Transient complete or partial monocular blindness due to retinal ischemia. This may be caused by emboli from the CAROTID ARTERY (usually in association with CAROTID STENOSIS) and other locations that enter the central RETINAL ARTERY. (From Adams et al., Principles of Neurology, 6th ed, p245)
The inability to see or the loss or absence of perception of visual stimuli. This condition may be the result of EYE DISEASES; OPTIC NERVE DISEASES; OPTIC CHIASM diseases; or BRAIN DISEASES affecting the VISUAL PATHWAYS or OCCIPITAL LOBE.
A rare degenerative inherited eye disease that appears at birth or in the first few months of life that results in a loss of vision. Not to be confused with LEBER HEREDITARY OPTIC NEUROPATHY, the disease is thought to be caused by abnormal development of PHOTORECEPTOR CELLS in the RETINA, or by the extremely premature degeneration of retinal cells.
Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)
Sudden ISCHEMIA in the RETINA due to blocked blood flow through the CENTRAL RETINAL ARTERY or its branches leading to sudden complete or partial loss of vision, respectively, in the eye.
Branch of the common carotid artery which supplies the anterior part of the brain, the eye and its appendages, the forehead and nose.
Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)
The excision of the thickened, atheromatous tunica intima of a carotid artery.
Enzymes that catalyze the rearrangement of geometry about double bonds. EC 5.2.
Surgical excision, performed under general anesthesia, of the atheromatous tunica intima of an artery. When reconstruction of an artery is performed as an endovascular procedure through a catheter, it is called ATHERECTOMY.
Radiography of blood vessels after injection of a contrast medium.
Central retinal artery and its branches. It arises from the ophthalmic artery, pierces the optic nerve and runs through its center, enters the eye through the porus opticus and branches to supply the retina.
The condition of an anatomical structure's being constricted beyond normal dimensions.
A spontaneous diminution or abatement of a disease over time, without formal treatment.
A maternally linked genetic disorder that presents in mid-life as acute or subacute central vision loss leading to central scotoma and blindness. The disease has been associated with missense mutations in the mtDNA, in genes for Complex I, III, and IV polypeptides, that can act autonomously or in association with each other to cause the disease. (from Online Mendelian Inheritance in Man,, MIM#535000 (April 17, 2001))
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
Ultrasonography applying the Doppler effect combined with real-time imaging. The real-time image is created by rapid movement of the ultrasound beam. A powerful advantage of this technique is the ability to estimate the velocity of flow from the Doppler shift frequency.
'Eye proteins' are structural or functional proteins, such as crystallins, opsins, and collagens, located in various parts of the eye, including the cornea, lens, retina, and aqueous humor, that contribute to maintaining transparency, refractive power, phototransduction, and overall integrity of the visual system.
Hereditary conditions that feature progressive visual loss in association with optic atrophy. Relatively common forms include autosomal dominant optic atrophy (OPTIC ATROPHY, AUTOSOMAL DOMINANT) and Leber hereditary optic atrophy (OPTIC ATROPHY, HEREDITARY, LEBER).
A retrogressive pathological change in the retina, focal or generalized, caused by genetic defects, inflammation, trauma, vascular disease, or aging. Degeneration affecting predominantly the macula lutea of the retina is MACULAR DEGENERATION. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p304)
Pathological developments in the RECTUM region of the large intestine (INTESTINE, LARGE).
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.
Hereditary, progressive degeneration of the neuroepithelium of the retina characterized by night blindness and progressive contraction of the visual field.
The bridge between the inner and the outer segments of a retinal rod or a cone photoreceptor cell. Through it, proteins synthesized in the inner segment are transported to the outer segment.
A group of disorders involving predominantly the posterior portion of the ocular fundus, due to degeneration in the sensory layer of the RETINA; RETINAL PIGMENT EPITHELIUM; BRUCH MEMBRANE; CHOROID; or a combination of these tissues.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Recording of electric potentials in the retina after stimulation by light.

Axillary-to-carotid artery bypass grafting for symptomatic severe common carotid artery occlusive disease. (1/38)

PURPOSE: Revascularization of the internal or external carotid arteries is occasionally indicated for symptomatic atherosclerotic common carotid artery occlusion or long-segment high-grade stenosis beginning at its origin. I report the outcome of axillary artery-based bypass grafts to the distal common, internal, or external carotid arteries. METHODS: Between 1981 and 1997, 29 axillary-to-carotid bypass grafting procedures were performed on 28 patients, 15 men and 13 women, with a mean age of 68 years. Indications were transient ischemia in nine patients, amaurosis fugax in four patients, completed stroke in six patients, and nonlateralizing global ischemia in nine patients. Twenty-three common carotid arteries were totally occluded, and six had long-segment stenosis of 90% or greater beginning at the origin. Saphenous vein grafts were used in 25 procedures, and synthetic grafts were used in four. Grafts were placed to 13 internal, eight distal common, and eight external carotid arteries. RESULTS: There were no perioperative deaths; one stroke occurred (3.4%). No lymphatic or peripheral nerve complications occurred. In a 1- to 11-year follow-up period (mean, 4.5 years), there were no graft occlusions, one restenosis of 50% or greater, and two restenoses of 70% or greater. The 1-year stenosis-free rate for 50% or greater stenosis was 93%, and the 5- and 10-year rates were 87%. No late ipsilateral strokes occurred. The 5- and 10-year survival rates were 64% and 28%, respectively. Coronary artery disease was the major cause of late mortality. CONCLUSION: Axillary-to-carotid bypass grafting for severe symptomatic common carotid occlusive disease is safe, well tolerated, durable, and effective in stroke prevention. There is a high late mortality rate because of coronary artery disease in patients with severe proximal common carotid occlusive disease.  (+info)

Hemispheric symptoms and carotid plaque echomorphology. (2/38)

PURPOSE: In patients with carotid bifurcation disease, the risk of stroke mainly depends on the severity of the stenosis, the presenting hemispheric symptom, and, as recently suggested, on plaque echodensity. We tested the hypothesis that asymptomatic carotid plaques and plaques of patients who present with different hemispheric symptoms are related to different plaque structure in terms of echodensity and the degree of stenosis. METHODS: Two hundred sixty-four patients with 295 carotid bifurcation plaques (146 symptomatic, 149 asymptomatic) causing more than 50% stenosis were examined with duplex scanning. Thirty-six plaques were associated with amaurosis fugax (AF), 68 plaques were associated with transient ischemic attacks (TIAs), and 42 plaques were associated with stroke. B-mode images were digitized and normalized using linear scaling and two reference points, blood and adventitia. The gray scale median (GSM) of blood was set to 0, and the GSM of the adventitia was set to 190 (gray scale range, black = 0; white = 255). The GSM of the plaque in the normalized image was used as the objective measurement of echodensity. RESULTS: The mean GSM and the mean degree of stenosis, with 95% confidence intervals, for plaques associated with hemispheric symptoms were 13.3 (10.6 to 16) and 80.5 (78.3 to 82.7), respectively; and for asymptomatic plaques, the mean GSM and the mean degree of stenosis were 30.5 (26.2 to 34.7) and 72. 2 (69.8 to 74.5), respectively. Furthermore, in plaques related to AF, the mean GSM and the mean degree of stenosis were 7.4 (1.9 to 12. 9) and 85.6 (82 to 89.2), respectively; in those related to TIA, the mean GSM and the mean degree of stenosis were 14.9 (11.2 to 18.6) and 79.3 (76.1 to 82.4), respectively; and in those related to stroke, the mean GSM and the mean degree of stenosis were 15.8 (10.2 to 21.3) and 78.1 (73.4 to 82.8), respectively. CONCLUSION: Plaques associated with hemispheric symptoms are more hypoechoic and more stenotic than those associated with no symptoms. Plaques associated with AF are more hypoechoic and more stenotic than those associated with TIA or stroke or those without symptoms. Plaques causing TIA and stroke have the same echodensity and the same degree of stenosis. These findings confirm previous suggestions that hypoechoic plaques are more likely to be symptomatic than hyperechoic ones. They support the hypothesis that the pathophysiologic mechanism for AF is different from that for TIA and stroke.  (+info)

