Transient Monocular Visual Loss Research Articles

Gaze-Evoked Amaurosis From Orbital Breast Carcinoma Metastasis

Gaze-evoked amaurosis (GEA) is a transient monocular vision loss provoked by eccentric gaze. Gaze-evoked amaurosis has been associated with a variety of orbital lesions, most commonly optic nerve sheath meningiomas and cavernous hemangiomas. The authors describe the first report in the literature of GEA as the presenting symptom of an orbital metastasis. The patient was a 47-year-old woman with a history of breast cancer with no known history of metastasis or active disease who presented with several weeks of vision loss in the OD upon rightward gaze. She was found to have enophthalmos and optic disc edema of the OD. Imaging revealed an intraorbital lesion, and a biopsy was consistent with a scirrhous metastasis of her breast carcinoma. This case highlights the importance of considering orbital metastases among the differential for gaze-evoked amaurosis.

Patterns of non-embolic transient monocular visual field loss

The aim of this study was to systematically describe the semiology of non-embolic transient monocular visual field loss (neTMVL). We conducted a retrospective case note analysis of patients from Moorfields Eye Hospital (1995-2007). The variables analysed were age, age of onset, gender, past medical history or family history of migraine, eye affected, onset, duration and offset, perception (pattern, positive and negative symptoms), associated headache and autonomic symptoms, attack frequency, and treatment response to nifedipine. We identified 77 patients (28 male and 49 female). Mean age of onset was 37 years (range 14-77 years). The neTMVL was limited to the right eye in 36 % to the left in 47 % and occurred independently in either eye in 5 % of cases. A past medical history of migraine was present in 12 % and a family history in 8 %. Headache followed neTMVL in 14 % and was associated with autonomic features in 3 %. The neTMB was perceived as grey in 35 %, white in 21 %, black in 16 % and as phosphenes in 9 %. Most frequently neTMVL was patchy 20 %. Recovery of vision frequently resembled attack onset in reverse. In 3 patients without associated headache the loss of vision was permanent. Treatment with nifedipine was initiated in 13 patients with an attack frequency of more than one per week and reduced the attack frequency in all. In conclusion, this large series of patients with neTMVL permits classification into five types of reversible visual field loss (grey, white, black, phosphenes, patchy). Treatment response to nifidipine suggests some attacks to be caused by vasospasm.

Migraine is a marker for systemic disease

Dear Editor, We read with interest the article titled “Retinal arterial occlusions in the young: Systemic[1] associations in Indian population by Ratra et al. Authors have mentioned severe headache, floaters and transient blurring of vision as the presenting symptoms in a subset of patients. Visual aura (migraine) are fully reversible symptoms including positive features (e.g., flickering of lights, spots or lines) and negative features (i.e., loss of vision). A migraine diathesis may be a marker for an underlying defect such as hypertension, hypercoagulability, lupus erythematosis or mitral valve prolapse and therefore might occasionally co-occur with[2] vascular occlusion or retinal vasospasm. Experts disagree whether retinal migraine is a rare or common cause of monocular visual loss and whether the mechanism is spreading depression or vasospasm. Complicated migraine refers to a permanent neurologic deficit whether it is visual, motor or sensory in origin. In some instances the stroke does not respect the usual middle or posterior cerebral artery territories suggesting that a strict vascular mechanism is insufficient to[3] explain all migraine-related stroke phenomena. Cocaine abuse cause hypertensive surges, stroke, arterial and venous thrombosis. Neuroimaging studies in cocaine abusers demonstrated abnormal perfusion involving the infraparietal,[4] temporal and anterofrontal cortex and basal ganglia. Dopamine-rich brain regions appear to be relatively specific targets for cocaine-induced cerebral ischemia. Dopamine is one of the[5] numerous neurotransmitters present in outer and inner layers of the retina. Cocaine abuse,[3] exercise and lupus cause non-migrainous retinal vasospasm and transient monocular visual loss. Authors have documented hypertension, cerebrovascular accident and basal ganglia infarction in a 37-year-old patient. In our practice we routinely inform the possibility of underlying systemic disease and importance of physician consultation in all patients with migraine. Perimetry may be useful to identify coexisting cerebral ischemia in patients with retinal vascular occlusion and normal neuroimaging study. We appreciate the authors’ effort and research work.

