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Late seizures following a first symptomatic brain infarct are related to large infarcts involving the posterior area around the lateral sulcus.

Controversies exist concerning factors that contribute to the occurrence of epileptic seizures after stroke. Therefore, we studied prospectively the occurrence of seizures in 322 patients with a first-ever CT-confirmed symptomatic territorial brain infarct involving the cortex. We also studied potential risk factors for seizures, and gave special attention to cortical infarct location. Fifty-four patients developed post-stroke seizures. We distinguished between early- and late-onset seizures, occurring within two weeks following stroke-onset, or later than two weeks, respectively. We found that patients of 65 years or older with a cardioembolic brain infarct involving the middle temporal or post-central gyrus, had an almost eight times increased risk of early-onset seizures, whereas patients with a large brain infarct involving the supramarginal or superior temporal gyrus, had a five times increased risk of late-onset seizures. We conclude that risk factors and epileptogenic cortical areas for post brain infarct seizures can be identified, which however, differ between early- and late-onset seizures. These two seizure types may also differ in terms of seizure mechanism. Our findings may influence the decision on prophylactic treatment with antiepileptic drugs in stroke patients.

Adult↗

Education and the cognitive decline associated with MRI-defined brain infarct.

OBJECTIVE: To assess whether educational attainment, a correlate of cognitive reserve, predicts the amount of cognitive decline associated with a new brain infarct. METHODS: The Cardiovascular Health Study is a population-based, longitudinal study of people aged 65 years and older. Cognitive function was measured annually using the Modified Mini-Mental State Examination (3MS) and the Digit-Symbol Substitution Test (DSST). The authors tested whether education level modified 1) the cross-sectional association between cognitive performance and MRI-defined infarct and 2) the change in cognitive function associated with an incident infarct at a follow-up MRI. RESULTS: In cross-sectional analysis (n = 3,660), MRI-defined infarct was associated with a greater impact on 3MS performance in the lowest education quartile when compared with others (p for heterogeneity = 0.012). Among those with a follow-up MRI who had no infarct on initial MRI (n = 1,433), education level was not associated with the incidence, size, or location of new brain infarct. However, a new MRI-defined infarct predicted substantially greater decline in 3MS scores in the lowest education group compared with the others (6.3, 95% CI 4.4- to 8.2-point decline vs 1.7, 95% CI 0.7- to 2.7-point decline; p for heterogeneity < 0.001). Higher education was not associated with smaller declines in DSST performance in the setting of MRI-defined infarct. CONCLUSIONS: Education seems to modify an individual's decline on a test of general cognitive function when there is incident brain infarct. These findings are consistent with the hypothesis that cognitive reserve influences the impact of vascular injury in the brain.

Cerebral Infarction↗

Preceding infection as an important risk factor for ischaemic brain infarction in young and middle aged patients.

The role of preceding infection as a risk factor for ischaemic stroke was investigated in a case-control study of 54 consecutive patients under 50 years of age with brain infarction and 54 randomly selected controls from the community matched for sex and age. Information about previous illnesses, smoking, consumption of alcohol, and use of drugs was taken. A blood sample was analysed for standard biochemical variables and serum cholesterol, high density lipoprotein cholesterol, triglyceride, and fasting blood glucose concentrations determined. Titres of antimicrobial antibodies against various bacteria, including Staphylococcus, Streptococcus, Yersinia, and Salmonella and several viruses were determined. Febrile infection was found in patients during the month before the brain infarction significantly more often than in controls one month before their examination (19 patients v three controls; estimated relative risk 9.0 (95% confidence interval 2.2 to 80.0)). The most common preceding febrile infection was respiratory infection (80%). Infections preceding brain infarction were mostly of bacterial origin based on cultural, serological, and clinical data. In conditional logistic regression analysis for matched pairs the effect of preceding febrile infection remained significant (estimated relative risk 14.5 (95% confidence interval 1.9 to 112.3)) when tested with triglyceride concentration, hypertension, smoking, and preceding intoxication with alcohol. Although causality cannot be inferred from these data and plausible underlying mechanisms remain undetermined, preceding febrile infection may play an important part in the development of brain infarction in young and middle aged patients.

