Bilateral Occipital Lobe Infarction Research Articles

Optic Nerve Infarction in a Patient With Coronavirus Disease 2019.

Severe acute respiratory syndrome 2 (SARS-CoV2), also called coronavirus disease 2019 (COVID-19), has spread worldwide and affected millions of lives. Although there are many unaddressed questions about the pathogenesis of the virus and the best treatment, it is known that the virus affects several organ systems, including respiratory, gastrointestinal, and neurologic (1–4). Neurologic manifestations reported in COVID-19 patients include headache, anosmia, seizure, stroke, encephalitis, and Guillain–Barre syndrome (4); However, neuro-ophthalmic manifestations have infrequently been reported (5–8). We describe a patient with COVID-19 who developed thrombosis of the left internal carotid artery leading to infarction of the left optic nerve. A 50-year-old man was found to have a positive polymerase chain reaction (PCR) test for COVID-19. Twelve days later, he developed fever, cough, and dyspnea. His respiratory symptoms worsened, and 2 days later, he was admitted to hospital for acute onset of aphasia and right hemiparesis. After computed tomography (CT) of the brain excluded a hemorrhagic stroke, the patient was given intravenous tissue plasminogen activator and referred to our medical center. His medical history included poorly controlled diabetes mellitus, hypertension, and hyperlipidemia. On admission, the patient was lethargic, oriented to self, aphasic, and not following commands. He had right hemiplegia and left gaze preference. Nasal and oropharyngeal swabs for real-time PCR confirmed infection with SARS-CoV2, and due to his respiratory failure, he was intubated and transferred to the intensive care unit. His hematologic studies included white blood cells of 12.6 × 103/µL (normal, 4–11/µL) with 4% lymphocyte (normal, 15%–52%), C-reactive protein 214 mg/L (normal, 0–10.9 mg/L), d-dimer >20,000 ng/mL (normal, 0–240 ng/mL), lactate dehydrogenase 280 U/L (normal, 120–240 U/L), and fibrinogen 1,228 mg/dL (normal, 220–498 mg/dL). Neuroimaging studies were obtained. CT angiography (CTA) was consistent with occlusion of the cervical and intracranial portion of the left internal carotid artery (Fig. 1). Subsequent brain MRI demonstrated scattered acute infarcts in the distribution of the left middle cerebral artery. Diffusion-weighted imaging (DWI) showed restricted diffusion along the intraorbital portion of the left optic nerve (Fig. 2).FIG. 1.: CTA. Sagittal and axial images reveal total occlusion of the left internal carotid artery (A, arrow) and absent flow in the artery at the skull base (B, arrow).FIG. 2.: A. Diffusion-weighted scan shows multiple areas of ischemia in the left cerebral hemisphere. B. Diffusion-weighted scan demonstrates restricted diffusion in the left intraorbital optic nerve (arrow). C. The apparent diffusion coefficient (ADC) map confirms restricted diffusion of the left optic nerve (arrow).After 3 weeks, as the patient's respiratory condition and mental status improved, he reported loss of vision in his left eye. At that time, visual acuity was 20/50 in the right eye and no light perception in the left eye. There was a left relative afferent pupillary defect, eye movements were intact, and the fundi were unremarkable. Six weeks later, visual function was unchanged, but the left optic disc was now pale. Cerebrovascular ischemia is a recognized complication of the COVID-19. A series of 219 patients with COVID-19 from Wuhan, China, revealed a 4.6% rate for acute ischemic stroke (1). In this series, patients with COVID-19 who developed stroke were significantly older than non-COVID-19 stroke patients (75.7 ± 10.8 vs 52.1 ± 15.3 years) and had other cardiovascular risk factors. In contrast, Oxley et al (2) reported 5 patients younger than 50 years with COVID-19 who were diagnosed with acute stroke; 2 had no cardiovascular risk factors. Our patient had several risk factors for stroke, including diabetes mellitus, hypertension, and hypercholesterolemia. The mechanism of thromboembolic events in COVID-19 is controversial. Connor and colleagues (3) suggested that a contributing factor is the elevated level of coagulative factors, including platelet, fibrinogen, and d-dimer. Vascular endothelial dysfunction that impairs its antithrombotic properties is another proposed mechanism (4). There are few reports of visual loss associated with COVID-19 disease. Four patients have been documented with profound visual loss due to bilateral parieto-occipital or bilateral occipital lobe infarctions (5–7). In addition, Zhou et al (8) described a patient with COVID-19 who developed bilateral myelin oligodendrocyte glycoprotein (MOG)–associated optic neuritis. The authors speculated that COVID-19 provided a “potential connection” between the viral disease and central nervous system demyelination. DWI in our patient demonstrated acute infarction of the intraorbital portion of the left optic nerve due to thrombosis of the left internal carotid artery. Our report expands the spectrum of neuro-ophthalmic findings in patients with COVID-19.