Factors associated to temporal artery biopsy result in suspects of giant cell arteritis: a retrospective, multicenter, case-control study

To evaluate the positivity rate of temporal artery biopsies (TAB) performed in suspects of giant cell arteritis (GCA) and to study the epidemiological and clinical factors associated to the biopsy result. A retrospective, multicenter, case-control study was performed, including three hundred and thirty-five patients who underwent TAB for a suspicion of GCA from 2001 to 2010. Clinical, epidemiological and pathology data were recovered from the patients' clinical records. Histologic diagnosis of GCA was made when active inflammation or giant cells were found in the arterial wall. Eighty-one biopsies (24.2%) were considered positive for GCA. Clinical factors independently associated to TAB result in a logistic regression analysis were temporal cutaneous hyperalgesia (OR = 10.8; p < 0.001), jaw claudication (OR = 4.6; p = 0.001), recent-onset headache (OR = 4.4; p = 0.001), decreased temporal pulse (OR = 2.8; p = 0.02), pain and stiffness in neck and shoulders (OR = 2.3; p = 0.05), unintentional weight loss (OR = 1.33; p = 0.003) and age (OR = 1.085; p = 0.004). Other factors such as length of the surgical specimen (OR = 1.079; p = 0.028) and erythrocyte sedimentation rate (OR = 1.042; p < 0.001) were also statistically significant. The model was accurate (C-index = 0.921), reliable (pHosmer-Lemeshow = 0.733) and consistent in the bootstrap sensitivity analysis. No significant association was detected between TAB result and number of days of previous systemic corticosteroid treatment (p = 0.146). However, an association was observed between TAB result and the total accumulated dose of previous systemic corticotherapy (p = 0.043). Exhaustive anamnesis and clinical examination remain of paramount importance in the diagnosis of GCA. To improve the yield of TAB, it should be performed specially in older patients with GCA-compatible clinic. TAB could be avoided in patients with an isolated elevation of acute phase reactants, without GCA-compatible clinic.

Recurrent Amaurosis Fugax in a Patient after Stanford Type A Dissection Depending on Blood Pressure and Haemoglobin Level

Purpose. A transient painless monocular visual loss due to a decrease in retinal circulation—also known as “amaurosis fugax”—often precedes acute territorial cerebral ischaemia. The case we present underlines the importance of a comprehensive diagnostic workup in patients with amaurosis fugax. Case Report. A 44-year-old man who had suffered from a dissection of the ascending aorta (Stanford Type A) five months ago presented with recurrent monocular vision problems. Episodes with sectional vision loss mainly occurred in combination with low blood pressure levels. Furthermore, the haemoglobin level was chronically low (Hb 9.7 mg/dL), and the patient was by mistake on a simultaneous therapy with phenprocoumon and unfractionated heparin. Carotid artery duplex scanning revealed a high-grade stenosis of the proximal right common carotid artery. MR imaging corroborated hypoperfusion in brain area corresponding to the right MCA. Conclusion. Our patient is an example in whom transient retinal ischaemic attacks may originate from haemodynamic reasons.

Transient monocular visual loss due to multiple CNS vascular pathology: report of two cases

