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Background and Purpose: Research suggests that women and men may present with different transient ischemic attack (TIA) and stroke symptoms. We aimed to explore symptoms and features associated with a definite TIA/stroke diagnosis and whether those associations differed by sex., Methods: We completed a retrospective cohort study of patients referred to The Ottawa Hospital Stroke Prevention Clinic in 2015. Exploratory multinomial logistic regression was used to evaluate candidate variables associated with diagnosis and patient sex. Backwards elimination of the interaction terms with a significance level for staying in the model of 0.25 was used to arrive at a more parsimonious model., Results: Based on 1770 complete patient records, sex-specific differences were noted in TIA/stroke diagnosis based on features such as duration of event, suddenness of symptom onset, unilateral sensory loss, and pain., Conclusions: This preliminary work identified sex-specific differences in the final diagnosis of TIA/stroke based on common presenting symptoms/features. More research is needed to understand if there are biases or sex-based differences in TIA/stroke manifestations and diagnosis.

Introduction: Atrial fibrillation (AF) is a major cause of ischemic stroke and Transient Ischemic Attack (TIA) and investigation for paroxysmal AF is recommended following an embolic brain event. In contrast, retinal ischemic monocular blindness is traditionally considered most linked to carotid artery disease (CAS) and investigating for AF is less vigilant. We aimed to determine the prevalence of AF in patients with ischemic monocular blindness., Methods: Consecutive records of all patients presenting to a daily TIA clinic with transient or permanent ischemic monocular blindness were reviewed, January 2014-October 2016., Results: Of 400 patients, 224 (56.0%) were male, mean age 64.5 years (SD 15.1). A total of 263 (66%) presented with transient and 137 (34%) with permanent ischemic monocular blindness. ECG was performed in 364 patients (91%) but only 211 (52%) had further cardiac monitoring. The vast majority (97.3%) had carotid imaging. Thirty-six patients (9%) were found to have AF while 53 (14%) had ipsilateral CAS. Median ABCD2 score was 1 in AF and non-AF groups. Only 55% of known AF patients were anticoagulated at presentation, despite all having CHADVASC2 score greater than or equal to 1. Patients with AF had more hypertension (P = .004), previous TIA (P = .002), previous stroke (P = .044) and ischemic heart disease (P = .022) with no difference in age (P = .791), diabetes (P = .563), smoking (P = .460) nor hypercholesterolaemia (P = .083)., Conclusions: A total of 9% of patients with ischemic monocular blindness had AF. This is an underestimate, as only 53% of patients had prolonged cardiac monitoring. Known AF was suboptimally managed with only 55% receiving anticoagulation despite being eligible., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Purpose: To report a case with monocular transient vision loss (TVL) associated with Hyperhomocysteinemia. Methods: We present a case with persistent TVL attacks and high level of homocysteine. Results: A 32-year-old male had a history of episodes of recurrent monocular TVL. Extensive ophthalmic, systemic and laboratory studies were unremarkable with the exception of high plasma homocysteine level. He never experienced TVL during the 36-month follow-up after starting folate, B12 and B6 except for one episode in which he had discontinued the treatment for three months. Conclusion: This case may suggest hyperhomocysteinemia as one of the underlying causes of recurrent attacks of TVL without any known source of emboli.

Central retinal artery occlusion (CRAO) is a medical emergency that, if not treated, may result in irreversible loss of vision. It continues to be an important cause for acute painless loss of vision. Amaurosis fugax or "transient CRAO" has long been considered an equivalent of transient cerebral ischemic event. Animal models, in addition to data from retrospective and randomized clinical studies, provide valuable insights into the time interval for irreversible retinal ischemia. Subset analyses from 2 large studies of patients with CRAO show benefit from treatment with thrombolysis within 6 hours from symptoms onset. Significant workflow improvements after the intra-arterial therapy trials for acute ischemic stroke have occurred world over in last 5 years. Patients with CRAO are uniquely suited to receive maximum benefits from the changes in workflow for treatment of patient's acute ischemic stroke. Just as in clinical triage of acute ischemic stroke, correct and timely diagnosis of patients with CRAO may help in preventing visual loss. The approach to acute ocular ischemia should mimic that used for acute brain ischemia. Comprehensive stroke centers would be ideal triage centers for these patients in view of availability of multidisciplinary participation from vascular neurology, neuroendovascular surgery, and ophthalmology. Time is Retina!, (Copyright © 2018. Published by Elsevier Inc.)