Clinical and pathophysiological features of amaurosis fugax in Japanese stroke patients. (3/38)

OBJECTIVE: It has been emphasized that amaurosis fugax (AmF) is caused by thromboembolism due to atheromatous lesions of the extracranial carotid artery (EC-CA) in Caucasian populations. However, there have been few studies of AmF in Japan. We analyzed the clinical and pathophysiologic features of AmF in 43 Japanese AmF patients. SUBJECTS AND METHODS: Forty-three patients presented with AmF from a group of 2,056 Japanese patients with acute ischemic stroke. We investigated angiographic and transcranial Doppler findings, precipitating factors, medical treatment and prognosis, to elucidate the pathogenetic mechanism of AmF. RESULTS: Angiographic findings revealed an intracranial lesion in 22 patients (51%), extracranial lesion in 16 (37%), and no abnormality in 5 (12%). Blood flow in the ophthalmic artery (OA) examined by the transcranial Doppler ultrasonography (TCD) showed normal antegrade flow in 24 patients and reversed flow in 7. Precipitating factors for AmF were seen in 7 out of 43 patients. Regarding the pathogenesis of AmF, the micro-thromboembolism originated from the internal carotid artery (ICA) in 25 patients, the thromboembolism was via the external carotid artery (ECA) in 7, the hemodynamic retinal vascular insufficiency in 6 patients showed various atheromatous changes in the intracranial carotid artery (IC-CA) or EC-CA, and the cause was unknown in 5. CONCLUSION: In this series of patients, AmF was mainly caused by thromboembolism from IC-CA atheromatous lesions. Micro-thromboemboli from the ECA or hemodynamic retinal vascular insufficiency, although less frequent, should also be considered as possible etiologies for AmF.  (+info)

Echomorphologic and histopathologic characteristics of unstable carotid plaques. (4/38)

BACKGROUND AND PURPOSE: Our hypothesis was that the carotid plaques associated with retinal and cerebrovascular symptomatology and asymptomatic presentation may be differ from each other. The aim of this study was to identify the sonographic and histopathologic characteristics of plaques that corresponded to these three clinical manifestations. METHODS: The echo process involved duplex preoperative imaging of 71 plaques (67 patients, 21 plaques were associated with retinal, 25 with cerebrovascular symptoms, and 25 were asymptomatic), which was performed in a longitudinal fashion. Appropriate frames were captured and digitized via S-video signal in a computer and digitized sonograms were normalized by two echo-anatomic reference points: the gray scale median (GSM) of the blood and that of the adventitia. The GSM of the plaques was evaluated to distinguish dark (low-GSM) from bright (high-GSM) plaques. Subsequent to endarterectomy, the plaques were sectioned transversely, and a slice at the level of the largest plaque area was examined for the relative size of necrotic core and presence of calcification and hemorrhage. RESULTS: Retinal symptomatology was associated with a hypoechoic plaque appearance (median GSM: 0), asymptomatic status with a hyperechoic plaque appearance (median GSM: 34), and cerebrovascular symptomatology with an intermediate plaque appearance (median GSM: 16) (P = .001). The histopathologic characteristics did not disclose differences between the three clinical groups. The hypoechoic plaque appearance was associated only with the presence of hemorrhage (median GSM for the hemorrhagic plaques, 6, and for the non-hemorrhagic ones, 20 [P = .04]). The relative necrotic core size and the presence of calcification did not show any echomorphologic predilection. CONCLUSION: Our results showed that distinct echomorphologic characteristics of plaques were associated with retinal and cerebrovascular symptomatology and asymptomatic status. Histopathologically, only the presence of hemorrhage proved to have an echomorphologic predilection.  (+info)

Types of neurovascular symptoms and carotid plaque ultrasonic textural characteristics. (5/38)

The aim of this study was to identify the echo morphology and stenosis of carotid plaques that corresponded to ipsilateral asymptomatic status, amaurosis fugax, hemispheric transient ischemic attack, and stroke. One hundred ninety-two plaques (150 patients), producing stenosis in the range of 50% to 99% and associated with various neurovascular manifestations, were studied. These plaques were imaged on duplex scans, and a series of textural features was produced in a computer to distinguish quantitatively their various echo patterns. Amaurosis fugax corresponded to dark, severely stenosed atheromas (90%); hemispheric transient ischemic attack and stroke corresponded to plaques with intermediate echoic characteristics and intermediate stenosis (80%); and asymptomatic status corresponded to bright, moderately stenosed plaques (70%; P < .05). The significance of these findings is discussed.  (+info)

Delayed onset of amaurosis fugax in a patient with type A aortic dissection post surgical repair. (6/38)

Stroke is an important complication for the surgical treatment of type A aortic dissection and it occurs immediately post operation. Many surgical techniques such as deep hypothermic circulatory arrest and retrograde cerebral perfusion have been reported to ameliorate this complication. We report here a male Taiwanese patient with type A aortic dissection involving the arch who underwent surgical repair. Amaurosis fugax appeared on the 4th day post operation. Funduscopic findings demonstrated multi focal embolization and carotid sonography revealed normal carotid arteries. The symptoms and signs improved after anticoagulation therapy. This is a rare case of delayed onset of amaurosis fugax in a patient with type A aortic dissection post surgical repair. The thromboemboli might have originated from the internal surface of the sawing area.  (+info)

Reoperation for recurrent carotid stenosis: early results and late outcome in 199 patients. (7/38)