BACKGROUND: The frequency of the transient monocular visual loss (TMVL), lasting minutes or longer, varies from a single to many episodes, which are usually followed by complete recovery of vision. TMVL is related most commonly o occlusive carotid disease. The therapy of patients with TMCL is divided into surgical and medical. CASE1: A55-year-old female was admitted to the clinic, with 4 months history of TMVL of the right eye, lasting 2-3 minutes, followed by complete recovery. Neuro-ophthalmological examination was normal. Neuro imaging investigations revealed proximal part right internal carotid artery (ICA) stenosis of 70%, left ICA stenosis of 40%, King-King in the middle segment of ICA, causing stenosis of 14%, and incidental aneurysms of the intracranial part of right ICA andin M2 segment of right middle cerebral artery. CASE2: A 74-year-old female was admitted to the clinic, with 1 year history of TMVL of the right eye, lasting 4-5 minutes, followed by complete recovery. Neuro-ophthalmological examination was normal. Duplex scaning showed hemodynamically significant stenosis of the right ICA, with King-Kingintheleft. MRI reveale diffuse vascular pathology. CONCLUSION: These cases demonstrated a co-occurrence of hemodynamically significant carotid artery occlusion with multiple or diffuse vascular pathology in patients with TMVL. We suggest that the detailed history, neuro-ophthalmological, and neuroimaging examinations might be useful to determine the correct etiologic diagnosis and discuss the most effective therapeutic strategy in TMVL patients. Scripta Scientifica Medica 2011;43(2):83-85

Sleep-induced amaurosis fugax

Amaurosis fugax is a manifestation of retinal ischemia, commonly described in the setting of carotid atherosclerotic disease. Thromboembolic, and less frequently, hemodynamic mechanisms have been described as responsible for producing negative symptoms of transient monocular vision loss during periods of wakefulness. We report an unusual presentation in which the patient became symptomatic during sleep. Initially, photopsias-positive symptoms were experienced, which caused the patient to awaken; this was immediately followed by transient monocular vision loss. Carotid endarterectomy was curative.

Occult Temporal Arteritis in a 54-Year-Old Man

A 54-year-old white man with a remote history of pars planitis reported transient monocular visual loss (TMVL) in the left eye on standing. The following week he experienced multiple similar episodes. He denied associated systemic symptoms. Initial examination showed old peripheral retinal vascular sheathing and delayed retinal arterial filling time. Complete blood count, erythrocyte sedimentation rate, and MRI studies of the head and neck were normal. One week later, there were multiple cotton wool spots in the posterior pole, a relative afferent pupillary defect, and subtle visual field loss in the left eye. Evaluation for infectious, inflammatory, or embolic etiologies was nonrevealing. Biopsy of the prominent but nontender temporal arteries showed granulomatous inflammation, fragmentation, and duplication of the internal elastic lamina consistent with the temporal arteritis (TA). Radiography and MRI of the chest revealed dilation of the ascending aorta. The patient began treatment with high-dose oral steroids with resolution of his TMVL and retinal cotton wool spots and decrease in the size of the temporal arteries. Our case demonstrates the importance of considering TA in the setting of TMVL, visual loss, cotton wool spots, or dilated nontender temporal arteries in an otherwise asymptomatic patient even with normal inflammatory markers. Long-term follow-up is essential in unusual cases such as this one, given the high risk of ocular and systemic morbidity with TA.

Clinical features and carotid artery color Doppler imaging in patients with ocular ischemic syndrome