A 66-year-old woman with chronic myeloid leukaemia in nilotinib-induced remission was diagnosed with amaurosis fugax, caused by carotid stenosis. Serum cholesterol was 316 mg/dL (Low-Density Lipoprotein (LDL) cholesterol 213 mg/dL). Nilotinib was discontinued and replaced by interferon. Antiplatelet therapy and atorvastatin 40 mg/day were prescribed. Muscle pain and elevation of serum creatine kinase (CK) occurred; thus, atorvastatin was replaced by ezetimibe. Afterwards, muscle pain subsided and CK reverted to normal, but 2 years later serum cholesterol was still elevated at 218 mg/dL with LDL cholesterol 126 mg/dL. Simvastatin 5 mg/day was then started, but again muscle pain occurred and CK rose to 267 U/L. Simvastatin was stopped and serum cholesterol climbed to 252 mg/dL. Creatine was prescribed and simvastatin was reintroduced. Two months later, cholesterol was 171 mg/dL, CK was 72 U/L and there was no muscle pain. This case supports the view that creatine may prevent statin-induced myopathy., Competing Interests: Competing interests: MB and EA are founding members of NovaNeuro Srl, an academic spin-off that ideates, produces and commercialises dietary supplements based on creatine., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: A transient visual symptom (TVS) is a clinical manifestation of transient ischemic attack (TIA). The aim of this study was to investigate differences in clinical characteristics among subtypes of TVS using multicenter TIA registry data., Materials and Methods: Patients with TIA visiting within 7 days of onset were prospectively enrolled from 57 hospitals between June 2011 and December 2013. Clinical characteristics were compared between patients with 3 major subtypes of TVS (transient monocular blindness [TMB], homonymous lateral hemianopia [HLH], and diplopia)., Results: Of 1365 patients, 106 (7.8%) had TVS, including 40 TMB (38%), 34 HLH (32%), 17 diplopia (16%), and 15 others/unknown (14%). Ninety-one patients with 1 of the 3 major subtypes of TVS were included. Symptoms persisted on arrival in 12 (13%) patients. Isolated TVS was significantly more common in TMB than in HLH and diplopia (88%, 62%, and 0%, respectively; P < .001). Duration of symptoms was shorter in patients with TMB than those with HLH (P = .004). The ABCD 2 score was significantly lower in patients with TMB compared with those with HLH and diplopia (median 2 [interquartile range 2-3] versus 3 [2-4] and 4 [2-5], respectively; P = .005). Symptomatic extracranial internal carotid artery stenosis or occlusion was seen in 14 (16%) patients, and was more frequent in TMB than in HLH and diplopia (28%, 9%, and 0%, respectively; P = .015)., Conclusions: TVS was an uncommon symptom in our TIA multicenter cohort. Some differences in clinical characteristics were found among subtypes of TVS., (Copyright © 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Transient monocular blindness is an acute episode of ischemic origin in which one eye has profound visual loss, followed by full recovery within one hour. Transient monocular blindness most often occurs in the setting of retinal ischemia secondary to carotid embolism, but other mechanisms have been reported, including thrombosis (most often in the setting of giant cell arteritis), hemodynamic disorders (secondary to severe carotid stenosis), or vasospasm. Transient monocular blindness is considered a transient ischemic attack originating in the carotid arteries, and must be managed the same as transient ischemic attack involving the brain, in order to prevent a subsequent stroke., (Copyright © 2017. Published by Elsevier Masson SAS.)