PURPOSE: This study was undertaken to determine the safety and efficacy of reoperations for recurrent carotid stenosis (REDOCEA) at the Cleveland Clinic. MATERIALS AND METHODS: From 1989 to 1999, 206 consecutive REDOCEAs were performed in 199 patients (131 men, 68 women) with a mean age of 68 years (median, 69 years; range, 47-86 years). A total of 119 procedures (57%) were performed for severe asymptomatic stenosis, 55 (27%) for hemispheric transient ischemic attacks or amaurosis fugax, 26 (13%) for prior stroke, and 6 (3%) for vertebrobasilar symptoms. Eleven REDOCEAs (5%) were combined with myocardial revascularization, and another 19 (9%) represented multiple carotid reoperations (17 second reoperations and 2 third reoperations). Three REDOCEAs (1%) were closed primarily, and nine (4%) required interposition grafts, whereas the remaining 194 (95%) were repaired with either vein patch angioplasty (139 [68%]) or synthetic patches (55 [27%]). Three patients (2%) were lost to follow-up, but late information was available for 196 patients (203 operations) at a mean interval of 4.3 years (median, 3.9 years; maximum, 10.2 years). RESULTS: Considering all 206 procedures, there were 7 early (< 30 days) postoperative neurologic events (3.4%), including 6 perioperative strokes (2.9%) and 1 occipital hemorrhage (0.5%) on the 12th postoperative day. Seventeen additional neurologic events occurred during the late follow-up period, consisting of eight strokes (3.9%) and nine transient ischemic attacks (4.4 %). With the Kaplan-Meier method, the estimated 5-year freedom from stroke was 92% (95% CI, 88%-96%). There were two early postoperative deaths (1%), both from cardiac complications after REDOCEAs combined with myocardial revascularization procedures. With the Kaplan-Meier method, the estimated 5-year survival was 81% (range, 75%-88%). A univariate Cox regression model yielded the presence of coronary artery disease as the only variable that was significantly associated with survival (P =.024). The presence of pulmonary disease (P =.036), diabetes (P =.01), and advancing age (P =.006) was found to be significantly associated with stroke after REDOCEA. Causes of 53 late deaths were cardiovascular problems in 25 patients (47%), unknown in 14 (26%), renal failure in 4 (8%), stroke in 3 (6%), and miscellaneous in 7 (13%). CONCLUSIONS: We conclude that REDOCEA may be safely performed in selected patients with recurrent carotid stenosis and that most of these patients enjoy long-term freedom from stroke.  (+info)

Clinical features of transient monocular blindness and the likelihood of atherosclerotic lesions of the internal carotid artery. (8/38)

To assess which features of transient monocular blindness (TMB) are associated with atherosclerotic changes in the ipsilateral internal carotid artery (ICA), 337 patients with sudden, transient monocular loss of vision were prospectively studied. History characteristics of the attack were compared with the presence of atherosclerotic lesions of the ipsilateral ICA. All patients were directly interviewed by a single investigator. Of all patients, 159 had a normal ICA on the relevant side, 33 had a stenosis between 0%-69%, 100 had a stenosis of 70%-99%, and 45 had an ICA occlusion. An altitudinal onset or disappearance of symptoms was associated with atherosclerotic lesions of the ipsilateral ICA. A severe (70%-99%) stenosis was also associated with a duration between 1 and 10 minutes, and with a speed of onset in seconds. An ICA occlusion was associated with attacks being provoked by bright light, an altitudinal onset, and the occurrence of more than 10 attacks. Patients who could not remember details about the mode of onset, disappearance, or duration of the attack were likely to have a normal ICA. Our findings may facilitate the clinical decision whether or not to perform ancillary investigations in these patients.  (+info)

Amaurosis fugax is a medical term that describes a temporary loss of vision in one eye, which is often described as a "shade or curtain falling over the field of vision." It's usually caused by a temporary interruption of blood flow to the retina or optic nerve. This condition is often associated with conditions such as giant cell arteritis, carotid artery stenosis, and cardiovascular disease.

It's important to note that Amaurosis fugax can be a warning sign for a more serious medical event, such as a stroke, so it's essential to seek medical attention promptly if you experience any symptoms of this condition.

Blindness is a condition of complete or near-complete vision loss. It can be caused by various factors such as eye diseases, injuries, or birth defects. Total blindness means that a person cannot see anything at all, while near-complete blindness refers to having only light perception or the ability to perceive the direction of light, but not able to discern shapes or forms. Legal blindness is a term used to define a certain level of visual impairment that qualifies an individual for government assistance and benefits; it usually means best corrected visual acuity of 20/200 or worse in the better eye, or a visual field no greater than 20 degrees in diameter.

Leber Congenital Amaurosis (LCA) is a group of inherited retinal degenerative disorders that affect the development and function of the retina, a light-sensitive tissue at the back of the eye. It is characterized by severe visual impairment or blindness from birth or early infancy.

The condition is caused by mutations in various genes involved in the normal functioning of photoreceptor cells (rods and cones) in the retina, which are responsible for capturing light and transmitting visual signals to the brain. As a result, the photoreceptors fail to develop properly or degenerate over time, leading to vision loss.

Symptoms of LCA may include roving eye movements (nystagmus), lack of fixation, decreased or absent response to light, and abnormal pupillary reflexes. Some individuals with LCA may also have other ocular abnormalities such as keratoconus, cataracts, or glaucoma.

LCA is typically inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition. Currently, there is no cure for LCA, but various treatments such as gene therapy and assistive devices may help improve visual function and quality of life for affected individuals.

Carotid artery diseases refer to conditions that affect the carotid arteries, which are the major blood vessels that supply oxygen-rich blood to the head and neck. The most common type of carotid artery disease is atherosclerosis, which occurs when fatty deposits called plaques build up in the inner lining of the arteries.

These plaques can cause the arteries to narrow or become blocked, reducing blood flow to the brain and increasing the risk of stroke. Other carotid artery diseases include carotid artery dissection, which occurs when there is a tear in the inner lining of the artery, and fibromuscular dysplasia, which is a condition that affects the muscle and tissue in the walls of the artery.

Symptoms of carotid artery disease may include neck pain or pulsations, transient ischemic attacks (TIAs) or "mini-strokes," and strokes. Treatment options for carotid artery disease depend on the severity and type of the condition but may include lifestyle changes, medications, endarterectomy (a surgical procedure to remove plaque from the artery), or angioplasty and stenting (procedures to open blocked arteries using a balloon and stent).

A Transient Ischemic Attack (TIA), also known as a "mini-stroke," is a temporary period of symptoms similar to those you'd get if you were having a stroke. A TIA doesn't cause permanent damage and is often caused by a temporary decrease in blood supply to part of your brain, which may last as little as five minutes.

Like an ischemic stroke, a TIA occurs when a clot or debris blocks blood flow to part of your nervous system. However, unlike a stroke, a TIA doesn't leave lasting damage because the blockage is temporary.

Symptoms of a TIA can include sudden onset of weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body. You could also experience slurred or garbled speech, or difficulty understanding others. Other symptoms can include blindness in one or both eyes, dizziness, or a severe headache with no known cause.

Even though TIAs usually last only a few minutes, they are a serious condition and should not be ignored. If you suspect you or someone else is experiencing a TIA, seek immediate medical attention. TIAs can be a warning sign that a full-blown stroke is imminent.

Retinal artery occlusion (RAO) is a medical condition characterized by the blockage or obstruction of the retinal artery, which supplies oxygenated blood to the retina. This blockage typically occurs due to embolism (a small clot or debris that travels to the retinal artery), thrombosis (blood clot formation in the artery), or vasculitis (inflammation of the blood vessels).