To report the clinical manifestations and results of carotid artery color Doppler imaging (CDI) of ocular ischemic syndrome (OIS). It was a retrospective case series study. Consecutive patients suspected with OIS were retrospectively studied from 1995 to 2009. We evaluated all patients with medical history, visual acuity, slit lamp, direct and indirect funduscopy, Fundus fluorescence angiography. CDI for internal carotid artery (ICA), Diagnostic Cerebral Angiography and magnetic resonance imaging were also performed. 17 patients (20 eyes) with OIS were studied, 13 males and 4 females. The age range of patients was 46 to 83 years old (median 70). 13 right eyes and 7 left eyes (3 bilateral) were involved. (1) SYMPTOMS: 70.6% (12/17) of the patients complained of visual decrease. 17.6% (3/17) had history of repeated amaurosis fugax (transient monocular visual loss); 11.8% (2/17) patients presented with floaters. The course before the first presentation was 2 days to 6 years (median 3 months). (2) Visual Acuity (VA): among the 20 involved eyes, the best corrected VA < 0.05 in 3 eyes (15.0%); 0.05 to < 0.3 in 7 eyes (35.0%); 0.3 to < 0.7 in 7 eyes (35.0%); ≥ 0.7 in 3 eyes (15.0%). (3) Fundus manifestations: 15.0% (3/20) eyes had cotton-wool spots; 25.0% (5/20) had retinal hemorrhages; retinal arterioles and vein became narrow; venous beading could be seen in severe cases. 30.0% (6/20) had microaneurysms in mid-peripheral area. The pressure of central retinal artery decreased; 25.0% (5/20) had optic disc or retinal neovascularization; 10.0% (2/20) had iris neovascularization. 5.0% (1/20) had neovascular glaucoma; 5.0% (1/20) had optic atrophy. (4) Fundus fluorescence angiography: arm-retinal circulation time prolonged to 14.5 to 39.9 seconds, (median 20.9 seconds). The retinal and choroidal circulation time was also prolonged. The wall of artery and venous could be staining. Hyperfluorescence dots indicating microaneurysms could be seen in the mid-peripheral area. Arterio-venous shunts, non-perfusion area and the leakage of new vessels were observed in some cases. (5) Internal carotid artery CDI examination: The ipsilateral ICA of the 19 involved eyes (another patient with pulseless disease had abnormal subclavian arterial flow) showed completely occluded in 5 cases (26.4%), > 80.0% to 95.0% stenosis in 7 cases (36.8%), 52.0% to 80.0% stenosis in 7 cases (36.8%). Among the 14 contralateral eyes of the same group of patients, CDI showed stenosis of 80.0%, 70.0%, 60.0%, 50.0% and 40.0% in 5 eyes, whereas no fundus abnormal was found. Peak of systolic velocity (PSV): Among the 20 involved eyes of the 17 patients, PSV of the ipsilateral ICA was undetectable in 8 cases which occluded completely or stenosis severely. Among the ipsilateral ICA of the other 12 eyes, 11 cases showed abnormal PSV; PSV increased to 92 to 524 cm/s in 9 cases and decreased to 41 cm/s in 1 case. The blood flow of subclavian artery reduced to 20 cm/s in one patient with pulseless disease. The blood flow of subclavian artery reduced to 20 cm/s in one patient with pulseless disease. The patients with OIS are usually older than 60 years of age. It is a chronic disease with unnoticed symptoms. The clinical manifestations may include: amaurosis fugax (transient monocular visual loss), hypoperfusion retinopathy and ischemic optic neuropathy. Internal carotid artery severe stenosis or occlusion are the most frequent cause of this disease. CDI is the best safe, reliable and non-invaded method for carotid artery examination.

A Case of Recurrent Transient Monocular Visual Loss after Receiving Sildenafil

A 53-year-old man was attended to the Clinic Ophthalmic Center, Mansoura University, Egypt, with recurrent transient monocular visual loss after receiving sildenafil citrate (Viagra) for erectile dysfunction. Examination for possible risk factors revealed mild hypercholesterolemia. Family history showed that his father had suffered from bilateral nonarteritic anterior ischemic optic neuropathy (NAION). Physicians might look for arteriosclerotic risk factors and family history of NAION among predisposing risk factors before prescribing sildenafil erectile dysfunction drugs.

Les troubles visuels monoculaires transitoires d’origine vasculaire

Diagnosis and management of transient monocular visual loss is an emergency. Ocular conditions causing transient visual loss are routinely managed by ophthalmologists. Vascular transient monocular visual loss may result from emboli, hypoperfusion, vasospasm, or venous congestion. Evaluation focuses on the carotid arteries, ophthalmic arteries, the aortic arch, the heart, and rarely hypercoagulable states. Secondary prevention of ischemic events is essential in order to prevent permanent visual loss as well as cerebral ischemic and cardiovascular death. Aggressive treatment of vascular risk factors is usually associated with antiplatelet agents. Anticoagulant and carotid surgery are only rarely required after vascular transient monocular visual loss.

Troubles visuels binoculaires transitoires : une approche diagnostique

It is rarer for a patient to present with transient binocular visual loss than transient monocular visual loss. This symptom usually results from a cerebral dysfunction. When transient binocular visual loss results from papilledema, ophthalmological examination is critical for an accurate diagnosis. In other cases, examination may be normal and a thorough history is of paramount importance for making a diagnosis and deciding whether or not imaging is necessary. The three main cerebral causes for transient binocular visual loss are migraine with visual aura, partial seizures occurring in the occipital lobe, and vertebrobasilar ischemia.