Background and Purpose: Ischaemic visual loss is often considered a lower risk factor than other transient ischaemic attacks (TIA). We aimed to determine the recurrence risk, prevalence and management of vascular risk factors in these patients., Methods: The study took place in the University College Hospital London daily TIA clinic, main referral centre for North-Central London and Moorfields Eye Hospital. Consecutive records for patients with transient (< 24 h) or permanent (> 24 h) ischaemic visual loss were reviewed during the period January 2014-October 2016. Patients diagnosed with temporal arteritis were excluded., Results: Of 400 patients, 224 (56%) were male with mean age 64.5 years (SD 15.1); 263 patients (65.8%) presented with transient and 137 patients (34.2%) with permanent ischaemic visual loss; 51.3% had hypertension (HTN), 35.3% hypercholesterolaemia, 14.5% diabetes, 11.8% ischaemic ocular events, 10.0% ischaemic heart disease, 7.3% atrial fibrillation (AF), 6.3% TIA, 5.3% stroke, and 12.3% were smokers. Median vascular risk factors were 2 (range 1-6), but 122 (30.5%) had ≥3. Those with diabetes (p < 0.001), HTN (p = 0.008), previous myocardial infarction (p = 0.005), or ≥3 vascular risk factors (p = 0.012) were more likely to present with permanent visual loss, while patients with history of transient events, TIA (p = 0.002), or ocular (p = 0.002) presented with transient visual loss. Ninety-day recurrence was 10.5%; this was higher in patients with ≥3 risk factors (hazard ratio 1.42, 95% CI 0.95-2.11, p = 0.111). Patients with past TIA were more likely to be on secondary prevention than those with ocular ischaemia; 60.0 vs. 34.1% received antiplatelets and 76.0 vs. 43.9% statins. At presentation, only 55.2% (16 patients) with known AF were anticoagulated, despite all of them having CHADSVASC ≥1., Conclusions: Approximately one-third of patients with ocular ischaemia had ≥3 vascular risk factors with recurrences higher in these patients. Yet only half of those with previous ischaemic ocular events were on antiplatelets or statins. These patients should be investigated and treated as aggressively as other forms of TIA or stroke., (© 2018 S. Karger AG, Basel.)

In previous studies of transverse sinus (TS) hypoplasia, discrepancies between TS diameter measured by magnetic resonance venography (MRV) and contrast T1-weighted magnetic resonance (contrast T1) were observed. To investigate these discrepancies, and considering that TS hypoplasia is associated with neurological disorders, we performed a post hoc analysis of prospectively collected data from 3 case-control studies on transient global amnesia (TGA), transient monocular blindness (TMB), and panic disorders while retaining the original inclusion and exclusion criteria. Magnetic resonance (MR) imaging of 131 subjects was reviewed to evaluate TS diameter and the location and degree of venous flow stenosis and obstruction.MRV without contrast revealed that TS hypoplasia was observed in 69 subjects, whom we classified into 2 subgroups according to the concordance with contrast T1 observations: concordance indicated anatomically small TS (30 subjects), and discrepancy indicated that the MRV diagnosis is in fact flow-related and that TS is not anatomically small (39 subjects). The latter subgroup was associated with at least 1 site of venous compression/stenosis in the internal jugular vein (IJV) or the left brachiocephalic vein (BCV) (P < 0.001), which was significantly larger in patients than controls. Compensatory dilatation of contralateral TS diameter was only observed with MRV, not with contrast T1 imaging.The clinical implication of these results is that using MRV only, IJV/BCV compression/stenosis may be misdiagnosed as TS hypoplasia. And contralateral TS have no compensatory dilatation in its diameter in contrast T1 imaging, just compensatory increased flow volume., Competing Interests: The authors have no conflicts of interest to disclose.

Objective: To investigate the correlation of amaurosis fugax and carotid stenosis as well as posterior ocular blood vessel hemodynamic changes., Methods: Case series studies. 32 patients (19 men and 13 women whose age were 50 to 80 years old and average age was 64.31 ± 8.15) who were diagnosed as amaurosis fugax with 32 eyes were enrolled from 2011.5-2012.12. During the same period 30 cases without posterior ocular ischemic diseases were collected as the control group. Their ophthalmic artery, central retinal artery and carotid artery were examinated by color Doppler ultrasound, to detect vascular peak systolic velocity, end diastolic velocity, resistance index, the degree of carotid stenosis, carotid artery plaque area and type. All data were analyzed by chi-square test and t-test., Results: PSV (25.95 ± 2.45) cm/s, EDV (6.01 ± 0.87) cm/s of the ophthalmic artery in AmF group were lower compared with the control group [PSV:(27.53 ± 1.41) cm/s, EDV: (6.89 ± 0.56) cm/s]. The differences were statistically significant (t = 3.087, 0.712, P = 0.003, 0.048). There was no statistical difference of RI between AmF and the control group (t = 0.188, P = 0.852) . PSV (7.13 ± 0.96) cm/s, EDV (1.78 ± 0.26) cm/s of the central retinal artery in AmF group were lower compared with the control group[PSV:(8.23 ± 0.92) cm/s, EDV:(2.13 ± 0.29) cm/s]. The differences were statistically significant (t = 4.648, 4.976, P = 0.000, 0.000). There was no statistical difference of RI between AmF and the control group (t = 0.180, P = 0.855). Detection rate of carotid artery moderately and severe stenosis (59.4%) was significantly higher compared with the control group (6.7%) . The difference was statistically significant (χ(2) = 19.205, P = 0.000)., Conclusions: The blood flow velocity of ophthalmic artery and central retinal artery in amaurosis fugax patients reduced significantly, while the resistance was normal. About 60% of the patients had carotid artery moderately and severe stenosis. There was significant correlation between amaurosis fugax and carotid artery stenosis.