Adolescent↗

Silent brain infarction in nonrheumatic atrial fibrillation. EAFT Study Group. European Atrial Fibrillation Trial.

BACKGROUND: Cerebral infarction associated with atrial fibrillation usually causes permanent neurologic disability, but several studies also reported patients with silent cerebral infarcts on CT. The clinical relevance of this findings is unknown, partly because of variable criteria for the diagnosis of "silent" brain infarction. METHODS: This report describes the frequency of silent brain infarcts in 985 patients with nonrheumatic atrial fibrillation, who shortly before suffered a symptomatic transient ischemic attach or nondisabling ischemic stroke, and evaluates the predictive value of silent infarcts for the future development of recurrent vascular events. RESULTS: Of 985 patients, 14% had CT evidence of brain infarcts not explainable by current or previous episodes of cerebral ischemia. In comparison with symptomatic infarcts, these silent infarcts were more often of the small deep lacunar type (odds ratio 5.1; 95% confidence interval 3.4-7.7). If silent and zone infarcts occurred, these often involved the territory of the posterior cerebral artery or the right hemisphere. The presence of a silent infarct at entry was associated with an increased risk of vascular events in general and of recurrent stroke in particular. This was due largely to the presence of multiple infarcts on CT. CONCLUSION: Silent infarcts reflect advanced vascular disease.

Aged↗

Cervical and intracranial atherosclerosis and silent brain infarction in Japanese patients with coronary artery disease.

PURPOSE: To investigate the prevalence of cervical and intracranial atherosclerosis and silent brain infarction in patients with coronary artery disease (CAD). METHODS: Cervical and intracranial atherosclerotic lesions on magnetic resonance angiography (MRA) and silent brain infarctions on magnetic resonance imaging (MRI) were investigated in comparison with the findings of coronary angiography in 133 consecutive patients with CAD. RESULTS: The mean severity scores of cervical and intracranial MRA lesions were significantly higher in the three-vessel CAD (0.40 and 0.53, respectively) than in the zero-vessel CAD group (0.04 and 0.11). The mean scores of the maximal size and multiplicity of MRI lesion were also significantly greater in the two-vessel (1.00 and 1.44) and three-vessel CAD (0.94 and 1.26) than in the zero-vessel CAD group (0.27 and 0.50). The incidence of MRA lesion was markedly higher in patients with brain MRI lesion than in those without (51.1 vs. 6.5%). CONCLUSIONS: Serious coronary artery lesions were commonly accompanied by latent atherosclerotic lesions in the cervical and intracranial arteries besides silent brain infarction in patients with CAD.

Adult↗

Risk of brain infarction in familial hypercholesterolemia.

We followed 54 subjects with heterozygous familial hypercholesterolemia for an average of 10 (range 3-14) years. Half were treated surgically with partial ileal bypass and the other half (matched for age, sex, coronary heart disease, blood pressure, diabetes mellitus, smoking, obesity, and serum cholesterol concentration) were treated conservatively with diet and hypolipidemic drugs. The mean decrease in serum cholesterol concentration from the average value of 522 mg/dl on entry into the study was 32% in the surgically treated group and 10% in the conservatively treated group. One quarter of the subjects (14 of 54) had symptomatic cerebrovascular disorders and one tenth (six of 54) suffered a brain infarction at a mean age of 43 (range 30-57) years. Two thirds of the brain infarctions occurred during follow-up. The method of treatment of familial hypercholesterolemia did not affect the number of new cerebrovascular events. The incidence of brain infarction was 7.4/1000/yr. The risk of brain infarction in these subjects with familial hypercholesterolemia was at least 20 times higher than in the general population. We conclude that symptomatic subjects with familial hypercholesterolemia have not only a high risk of coronary heart disease but also a high risk of cerebrovascular disorders.