There are two types of retinal artery occlusions:

1. Central Retinal Artery Occlusion (CRAO): This type occurs when the main retinal artery is obstructed, affecting the entire inner layer of the retina. It can lead to severe and sudden vision loss in the affected eye.
2. Branch Retinal Artery Occlusion (BRAO): This type affects a branch of the retinal artery, causing visual field loss in the corresponding area. Although it is less severe than CRAO, it can still result in noticeable vision impairment.

Immediate medical attention is crucial for both types of RAO to improve the chances of recovery and minimize potential damage to the eye and vision. Treatment options may include medications, laser therapy, or surgery, depending on the underlying cause and the severity of the condition.

The internal carotid artery is a major blood vessel that supplies oxygenated blood to the brain. It originates from the common carotid artery and passes through the neck, entering the skull via the carotid canal in the temporal bone. Once inside the skull, it branches into several smaller vessels that supply different parts of the brain with blood.

The internal carotid artery is divided into several segments: cervical, petrous, cavernous, clinoid, and supraclinoid. Each segment has distinct clinical significance in terms of potential injury or disease. The most common conditions affecting the internal carotid artery include atherosclerosis, which can lead to stroke or transient ischemic attack (TIA), and dissection, which can cause severe headache, neck pain, and neurological symptoms.

It's important to note that any blockage or damage to the internal carotid artery can have serious consequences, as it can significantly reduce blood flow to the brain and lead to permanent neurological damage or even death. Therefore, regular check-ups and screening tests are recommended for individuals at high risk of developing vascular diseases.

Carotid stenosis is a medical condition that refers to the narrowing or constriction of the lumen (inner space) of the carotid artery. The carotid arteries are major blood vessels that supply oxygenated blood to the head and neck. Carotid stenosis usually results from the buildup of plaque, made up of fat, cholesterol, calcium, and other substances, on the inner walls of the artery. This process is called atherosclerosis.

As the plaque accumulates, it causes the artery to narrow, reducing blood flow to the brain. Severe carotid stenosis can increase the risk of stroke, as a clot or debris from the plaque can break off and travel to the brain, blocking a smaller blood vessel and causing tissue damage or death.

Carotid stenosis is typically diagnosed through imaging tests such as ultrasound, CT angiography, or MRI angiography. Treatment options may include lifestyle modifications (such as quitting smoking, controlling blood pressure, and managing cholesterol levels), medications to reduce the risk of clots, or surgical procedures like endarterectomy or stenting to remove or bypass the blockage.

Carotid endarterectomy is a surgical procedure to remove plaque buildup (atherosclerosis) from the carotid arteries, which are the major blood vessels that supply oxygen-rich blood to the brain. The surgery involves making an incision in the neck, opening the carotid artery, and removing the plaque from the inside of the artery wall. The goal of the procedure is to restore normal blood flow to the brain and reduce the risk of stroke caused by the narrowing or blockage of the carotid arteries.

Cis-trans isomeres are molecules that have the same molecular formula and skeletal structure, but differ in the arrangement of their atoms around a double bond. In a cis isomer, the two larger groups or atoms are on the same side of the double bond, while in a trans isomer, they are on opposite sides.

Cis-trans isomerases are enzymes that catalyze the interconversion between cis and trans isomers of various molecules, such as fatty acids, steroids, and retinals. These enzymes play important roles in various biological processes, including membrane fluidity, vision, and the biosynthesis of hormones and other signaling molecules.

Examples of cis-trans isomerases include:

* Fatty acid desaturases, which introduce double bonds into fatty acids and can convert trans isomers to cis isomers
* Retinal isomerases, which interconvert the cis and trans isomers of retinal, a molecule involved in vision
* Steroid isomerases, which catalyze the interconversion of various steroids, including cholesterol and its derivatives.

Endarterectomy is a surgical procedure in which the inner lining of an artery (the endothelium) that has become thickened, damaged, or narrowed due to the buildup of fatty deposits, called plaques, is removed. This process helps restore normal blood flow through the artery and reduces the risk of serious complications such as stroke or limb loss.

The procedure typically involves making an incision in the affected artery, carefully removing the plaque and inner lining, and then closing the artery with sutures or a patch graft. Endarterectomy is most commonly performed on the carotid arteries in the neck, but it can also be done on other arteries throughout the body, including the femoral artery in the leg and the iliac artery in the pelvis.

Endarterectomy is usually recommended for patients with significant narrowing of their arteries who are experiencing symptoms such as pain, numbness, or weakness in their limbs, or who have a high risk of stroke due to carotid artery disease. The procedure is generally safe and effective, but like any surgery, it carries risks such as bleeding, infection, and damage to nearby nerves or tissues.

Angiography is a medical procedure in which an x-ray image is taken to visualize the internal structure of blood vessels, arteries, or veins. This is done by injecting a radiopaque contrast agent (dye) into the blood vessel using a thin, flexible catheter. The dye makes the blood vessels visible on an x-ray image, allowing doctors to diagnose and treat various medical conditions such as blockages, narrowing, or malformations of the blood vessels.

There are several types of angiography, including:

* Cardiac angiography (also called coronary angiography) - used to examine the blood vessels of the heart
* Cerebral angiography - used to examine the blood vessels of the brain
* Peripheral angiography - used to examine the blood vessels in the limbs or other parts of the body.

Angiography is typically performed by a radiologist, cardiologist, or vascular surgeon in a hospital setting. It can help diagnose conditions such as coronary artery disease, aneurysms, and peripheral arterial disease, among others.

A retinal artery is a small branch of the ophthalmic artery that supplies oxygenated blood to the inner layers of the retina, which is the light-sensitive tissue located at the back of the eye. There are two main retinal arteries - the central retinal artery and the cilioretinal artery. The central retinal artery enters the eye through the optic nerve and divides into smaller branches to supply blood to the entire retina, while the cilioretinal artery is a smaller artery that supplies blood to a small portion of the retina near the optic nerve. Any damage or blockage to these arteries can lead to serious vision problems, such as retinal artery occlusion or retinal artery embolism.

Pathological constriction refers to an abnormal narrowing or tightening of a body passage or organ, which can interfere with the normal flow of blood, air, or other substances through the area. This constriction can occur due to various reasons such as inflammation, scarring, or abnormal growths, and can affect different parts of the body, including blood vessels, airways, intestines, and ureters. Pathological constriction can lead to a range of symptoms and complications depending on its location and severity, and may require medical intervention to correct.

Spontaneous remission in a medical context refers to the disappearance or significant improvement of symptoms of a disease or condition without any specific treatment being administered. In other words, it's a situation where the disease resolves on its own, without any apparent cause. While spontaneous remission can occur in various conditions, it is relatively rare and not well understood. It's important to note that just because a remission occurs without treatment doesn't mean that medical care should be avoided, as many conditions can worsen or lead to complications if left untreated.

Hereditary Optic Atrophy, Leber type (LOA) is a mitochondrial DNA-associated inherited condition that primarily affects the optic nerve and leads to vision loss. It is characterized by the degeneration of retinal ganglion cells and their axons, which make up the optic nerve. This results in bilateral, painless, and progressive visual deterioration, typically beginning in young adulthood (14-35 years).

