Diagnosis of Transient Ischemic Attack: Sex-Specific Differences From a Retrospective Cohort Study.

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.

Homocysteinemia as a cause for amaurosis fugax in a patient without an apparent embolic source.

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.

Atrial Fibrillation: An Underestimated Cause of Ischemic Monocular Visual Loss?

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.

Is Management of Central Retinal Artery Occlusion the Next Frontier in Cerebrovascular Diseases?

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!

Statin-induced myopathy prevented by creatine administration.

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.

Undertreatment of Vascular Risk Factors in Patients with Monocular Ischaemic Visual Loss.

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.

Transient monocular blindness: Vascular causes and differential diagnoses.

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.

Comparison of Clinical Characteristics among Subtypes of Visual Symptoms in Patients with Transient Ischemic Attack: Analysis of the PROspective Multicenter registry to Identify Subsequent cardiovascular Events after TIA (PROMISE-TIA) Registry.

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 ABCD2 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.

Diagnosis of Transverse Sinus Hypoplasia in Magnetic Resonance Venography: New Insights Based on Magnetic Resonance Imaging in Combined Dataset of Venous Outflow Impairment Case-Control Studies: Post Hoc Case-Control Study.

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.

[Correlation analysis on retrobulbar vascular hemodynamic characteristics and carotid artery color Doppler ultrasonographic features of amaurosis fugax].

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.

Flow velocities in the external carotid artery following carotid revascularization.

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.

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.

[Role of ocular ischaemic syndrome in establishing indications for revasculization of the carotid basin in stenotic lesions of extracranial portions of carotid arteries].

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.

Inhibition of matrix metalloproteinases prevents the potentiation of nondeprived-eye responses after monocular deprivation in juvenile rats.

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.

[Long-term follow-up results of carotid endarterectomy in patients with carotid stenosis and transient monocular blindness].

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.