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Cortical blindness is a type of cerebral blindness characterized as vision loss caused by injury to the visual pathway’s posterior to the lateral geniculate nuclei, with intact pupillary reflexes and without any other ocular impairments. In this report, we describe a 42-year-old female who presented with bilateral acute painless loss of eyesight following cardiac arrest, as well as bilateral plantar extensor weakness with varied weakening of both lower limbs. Recognising it may contribute to better management and outcomes. Education of health care personnel is critical because many scenarios are initially misdiagnosed as conversion disorder or malingering, postponing diagnosis while potentially harming the patient.
Cortical blindness (CB) is a type of cerebral blindness characterized as vision loss caused by injury to the visual pathways posterior to the lateral geniculate nuclei, with intact pupillary reflexes and without any other ocular impairments.1,2 In adulthood, it occurs in lesions of the primary visual cortex of the occipital lobes resulting from various conditions including cardiac embolism, stroke, head trauma, hyponatremia, extreme hypoglycemia, occipital lobe epilepsy, Creutzfeldt-Jacob disease, eclampsia, infection, cardiac surgery, and cerebral angiography. Transient CB can be induced by infectious endocarditis, hypertensive encephalopathy, or posterior reversible encephalopathy syndrome.3
Anton syndrome is an uncommon and peculiar type of blindness characterized by bilateral CB, visual anosognosia (disregard of loss of vision), and visual confabulation (the appearance of incidents and sensations that never occurred). CB occurs when the occipital lobe's visual cortex is damaged while the anterior visual pathways remain intact. The most prevalent cause of CB is an infarction.4 In this case report, we presented a female patient with bilateral acute painless loss of eyesight following cardiac arrest, as well as bilateral plantar extensor weakness with varied weakening of both lower limbs.
The 42-year-old woman reported bilateral vision loss for the past two weeks. The patient, who seemed stable three weeks ago, suffered abrupt onset dyspnea. She was promptly transported to a neighboring hospital. She was unconscious while on her way to the hospital. It lasted roughly ten minutes. When she arrived at the hospital, the caretakers were told that she was in cardiac arrest. However, three rounds of CPR resulted in the return of spontaneous circulation. She was admitted with the following diagnoses: ACS NSTEMI, hypertensive emergency, acute pulmonary edema, and s/p sudden cardiac arrest.
She was intubated and was on ventilator support for two days. She was moved to her room after being extubated. Two days later, the patient reported painless loss of vision in both eyes. An emergency MRI revealed no signs of parenchymal alterations; nonetheless, the left ICA was severely narrowed. Three days later, she was discharged. The patient stayed conscious throughout the days. She could swallow food. However, she needs assistance in getting food into her mouth. She was unable to walk on her own and began physiotherapy. The patient now had decreased urine production and pus in the catheter.
There was no history to indicate a Cranial nerve palsy. The patient had a history of diabetes mellitus, systemic hypertension, and dyslipidemia. The patient was conscious, medium built, and moderately nourished, with a BMI of 20.3 kg/m2. No icterus, cyanosis, clubbing, lymphadenopathy, or pedal edema. The patient was afebrile and had pallor. The pulse rate was 84 beats per minute, with regular rhythm, normal volume, and character. There was no thickening of the vessel wall or radioradial/radiofemoral delay. All peripheral pulses are perceived equally bilaterally. In the sitting position, the right arm and lower limb had blood pressures of 180/100 mmHg. The respiration rate was 16 per minute (thoracoabdominal). There are no neurocutaneous markers. There is no peripheral nerve thickening and no trophic ulcers. Superficial reflexes revealed a bilateral plantar extensor with varying weakening in both the lower and upper limbs.
The patient was taken to the Medicine department after initial investigations revealed anemia, elevated ESR, disordered RFT, and evidence of UTI, and was treated with antibiotics (Intravenous Ceftriaxone). The ECG indicated a normal sinus rhythm. The hemoglobin level was 8.4 g%. The total WBC was 11300 mm3. The ESR was increased to 106 mm/hour. The CRP level was 116 mg/dL. Platelet, RBS, sodium, and potassium levels were all within normal range. URE indicated no albumin or sugar, with many WBC and RBC (10-20), urea (164 mg/dl), and creatinine (5.1 mg/dl). The liver function tests were within the normal range. The USG revealed bilateral increased cortical echogenicity with stable CMD. The 2D Echo showed no RWMA and good biventricular systolic function. The MRI revealed cortical diffusion limitation and areas of aberrant blooming in bilateral parieto-occipital regions, raising the potential of hypoxic ischemic encephalopathy (HIE) with bilateral parieto-occipital cortical ischemia (Figure 1).