Leber's hereditary optic atrophy is caused by mutations in the mitochondrial DNA (mtDNA) gene MT-ND4 or MT-ND6. The condition follows a maternal pattern of inheritance, meaning that it is passed down through the mother's lineage.

The onset of LOA usually occurs in one eye first, followed by the second eye within weeks to months. Central vision is initially affected, leading to blurriness and loss of visual acuity. Color vision may also be impaired. The progression of the condition generally stabilizes after a few months, but complete recovery of vision is unlikely.

Currently, there is no cure for Leber's hereditary optic atrophy. Treatment focuses on managing symptoms and providing visual rehabilitation to help affected individuals adapt to their visual impairment.

Cerebrovascular disorders are a group of medical conditions that affect the blood vessels of the brain. These disorders can be caused by narrowing, blockage, or rupture of the blood vessels, leading to decreased blood flow and oxygen supply to the brain. The most common types of cerebrovascular disorders include:

1. Stroke: A stroke occurs when a blood vessel in the brain becomes blocked or bursts, causing a lack of oxygen and nutrients to reach brain cells. This can lead to permanent damage or death of brain tissue.
2. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA occurs when blood flow to the brain is temporarily blocked, often by a blood clot. Symptoms may last only a few minutes to a few hours and typically resolve on their own. However, a TIA is a serious warning sign that a full-blown stroke may occur in the future.
3. Aneurysm: An aneurysm is a weakened or bulging area in the wall of a blood vessel. If left untreated, an aneurysm can rupture and cause bleeding in the brain.
4. Arteriovenous malformation (AVM): An AVM is a tangled mass of abnormal blood vessels that connect arteries and veins. This can lead to bleeding in the brain or stroke.
5. Carotid stenosis: Carotid stenosis occurs when the carotid arteries, which supply blood to the brain, become narrowed or blocked due to plaque buildup. This can increase the risk of stroke.
6. Vertebrobasilar insufficiency: This condition occurs when the vertebral and basilar arteries, which supply blood to the back of the brain, become narrowed or blocked. This can lead to symptoms such as dizziness, vertigo, and difficulty swallowing.

Cerebrovascular disorders are a leading cause of disability and death worldwide. Risk factors for these conditions include age, high blood pressure, smoking, diabetes, high cholesterol, and family history. Treatment may involve medications, surgery, or lifestyle changes to reduce the risk of further complications.

The carotid arteries are a pair of vital blood vessels in the human body that supply oxygenated blood to the head and neck. Each person has two common carotid arteries, one on each side of the neck, which branch off from the aorta, the largest artery in the body.

The right common carotid artery originates from the brachiocephalic trunk, while the left common carotid artery arises directly from the aortic arch. As they ascend through the neck, they split into two main branches: the internal and external carotid arteries.

The internal carotid artery supplies oxygenated blood to the brain, eyes, and other structures within the skull, while the external carotid artery provides blood to the face, scalp, and various regions of the neck.

Maintaining healthy carotid arteries is crucial for overall cardiovascular health and preventing serious conditions like stroke, which can occur when the arteries become narrowed or blocked due to the buildup of plaque or fatty deposits (atherosclerosis). Regular check-ups with healthcare professionals may include monitoring carotid artery health through ultrasound or other imaging techniques.

Ultrasonography, Doppler, and Duplex are diagnostic medical techniques that use sound waves to create images of internal body structures and assess their function. Here are the definitions for each:

1. Ultrasonography: Also known as ultrasound, this is a non-invasive imaging technique that uses high-frequency sound waves to produce images of internal organs and tissues. A small handheld device called a transducer is placed on the skin surface, which emits and receives sound waves. The returning echoes are then processed to create real-time visual images of the internal structures.
2. Doppler: This is a type of ultrasound that measures the velocity and direction of blood flow in the body by analyzing the frequency shift of the reflected sound waves. It can be used to assess blood flow in various parts of the body, such as the heart, arteries, and veins.
3. Duplex: Duplex ultrasonography is a combination of both gray-scale ultrasound and Doppler ultrasound. It provides detailed images of internal structures, as well as information about blood flow velocity and direction. This technique is often used to evaluate conditions such as deep vein thrombosis, carotid artery stenosis, and peripheral arterial disease.

In summary, ultrasonography is a diagnostic imaging technique that uses sound waves to create images of internal structures, Doppler is a type of ultrasound that measures blood flow velocity and direction, and duplex is a combination of both techniques that provides detailed images and information about blood flow.

Eye proteins, also known as ocular proteins, are specific proteins that are found within the eye and play crucial roles in maintaining proper eye function and health. These proteins can be found in various parts of the eye, including the cornea, iris, lens, retina, and other structures. They perform a wide range of functions, such as:

1. Structural support: Proteins like collagen and elastin provide strength and flexibility to the eye's tissues, enabling them to maintain their shape and withstand mechanical stress.
2. Light absorption and transmission: Proteins like opsins and crystallins are involved in capturing and transmitting light signals within the eye, which is essential for vision.
3. Protection against damage: Some eye proteins, such as antioxidant enzymes and heat shock proteins, help protect the eye from oxidative stress, UV radiation, and other environmental factors that can cause damage.
4. Regulation of eye growth and development: Various growth factors and signaling molecules, which are protein-based, contribute to the proper growth, differentiation, and maintenance of eye tissues during embryonic development and throughout adulthood.
5. Immune defense: Proteins involved in the immune response, such as complement components and immunoglobulins, help protect the eye from infection and inflammation.
6. Maintenance of transparency: Crystallin proteins in the lens maintain its transparency, allowing light to pass through unobstructed for clear vision.
7. Neuroprotection: Certain eye proteins, like brain-derived neurotrophic factor (BDNF), support the survival and function of neurons within the retina, helping to preserve vision.

Dysfunction or damage to these eye proteins can contribute to various eye disorders and diseases, such as cataracts, age-related macular degeneration, glaucoma, diabetic retinopathy, and others.

Hereditary optic atrophies (HOAs) are a group of genetic disorders that cause degeneration of the optic nerve, leading to vision loss. The optic nerve is responsible for transmitting visual information from the eye to the brain. In HOAs, this nerve degenerates over time, resulting in decreased visual acuity, color vision deficits, and sometimes visual field defects.

There are several types of HOAs, including dominant optic atrophy (DOA), Leber hereditary optic neuropathy (LHON), autosomal recessive optic atrophy (AROA), and Wolfram syndrome. Each type has a different inheritance pattern and is caused by mutations in different genes.

DOA is the most common form of HOA and is characterized by progressive vision loss that typically begins in childhood or early adulthood. It is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disease-causing mutation from an affected parent.

LHON is a mitochondrial disorder that primarily affects males and is characterized by sudden, severe vision loss that typically occurs in young adulthood. It is caused by mutations in the mitochondrial DNA and is inherited maternally.

AROA is a rare form of HOA that is inherited in an autosomal recessive manner, meaning that both copies of the gene must be mutated to cause the disease. It typically presents in infancy or early childhood with progressive vision loss.

Wolfram syndrome is a rare genetic disorder that affects multiple organs, including the eyes, ears, and endocrine system. It is characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and hearing loss. It is inherited in an autosomal recessive manner.