Objective: To study the changes in peak systolic velocities of the ipsilateral external carotid artery (ECA) following carotid revascularization., Methods: All patients randomized to carotid artery stenting (CAS) or carotid endarterectomy (CEA) in the International Carotid Stenting Study (ICSS; ISRCTN25337470) in our center were included. Peak systolic velocities (PSV) were assessed with duplex ultrasound (DUS) at baseline, at 30 days, and at 12 and 24 months after treatment. Our primary outcome measure was the change in blood flow velocities in the ECA (ΔPSVECA). Secondary outcome measure was the prevalence of post interventional ECA occlusion., Results: Of 270 patients enrolled in ICSS at our center, 224 patients (mean age, 68.8 years; 154 males) were included in the present study (116 CAS, 108 CEA). Baseline PSV in the ipsilateral ECA was similar between the groups. Following CAS, PSV gradually increased during follow-up, whereas PSV remained relatively stable after CEA; mean difference of PSV between CAS and CEA: 23 cm/s (95% CI, -5 to 52), 58 cm/s (95% CI, 27-89), and 69 cm/s (95% CI, 31-107) at 30 days, 12 months, and 24 months. One new ECA occlusion occurred after CAS and two after CEA., Conclusion: Blood flow velocities in the ipsilateral ECA increase significantly after CAS but not after CEA. However, this does not lead to a higher rate of ECA occlusion in the first 2 years after revascularization. We conclude that CAS is not inferior to CEA in preserving the ECA as a possible potential collateral pathway for cerebral blood supply within 2 years following revascularization., (Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.)

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.

The ocular dominance (OD) shift induced by monocular deprivation (MD) during the critical period is mediated by an initial depression of deprived-eye responses followed by an increased responsiveness to the nondeprived eye. It is not fully clear to what extent these 2 events are correlated and which are their physiological and molecular mediators. The extracellular synaptic environment plays an important role in regulating visual cortical plasticity. Matrix metalloproteinases (MMPs) are a family of activity-dependent zinc-dependent extracellular endopeptidases mediating extracellular matrix remodeling. We investigated the effects of MMP inhibition on OD plasticity in juvenile monocularly deprived rats. By using electrophysiological recordings, we found that MMP inhibition selectively prevented the potentiation of neuronal responses to nondeprived-eye stimulation occurring after 7 days of MD and potentiation of deprived-eye responses occurring after eye reopening. Three days of MD only resulted in a depression of deprived-eye responses insensitive to MMP inhibition. MMP inhibition did not influence homeostatic plasticity tested in the monocular cortex but significantly prevented an increase in dendritic spine density present after 7 days MD in layer II-III pyramids.

The article is dedicated to the problem concerning indications for revascularization of the carotid basin. The aim was to determine significance of ocular ischaemic syndrome in establishing indications for revascularization of the carotid basin in stenotic lesions of extracranial portions of carotid arteries.

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., (Copyright © 2011 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.)

