Recovery from cortical blindness with mepivacaïne.

We report the case of a patient suffering from cortical blindness following bilateral occipital stroke, who recovered normal vision in his right visual field following injection of the local anesthetic mepivacaïne. The effect was transient but reproducible, allowing the patient to lead a normal life. Effect duration increased after adjunction of paroxetine. We provide anatomical and functional brain imaging correlates of this improvement, showing particularly how functional connectivity is restored between intact perilesional cortex and distant brain regions. This serendipitous finding may potentially benefit patients suffering from visual but also nonvisual handicap following brain lesions.

Bioccipital Lobe Hypoperfusion and Anton's Syndrome Resolution with Intravenous Thrombolysis.

BACKGROUND: Anton's syndrome is a rare neurological disorder characterized by a combination of visual anosognosia and confabulation of visual experience, most often seen after bilateral ischemic damage to the posterior occipital cortex. CASE REPORT: We report the first case of an acute synchronous P2 occlusion as confirmed by multiparametric computed tomography (CT) including perfusion. After the administration of Recombinant tissue plasminogen activator (rtPA), Anton's syndrome completely resolved. CONCLUSION: Multiparametric CT imaging may aid in quickly proving the underlying stroke in Anton's syndrome, especially helpful considering the discrepancy between the patient's perception and clinical examination results.

Transient Cortical Blindness Associated with Endovascular Procedures for Intracranial Aneurysms.

BACKGROUND: We presented 3 cases of transient cortical blindness secondary to contrast medium toxicity after endovascular procedures for intracranial aneurysms. We also reviewed the literature and found 12 cases of contrast-induced cortical blindness after endovascular procedures for intracranial aneurysms. CASE DESCRIPTION: Two patients (cases 1 and 2) noted bilateral blindness 5 and 6 hours, respectively, after awakening from general anesthesia following aneurysm treatment. The third patient (case 3) noted bilateral blindness during vertebral angiography under local anesthesia. Immediate angiography was performed in case 1 and showed no arterial occlusion. Computed tomography was performed in case 2 and showed brain edema. Magnetic resonance imaging was performed in all 3 cases, and cases 2 and 3 showed abnormal presentation on fluid attenuated inversion recovery sequences. With the use of corticosteroid and intravenous hydration, cortical blindness resolved within 1 week in 2 patients (Cases 1 and 2). The remaining patient (case 3) had incomplete quadrantanopia 3 months after blindness onset. CONCLUSIONS: Based on our experience and the literature reports, we advocate corticosteroid and intravenous hydration for patients with contrast-induced cortical blindness after endovascular procedures for intracranial aneurysms.

Bilateral visual loss and cerebral infarction after spleen embolization in a trauma patient with idiopathic thrombocytopenic purpura: A case report.

RATIONALE: Splenic artery embolization (SAE) is a common procedure in trauma patients with blunt splenic injuries. We report a case of acute ischemic stroke following orthopedic surgery in a patient with post-SAE reactive thrombocytosis. PATIENT CONCERNS: A 37-year-old woman with idiopathic thrombocytopenic purpura (ITP) suffered from multiple trauma scheduled for open reduction and internal fixation for right tibial and left radius fracture five days after SAE. The patient did not have any thromboembolic complications, although the platelet counts increased from 43 × 10/L to 568 × 10/L within two days after SAE. Surgery was completed under general anesthesia with tracheal intubation without complications. The patient complained of visual loss followed by limb weakness on the fourth and eighth hour postoperatively. DIAGNOSES: Magnetic resonance imaging (MRI) of head demonstrated ischemic change over bilateral basal ganglia, and occipital areas, suggesting the diagnosis of cortical blindness. INTERVENTIONS: To suppress platelet count and avoid platelet hyper-aggregation, anti-platelet drug (i.e., oral aspirin 100 mg daily), hydration, and hydroxyurea (i.e., 20 mg/kg daily) were used for the treatment of reactive thrombocytosis. OUTCOMES: Although right-sided hemiparesis persisted, the patient reported mild visual recovery. She was discharged four months after SAE with active rehabilitation. LESSONS: Our report highlights an increased risk of acute arterial thromboembolic events in patients with reactive thrombocytosis, especially those undergoing surgery.

Late onset reversible cortical blindness following electrocution.

An elderly gentleman presented with acute onset of bilateral visual blurring and generalized headache after 1 week post electrocution injury. Clinically, the symptoms were attributed to cortical lesion. Magnetic resonance imaging (MRI) of brain revealed bilaterally symmetrical diffusion restriction in parietal and occipital areas. Treatment with intravenous steroids resulted in remarkable improvement in symptoms. Neurological injury secondary to electrocution is a well described entity having a variety of clinical presentation. We put forward our experience with this unique case presenting as post electrocution delayed onset of visual symptoms. Discussion and review of literature related to this clinical entity will also be presented.

Importance of diazepam administration during electroencephalography in the differential diagnosis of cortical visual loss.