Adult↗

[Advantages and disadvantages of fast fluid-attenuated inversion recovery sequence in the evaluation of brain infarction].

This study was performed to determine the advantages and disadvantages of fast fluid attenuated inversion recovery (fast FLAIR) images in diagnosing brain infarction compared with fast spin-echo (fast SE) images. Fast FLAIR and fast SE images were obtained in 32 patients with brain infarction. Infarctions close to the sulci were difficult to differentiate from the real sulci on fast SE images, but were clearly depicted on FLAIR images. Linear foci along with cortex were especially well demonstrated on FLAIR images. On the other hand, foci that showed high signal intensity on fast SE images were sometimes appeared as having low or iso signal intensity on FLAIR images. These foci, suspected of being cystic lesions, were sometimes difficult to identify on fast FLAIR images. For the above reasons, we concluded that fast FLAIR and fast SE each have advantages and disadvantages in the detection of brain infarctions.

Cerebral Infarction↗

Experimental brain infarcts in cats. II. Ischemic brain edema.

In cats, the early development of ischemic brain edema was studied 1 to 4 hours after transorbital occlusion of the left middle cerebral artery (MCA). Two groups of animals were compared: those in which blood flow in the territory of the MCA decreased below the threshold of 10--15 ml/100 g/min (critical ischemia) and those in which it remained above this level (non-critical ischemia). In animals with critical ischemia, water content in the cortex of the MCA territory increased from 80.7 +/- 0.4 to 83.0 +/- 0.3 vol. % (means +/- SE) within 4 h. Edema was associated with an increase in tissue osmolality by 16--22 mosm/kg w.w., and a rise of sodium from 262 +/- 9 to 454 +/- 13 meq/kg d.w. and a decrease of potassium from 442 +/- 20 to 305 +/- 32 meq/kg d.w. The sodium/potassium ratio rose from 0.60 +/- 0.03 to 1.55 +/- 0.17. The water and electrolyte disturbances were accompanied by a major shift of extracellular fluid into the intracellular compartment, as evidenced by the increase in cortical impedance from 282 to 660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was continuously monitored using an induction transducer; swelling began within a few minutes of vascular occlusion, and it continued throughout the 4 h observation period. During this time the blood-brain barrier remained intact as evidenced by the absence of Evans blue staining. Edema was associated with disturbances of the energy producing metabolism, but there was no strict correlation with either lactate or the concentration of high energy phosphates. In animals without critical ischemia, i.e. in which blood flow remained above 10--15 ml/100 g/min, edema was absent despite a distinct deterioration of the energy state of the brain. Edema was also absent in the border zone, in the territory of the posterior cerebral artery and in the contralateral hemisphere of animals with both critical and non-critical ischemia. It is concluded that the early ischemic brain edema following middle cerebral artery occlusion is of the cytotoxic type, that it develops at a flow rate below 10--15 ml/100 g/min, and that it is not strictly correlated with the energy state of the brain.

Animals↗

Electrobehavioral characteristics of epileptic rats following photothrombotic brain infarction.

The goal of this study was to characterize the electroencephalographic (EEG) and behavioral properties of young adult rats during extended video-EEG monitoring following photothrombotic brain infarction. Two-month-old male Sprague-Dawley rats underwent photothrombotic brain infarction of the left sensorimotor cortex with the photosensitive dye rose bengal (n=10) or were used as controls (n=9). Qualitative and quantitative EEG analysis was performed on digital video-EEG records obtained during 6 months of recording. The main finding of this study was that 5/10 (50%) lesioned animals developed focal epileptic seizures ipsilateral to the cortical infarct characterized by rhythmic spike-wave discharges with or without behavioral change. Epileptic animals demonstrated increased delta, theta, and low beta-range power ipsilateral to the infarct that reliably distinguished them from lesioned nonepileptic and control animals. Lesioned animals (epileptic and nonepileptic) also demonstrated a distinct pattern of focal rhythmic theta activity before or after generalized high beta-range discharges. Electrical and behavioral characteristics common to both lesioned and control animals included: (1) focal rhythmic theta activity in either hemisphere; (2) focal low beta-range discharges in either hemisphere; (3) generalized high beta-range discharges; (4) absence seizures; (5) generalized pseudoperiodic spike discharges associated with mild multifocal body jerks; (6) tonic-clonic seizures (one nai;ve control; one lesioned animal). Cresyl violet staining of lesioned animals' brains showed consistent infarcts of the sensorimotor cortex extending to the subcortical white matter. These results provide an expanded electrobehavioral description of young adult rats following photothrombotic brain infarction and augment further investigation into the molecular, cellular, and network alterations that contribute to the establishment of post-stroke epilepsy.