The study aimed to prove the efficacy of carotid endarterectomy in patients with transient monocular blindness caused by carotid arterial stenosis. 31 patients, aged 45-80 years, were included in the study. All patients were divided in 2 groups: 16 patients from the first group had classic carotid endarterectomy with synthetic patch; 15 patients from the second group were treated conservatively. All operated patients had no stroke or transient ischemic attack and were spared from amaurosis attacks and even showed certain vision sharpness improvement. Whereas the majority of patients from the second group showed the recurrence of the amaurosis fugax attacks after the treatment. Carotid endarterectomy significantly improves the condition of an eye and prevents brain ischemia in patients with transient monocular blindness caused by carotid arterial stenosis.

Postnatal cortical circuit development is characterized by windows of heightened plasticity that contribute to the acquisition of mature connectivity and function. What drives the transition between different critical plasticity windows is not known. Here we show that a switch in sign of inhibitory plasticity correlates with the reported transition between the precritical period (pre-CP) and the critical period (CP) for ocular dominance plasticity (ODP). In layer 4 of binocular visual cortex (V1b), depression of inhibitory synapses onto pyramidal neurons is induced when rats are monocularly deprived for 2 d at the end of the third postnatal week (pre-CP), whereas potentiation is induced if the monocular deprivation is started in the fourth postnatal week (CP). The magnitude of potentiation increases with deprivations started close to the peak of the CP for ODP. The direction of inhibitory plasticity depends on the differential manipulation of circuits activated by the two eyes. During development, these two forms of plasticity shift the balance between excitation and inhibition of the circuit in opposite directions, whereas the excitatory synaptic drive remains unaffected. Inhibitory plasticity is thus fundamental in modulating cortical circuit refinement and might be one of the mechanisms promoting ocular dominance shifts.

Neuronal circuits in the cerebral cortex consist mainly of glutamatergic/excitatory and GABAergic/inhibitory neurons. In the visual cortex, the binocular responsiveness of neurons is modified by monocular visual deprivation during the critical period of postnatal development. Although GABAergic neurons are considered to play a key role in the expression of the critical period, it is not known whether their binocular responsiveness and ocular dominance plasticity are different from those of excitatory neurons. Recently, the end of the critical period was found to be not strict so that cortical neurons in the adult still have some ocular dominance plasticity. It is not known, however, which type of neurons or both maintain such plasticity in adulthood. To address these issues, we applied in vivo two-photon functional Ca(2+) imaging to transgenic mice whose GABAergic neurons express a yellow fluorescent protein called Venus. We found that GABAergic neurons are more binocular than excitatory neurons in the normal visual cortex, and both types of neurons show the same degree of modifiability to monocular visual deprivation during the critical period, but the modifiability of GABAergic neurons is stronger than that of excitatory neurons after the end of the critical period.

Background: The frequency of jugular venous reflux (JVR) is higher in patients with transient monocular blindness (TMB). We hypothesize that JVR influences ocular venous outflow, and resulting disturbances in cerebral and ocular venous circulation might be a cause of TMB. To substantiate this hypothesis, we aimed to demonstrate that: (1) TMB patients have vasculature changes in their retinal venules, and (2) JVR could influence ocular venous outflow, as revealed by dilated retinal venules., Methods: This study has 2 parts. The case-control study included 31 TMB patients and 31 age/gender-matched normal individuals, who all received fundus photography for retinal venule diameter comparisons. The Valsalva maneuver (VM) experiment included 30 healthy volunteers who received both color Doppler imaging of the internal jugular vein and fundus photography for retinal venule diameter measurement., Results: In the case-control study, TMB patients had a wider retinal venule diameter (184.5 +/- 17.5 vs. 174.3 +/- 16.2 microm, right eye, p = 0.023; 194.20 +/- 24.6 vs. 176.6 +/- 19.5 microm, left eye, p = 0.017), especially TMB patients with JVR. The VM experiments showed that the presence of JVR was associated with a greater increase in retinal venule diameters during VM in the subjects' right eye (14.27 +/- 11.16 vs. 2.75 +/- 3.51%, JVR vs. non-JVR, p = 0.0002) and left eye (10.06 +/- 6.42 vs. 1.80 +/- 2.03%, p = 0.0003)., Conclusions: These findings provide evidence that frequently occurring JVR associated with TMB impedes ocular venous outflow, and the subsequent disturbances in ocular venous circulation may be a cause of TMB., ((c) 2009 S. Karger AG, Basel.)