A 14-year-old boy presented with acute visual loss due to cortical blindness. Two weeks after the visual symptoms, the patient developed behavioral abnormalities. Brain magnetic resonance imaging (MRI) revealed hyperintense lesions at parieto-occipital lobes on T2-weighted and fluid attenuated inversion recovery images. Sleep and awake electroencephalography (EEG) were normal, but diazepam administration revealed bilateral periodic synchronous complexes occurring every 20 to 30 seconds. Elevated measles antibody titers in cerebrospinal fluid confirmed the diagnosis of subacute sclerosing panencephalitis. We conclude that visual loss due to cortical blindness is an important finding of subacute sclerosing panencephalitis. Diazepam administration during EEG should be a part of investigation in cases with unexplained cortical blindness.

Acute cortical blindness in preeclampsia--a case of reversible posterior encephalopathy syndrome.

BACKGROUND: Cortical blindness is one the most disturbing symptoms of reversible posterior encephalopathy syndrome in preeclamptic and eclamptic patients. The disease has been previously associated with a hypertensive breakthrough in the autoregulation of posterior cerebral arterioles followed by extravasation of the fluid into the brain tissue. CASE: 22-year-old primigravida in the 39th week of gestation diagnosed with gestational diabetes mellitus presented with mild preeclampsia and was admitted to our hospital. Antihypertensive treatment was initiated. Her blood pressure remained between 120/80 to 140/90 mm Hg. Glucose levels were within acceptable range. Before the labor induction she developed acute cortical blindness. Magnetic resonance imaging showed vasogenic edema localized in occipital lobes. Cesarean section was performed and anti-edematous treatment initiated. Blindness resolved by the fifth day postpartum. CONCLUSIONS: Reversible posterior encephalopathy developed in our patient in spite of normalized blood pressure that remained within autoregulation limits. Alternative pathogenesis and precipitating factors are discussed.

Cortical blindness and posterior reversible encephalopathy syndrome in an older patient.

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological entity. It associates, to varying extents, neurological symptoms such as headaches, confusion, seizures and visual alterations from haemianopsia to cortical blindness. The diagnosis relies on brain MRI, showing signs of subcortical and cortical oedema in the posterior regions of the brain, with hypersignals in T2/fluid attenuated inversion recovery (FLAIR) or diffusion sequences. With early diagnosis and control of the causal factors, the symptoms and radiological signs can be - as the name implies - totally regressive. PRES can be caused by various heterogeneous factors, such as hypertension, side effect of drug therapies, eclampsia, sepsis or autoimmune diseases. The authors report here the case of an 86-year-old woman, presenting totally regressive cortical blindness and seizures, with compatible imaging.

Cerebral venous thrombosis presenting with cerebellar ataxia and cortical blindness.

Venous infarction in the cerebellum has been reported only rarely, probably because of the abundant venous collateral drainage in this region. Bilateral occipital infarction is a rare cause of visual loss in cerebral venous thrombosis. We describe a 50-year-old woman with a history of ulcerative colitis who developed acute cerebellar ataxia and cortical blindness. She had bilateral cerebellar and occipital lesions related to sigmoid venous thrombosis and achieved complete recovery with anticoagulation therapy. Cerebral venous thrombosis should be considered in cases of simultaneous cerebellar and occipital vascular lesions.

Cysticercal encephalitis with cortical blindness.

The authors report a 6-year-old boy, who had presented with low-grade fever, altered sensorium, headache and seizure for 5 days. On examination, he had features of raised intracranial pressure with left VI cranial-nerve palsy and bilateral extensor plantar response. CT scan showed multiple calcifications in cerebral cortex. MRI cranium showed multiple cysts involving whole of the brain. He was diagnosed as having cysticercal encephalitis, based on immunological and imaging study. He was managed with 20% mannitol, phenytoin and albendazole, and regained consciousness 7 days later, but had residual neurological deficit as left-lower-limb monoparesis and visual acuity of just projection of rays (PR+) and perception of light (PL+).

Reversible cortical blindness: posterior reversible encephalopathy syndrome.

Cortical blindness is defined as visual failure with preserved pupillary reflexes in structurally intact eyes due to bilateral lesions affecting occipital cortex. Bilateral oedema and infarction of the posterior and middle cerebral arterial territory, trauma, glioma and meningioma of the occipital cortex are the main causes of cortical blindness. Posterior reversible encephalopathy syndrome (PRES) refers to the reversible subtype of cortical blindness and is usually associated with hypertension, diabetes, immunosuppression, puerperium with or without eclampsia. Here, 3 cases of PRES with complete or partial visual recovery following treatment in 6-month follow-up are reported.

Postpartum cortical blindness.

A 30-years-old third gravida with previous normal pregnancies and an unremarkable prenatal course had an emergency lower segment caesarean section at a periphery hospital for failure of labour to progress. She developed bilateral cortical blindness immediately after recovery from anesthesia due to cerebral angiopathy shown by CT and MR scan as cortical infarct cerebral angiopathy, which is a rare complication of a normal pregnancy.

[An old woman with sudden pareses and blindness]. / En eldre kvinne med akutte pareser og synstap.