Animals↗

Components of blood pressure and risk of atherothrombotic brain infarction: the Framingham study.

From a study of the evolution of atherothrombotic brain infarction (ABI) in the Framingham cohort of 5,209 men and women over 18 years of follow-up, it has been ascertained that hypertensionis the most common and most powerful precursor. Atherothrombotic brain infarction developed in hypertensive patients seven times more often than in normotensive patients, and the risk was proportional to the blood pressure throughout its range.

Adult↗

Texture analysis of ultrasonic images of symptomatic carotid plaques can identify those plaques associated with ipsilateral embolic brain infarction.

OBJECTIVES: The aim of our study was to determine the association between objective, computerised texture analysis of carotid plaque ultrasonic images and embolic CT-brain infarction in patients presenting with hemispheric neurological symptoms. DESIGN: Cross-sectional study in patients with 50%-99% (ECST) carotid stenosis. PATIENTS AND METHODS: Carotid plaque ultrasonic images (n=54, 26 with TIAs and 28 with stroke) obtained during carotid ultrasound were normalised and standardised for resolution and subsequently assessed visually for the presence of discrete echogenic or juxtaluminal echolucent components and overall echogenicity (plaque type). Using computer software, 51 histogram/textural features of the plaque outlines were calculated. Factor analysis was subsequently applied to eliminate redundant variables. Small cortical, large cortical and discrete subcortical infarcts on CT-brain scan were considered as being embolic. RESULTS: Twenty-five cases (46%) had embolic infarcts. On logistic regression, grey-scale median (GSM), a measure of echolucency, spatial grey level dependence matrices (SGLDM) correlation and SGLDM information measure of correlation-1, measures of homogeneity were significant (p<0.05), but not grey level runlength statistics (RUNL) Run Percentage (RP), stenosis severity, type of symptoms or echolucent juxtaluminal components. Using ROC curves methodology, SGLDM information measure of correlation-1 improved the value of GSM in distinguishing embolic from non-embolic CT-brain infarction. CONCLUSION: Computerised texture analysis of ultrasonic images of symptomatic carotid plaques can identify those that are associated with brain infarction, improving the results achieved by GSM alone. This methodology could be applied to prospective natural history studies of symptomatic patients not operated on or randomised trials of patients undergoing carotid angioplasty and stenting in order to identify high-risk subgroups for cerebral infarction.

Algorithms↗

Clinical characteristics of patients with ischemic ocular nerve palsies and lacunar brain infarcts: a retrospective comparative study.

