Late onset reversible cortical blindness following electrocution

Visual stimulation rehabilitation for cortical blindness after vertebral artery interventional surgery: A case report and literature review

“…We searched the PubMed database for clinical studies conducted in patients with complete cortical blindness due to various causes over the past 10 years and summarized in Table 1 . We focused on the type of neurophysiological examination performed, treatment modality, and outcomes [ 7 , 8 , 15 , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] ]. The search strategy was “Blindness, cortical/rehabilitation”[Mesh] OR “Blindness, Cortical/therapy”[Mesh].…”

“…Physical therapists should consider the use of medications such as valproic acid, carbamazepine, and antipsychotics to improve recovery engagement. Furthermore, in terms of medicine for cortical blindness, injection of the local anesthetic mepivacaine [ 32 ] and treatment with cortisol [ 33 , 36 ] and plasma exchange [ 31 ] have been shown in case studies to bring about visual recovery. However, due to the variable pathogenic factors of cortical blindness, the effectiveness of such drugs needs to be verified in large clinical samples and multi-etiological populations.…”

Delayed-onset Reversible Cortical Blindness after Resuscitation from Cardiac Arrest

“…Based on extrapolations from similar cases, in which CB or other neurological symptoms occurred a few days after diverse brain insults, it may be linked to delayed and cumulative oxidative stress, delayed effects of anoxia, or cortical laminar necrosis affecting layers 3 and 4 of the striate cortex. [ 1 5 6 ] Other aspects of pathogenesis such as variability in delay of onset, involvement of isolated areas of the neuraxis in an individual, severity of symptoms, and underlying pathological variations still remain unexplained.…”

Electrifying Consequences: Posterior Reversible Encephalopathy Syndrome After an Electric Shock Injury

“…These symptoms may develop due to infarction, ischemia, edema, or demyelination. Various anatomical substrates are involved in the neurological manifestations that occur after electrical injury and temporal variability exists concerning electrocution [ 1 ].…”

“…Preeclampsia, eclampsia, the administration of cyclosporine post-organ transplantation, or severe hypertension were the primary settings in which PRES was first reported. However, it can also occur in a wide range of other clinical conditions, including sepsis, infections, shock, chemotherapy, autoimmune illnesses, and hypercalcemia [ 1 ]. While PRES has a typical neuroradiological pattern of brain lesion distribution, MRI reveals a symmetrical zone of vasogenic edema of the white matter, largely localized in the areas of posterior circulation [ 3 ].…”