We present a patient with Posterior Reversible Encephalopathy Syndrome (PRES). A 74-year-old woman was admitted with sepsis, which originated from erysipelas on her neck the following day. She developed respiratory obstruction due to oedema, septic shock, disseminated intravascular coagulation (DIC), acute renal failure and atrial fibrillation. She responded well to treatment and improved rapidly, despite of her serious condition. When she had almost fully recovered after 15 days, her general condition worsened, and she developed confusion, blindness and pareses. MRI showed vasogenic oedema in the parietooccipital regions of the brain and in the cerebellum, consistent with PRES. PRES is a clinical and radiological diagnosis consisting of headache, confusion, cortical blindness, convulsions and sometimes pareses. MRI of the cerebrum with diffusion-weighted imaging (DWI) and Apparent Diffusion Coefficient (ADC) map are decisive to the diagnosis, and usually shows a characteristic bilateral vasogenic oedema in the parietooccipital region. This can distinguish PRES from brain infarction, which shows a cytotoxic oedema on MRI. We discuss our patient in the light of different conditions leading to PRES, possible pathophysiological factors and treatment options.

Clinical, electrophysiological and brain imaging features during recurrent ictal cortical blindness associated with chronic liver failure.

Transient neuroimaging features indicating primary cortical and secondary subcortical white matter cytotoxic oedema have been described in association with prolonged or intense seizures. We describe the unusual condition of recurrent ictal cortical blindness due to focal occipital status epilepticus, in the context of chronic hepatic failure. There was a close association between the onset and disappearance of clinical, electrophysiological and magnetic resonance imaging abnormalities.

Cortical blindness: clinical and radiologic findings in reversible posterior leukoencephalopathy syndrome: case report and review of the literature.

PURPOSE: To alert ophthalmologists to the recognition of cortical visual loss as the presenting feature in patients with reversible posterior leukoencephalopathy syndrome (RPLES). Unique radiologic findings are paramount to the diagnosis. DESIGN: Interventional case report. METHODS: A patient was seen with perioperative bilateral cerebral visual loss that was misinterpreted initially as an irreversible ischemic event. Further detailed analysis of the radiologic findings and clinical history led to the correct diagnosis. MAIN OUTCOME MEASURES: Visual acuity and magnetic resonance imaging (MRI) of the brain. RESULTS: Recognition of the correct diagnosis of RPLES led to the institution of antihypertensive therapy and recovery of normal vision. CONCLUSIONS: The diagnosis of RPLES should be considered in all patients with acute cerebral visual loss, especially in the setting of recent surgery, blood transfusion, chemotherapy, immunosuppressant use, hypertension, eclampsia, or seizures. Prompt diagnosis requires close collaboration with a radiologist and an emergent MRI study, which ideally should include diffusion-weighted imaging with calculation of an apparent diffusion coefficient map. Differentiation from acute cerebral ischemia is important in order to avoid permanent visual loss by prompt and vigorous treatment of exacerbating factors such as intermittent hypertension. Prompt diagnosis will also help to avoid potentially dangerous invasive procedures such as thrombolytic therapy.

Migraine, cortical blindness, multiple cerebral infarctions and hypocoagulopathy in celiac disease.

We describe the case of a female patient affected by migraine and untreated adult celiac disease who presented with a state of acute migraine accompanied by multiple neurological deficits, including transient cortical blindness with ischemic CT and MRI alterations, and hypocoagulation due to factor VII deficiency. She was receiving estroprogestin therapy. There was a prompt response to cortisone therapy followed by a state of complete well-being, which also led to the disappearance of migraine attacks after five years of dietary treatment alone.

Favorable outcome of epileptic blindness in children.

Acute blindness is a rare presentation of epileptic seizures, referring to loss of sight without loss of consciousness associated with electroencephalographic (EEG) epileptic discharges, mainly representing an ictal phase but also either pre- or postictal. We report a series of 14 children with documented epileptic blindness, describing the accompanying fits and thereafter the response to therapy to resolve the blindness and control associated seizures. All patients experienced episodes of acute complete visual obscuration lasting for 1 to 10 minutes. Seven patients hadaccompanying generalized seizures, with a photosensitive response recorded in three of them. All of these seven children were treated with valproic acid, regaining full vision, and six of them became seizure free. Three patients with acute blindness who had accompanying focal motor seizures and unilateral temporooccipital posterior epileptic discharges were treated with carbamazepine regained full vision and complete seizure control. Four additional children had the constellation of migrainous headaches, focal motor phenomena, and complete blindness, along with occipital discharges compatible with Gastaut syndrome, benign childhood epilepsy with occipital paroxysms. All four patients were started on carbamazepine and became asymptomatic. Our overall experience suggests that epileptic blindness in children is associated with a favorable outcome when promptly diagnosed and treated appropriately, resulting in complete resolution of blindness in all children and satisfactory control of seizures in most of them. We therefore recommend performing a prompt EEG in any child presenting with acute visual obscuration, even in the absence of other epileptic phenomena.