BACKGROUND: Ischemic ocular motor nerve palsies (IOMP) and lacunar brain infarcts share a similar pathological mechanism. The clinical characteristics of patients as well as the protective role of aspirin should therefore be similar in both conditions. METHODS: The medical records of 107 consecutive patients with IOMP and 160 patients with lacunar cerebrovascular accidents (CVA) were reviewed and analyzed with respect to patient characteristics, vascular risk factors, and aspirin intake. The data on patients with and without aspirin were compared within each group as well as between both groups. RESULTS: Hyperlipidemia, smoking, high carotid stenosis (>70%) and the presence of more than one vascular risk factor in an individual patient were found to be more common in patients with lacunar brain infarcts regardless of aspirin intake. Absence of vascular risk factors was encountered more in IOMP patients. The recurrence of lacunar CVA was significantly higher than recurrence of IOMP. A history of Bell's palsy was more common in IOMP patients than in patients with lacunar CVA. Within the IOMP group, the prevalence of vascular risk factors did not differ between the aspirin and non-aspirin group. Ischemic heart disease (IHD), CVA and recurrence were found more often in the aspirin group. Within the CVA group hypertension, IHD, cardiac arrhythmia and recurrence rate were more common in the aspirin group whereas smoking was found to be more common in the non-aspirin group of patients. CONCLUSIONS: Arteriosclerosis is the main cause of lacunar CVA and IOMP. However, IOMP depends less on the presence of vascular risk factors than does lacunar CVA. Furthermore, aspirin - at least at low doses - does not seem to have a protective effect on either of these conditions, but more extensive prospective studies of homogeneous groups of patients are needed to clarify the preventive role of antiplatelet agents in IOMP.

Aged↗

Alcohol abuse and brain infarction.

Recent findings on the relation between alcohol abuse and ischaemic brain infarction are reviewed. Much of the association has hitherto been explained by the effects of confounding factors such as smoking. Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. Analysis of case histories shows that alcohol abuse has precipitated cerebral embolism in conjunction with cardiac diseases including alcoholic cardiomyopathy and paradoxical embolism due to deep vein thrombosis via atrial septal defect. Among young adults, falling when intoxicated with alcohol has caused traumatic dissection of the carotid artery and consequent brain infarction. Alcohol may predispose individuals to cerebral embolism, thrombosis and ischaemia via its effects on the coagulation cascade, platelet count and function and contractility of the cerebral vessels. Further studies are needed to prove that these mechanisms are significant and to identify any other mechanisms which may mediate the risk associated with alcohol abuse. On the basis of current data, alcohol should be considered as an independent risk factor for ischaemic cerebral infarction in young adults.

Alcohol Drinking↗

Cardiovascular autonomic reflexes in brain infarction.

BACKGROUND AND PURPOSE: Increased sympathetic activity is associated with cardiovascular complications in stroke, but the role of the parasympathetic nervous system has not been carefully outlined. In the present study our purpose was to assess quantitatively autonomic cardiovascular disturbances in brain infarction by measuring cardiovascular autonomic reflexes. METHODS: We studied the autonomic regulation of cardiovascular functions prospectively in 40 patients with brain infarction (acute phase, 1 month, and 6 months) and in 55 healthy control subjects by recording heart rate and blood pressure responses to normal and deep breathing, the Valsalva maneuver, tilting, and isometric work. RESULTS: In the acute phase, heart rate responses to normal breathing, deep breathing, the Valsalva maneuver, and tilting were significantly (P < .05) impaired in both hemispheric and brain stem infarctions, thus indicating hypofunction of the parasympathetic nervous system. At 1 month heart rate responses to normal breathing (brain stem, P < .05), the Valsalva maneuver (brain stem, P < .01), and tilting (hemispheric, P < .05) were still significantly lower than those of the control subjects, but at 6 months significant suppression of the response was found only in tilting (hemispheric, P < .05). CONCLUSIONS: These findings suggest that in addition to the previously well-established sympathetic hyperfunction, brain infarction also seems to cause parasympathetic hypofunction, brain which may be involved in cardiovascular and other known manifestations of autonomic failure associated with stroke.

Adult↗

[Prevalence of cervical and cerebral atherosclerosis and silent brain infarction in patients with multivessel coronary artery disease].