Retinal Arteriolar Spasm During Transient Monocular Visual Loss in Eosinophilic Vasculitis

A patient with eosinophilic vasculitis and acquired immunodeficiency syndrome (AIDS) developed episodic transient monocular visual loss. During or immediately after two visual loss episodes, we demonstrated narrowed retinal arterioles, delayed arterial filling time, and segmented retinal venous flow in the affected eye on fundus photography and fluorescein angiography (FA). Such findings have only rarely been reported in patients with transient monocular visual loss in other conditions, probably because the episodes have ended before fundus photography and FA could be performed. This is the first report to capture retinal vascular changes associated with transient monocular visual loss in a patient with eosinophilic vasculitis.

RESOLUTION OF MYDRIATIC PUPIL AFTER ANGIOPLASTY AND STENTING OF CERVICAL INTERNAL CAROTID ARTERY DISSECTION

A patient with cervical internal carotid artery (ICA) dissection presented with visual loss and a mydriatic pupil that resolved after angioplasty and stenting. A 49-year-old woman presented with a unilateral dilated tonic pupil and transient monocular visual loss and subsequently developed speech disturbance. Angiography revealed a left cervical ICA dissection with significant luminal narrowing. The ophthalmic artery filled retrograde through external carotid artery branches and reconstituted the supraclinoid ICA. Computed tomographic perfusion showed significant hypoperfusion of the left hemisphere. Magnetic resonance imaging showed punctate boundary zone infarcts. The patient experienced pressure-dependent left hemispheric transient ischemic attacks and pressure-dependent ocular findings despite anticoagulation. She underwent uncomplicated left ICA angioplasty and stenting. The flow through the ophthalmic artery became anterograde. The tonic pupil returned to symmetry with the contralateral pupil, and the patient's symptoms resolved completely. Cervical ICA dissection can manifest with a tonic mydriatic pupil. Treatment with angioplasty and stenting of the dissected segment can restore flow and resolve the pupillary abnormality. A pathophysiological mechanism for the mydriasis is proposed.

Expert Opinion: Sexual Intercourse Followed by Headache and Transient Monocular Visual Loss

CLINICAL HISTORY Thirty minutes after sexual intercourse, this 48-year-old woman noticed a slight headache on the top of her head. Fifteen minutes later, she developed a severe left-sided throbbing headache with visual symptoms but without nausea, light, or noise sensitivity. She had a sudden warm liquid feeling in the left eye and then vision in the inferior field of the left eye became dark and, within about 3 seconds, vision in the entire field of the left eye was dark.The vision cleared completely in a segmental fashion in about 30 to 45 minutes. Acetaminophen with codeine decreased the intensity of the headache. A computerized tomography (CT) of the brain without contrast performed about 2 hours after the onset of the symptoms was negative. When I saw her the next afternoon, the left-sided headache was slight. She had no further visual symptoms. She reported a 26-year history of headaches about once or twice per month described as a top or back of the head throbbing with light and noise sensitivity decreased by acetaminophen with codeine and lasting about 8 hours. Her menses was a common trigger. Past medical history was negative. Blood pressure and pulse were normal. There were no carotid bruits. Cardiac auscultation was normal. The neurological examination was normal. Questions.—Is this a case of retinal migraine? Is further testing indicated?

Recurrent Vision Loss After Endoscopic Sinus Surgery Managed With Palmar Pressure

A 41-year-old woman underwent endoscopic sinus surgery and 24 hours later, she developed acute orbital emphysema with marked vision loss. CT showed disruption of the inferior aspect of the medial wall of the orbit with fat herniation. She was immediately treated with the application of bedside palmar pressure to the globe with complete return of her vision without the need for a needle aspiration or orbital decompression. Weeks later, the patient experienced 2 more episodes of transient monocular visual loss that were again successfully treated with the same palmar pressure. Bedside digital decompression may be a potentially helpful method of restoring vision in cases of orbital emphysema with acute vision loss. We advise attempting this simple bedside procedure before committing the patient to a more invasive needle aspiration or surgical decompressive procedure.