Review of the ophthalmic symptoms of preeclampsia

AbstractPreeclampsia is a severe, sometimes life-threatening complication of pathological pregnancies. The incidence of neonatal morbidity and mortality is usually increased. Besides general maternal symptoms like hemolysis, low platelet number, elevated liver enzyme level, proteinuria, cardiovascular problems, neurological and cerebral complications, serious ophthalmic symptoms might occur. These include focal or generalized narrowing of the arterioles, flame-shaped retinal haemorrhages, and cotton-wool spots. Rarely, disc swelling, exudative retinal detachment, cystoid macular edema, bilateral occipital lobe infarction, or cortical blindness might occur. In this article, I review the retinal and macular changes, retinal detachment, and the cause of blindness. Optical coherence tomography (OCT) allows ophthalmologists to diagnose early and late changes in choroid vasculature and circulation, and consequent retinal morphological changes. Spectral-domain OCT and enhanced depth imaging provide important insight and possible prognosis for the course of the disease. After termination of the pathological pregnancy, vision returns to normal in most cases; unfortunately, there are some exceptions.

Multiple Cerebral and Cerebellar Infarctions following Russell's Viper (Daboia Russelii) Envenomation - A Case Report

Ischemic stroke is a rare neurological complication following SriLankan Russell's viper envenomation. We report a case of a 44-year-old person, who developed multiple cerebral and cerebellar infarctions following SriLankan Russell's viper envenomation. The patient developed both local and systemic envenomation and was treated with Snake Venom Anti-Serum I.P. (VinsBioproducts Ltd). On day six, this patient developed left-sided hemiparesis. CT scan of the brain showed bilateral cerebellar, bilateral occipital, and right-sideparietal lobe infarctions.

Bilateral Occipital Lobe Infarction Presenting as Bilateral Inferior Altitudinal Defects

Bilateral Occipital Lobe Infarction Presenting as Bilateral Inferior Altitudinal Defects

Seeing without knowing: Operational principles along the early visual pathway

Single cases may lead to unexpected hypotheses in psychology. We retrospectively analyzed single case studies that suggested organizational principles along the early visual pathway, which have remained unanswered until now. In spite of the inhomogeneity of sensitivity, paradoxically the visual field on the subjective level appears to be homogeneous; constancy of brightness of supra-threshold stimuli throughout the visual field is claimed to be responsible for homogeneity; specific summation properties of retinal ganglion cells are hypothesized to guarantee this effect. With a brain-injured patient having suffered a partial visual field loss it can be shown that color induction is a retinal phenomenon; lateral inhibitory processes at the level of amacrine cells are hypothesized as neural network. Third case: In a patient having suffered a bilateral occipital lobe infarction, some functional recovery has been demonstrated; divergence and convergence of projection in the ascending neural pathway are suggested as a structural basis for recovery. Slowed down binocular rivalry discloses a sequential mechanism in the construction of a visual percept. Fourth case: The pre-wired projection of the retina to the visual cortex in spite of a severe squint of one eye is confirmed, but paradoxically some local neuroplasticity is also suggested. Fifth case: Using habituation of local sensitivity in the visual field and its resetting by interhemispheric interactions as an experimental paradigm, it is suggested that spatial attention is controlled at the midbrain level. Sixth case: Observations on residual vision or "blindsight" support the hypothesis that the visual cortex is the one and only structure responsible for visual perception on a conscious level. The unifying principle of these retrospective analyses is that subjective visual phenomena can lead to unexpected but testable hypotheses of neural processing on the structural and functional level in the early visual pathway.