Objective: Transient monocular blindness (TMB) attacks may occur during straining activities that impede cerebral venous return. Disturbance of cerebral and orbital venous circulation may be involved in TMB., Methods: Duplex ultrasonography and Doppler-flow measurement of jugular and retrobulbar veins were performed in 134 consecutive patients with TMB and 134 age- and sex-matched control subjects. All recruited patients received thorough examinations to screen for possible underlying causes., Results: Of the 134 patients with TMB, 48 patients had ipsilateral carotid arterial lesion and 7 patients had TMB attack(s) caused by cardiac embolism. Of the remaining 79 patients with undetermined cause, 46 had 3 or more TMB attacks (undetermined-frequent group) and 33 had fewer than 3 attacks. In comparison with the control subjects, the TMB patients had greater frequencies of jugular venous reflux (57 vs 30%; p < 0.0001; odds ratio [OR]: 3.079, 95% confidence intervals [CI]: 1.861-5.096) and flow reversal in the superior ophthalmic vein (RSOV; 37 vs 9%; p < 0.0001; OR: 6.052, CI: 3.040-12.048). The undetermined-frequent group had the greatest frequencies of jugular venous reflux (74%, 34 patients; OR: 6.66, CI: 3.13-14.17) and RSOV (59%, 27 patients; OR: 6.51, CI: 3.12-13.58). Of the 50 patients with RSOV, 47 (94%) had RSOV on the side of the TMB attacks., Interpretation: The increased incidences of jugular and orbital venous reflux in TMB patients suggest that disturbance of cerebral and orbital venous circulation is involved in the pathogenesis of TMB, especially among patients with frequent attacks of undetermined cause.

Background: Clinical characteristics of common carotid artery (CCA) stenosis have been reported relatively rarely, compared with those of internal carotid artery (ICA) stenosis. The current retrospective study aimed to clarify the symptomatology of CCA stenosis., Methods: Summarized records of patients admitted were reviewed to identify patients with CCA stenosis or extracranial ICA stenosis. Clinical histories and neurologic symptoms were identified and analyzed., Results: CCA stenosis was present in 12 patients (symptomatic, n = 8; asymptomatic, n = 4). Among symptomatic patients, 4 (50%) had amaurosis fugax. Among 137 patients with symptomatic extracranial ICA stenosis, amaurosis fugax occurred in 9 patients (6.6%)., Conclusions: Frequency of amaurosis fugax was significantly higher in CCA stenosis than in ICA stenosis. Patients with CCA stenosis may be susceptible to transient hemodynamic insufficiency of the retina as a result of simultaneous reductions in blood supplies from both the external carotid artery and the ICA.

Purpose: Release hallucinations (RH) with insight into the unreality of the hallucination have been reported in association with severe vision loss. Postoperative blindness following nonocular surgery may appear associated with central retinal artery occlusion (CRAO) caused by incorrect head positioning during surgery, intraoperative hypotension, and atherosclerosis. RH may initially mask the loss of vision., Methods: Case report., Results: A 27-year-old woman who had undergone lumbar spinal surgery for right L4-L5 discal herniation developed left eye visual loss and complex visual hallucinations immediately after surgery. Her symptoms were initially considered hallucinations related to the anesthesia and not taken into consideration until 4 days later. Ophthalmic examination disclosed CRAO probably caused by ocular compression during surgery. Optic nerve atrophy appeared during the following 6 years., Conclusions: Doctors and auxiliary personnel should be aware that visual hallucinations may be a sign of actual vision damage.

Background and Purpose: This study was to evaluate the retrobulbar hemodynamics in patients who have transient monocular blindness (TMB) without carotid stenosis., Methods: Fifty-nine patients who have TMB without carotid stenosis were studied along with 59 age- and sex-matched controls. Color Doppler-imaging was used to study the retrobulbar hemodynamic by measuring the flow velocities (peak-systolic velocity, and end-diastolic velocity), vascular resistance indices (pulsatility index, and resistance index) in central retinal arteries, short posterior ciliary arteries, and ophthalmic arteries. The patients were divided into 2 groups according to the attack frequency: group 1 (occasional TMB, 2 or fewer attacks, 26 patients) and group 2 (frequent TMB, 3 or more attacks, 33 patients)., Results: The risk factors for atherosclerosis were similar between the cases and controls. The means of end-diastolic velocity were significantly lower in central retinal arteries and ophthalmic arteries, and the pulsatility index and resistance index were significantly higher in all the 3 retrobulbar vessels in TMB patients than for the controls. The differences between patients and controls were greater for the group-2 patients., Conclusions: Patients who have TMB without carotid stenosis had altered retrobulbar hemodynamics with a generalized increase in vascular resistance in the retrobulbar arteries. The role of venous hypertension as an etiology needs further study.

