Circle of Willis and eca are compromised. In these cases symptoms may be inducible by change in position or eating, or when distal flow is inadequate such as chronic ocular ischemia or bright light amaurosis. The latter occurs with TMB after sunlight or looking at a white wall, in the setting of carotid occlusion and is a well known phenomenon.
Risk of stroke per annum is 2 % with 1 % risk of permanent visual loss, v. 5-8 % risk of stroke with hemispheric tia's.
Symptoms are abrupt onset, painless, lasts 1-5 minutes, darkening or fogging (not blurring) of visual field, altitudinal pattern (shade closing) of vision loss, and return of vision over minutes.
Vision loss may be altitudinal, peripheral, central or even vertical. A nasal field defect may suggest emboli due to lodging in temporal retinal circulation. Rarely, scintillating scotomas occur. Pain which is rare may suggest temporal arteritis.
Neuroopthalmic signs-- the most common are retinal emboli, including cholesterol (Hollenhorst) plaques which are refractile, metallic gold appearance and indicate carotid disease and platelet fibrin emboli which are creamy white grey longitudinal intravascular opacifications that fill the lumen, and indicate either carotid thrombosis or thrombosis with recent MI. Chronic severe carotid disease leads to chronic ocular ischemia including episcleral and conjunctival injection, corneal edema, and neovascular glaucoma. Venous stasis causes microaneurysms and blot hemorrhages. Unlike diabetes they are unilateral (ipsilateral to stenosis) and mid periphery instead of posterior pole. Rarely retinal calcific emboli occur in patients with cardiac valvular disease. They are grey white and ovoid and infarct the retina.
In papilledema, episodes of grey black and white vision lasting seconds may occur. Its fleeting and associated with changes in position. This also occurs in pseudopappilledema drusen or colobomas. Gaze evoked amaurosis suggests intraorbital lesion such as glioma, nerve sheath meningioma, or intraconal mass such as cavernous hemangioma. Vision deteriorates seconds after eccentric gaze and returns to normal with straight ahead gaze.
Vision loss lasting seconds
papilledema, IIH, optic disc drusen, optic nerve sheath meningioma (need MRI with contrast),
gaze evoked (orbital tumor suspect). Get T1 image in 3 planes to differentiate MRV clot from physiologic narrowing of vessel
Vision loss can occur due to ACA aneurysm due to leakage of blood into opthalmic sheath
Consider: noninschemic
1. opthalmic surface disorders
a. tear film abnormalities-- visual blurring occurs many times a week often at the end of the day and under one environmental circumstance. Blinking and lubricating eye helps. Patients with blepharitis may be worse in the morning due to accumulated meibomian gland secretion overnight. With dry eyes causing epithelial breakdown, there may be foreign body sensation, pain or redness with a positive Schirmer's test. Patients with rosacea frequently have opthalmic involvement. Also PD.
2. Other ocular causes-- narrow angle glaucoma causes transient blurring with halos. Recurrent spontaneous anterior chamber hemorrhages is such patients needs to be differentiated from those occurring in juvenile xanthogranuloma, malpositioned lens with iris contact, and iris neovascularization.
Patients with corneal dysfunction have episodes of blurred vision that last for hours especially in the mornings, must examine during an episode. Episodes in patients with diabetes due to hyper or hypoglycemia occur.
Ischemic Causes
Causes-- 60 % are due to carotid stenosis/occlusion. Also called TMB, amaurosis fugax, or retinal tia. In usual cases , emboli from carotid are common but low flow also occurs when collaterals from the Circle of Willis and eca are compromised. In these cases symptoms may be inducible by change in position or eating, or when distal flow is inadequate such as chronic ocular ischemia or bright light amaurosis. The latter occurs with TMB after sunlight or looking at a white wall, in the setting of carotid occlusion and is a well known phenomenon.
Risk of stroke per annum is 2 % with 1 % risk of permanent visual loss, v. 5-8 % risk of stroke with hemispheric tia's.
Symptoms are abrupt onset, painless, lasts 1-5 minutes, darkening or fogging (not blurring) of visual field, altitudinal pattern (shade closing) of vision loss, and return of vision over minutes.
Vision loss may be altitudinal, peripheral, central or even vertical. A nasal field defect may suggest emboli due to lodging in temporal retinal circulation. Rarely, scintillating scotomas occur. Pain which is rare may suggest temporal arteritis.
Neuroopthalmic signs-- the most common are retinal emboli, including cholesterol (Hollenhorst) plaques which are refractile, metallic gold appearance and indicate carotid disease and platelet fibrin emboli which are creamy white grey longitudinal intravascular opacifications that fill the lumen, and indicate either carotid thrombosis or thrombosis with recent MI. Chronic severe carotid disease leads to chronic ocular ischemia including episcleral and conjunctival injection, corneal edema, and neovascular glaucoma. Venous stasis causes microaneurysms and blot hemorrhages. Unlike diabetes they are unilateral (ipsilateral to stenosis) and mid periphery instead of posterior pole. Rarely retinal calcific emboli occur in patients with cardiac valvular disease. They are grey white and ovoid and infarct the retina.
In papilledema, episodes of grey black and white vision lasting seconds may occur. Its fleeting and associated with changes in position. This also occurs in pseudopappilledema drusen or colobomas. Gaze evoked amaurosis suggests intraorbital lesion such as glioma, nerve sheath meningioma, or intraconal mass such as cavernous hemangioma. Vision deteriorates seconds after eccentric gaze and returns to normal with straight ahead gaze.
Vision loss lasting seconds
papilledema, IIH, optic disc drusen, optic nerve sheath meningioma (need MRI with contrast),
gaze evoked (orbital tumor suspect). Get T1 image in 3 planes to differentiate MRV clot from physiologic narrowing of vessel
Vision loss can occur due to ACA aneurysm due to leakage of blood into opthalmic sheath
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