There is currently no cure for HOAs, but treatments such as low-vision aids and rehabilitation may help to manage the symptoms. Research is ongoing to develop new therapies for these disorders.

Retinal degeneration is a broad term that refers to the progressive loss of photoreceptor cells (rods and cones) in the retina, which are responsible for converting light into electrical signals that are sent to the brain. This process can lead to vision loss or blindness. There are many different types of retinal degeneration, including age-related macular degeneration, retinitis pigmentosa, and Stargardt's disease, among others. These conditions can have varying causes, such as genetic mutations, environmental factors, or a combination of both. Treatment options vary depending on the specific type and progression of the condition.

Rectal diseases refer to conditions that affect the structure or function of the rectum, which is the lower end of the large intestine, just above the anus. The rectum serves as a storage area for stool before it is eliminated from the body. Some common rectal diseases include:

1. Hemorrhoids: Swollen veins in the rectum or anus that can cause pain, itching, bleeding, and discomfort.
2. Rectal cancer: Abnormal growth of cells in the rectum that can invade and destroy nearby tissue and spread to other parts of the body.
3. Anal fissures: Small tears in the lining of the anus that can cause pain, bleeding, and itching.
4. Rectal prolapse: A condition where the rectum slips outside the anus, causing discomfort, fecal incontinence, and other symptoms.
5. Inflammatory bowel disease (IBD): A group of chronic inflammatory conditions that affect the digestive tract, including the rectum, such as Crohn's disease and ulcerative colitis.
6. Rectal abscess: A collection of pus in the rectum caused by an infection, which can cause pain, swelling, and fever.
7. Fistula-in-ano: An abnormal connection between the rectum and the skin around the anus, which can cause drainage of pus or stool.
8. Rectal foreign bodies: Objects that are accidentally or intentionally inserted into the rectum and can cause injury, infection, or obstruction.

These are just a few examples of rectal diseases, and there are many other conditions that can affect the rectum. If you experience any symptoms related to the rectum, it is important to seek medical attention from a healthcare professional for proper diagnosis and treatment.

Postoperative complications refer to any unfavorable condition or event that occurs during the recovery period after a surgical procedure. These complications can vary in severity and may include, but are not limited to:

1. Infection: This can occur at the site of the incision or inside the body, such as pneumonia or urinary tract infection.
2. Bleeding: Excessive bleeding (hemorrhage) can lead to a drop in blood pressure and may require further surgical intervention.
3. Blood clots: These can form in the deep veins of the legs (deep vein thrombosis) and can potentially travel to the lungs (pulmonary embolism).
4. Wound dehiscence: This is when the surgical wound opens up, which can lead to infection and further complications.
5. Pulmonary issues: These include atelectasis (collapsed lung), pneumonia, or respiratory failure.
6. Cardiovascular problems: These include abnormal heart rhythms (arrhythmias), heart attack, or stroke.
7. Renal failure: This can occur due to various reasons such as dehydration, blood loss, or the use of certain medications.
8. Pain management issues: Inadequate pain control can lead to increased stress, anxiety, and decreased mobility.
9. Nausea and vomiting: These can be caused by anesthesia, opioid pain medication, or other factors.
10. Delirium: This is a state of confusion and disorientation that can occur in the elderly or those with certain medical conditions.

Prompt identification and management of these complications are crucial to ensure the best possible outcome for the patient.

Retinitis pigmentosa (RP) is a group of rare, genetic disorders that involve a breakdown and loss of cells in the retina - a light-sensitive tissue located at the back of the eye. The retina converts light into electrical signals which are then sent to the brain and interpreted as visual images.

In RP, the cells that detect light (rods and cones) degenerate more slowly than other cells in the retina, leading to a progressive loss of vision. Symptoms typically begin in childhood with night blindness (difficulty seeing in low light), followed by a gradual narrowing of the visual field (tunnel vision). Over time, this can lead to significant vision loss and even blindness.

The condition is usually inherited and there are several different genes that have been associated with RP. The diagnosis is typically made based on a combination of genetic testing, family history, and clinical examination. Currently, there is no cure for RP, but researchers are actively working to develop new treatments that may help slow or stop the progression of the disease.

A photoreceptor connecting cilium, also known as the connecting cilium or the outer segment initial segment, is a specialized structure found in the eye's photoreceptor cells (rods and cones). It is a thin, non-motile cilium that connects the inner segment of the photoreceptor cell to the outer segment. The outer segment contains the visual pigments that absorb light and initiate the process of vision.

The connecting cilium plays a crucial role in the maintenance and function of the outer segment by providing a passageway for the transport of proteins, lipids, and other molecules from the inner segment to the outer segment. This process is essential for the renewal and turnover of the visual pigments and other components of the outer segment. The connecting cilium also helps maintain the structural integrity of the photoreceptor cells and their sensitivity to light.

Defects in the connecting cilium can lead to various retinal disorders, such as retinitis pigmentosa and Leber congenital amaurosis, which are characterized by progressive vision loss due to the degeneration of the photoreceptor cells.

Retinal dystrophies are a group of genetic eye disorders that primarily affect the retina, a light-sensitive layer at the back of the eye. These conditions are characterized by progressive degeneration and death of photoreceptor cells (rods and cones) in the retina, leading to vision loss.

The term "dystrophy" refers to a condition that results from the abnormal or defective development and function of tissues or organs. In the case of retinal dystrophies, the photoreceptor cells do not develop or function properly, resulting in visual impairment.

Retinal dystrophies can present at any age, from infancy to adulthood, and can have varying degrees of severity. Some common symptoms include night blindness, decreased visual acuity, loss of peripheral vision, light sensitivity, and color vision abnormalities.

Examples of retinal dystrophies include retinitis pigmentosa, Stargardt disease, Usher syndrome, and Leber congenital amaurosis, among others. These conditions are typically inherited and can be caused by mutations in various genes that play a role in the development and function of the retina.

There is currently no cure for retinal dystrophies, but research is ongoing to develop treatments that may slow or halt the progression of these conditions, such as gene therapy and stem cell transplantation.

Retrospective studies, also known as retrospective research or looking back studies, are a type of observational study that examines data from the past to draw conclusions about possible causal relationships between risk factors and outcomes. In these studies, researchers analyze existing records, medical charts, or previously collected data to test a hypothesis or answer a specific research question.

Retrospective studies can be useful for generating hypotheses and identifying trends, but they have limitations compared to prospective studies, which follow participants forward in time from exposure to outcome. Retrospective studies are subject to biases such as recall bias, selection bias, and information bias, which can affect the validity of the results. Therefore, retrospective studies should be interpreted with caution and used primarily to generate hypotheses for further testing in prospective studies.

Electroretinography (ERG) is a medical test used to evaluate the functioning of the retina, which is the light-sensitive tissue located at the back of the eye. The test measures the electrical responses of the retina to light stimulation.

During the procedure, a special contact lens or electrode is placed on the surface of the eye to record the electrical activity generated by the retina's light-sensitive cells (rods and cones) and other cells in the retina. The test typically involves presenting different levels of flashes of light to the eye while the electrical responses are recorded.