OBJECTIVES: This clinical study investigated the prevalence of cervical and cerebral atherosclerosis and silent brain infarction in patients with coronary artery disease. METHODS: Cervical and cerebral magnetic resonance angiography(MRA) was performed in 133 patients (98 males, 35 females, mean age 65.3 years) with suspected coronary artery disease, who were divided into a zero- and one-vessel disease group(n = 71) and a two- and three-vessel disease group(n = 62) depending on the number of major coronary branches with 75% or more stenosis. The MRA lesion was defined as more than 50% stenosis. Magnetic resonance imaging(MRI) of the brain was performed within 1 week of MRA in 78 patients without symptomatic stroke and atrial fibrillation. Silent brain infarction on MRI was defined as a focal high intensity area on T2-weighted images larger than 3 mm. RESULTS: The prevalence of MRA lesions was significantly greater in the two- and three-vessel group than in the zero- and one-vessel group(53% vs 14%, p < 0.01). The prevalence of MRI lesion was significantly higher in the two- and three-vessel group than in the zero- and one-vessel group(77% vs 36%, p < 0.01). The size and number of the MRI lesions were also significantly greater in the two- and three-vessel group than in the zero- and one-vessel group(p < 0.01). Neither age nor percentage of male gender was different between the groups. Diabetes mellitus was the common risk factor for coronary artery disease, MRA lesion and MRI lesion. CONCLUSIONS: Cervical and cerebral atherosclerosis and silent brain infarction are frequently observed in patients with multivessel coronary artery disease.

Adult↗

Delayed treatment with magnesium: reduction of brain infarction and improvement of electrophysiological recovery following transient focal cerebral ischemia in rats.

OBJECT: The authors examined whether delayed treatment with Mg++ would reduce brain infarction and improve electrophysiological and neurobehavioral recovery following cerebral ischemia-reperfusion. METHODS: Male Sprague-Dawley rats were subjected to right middle cerebral artery occlusion for 90 minutes followed by 72 hours of reperfusion. Magnesium sulfate (750 micromol/kg) or vehicle was given via intracarotid infusion at the beginning of reperfusion. Neurobehavioral outcome and somatosensory evoked potentials (SSEPs) were examined before and 72 hours after ischemia-reperfusion. Brain infarction was assessed after the rats had died. Before ischemia-reperfusion, stable SSEP waveforms were recorded after individual fore- and hindpaw stimulations. At 72 hours of perfusion the SSEPs recorded from ischemic fore- and hindpaw cortical fields were depressed in vehicle-injected animals and the amplitudes decreased to 19 and 27% of baseline, respectively (p < 0.001). Relative to controls, the amplitudes of SSEPs recorded from both ischemic fore- and hindpaw cortical field in the Mg++-treated animals were significantly improved by 23% (p < 0.005) and 39% (p < 0.001) of baselines, respectively. In addition, Mg++ improved sensory and motor neurobehavioral outcomes by 34% (p < 0.01) and 24% (p < 0.05), respectively, and reduced cortical (p < 0.05) and striatal (p < 0.05) infarct sizes by 42 and 36%, respectively. CONCLUSIONS: Administration of Mg++ at the commencement of reperfusion enhances electrophysiological and neurobehavioral recovery and reduces brain infarction after cerebral ischemia-reperfusion. Because Mg++ has already been used clinically, it may be worthwhile to investigate it further to see if it holds potential benefits for patients with ischemic stroke and for those who will undergo carotid endarterectomy.

Animals↗

[MR imaging of acute hemorrhagic brain infarction].

Six patients with acute hemorrhagic brain infarct were imaged using spin-echo (SE) pulse sequences on a 1.5 Tesla MR scanner. Including two patients with repeated MR imaging, a total of eight examinations, all performed within 15 days after stroke, were analyzed retrospectively. Four patients revealed massive hemorrhages in the basal ganglia or cerebellum and three cases demonstrated multiple linear hemorrhages in the cerebral cortex. On T1-weighted images, hemorrhages were either mildly or definitely hyperintense relative to gray matter, while varied from mildly hypointense to hyperintense on T2-weighted images. T1-weighted images were superior to T2-weighted images in detection of hemorrhage. CT failed to detect hemorrhages in two of five cases: indicative of MR superiority to CT in the diagnosis of acute hemorrhagic infarcts.

Acute Disease↗

Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs.

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.

Animals↗