Transient Monocular Visual Loss Research Articles

Most Cases Labeled as “Retinal Migraine” Are Not Migraine

Monocular visual loss has often been labeled "retinal migraine." Yet there is reason to believe that many such cases do not meet the criteria set out by the International Headache Society (IHS), which defines "retinal migraine" as attacks of fully reversible monocular visual disturbance associated with migraine headache and a normal neuro-ophthalmic examination between attacks. We performed a literature search of articles mentioning "retinal migraine," "anterior visual pathway migraine," "monocular migraine," "ocular migraine," "retinal vasospasm," "transient monocular visual loss," and "retinal spreading depression" using Medline and older textbooks. We applied the IHS criteria for retinal migraine to all cases so labeled. To be included as definite retinal migraine, patients were required to have had at least two episodes of transient monocular visual loss associated with, or followed by, a headache with migrainous features. Only 16 patients with transient monocular visual loss had clinical manifestations consistent with retinal migraine. Only 5 of these patients met the IHS criteria for definite retinal migraine. No patient with permanent visual loss met the IHS criteria for retinal migraine. Definite retinal migraine, as defined by the IHS criteria, is an exceedingly rare cause of transient monocular visual loss. There are no convincing reports of permanent monocular visual loss associated with migraine. Most cases of transient monocular visual loss diagnosed as retinal migraine would more properly be diagnosed as "presumed retinal vasospasm."

Retinal Migraine Reappraised

Retinal migraine is usually characterized by attacks of fully reversible monocular visual loss associated with migraine headache. Herein we summarize the clinical features and prognosis of 46 patients (six new cases and 40 from the literature) with retinal migraine based upon the International Classification of Headache Disorders-2 (ICHD-2) criteria. In our review, retinal migraine is most common in women in the second to third decade of life. Contrary to ICHD-2 criteria, most have a history of migraine with aura. In the typical attack monocular visual features consist of partial or complete visual loss lasting <1 h, ipsilateral to the headache. Nearly half of reported cases with recurrent transient monocular visual loss subsequently experienced permanent monocular visual loss. Although the ICHD-2 diagnostic criteria for retinal migraine require reversible visual loss, our findings suggest that irreversible visual loss is part of the retinal migraine spectrum, perhaps representing an ocular form of migrainous infarction. Based on this observation, the authors recommend migraine prophylactic treatment in an attempt to prevent permanent visual loss, even if attacks are infrequent. We also propose a revision to the ICHD-2 diagnostic criteria for retinal migraine.

Three presentations of monocular vision loss

Background Carotid artery disease is estimated to affect 30% of persons older than 50. Risk factors include hypertension, cigarette smoking, hyperlipidemia and diabetes mellitus. Symptoms ascribed to carotid artery lesions with stenosis of the artery or plaque formation include monocular vision loss and transient ischemic attacks. Patients can present with transient monocular vision loss as their initial symptom. Case reports Three patients from a geriatric clinic in Wilmington, Delaware presented with different complaints of vision loss with similar overall outcomes. Patient A was an 87-year-old woman who presented with dimming of vision on extreme left head turn. Dilated fundus examination found a retinal arterial emboli in the left eye (O.S.). Carotid duplex examination found 50% to 79% left internal carotid stenosis with no hemodynamic stenosis of the right internal carotid. Patient B was a 78-year-old woman who presented with a right superior altitudinal defect and transient vision loss in the right eye. Dilated fundus examination found retinal arterial emboli in the right eye (O.D.). Carotid duplex examination found 50% to 79% carotid stenosis in both the left and right internal carotids. Patient C was an 84-year-old man who complained of a superior altitudinal visual field defect O.D. Dilated fundus examination found a retinal arterial emboli O.D. Carotid duplex results showed calcified atherosclerotic plaques present at the level of the common carotid artery bifurcations bilaterally, with 50% to 70% narrowing of the right internal carotid artery with no significant narrowing of the left internal carotid artery. Conclusions These 3 presentations show that in patients older than 50 who present with chief complaints of monocular vision loss, a differential diagnosis of carotid artery disease must be considered. Patients who exhibit retinal arterial emboli are at increased risk for stroke and vascular death. Appropriate measures for confirming a diagnosis include duplex ultrasound imaging, magnetic resonance angiography (MRA), and carotid angiography. Surgical techniques such as carotid angioplasty and carotid endarterectomy may be recommended.

Transient monocular visual loss and retinal migraine

The Case: A 40-year-old man was referred because of multiple events of transient monocular visual loss since adolescence. He described the events as small, translucent, grey-coloured spots similar to those seen after looking at a bright light. These visual defects affected both of his eyes equally

Carotid Endarterectomy for Ophthalmic Manifestations: Is It Ever Indicated?