Background: 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., Methods: 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., Results: 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., Conclusions: 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."

Gaze-evoked amaurosis is a quite unique symptom. We present a 37-year-old patient with unilateral gaze-evoked amaurosis caused by an orbital tumor. Possible mechanisms include transient ischemia of the optic nerve and the retina or inhibition of the axonal impulses. While not common as a cause of amaurosis fugax, an orbital mass should be considered in the differential diagnosis of gaze-evoked atypical monocular amaurosis fugax.

Purpose: To evaluate the blood flow velocity in the ophthalmic artery using color Doppler imaging in two patients who had diabetic retinopathy with amaurosis fugax caused by orthostatic hypotension., Design: Interventional case reports., Methods: A 40-year-old woman (Case 1) and a 65-year-old man (Case 2) had diabetic retinopathy and amaurosis fugax caused by orthostatic hypotension. We evaluated the blood flow velocity in the ophthalmic artery using color Doppler imaging in the two patients., Setting: Department of Ophthalmology, Diabetes Center Tokyo Women's Medical University, Tokyo, Japan., Results: For Case 1, the maximum systolic blood flow velocity in the ophthalmic artery (V max) was 10 cm/sec in the supine position. In a seated position, visual acuity was decreased from 20/20 to light perception as V max fell to 1 cm/sec. For Case 2, the V max was 14 cm/sec in the supine position, but it was too low to measure in a seated position., Conclusions: The decrease of V max by orthostatic hypotension may cause amaurosis fugax in patients with diabetic retinopathy.

Objective: To investigate the association between ischemic brain lesions and intracranial collateral blood flow in patients with unilateral occlusion of the internal carotid artery (ICA)., Methods: Sixty-eight consecutive patients were included. Ischemic lesions on MRI were identified on hard copies, and volume measurements of the lesions were performed on an MR workstation. Intracranial collateral pathways were studied with MR angiography, digital subtraction angiography, and transcranial Doppler sonography., Results: The presence of collateral flow via the anterior communicating artery (ACoA) was associated with a reduction in prevalence (p = 0.01) and volume (p = 0.008) of internal border zone infarcts in the hemisphere ipsilateral to the occluded ICA. Absence of collateral blood flow via the circle of Willis was associated with an increase in prevalence (p = 0.007) and volume (p = 0.005) of internal border zone infarcts. No association between any collateral flow pattern in the circle of Willis and periventricular lesions or lacunar, territorial, or external border zone infarcts was found. No association between collateral flow via the ophthalmic artery or leptomeningeal vessels with any type of ischemic lesion was found., Conclusion: Collateral flow via the ACoA is associated with a reduction of the prevalence and volume of internal border zone lesions but not with any other type of ischemic lesion. The presence of a functional posterior communicating artery or secondary collateral pathways is not associated with the prevalence of any type of ischemic lesion.

Background and Purpose: Carotid artery disease can cause chronic retinal ischemia, resulting in transient or permanent blindness, pupillary reflex dysfunction, and retinal degeneration. This experiment investigated the effects of chronic retinal ischemia in an animal model involving permanent carotid occlusion. The time course of retinal pathology and the role of light in this pathology were examined., Methods: Sprague-Dawley rats underwent permanent bilateral occlusion of the common carotid arteries or sham surgery. Half of the animals were postsurgically housed in darkness, and half were housed in a 12-hour light/dark cycle. Animals were killed at 3, 15, and 90 days after surgery. Stereological techniques were used to count the cells of the retinal ganglion cell layer. Thy-1 immunoreactivity was assessed to specifically quantify loss of retinal ganglion cells. The thicknesses of the remaining retinal sublayers were measured. Optic nerve degeneration was quantified with the Gallyas silver staining technique., Results: Permanent bilateral occlusion of the common carotid arteries resulted in loss of the pupillary reflex to light in 58% of rats. Eyes that lost the reflex showed (1) optic nerve degeneration at 3, 15, and 90 days after surgery; (2) a reduction of retinal ganglion cell layer neurons and Thy-1 immunoreactivity by 15 and 90 days; and (3) a severe loss of photoreceptors by 90 days when postsurgically housed in the light condition only., Conclusions: Ischemic damage to the optic nerve caused loss of pupillary reflex and death of retinal ganglion cells in a subset of rats. Subsequently, light toxicity induced death of the photoreceptors.