Bilateral Cortical Blindness due to Bilateral Occipital Infarcts without Anosognosia

Bilateral cortical blindness refers to the total loss of vision in the presence of normal pupillary reflexes and in the absence of Ophthalmological disease resulting from bilateral lesions of the striate cortex in the occipital lobes. In most cases, these patients deny their blindness and their behavior is as if they have an intact vision. We report the case of an 84-year-old man with bilateral cortical blindness resulting from bilateral occipital lobe infarcts. The patient presented this infrequent clinical condition after acute bilateral infarction of the occipital lobes possibly due to cardiac embolism resulting from atrial fibrillation of unknown duration. Subcutaneous administration of low molecular weight heparin in therapeutic doses resulted in neurological improvement in the first four days. Interestingly, the visual symptoms were complicated neither by anosognosia nor by memory impairment. Cortical blindness and Anton’s syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease could be the background in a bilateral cortical blindness, as in our patient. To our knowledge, this is the first reported case with bilateral cortical blindness due to simultaneous bilateral occipital infarcts but without anosognosia. Bilateral cortical blindness refers to the total loss of vision in the presence of normal pupillary reflexes and in the absence of Ophthalmological disease resulting from bilateral lesions of the striate cortex in the occipital lobes. In most cases, these patients deny their blindness and their behavior is as if they have an intact vision. We report the case of an 84-year-old man with bilateral cortical blindness resulting from bilateral occipital lobe infarcts. The patient presented this infrequent clinical condition after acute bilateral infarction of the occipital lobes possibly due to cardiac embolism resulting from atrial fibrillation of unknown duration. Subcutaneous administration of low molecular weight heparin in therapeutic doses resulted in neurological improvement in the first four days. Interestingly, the visual symptoms were complicated neither by anosognosia nor by memory impairment. Cortical blindness and Anton’s syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease could be the background in a bilateral cortical blindness, as in our patient. To our knowledge, this is the first reported case with bilateral cortical blindness due to simultaneous bilateral occipital infarcts but without anosognosia.

Teaching Neuro Images : Cortical blindness following acute obstructive hydrocephalus by a colloid cyst

A 46-year-old woman was admitted for acute headache, postseizure confusion, and visual loss. Urgent head CT scan showed obstructive hydrocephalus due to a colloid cyst (figure 1). External ventricular drains inserted emergently demonstrated CSF under pressure, above 40 mm H2O. MRI confirmed the suspected diagnosis of a colloid cyst and highlighted bilateral occipital lobe infarcts (figure 2). CT angiography showed no thrombosis of the posterior cerebral arteries (PCAs). After neurosurgical excision of the colloid cyst, the patient remained blind. The presumed mechanism of infarction was acute compression of the PCAs against the edge of the tentorium cerebelli.

Visual recovery demonstrated by functional MRI and diffusion tensor tractography in bilateral occipital lobe infarction

We report on a patient who showed visual recovery following bilateral occipital lobe infarct, as evaluated by follow up functional magnetic resonance imaging (fMRI) and diffusion tensor tractography (DTT). A 56-year-old female patient exhibited severe visual impairment since onset of the cerebral infarct in the bilateral occipital lobes. The patient complained that she could not see anything, although the central part of the visual field remained dimly at 1 week after onset. However, her visual function has shown improvement with time. As a result, at 5 weeks after onset, she notified that her visual field and visual acuity had improved. fMRI and DTT were acquired at 1 week and 4 weeks after onset, using a 1.5-T Philips Gyroscan Intera. The fiber number of left optic radiation (OR) increased from 257 (1-week) to 353 (4-week), although the fiber numbers for right OR were similar. No activation in the occipital lobe was observed on 1-week fMRI. By contrast, activation of the visual cortex, including the bilateral primary visual cortex, was observed on 4-week fMRI. We demonstrated visual recovery in this patient in terms of the changes observed on DTT and fMRI. It appears that the recovery of the left OR was attributed more to resolution of local factors, such as peri-infarct edema, than brain plasticity.