The resulting ERG waveform provides information about the overall health and function of the retina, including the condition of the photoreceptors, the integrity of the inner retinal layers, and the health of the retinal ganglion cells. This test is often used to diagnose and monitor various retinal disorders, such as retinitis pigmentosa, macular degeneration, and diabetic retinopathy.

The Amaurosis Fugax Study Group (February 1990). "Current management of amaurosis fugax. The Amaurosis Fugax Study Group". ... Amaurosis fugax (Greek amaurosis meaning darkening, dark, or obscure, Latin fugax meaning fleeting) is a painless temporary ... the causes of amaurosis fugax were better refined by the Amaurosis Fugax Study Group, which has defined five distinct classes ... leading to decreased blood flow manifesting as amaurosis fugax. Commonly, amaurosis fugax caused by giant cell arteritis may be ...
Amaurosis fugax is a form of acute vision loss caused by reduced blood flow to the eye; it may be a warning sign of an ... Kaiboriboon K, Piriyawat P, Selhorst JB (May 2001). "Light-induced amaurosis fugax". American Journal of Ophthalmology. 131 (5 ...
It was first described by Theodore Leber in the 19th century.[citation needed] Amaurosis fugax (Latin: fugax meaning fleeting) ... "Hersh: What causes amaurosis fugax, a temporary loss of vision?",, Dec 4, 2012 v t e (All articles with ... Quinidine toxicity can lead to cinchonism and also to quinine amaurosis.[citation needed] Those experiencing amaurosis are ... Amaurosis (Greek meaning darkening, dark, or obscure) is vision loss or weakness that occurs without an apparent lesion ...
Amaurosis fugax Entoptic phenomenon Scintillating scotoma Grosberg BM, Solomon S, Lipton RB (August 2005). "Retinal migraine". ...
... pelvic pain vaginal discharge Ocular amaurosis fugax (G45.3) and amaurosis blurred vision Dalrymple's sign double vision (H53.2 ... It is rare that a person would visit a doctor and complain as follows: "Doctor, I have amaurosis fugax." They are more likely ... odynophagia proctalgia fugax pyrosis (R12) Rectal tenesmus steatorrhea vomiting (R11) Integumentary Hair: alopecia hirsutism ...
His symptoms began at age 28 with a sudden transient visual loss (amaurosis fugax) after the funeral of a friend. During his ...
In addition to the various permanent conditions, fleeting temporary vision impairment, amaurosis fugax, may occur, and may ... known as Leber's congenital amaurosis or LCA. Leber's Congenital Amaurosis damages the light receptors in the retina and ... Leber congenital amaurosis can cause total blindness or severe sight loss from birth or early childhood. Retinitis pigmentosa ... May 2008). "Effect of gene therapy on visual function in Leber's congenital amaurosis" (PDF). The New England Journal of ...
... known as amaurosis fugax). Emboli to the eye can be seen by ophthalmoscopy and are known as plaques of Hollenhorst. Emboli to ...
Symptoms such as unilateral weakness, amaurosis fugax, and double vision have higher odds of representing TIA compared to ... Amaurosis fugax (painless, temporary loss of vision) One-sided facial droop One-sided motor weakness Diplopia (double vision) ...
Amaurosis fugax is a temporary loss of vision that occurs in two conditions which cause a temporary reduction in ophthalmic ... "Blood pressure and pressure amaurosis." Investigative Ophthalmology and Visual Science 1975 Mar;14(3):237-40. PMID 1116922 A ...
Central retinal vein occlusion Branch retinal artery occlusion Branch retinal vein occlusion Amaurosis fugax Ocular ischemic ...
... amaurosis fugax MeSH C23.888.592.763.941.162.250 - blindness, cortical MeSH C23.888.592.763.941.256 - color vision defects MeSH ...
Alien hand syndrome Allan-Herndon-Dudley syndrome Alternating hemiplegia of childhood Alzheimer's disease Amaurosis fugax ...
... , a type of non-permanent vision loss, may refer to: Amaurosis fugax, or fleeting blindness Conversion ...
968 Her right eye suffers from amaurosis fugax.Ch. 1106 Most likely, her name is meant to resemble "ASAKA RUM", the code from ...
... amaurosis fugax MeSH C10.597.751.941.162.250 - blindness, cortical MeSH C10.597.751.941.256 - color vision defects MeSH C10.597 ...
... either temporary due to amaurosis fugax or potentially permanent due to retinal detachment), or cortical blindness, which ...
... amaurosis fugax) in one eye. Less common symptoms are artery sounds (bruits), or ringing in the ears (tinnitus). In ...
... amaurosis fugax), other signs of a transient ischemic attack (TIA) or stroke Dizziness, fatigue Unusual bleeding, nosebleeds ...
... amaurosis fugax MeSH C11.966.075.250 - blindness, cortical MeSH C11.966.075.500 - hemianopsia MeSH C11.966.256 - color vision ...
The Amaurosis Fugax Study Group (February 1990). "Current management of amaurosis fugax. The Amaurosis Fugax Study Group". ... Amaurosis fugax (Greek amaurosis meaning darkening, dark, or obscure, Latin fugax meaning fleeting) is a painless temporary ... the causes of amaurosis fugax were better refined by the Amaurosis Fugax Study Group, which has defined five distinct classes ... leading to decreased blood flow manifesting as amaurosis fugax. Commonly, amaurosis fugax caused by giant cell arteritis may be ...
Amaurosis fugax is a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina. The retina is the ... Amaurosis fugax is a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina. The retina is the ... Treatment of amaurosis fugax depends on its cause. When amaurosis fugax is due to a blood clot or plaque, the concern is to ... Amaurosis fugax is not itself a disease. Instead, it is a sign of other disorders. Amaurosis fugax can occur from different ...
encoded search term (Transient Vision Loss (TVL) and Amaurosis Fugax) and Transient Vision Loss (TVL) and Amaurosis Fugax What ... Amaurosis fugax and ocular infarction in adolescents and young adults. Ann Neurol. 1989 Jul. 26(1):69-77. [QxMD MEDLINE Link]. ... Transient Vision Loss (TVL) and Amaurosis Fugax. Updated: Dec 22, 2022 * Author: Donny W Suh, MD, MBA, FAAP, FACS; Chief Editor ... Amaurosis fugax and a visual TIA are similar in several respects: Both are of sudden onset, last 2-30 minutes, and resolve ...
talk contribs‎ 376 bytes +376‎ Created page with __NOTOC__ {{Amaurosis fugax}} {{CMG}} Please help WikiDoc by adding content ...
by urednik1. Katja Šibli, dr. med., spec. interne medicine, opravljen ima tudi evropski subspecialistični izpit za angiologijo, je zaposlena na Oddelku za žilno kirurgijo Splošne bolnišnice v Celju, ultrazvočne preiskave pa opravlja v ambulantnem Centru za bolezni ožilja. V tem centru delajo skupaj internisti, kirurgi in tudi nevrologi. Takšen multidisciplinaren pristop je v Sloveniji edinstven in po […]. Preberi več ...
Amaurosis fugax Amaurosis fugax can result from blockage of the internal carotid artery. It is a temporary loss of vision in ... Amaurosis fugax. StatPearls [Internet]. September 2021.. Central retinal artery occlusion. StatPearls [Internet]. September ...