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.

A 71 year-old woman had 85% and 60% stenoses of the right and left internal carotid arteries, respectively. Right-sided endarterectomy was performed because of amaurosis fugax. Two days postoperatively, she developed classical symptoms and signs of acute glaucoma. Right-sided acute angle closure glaucoma was diagnosed by tonometry and gonioscopy, and treated with laser-iridectomy. The patient was discharged two days later without neurological or ophthalmological deficits. Manifest acute glaucoma postoperatively seems never to have been reported. However, the choroid is not autoregulated, and the intraocular pressure has been reported to increase after internal carotid-endarterectomy.

Purpose: To assess whether patients with transient monocular blindness (TMB) and patients with hemispheric transient ischemic attacks (hTIA) differ from each other with respect to cerebral hemodynamic parameters., Methods: Seventeen TMB patients and 23 hTIA patients with a moderate to severe stenosis or an occlusion of the internal carotid artery (ICA) underwent magnetic resonance (MR) angiography, (1)H MR spectroscopy and transcranial Doppler sonography. Thirty-one control subjects were investigated to obtain reference values for the MR investigations. Quantitative flow was measured in the ICAs, the basilar artery and the middle cerebral arteries (MCA). Metabolic changes in the MCA territory were studied by assessing N-acetyl-aspartate (NAA)/choline ratios and prevalences of lactate. The prevalence of collateral flow was assessed in the circle of Willis and the ophthalmic arteries. The vasomotor reactivity was studied by measuring the CO(2) reactivity of the MCA territories., Results: Quantitative flow in the cerebropetal arteries and the MCAs did not differ between TMB patients and hTIA patients. Also patterns of collateral flow, prevalence of lactate and CO(2) reactivity were similar. The mean ipsilateral NAA/choline ratio was lower in hTIA patients compared with TMB patients (p < 0.01), and was predominantly correlated with symptomatology (p < 0.01), i.e. whether patients had TMB or hTIA, and not with ipsilateral MCA flow (p = 0.2) or ipsilateral CO(2) reactivity (p = 0.7)., Conclusion: The results of this study indicate that there are no cerebral hemodynamic differences between TMB patients and hTIA patients. It is therefore unlikely that hemodynamic factors account for differences in clinical characteristics between the two patient groups., (Copyright 2000 S. Karger AG, Basel)

The objective of this 1H magnetic resonance spectroscopy study was to investigate the time course of the brain metabolites N-acetyl-aspartate (NAA), choline, and lactate in patients with transient or minor disabling neurological deficits associated with an occlusion of the internal carotid artery (ICA). Fifty patients had had symptoms of hemispheric ischemia, and 16 had suffered symptoms of retinal ischemia. Single-voxel proton spectra were obtained from uninfarcted cerebral regions on three occasions: 0-6, 6-12, and 12-18 months after symptoms. Reference values were obtained from 29 control subjects. In the 0-6 month period, patients with hemispheric ischemia showed a significantly lower NAA/creatine ratio in the hemisphere ipsilateral to the ICA occlusion, compared with control subjects and patients with retinal ischemia, and a significantly higher choline/creatine ratio, compared with control subjects. The prevalence of lactate did not differ significantly between patient groups. In the following time periods, the NAA/creatine ratio in patients with hemispheric ischemia tended to return to control values and no longer differed from that in patients with retinal ischemia; the choline/creatine ratio decreased significantly and returned to control values. These results demonstrate that cerebral metabolism is altered in patients with an ICA occlusion who have had a hemispheric ischemic event, but returns (choline) or tends to return (NAA) to control values over time. The metabolic changes occur primarily in the hemisphere ipsilateral to the symptomatic ICA occlusion and are related to the occurrence of the hemispheric ischemic event.

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.