A case of bilateral occipital lobe infarcts following Indian tree viper bite.

A case of bilateral occipital lobe infarcts following Indian tree viper bite.

A rare complication following general anaesthesia for gynaecological laparotomy: postoperative visual loss due to bilateral occipital lobe infarction

A rare complication following general anaesthesia for gynaecological laparotomy: postoperative visual loss due to bilateral occipital lobe infarction

The Rehabilitation of Anton Syndrome

Anton syndrome is a rare stroke syndrome that can occur after injury to the bilateral occipital lobes of the brain and result in cortical blindness with a lack of awareness of visual deficits. Patients with this syndrome tend to dismiss their blindness, resolutely insist that their vision is intact, and confabulate responses when asked to describe their visual perceptions. This syndrome can theoretically occur in any person with cortical blindness despite the mechanism of injury to the occipital lobe. We describe a patient who developed cortical blindness with Anton syndrome after bilateral occipital lobe infarctions.

Cortical Blindness Following Spinal Surgery: Very Rare Cause of Perioperative Vision Loss

A 38-year-old man was operated with posterior spinal decompression and pedicle screw instrumentation for his L2 fracture with incomplete neurological deficit. In the recovery, he complained of blindness in both eyes after twelve hours. Computed tomographic scan and magnetic resonance angiography revealed bilateral occipital lobe infarcts. He remained permanently blind even after three years follow-up. Though rare, perioperative vision loss is a potential complication following spine surgery in prone position. We report a rare occurrence of cortical blindness following lumbar spine surgery.

Cortical Blindness Following a Near-Drowning Incident

Victims of near-drowning incidents often suffer neurologic injury with long-term sequelae secondary to hypoxic-ischemic injury. We describe a case of profound visual loss due to bilateral occipital lobe infarcts in a 23-year-old male victim of a near-drowning incident.

Bilateral occipital lobe infarction with altitudinal field loss following radiofrequency cardiac catheter ablation

BackgroundBilateral stroke following radiofrequency catheter ablation is an unusual complication and may result in bilateral altitudinal visual field defects. Bilateral altitudinal visual field defects usually result from prechiasmal pathology causing damage to both retinas or optic nerves and rarely from bilateral symmetric damage to the post chiasmal visual pathways.Case presentationA 48-year-old man complained of visual disturbance on wakening following radiofrequency catheter ablation. The patient had a CHADS score of 1 pre-operatively and no complications were noted intra-operatively. Examination revealed a bilateral superior altitudinal defect and MRI of the brain showed multifocal areas of infarction predominantly involving the occipital lobes which correlated to with the visual deficits.ConclusionWhile the risk of thromboembolism and perioperative stroke during radiofrequency catheter ablation is small, it is not insignificant.

Bilateral Superior Altitudinal Hemianopia due to Bilateral Occipital Lobe Infarction

ABSTRACTWe report a 77-year-old man showing bilateral superior altitudinal hemianopia (BSAH) caused by bilateral occipital lobe infarction. The lesions existed into the lingual gyri and involved V1, V2 and V3 in the visual cortex on both sides. The location of the lesions correlated well with visual field defects in our patient. There have been 8 case reports of BSAH caused by occipital lobe lesions, however, the extent of the lesions inside the visual cortex was not evaluated in the previously reported patients. The analysis in our patient showed a close clinico-radiological correlation of BSAH.

Anton's syndrome due to cerebrovascular disease: a case report.