The Vascular Doppler Lab provides objective diagnostic information evaluating the presence, location and physiological extent of peripheral arterial, venous and cerebrovascular disease.
Unexplained amaurosis fugax. * Autoimmune thrombocytopenia. * Autoimmune hemolytic anemia. * Unexplained prolongation of a ...
Shaw, H.E.J., Lawson, J.G. and Stulting, R.D. (1985) Amaurosis fugax and retinal vasculitis associated with methamphetamine ...
Visual loss ranging from unilateral visual field loss (amaurosis fugax) to bilateral total blindness ...
Left ventricular pseudoaneyrysm with amaurosis fugax as first presentation Speaker: Doctor A. Siama (Maroussi-Athens, GR) ...
... managed the amaurosis fugax. Due to repeated amaurosis attacks, with the ophthalmic assessments to exclude other ocular or ... Recently, the left amaurosis fugax reappeared, and the patient was referred to our hospital. Oral administration of clopidogrel ... Recently, he experienced a third amaurosis fugax attack. Digital subtraction angiography and cone-beam computed tomography ... Six years ago, he had a left transient amaurosis attack and magnetic resonance angiography (MRA) revealed a decreased signal of ...
Transient monocular blindness (amaurosis fugax), which usually lasts , 5 minutes, may occur when the ophthalmic artery is ...
Amaurosis fugax. *Central retinal artery occlusion (CRAO)†. *Central retinal vein occlusion (CRVO)† ...
amaurosis fugax G45.3 *transient retinal artery occlusion H34.0 Index to Diseases and Injuries References. The following ...
Amaurosis Fugax Whats New Last Posted: Feb 15, 2023 * Patients with laboratory criteria of anti-phospholipid syndrome and non ...
362.34G45.3Amaurosis fugax. *372.40H11.013Amyloid pterygium of eye- bilateral. *372.40H11.012Amyloid pterygium of left eye ...
Diagnostic: Event of Amaurosis fugax. Recommendation: You need to consult with Cardiology for vascular problems ...
Monocular visual obscuration (amaurosis fugax) inokonzera retinal ischemia. *Contralateral hemiparesis. *Kukanganisa ...
Transient Vision Loss (TVL) and Amaurosis Fugax Slideshow. * 2 Cases of Arrhythmogenic Syncope in Adolescents ...
Amaurosis fugax: pode viagra causar avc Risk factors 348. Jayet c, deperthes d, leisinger hj: Angiogenesis and of hiv because ...
Latex Hypersensitivity Laurence-Moon Syndrome Laurence-Moon-Biedl Syndrome Lazy Eye Lead Poisoning Lebers Congenital Amaurosis ... Amaurosis Fugax. *Amblyopia. *Ambulation Disorders Neurologic. *Amebiasis. *Ameboma. *Ametropia. *Amino Acid Metabolism Inborn ...
Amaurosis fugax (Transient loss of vision due to vascular abnormality in retina or brain) ...
  • Certainly, additional symptoms may be present with the amaurosis fugax, and those findings will depend on the cause of the transient monocular vision loss. (
  • While, most commonly, emboli causing amaurosis fugax are described as coming from an atherosclerotic carotid artery, any emboli arising from vasculature preceding the retinal artery, ophthalmic artery, or ciliary arteries may cause this transient monocular blindness. (
  • citation needed] Atherosclerotic carotid artery: Amaurosis fugax may present as a type of transient ischemic attack (TIA), during which an embolus unilaterally obstructs the lumen of the retinal artery or ophthalmic artery, causing a decrease in blood flow to the ipsilateral retina. (
  • Some authors refer to ischemic transient vision loss as amaurosis fugax syndrome, so transient vision loss can be a symptom of a serious vision or life-threatening condition, requiring urgent investigation and treatment, or it may have a more benign origin (eg, migraine, dry eye). (
  • Gaze-evoked amaurosis (compression) is transient vision loss occurring when looking in a particular direction. (
  • Four years ago, he experienced another transient amaurosis attack and was treated with antiplatelet therapy because no embolic source was detected using ultrasonography examination, and he was diagnosed with idiopathic ICA dissection. (
  • Four years ago, he experienced another transient amaurosis attack on the left side and visited our hospital. (
  • Amaurosis fugax is a transient episode of complete or partial monocular blindness, lasting for a period of less than 10 minutes. (
  • Amaurosis fugax (Greek amaurosis meaning darkening, dark, or obscure, Latin fugax meaning fleeting) is a painless temporary loss of vision in one or both eyes. (
  • minor stroke in 39.4 %, transitory ischemic attack in 36.7 %, amaurosis fugax in 17.4 %, and major stroke in 6.0 % of the patients. (
  • When amaurosis fugax is due to a blood clot or plaque, the concern is to prevent a stroke. (
  • Amaurosis fugax increases your risk for stroke. (
  • Giant cell arteritis: Giant cell arteritis can result in granulomatous inflammation within the central retinal artery and posterior ciliary arteries of eye, resulting in partial or complete occlusion, leading to decreased blood flow manifesting as amaurosis fugax. (
  • Symptoms can include amaurosis fugax, gradual or sudden visual loss, and pain. (
  • citation needed] Temporary vasospasm leading to decreased blood flow can be a cause of amaurosis fugax. (
  • Amaurosis fugax is a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina . (
  • 15:10 15:10, 26 November 2012 ‎ Charmaine Patel talk contribs ‎ 376 bytes +376 ‎ Created page with '__NOTOC__ {{Amaurosis fugax}} {{CMG}} Please help WikiDoc by adding content here. (
  • Us justice foundation forum - member profile activity page, venta de esteroides en santa cruz bolivia köpa steroider flashback. (
  • One comprehensive review found a two to nineteen percent incidence of amaurosis fugax among these patients. (
  • A history of amaurosis fugax is elicited in 9-15% of patients with OIS. (
  • Some authors refer to ischemic transient vision loss as amaurosis fugax syndrome, so transient vision loss can be a symptom of a serious vision or life-threatening condition, requiring urgent investigation and treatment, or it may have a more benign origin (eg, migraine, dry eye). (
  • Gaze-evoked amaurosis (compression) is transient vision loss occurring when looking in a particular direction. (
  • Vision loss with negative scotoma may be seen with amaurosis fugax or retinal transient ischemic attack. (
  • The 39-year-old white male proband, with amaurosis fugax and transient ischemic attacks (TIA), was found to be a compound heterozygote for FVL and PTG mutations. (
  • Symptomatic presentation: Transient ischemic attacks, amaurosis fugax, contralateral weakness/sensory deficit. (
  • INTRODUCTION AND DEFINITIONS-Amaurosis fugax (from the Greek "amaurosis," meaning dark, and the Latin "fugax," meaning fleeting) refers to a transient loss of vision in one or both eyes. (
  • 2 As the ophthalmic artery directly arises from the internal carotid artery (ICA), ophthalmic manifestations, such as visual impairment 3 and amaurosis fugax, 4 are commonly reported in patients with CAS. (