Four ophthalmic manifestations make up a substantial proportion of the indications for carotid endarterectomy (CE). They include transient monocular visual loss (TMVL), ocular ischemic syndrome (OIS), retinal artery occlusion (RAO), and asymptomatic Hollenhorst plaque. Critical review of the literature shows that the evidence to support the efficacy of CE in these four settings is tenuous.

Carotid Endarterectomy for Transient Monocular Visual Loss and Other Ocular Ischemic Conditions

Carotid Endarterectomy for Transient Monocular Visual Loss and Other Ocular Ischemic Conditions

Transient Monocular Visual Loss

To provide a practical update on the diagnosis and management of transient monocular visual loss (TMVL). Perspective. Review of the literature. TMVL is an important clinical symptom. It has numerous causes but most often results from transient retinal ischemia. It may herald permanent visual loss or a devastating stroke, and patients with TMVL should be evaluated urgently. A practical approach to the evaluation of the patient with TMVL must be based on the patient's age and the suspected underlying etiology. In the older patient, tests should be performed to investigate giant cell arteritis, atherosclerotic large vessel disease, and cardiac abnormalities. In the younger patient, TMVL is usually benign and the evaluation should be tailored to the particular clinical setting. Specific prevention strategies are tailored to the most likely cause of TMVL and the patient's underlying risk factors. Prevention of a future event should begin in the ophthalmologist's office with education and aggressive treatment of artherosclerotic risk factors.

Retinal migraine

Retinal migraine is a primary headache disorder, clinically manifested by attacks of transient monocular visual loss associated with migraine headache. Although isolated reports suggest that retinal migraine is rare, it likely is under-recognized. Retinal migraine usually is reported in women of childbearing age who have a history of migraine with aura. It typically is characterized by negative monocular visual phenomena lasting less than 1 hour. More than half of reported cases with recurrent transient monocular visual loss subsequently experienced permanent monocular visual loss. Although the International Headache Society diagnostic criteria for retinal migraine require reversible visual loss, our findings suggest that irreversible visual loss is part of the retinal migraine spectrum, likely representing an ocular form of migrainous infarction.

Retinal, ophthalmic, or ocular migraine.

Ocular migraine, an uncommon cause of transient monocular visual loss, is an entity physicians should be able to recognize in order to provide appropriate treatment and to avoid unnecessary testing. The following text provides an overview of ocular migraine, including discussion of accepted terminology, clinical presentation, and pathophysiology. An ocular and systemic differential diagnosis, appropriate evaluation, therapy, and prognosis are also discussed.

False and non-localizing signs in neuro-ophthalmology.

The absolute reliance on abnormal neuro-ophthalmologic findings as signposts for particular lesions of the neuraxis must be tempered by a working knowledge of false and nonlocalizing signs and symptoms. Transient monocular visual loss or complex visual hallucinations may lead to neuroanatomic ambiguity, and elevated intracranial pressure is not the most common cause of swollen optic disks in late life. Sixth nerve palsy associated with increased intracranial pressure is possibly the best-known false localizing sign, but other ocular motility disturbances (divergence paresis, convergence insufficiency, and skew deviation) also elude localization. Lastly, the localizing pitfalls of anisocoria--Horner and Raeder syndromes, physiologic anisocoria, pupil-involving third nerve palsy, and benign pupillary dilation--are discussed.

Retinal Ischemia and Embolism

Objectives: To identify the most likely mechanisms of retinal ischemia and embolism in a hospital-referred population, and to determine the frequency of recurrent vascular events during the 3-month period following initial presentation. Methods: Consecutive patients presenting to 2 tertiary medical centers and their outpatient clinics were prospectively enrolled over a 22-month period. Eligible patients presented with histories of transient or permanent monocular visual loss, or had evidence of asymptomatic retinal embolism on routine ophthalmological examination. They underwent a rapid and standardized evaluation that included imaging studies as well as blood tests, and follow-up was obtained at 1 and 3 months. Results: Seventy-seven patients were enrolled. Enrollment diagnoses consisted of amaurosis fugax (n = 32), asymptomatic retinal embolism (n = 34), and central or branch retinal artery occlusion (n = 11). Eight different presumed etiologies of retinal artery distribution embolism or hypoperfusion were identified. Extracranial internal carotid artery occlusion or more than 50% stenosis was observed in 17/77 (22.1%) cases, making it the largest etiologic subgroup. Uncommon but treatable conditions were identified in 8/77 (10.4%) patients, and an etiologic diagnosis could not be made in 35/77 (45.5%) patients. Recurrent events occurred in, respectively, 14/77 (18.2%) and 6/73 (8.2%) patients at the 1- and 3-month follow-ups. They included 2 infarcts and 2 deaths; ischemic events of the retina were more common than those involving the brain. Conclusion: Severe stenosis of the extracranial internal carotid artery is the most common identified condition associated with retinal ischemia and embolism, but a variety of other, potentially treatable, conditions can be diagnosed if appropriate and specific evaluations are conducted. The frequency of recurrent vascular ischemic events is highest during the 1st month of follow-up and decreases during the 2nd and 3rd months. Recurrences range from relatively innocuous episodes of amaurosis fugax to vascular death.