Figure 1: MRI findings of the reported case
The management of the patient generally involved addressing the underlying aetiology (cardiac arrest) while employing visual rehabilitation techniques, including "restitution treatment" aimed at recovering the impaired visual field, "compensation treatment" that utilises eye movements to acquire visual data from the blind region, and "substitution treatment" which incorporates devices involving prisms to transfer visual stimuli from the blind field to the seeing field.
CB is caused by reduced perfusion to the occipital (visual) cortex through the posterior cerebral artery, which is usually due to hypoperfusion or embolism. Epidemiological evidence is scarce, but evidence indicate that the incidence among individuals with stroke ranges between 20% and 57%.5 Anton syndrome is an extremely uncommon illness, with the most recent long-term epidemiology findings indicating only 28 published instances between 1965 and 2016.6 Hypoxic damage is an uncommon cause of CB.7 The prognosis for CB following a stroke appears to be bad, but with other causes such as infection and convulsions, significant recovery may be possible. CB prognosis varies according on age, medical history, origin, severity, length, and initial recovery rate. Visual function has recovered well in circumstances including hypertensive encephalopathy, heart surgery, cerebral angiography, and infective endocarditis. According to Aldrich et al.,8 younger patients over 40 years of age without any history of hypertension or diabetes, linguistic, cognitive, or memory impairment, and no CVA were shown to have a superior visual prognosis.
Visual disturbances can present in a variety of ways, including abrupt blindness, visual anosognosia, and perceptual problems. The right and left vertebral arteries combine to form the basilar artery, which gives rise to the posterior cerebral artery. The occipital lobes are supplied by the basilar artery's terminal branches. They are regarded as watershed zones, which makes them vulnerable to hypoxic effects from ischemia. When one side is afflicted, the patient appears with contralateral homonymous hemianopsia; nevertheless, if two sides are ischemic, the individuals may experience peripheral vision loss or become completely blind. A thorough assessment of heart, eyes, and nervous system are required.2 However, late-onset of symptom has been documented. Limaye et al. documented a case of CB that developed many days following an initial anoxic incident.7
Bilateral CB is typically caused by vascular insufficiency in the distal branches of the posterior cerebral artery. There are various ideas that explain the mechanism of visual anosognosia in persons with CB. The damaged visual areas are successfully isolated from functional portions. Because disconnected speech-language regions do not provide input, functioning speech areas provide confabulated responses. Another neuropsychological hypothesis suggests the elimination of sensory monitors, resulting in inaccurate visual interpretation. It has also been proposed that false feedback from another visual system may provide erroneous input. When there is no visual input, speech centres may be persuaded to produce a confabulated output by deceptive internal representations from the pulvinar, temporoparietal, and superior colliculus regions.9
While CB has a decent prognosis, optimum therapy is still uncertain. Corticosteroids, antiplatelets, and appropriate hydration have been proposed; however, recent literature has found little evidence for any specific treatment intervention other than vigilant monitoring, as the illness is typically reversible and disappears within a week. Since the disease is usually reversible and resolves away in a week, recent research has revealed little support for any particular treatment intervention other than careful monitoring. Visual training, rehabilitation, and restitution therapy, may aid in the recovery of visual field abnormalities.10 CT brain is useful when there are low attenuation areas in the occipital lobes or cerebral edema, which aids in the diagnosis of CB and the exclusion of bleeding or neoplastic causes. Some literature recommends MRI as the preferred diagnostic imaging technology. The advantages of MRI include improved identification of modest vasogenic edema and a thorough examination of the venous sinuses and anterior visual pathways. The function of EEG and VEP in assessing CB and its prognostic usefulness is still debated.8,11
CB is a common type of blindness caused by injury to the occipital cortex. Recognising it may contribute to better management and outcomes. Education of health care personnel is critical because many scenarios are initially misdiagnosed as conversion disorder or malingering, postponing diagnosis while potentially harming the patient.
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