Transient Monocular Vision Loss from Acute Rheumatic Fever

A 15-year-old male developed transient monocular visual loss secondary to retinal artery flow disturbance, vasospasm, and possible microemboli associated with acute rheumatic heart disease. He had insufficiently treated streptococcal pharyngitis. Inadequately treated rheumatic carditis should be considered among the causes of transient monocular visual loss in children.

Expert Opinion: Retinal Migraine: Migraine Associated With Monocular Visual Symptoms (CME)

Expert Opinion: Retinal Migraine: Migraine Associated With Monocular Visual Symptoms (CME)

The fate of patients with retinal artery occlusion and Hollenhorst plaque

Ocular symptoms and signs often herald hemispheric neurological events associated with extracranial cerebrovascular disease. However, the presence of a Hollenhorst plaque (HP) or retinal artery occlusion (RAO) and the risk of stroke is unclear. The purpose of this study was to review the outcomes of all patients who presented with a HP or RAO at a single institution. Between 2000 and 2005, the management and outcome of 130 consecutive patients with a diagnosis of HP, central RAO, or branch RAO (ICD-9 codes 362.30 to 362.33) were reviewed. Patients with transient monocular visual loss (amaurosis fugax), retinal venous occlusion, and other ocular pathologies were excluded. Electronic and hardcopy medical records were reviewed for demographic data, clinical variables, radiological, and noninvasive vascular lab testing. Duplex and magnetic resonance angiography (MRA) of the carotid arteries were reviewed to confirm the presence of a lesion and quantify the degree of stenosis. During the study interval, 70 males and 60 females, with a mean age of 68 +/- 16 (+/-SD) years underwent ophthalmologic evaluation. Symptoms were present in 61% of patients and included eye pain, blurred vision, or atypical visual symptoms, while 39% were asymptomatic. Atherosclerotic risk factors in this population included the presence of hypertension (73%), diabetes (33%), hyperlipidemia (75%), and tobacco use (38%). A majority of patients underwent carotid interrogation via Duplex imaging (68%). Carotid bifurcation stenoses ipsilateral to the ocular findings were <30% in 68% of the patients, between 30 and 60% in 22% and >60% in only 8% of patients. Six patients with lesions greater than 60% went on to have either a carotid endarterectomy or carotid stenting. Follow-up data on this group ranged from 1 to 49 months (median, 22 months), with no stroke or transient ischemic attack identified. There were five deaths during follow-up; none related to stroke. Serial carotid Duplex examinations failed to identify progression of carotid stenoses in this group of patients. Overall survival was 94% at 36 months for this cohort. The presence of a HP or RAO is associated with a low prevalence of extracranial cerebrovascular disease that requires intervention. Furthermore, in contradistinction to amaurosis fugax, these ocular findings are not associated with a high risk for hemispheric neurological events.

Painless Transient Monocular Loss of Vision Resulting From Angle‐Closure Glaucoma

The main symptoms of acute primary angle-closure glaucoma (PACG) include pain in the head and/or the eyes in addition to the characteristic halo and blurred vision. When loss of vision is accompanied by such pain, PACG is usually suspected. However, no information has been available regarding painless acute angle-closure glaucoma. Recently, we treated a patient with painless acute PACG mimicking amaurosis fugax as a type of transient ischemic attack. Generally, amaurosis fugax causes transient monocular loss of vision due to occlusion of the ophthalmic artery. The formation of microemboli derived from the heart or carotid artery and/or the occurrence of some hemodynamic abnormality due to arteriosclerosis is closely related to amaurosis fugax, and most cases are complicated by intracranial or extracranial arterial lesions. In the present case, we provisionally diagnosed transient amaurosis fugax which, however, was shown by additional ocular testing to be painless PACG. Herein we describe our diagnostic process and the outcome.