How do general practitioners diagnose and manage patients with transient monocular loss of vision of sudden onset?

Symptoms of transient loss of vision in one eye differ widely. They may have different causes and therefore carry a different prognosis. We studied the influence of differences between characteristics of transient monocular blindness on the diagnosis and management by general practitioners (GPs). A postal questionnaire, was sent to 1600 GPs in The Netherlands along with four case vignettes describing a case history of a 56-year-old man with transient monocular disturbances of vision of sudden onset. We introduced random permutations in the following four elements of the history: partial or complete visual field involved, blurring or blacking out of vision, attacks lasting minutes or hours, and patients having covered either eye during the attack or not. Respondents were asked about the probable diagnosis and the preferred management. For each of the 16 permutations about 50 responses were obtained (overall response rate 54%). Ischemic transient monocular blindness (ITMB) was chosen as the most likely diagnosis in 49%. In 12% primary ocular disease was suspected. Involvement of the complete visual field, blacking out of vision, and short attacks were identified as independent predictors of a diagnosis of ITMB. A diagnosis of ITMB would have resulted in referral to a specialist in 72% of patients. Antithrombotic treatment would have been initiated in only 36% of ITMB patients. GPs consider brief attacks with complete blacking out of vision most typical for retinal ischemia. They refer only three-quarters of patients with probable ITMB to a specialist and start antithrombotic medication in only one-third of these patients. Therefore further education with regard to transient monocular blindness is needed.

Ophthalmologic manifestions of internal carotid artery dissection

PURPOSE: To report the ophthalmologic symptoms and signs associated with extracranial internal carotid artery dissection. METHODS: One hundred forty-six consecutive patients with extracranial internal carotid artery dissection were evaluted; 29 were studied retrospectively from 1972 to 1984 and 117 prospectively from 1985 to 1997. RESULTS: Sixty-two percent of patients (91/146) with extracranial internal carotid artery dissection had ophthalmologic symptoms or signs that were the presenting symptoms or signs of dissection in 52% (76/146). Forty-four percent (65/146) had painful Horner syndrome, which remained isolated in half the cases (32/65). Twenty-eight percent (41/146) had transient monocular visual loss, which was painful in 31 cases, associated with Horner syndrome in 13 cases, and described as “scintillations” or “flashing lights”—often related to postural changes or exposure to bright lights—suggesting acute choroidal hypoperfusion in 23 cases. Four patients had ischemic optic neuropathy; one had diplopia. Among the 76 patients with ophthalmologic symptoms or signs as the presenting features of carotid dissection, a nonreversible ocular or hemispheric stroke later occurred in 27, within a mean of 6.2 days (range, 1 hour to 31 days). Eighteen patients had a stroke within the first week after the onset of neuro-ophthalmic symptoms and signs, and 24 had a stroke within the first 2 weeks. CONCLUSION: Ophthalmologic symptoms or signs are frequently associated with and are often the presenting features in internal carotid artery dissection. Painful Horner syndrome or transient monocular visual loss should prompt investigations to diagnose carotid artery dissection and begin early treatment to prevent a devastating ocular or hemispheric stroke.

Internal Carotid Artery Dissection Causing a Branch Retinal Artery Occlusion in a Young Adult

Purpose: To report a 34-year-old healthy man with an internal carotid artery dissection who presented with an ipsilateral branch retinal artery occlusion. Method: Case report. Results: Ophthalmic examination of a young adult presenting with transient monocular visual loss and a superior nasal field defect disclosed a left inferior branch retinal artery occlusion. After fluorescein angiography, the patient had a vasovagal response, and his condition worsened to a left central retinal artery occlusion. Neurologic evaluation followed by carotid angiography disclosed a left internal carotid artery dissection with total occlusion of the internal carotid artery. Conclusion: The differential diagnosis of retinal arterial occlusion in a young healthy adult without any notable ocular or medical history, including trauma, should include spontaneous internal carotid artery dissection.

Carotid disease and the eye.

Patients with carotid artery disease may present with monocular, ipsilateral ocular symptoms, and signs that can herald a devastating stroke. Asymptomatic retinal emboli, transient monocular visual loss, and central retinal artery occlusion are the most common. Venous stasis retinopathy and ocular ischemic syndrome are associated with severe hypoperfusion of the eye and usually reflect severe carotid occlusive disease. Embolic ischemic optic neuropathies and compression of the intracranial optic nerve by supraclinoid carotid arteries remain debated. Third-order Horner's syndrome and eye pain are common in carotid artery disease, particularly carotid dissection; carotid artery disease, however, is an uncommon cause of ocular motor nerve palsy. Several recent publications have highlighted the prognosis and management of patients with carotid artery occlusive disease, and have emphasized the role of the ophthalmologist in early diagnosis and prevention of further cerebral and systemic complications.