Anton's syndrome describes the condition in which patients deny their blindness despite objective evidence of visual loss, and moreover confabulate to support their stance. It is a rare extension of cortical blindness in which, in addition to the injury to the occipital cortex, other cortical centres are also affected, with patients typically behaving as if they were sighted. We present a case report of an 83-year-old white woman with cortical blindness as a result of bilateral occipital lobe infarcts. Despite her obvious blindness, illustrated by her walking into objects, the patient expressed denial of visual loss and demonstrated confabulation in her accounts of her surroundings, consistent with a diagnosis of Anton's syndrome. A suspicion of cortical blindness and Anton's syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease is the most common cause of Anton's syndrome, as in our patient. However, any condition that may result in cortical blindness can potentially lead to Anton's syndrome. Recovery of visual function will depend on the underlying aetiology, with cases due to occipital lobe infarction after cerebrovascular events being less likely to result in complete recovery. Management in these circumstances should accordingly focus on secondary prevention and rehabilitation.

Bilateral Mesial Occipital Lobe Infarction After Cardiogenic Hypotension Induced by Electrical Shock

A 28-year-old man developed cerebral blindness from infarction of both mesial occipital lobes after cardiogenic hypotension induced by electrical shock. He remained globally encephalopathic for several weeks, but his most enduring deficit was bilateral homonymous hemianopias with macular sparing. Cerebral visual loss after electrical injury has been sparsely reported. It has been attributed to direct thermal injury of the skull or posterior dural venous sinuses. We suggest that cerebral blindness after cardiogenic hypotension in which there is no thermal injury to the scalp be attributed to hypotensive infarction of the mesial occipital lobes, which lie in the terminal domain of the posterior cerebral arteries.

Anton's syndrome due to cerebrovascular disease: a case report

IntroductionAnton's syndrome describes the condition in which patients deny their blindness despite objective evidence of visual loss, and moreover confabulate to support their stance. It is a rare extension of cortical blindness in which, in addition to the injury to the occipital cortex, other cortical centres are also affected, with patients typically behaving as if they were sighted.Case presentationWe present a case report of an 83-year-old white woman with cortical blindness as a result of bilateral occipital lobe infarcts. Despite her obvious blindness, illustrated by her walking into objects, the patient expressed denial of visual loss and demonstrated confabulation in her accounts of her surroundings, consistent with a diagnosis of Anton's syndrome.ConclusionsA suspicion of cortical blindness and Anton's syndrome should be considered in patients with atypical visual loss and evidence of occipital lobe injury. Cerebrovascular disease is the most common cause of Anton's syndrome, as in our patient. However, any condition that may result in cortical blindness can potentially lead to Anton's syndrome. Recovery of visual function will depend on the underlying aetiology, with cases due to occipital lobe infarction after cerebrovascular events being less likely to result in complete recovery. Management in these circumstances should accordingly focus on secondary prevention and rehabilitation.

Recovery of visual functions after early acquired occipital damage

Plasticity of visual systems after early brain damage has been extensively studied in animal models but poorly documented in children after visual pathway lesions. This report describes the visual recovery of a male child who had a bilateral occipital lobe infarction at the age of 2 years 6 months, 10 days after colon resection for Hirschsprung disease. In the acute phase he had severe visual impairment without visual response. Some weeks later he could perceive movement. Since then, progressive recovery of his visual acuity and oculomotor abilities has been accompanied by a progressive reduction of the visual field defect. At 6 years 8 months, visual recognition acuity was 10/10 in both eyes and neuro-ophthalmological examination was normal, except for persistence of the visual field defect in the upper hemifield and a selective impairment of higher visual functions (recognition of object presented in a hard-to-decode way [e.g. overlapping figures], or use of complex visuospatial skills). The functional recovery observed in this patient confirms the adaptive plasticity of developing visual systems after early brain lesions. It suggests that in humans, as in animal models, processes related to cerebral plasticity may take place years after a brain lesion has been sustained.

Pseudo-subarachnoid hemorrhage and cortical visual impairment as the presenting sign of gliomatosis cerebri

A 49-year-old white male presented with a pseudo-subarachnoid hemorrhage and diffuse brain edema. Neuroimaging showed brain edema causing the unusual findings of a pseudo-subarachnoid hemorrhage and bilateral occipital lobe infarcts following herniation and compression of the posterior cerebral arteries. An enlarged corpus callosum was noted which led to a brain biopsy and a diagnosis of gliomatosis cerebri.