Retinal Vein Occlusion and Transient Monocular Visual Loss Associated With Hyperhomocystinemia

To report a 24-year-old man with bilateral central retinal vein occlusions who had preceding episodes of prolonged transient monocular visual loss during which ophthalmoscopic findings were not suggestive of vein occlusion. Case report. Extensive hematologic studies for causes of vein occlusion were unremarkable with the exception of increased plasma homocysteine in the patient and in his asymptomatic father. Impending vein occlusion should be considered in the differential diagnosis of transient monocular visual loss regardless of ophthalmoscopic appearance, and hyperhomocystinemia should be considered as a possible cause of retinal vein occlusion.

Subtypes of Transient Monocular Blindness and Subsequent Risk of Vascular Complications

Background and Purpose: Little is known about different varieties of transient monocular blindness (TMB) in relation to the subsequent occurrence of vascular outcome events. Very few studies have addressed the prognostic value of the form of the attack in patients with TMB. To try and distinguish benign and hazardous symptoms of TMB, we studied the prognosis of different subtypes of TMB in terms of subsequent vascular complications. Methods: We analysed the characteristics of transient monocular loss of vision, vascular risk factors, and vascular events during follow-up in patients with TMB, who were recorded in the Royal Victoria Infirmary, Newcastle, United Kingdom (n = 137) or were entered into the Dutch TIA Trial (n = 185). The mean follow-up period was 5.0 years. The attacks were categorized in different ''patterns''. These patterns were related to the occurrence of (1) the combined event of vascular death, stroke or myocardial infarction and (2) cerebral infarction (fatal or non-fatal). Results: Patients with attacks of blurred vision had a more than twofold risk of vascular outcome events than patients with blackened vision, complete or in part [hazard ratio (HR) 2.3; 95% confidence limits (CL) 1.2–4.5]. Involvement of only a part of the visual field of one eye during the attack (instead of complete loss of vision) carried a lower risk (HR 0.4; 95% CL 0.2–0.9). Conclusion: Our findings suggest a relation between different types of TMB and outcome, but this needs to be validated in a subsequent cohort.

Neuro-ophthalmic aspects of vascular disease

One of the most susceptible sites to vascular diseases is the optic nerve head. By innovative approaches using morphometry and in situ hybridization, vascular and extracellular characteristics of the human optic nerve head were examined. Nonarteritic ischemic optic neuropathy occurs due to vascular insufficiency within the optic nerve head. Various local and systemic risk factors have been proposed among which smoking and acute hypotension are now included. Anatomically abnormal discs such as the small optic disc, tilted disc, and optic nerve drusen are recognized as "disks at risk" and hyperopia may be an additional predisposing factor. Ocular, neurological, and vascular disorders due to giant cell arteritis were reviewed. Intravenous high-dose methylprednine should be administered in certain cases. Differentiating nonarteritic from arteritic ischemic optic neuropathy is sometimes difficult. Isolated choroidal ischemia or choroidal filling delay may be an indication of giant cell arteritis. Studies have been conducted on the vascular event, amaurosis fugax (transient monocular visual loss), and the results of some of these studies are discussed.

Transient Monocular Blindness Caused by Vasospasm

SPORADIC transient monocular loss of vision (amaurosis fugax) lasting a few seconds to several minutes has fascinated and perplexed clinicians for years. In the mid-19th century, von Graefe1 and later Gowers2 proposed an embolic pathogenesis. Temporary vasospasm, however, was later invoked to account for this type of visual loss.3 , 4 In 1959, Fisher5 observed platelet–fibrin emboli passing through the retinal vasculature during an episode of monocular blindness. This report helped establish the platelet–fibrin theory as an explanation of many transient and fixed ischemic visual deficits. We describe two patients with vasospastic transient monocular blindness, as demonstrated by photography of the fundus. . . .

Transient monocular visual loss patterns and associated vascular abnormalities.

To determine if certain transient monocular visual loss patterns predict the associated vascular abnormalities, we prospectively evaluated 100 consecutive patients. Each patient had hematologic tests, a carotid artery study (arteriography in 74, duplex ultrasonography in the remaining 26), and an ophthalmologic examination. Patients with altitudinal or lateralized transient monocular visual loss were more likely to have carotid artery stenosis, carotid artery ulceration, cardiac sources of emboli, or visible retinal emboli than patients with other visual loss patterns. Our findings suggest that altitudinal or lateralized transient monocular visual loss is primarily caused by embolism but that other visual loss patterns are usually caused by nonembolic mechanisms.