Chronic hyperglycemia‐induced gaze‐evoked visual seizures

Focal seizures can arise from various neurological or metabolic conditions. Some patients with hyperglycemia-associated focal seizures exhibit reflex epilepsy, characterized by seizures induced by active or passive movement of a body part, typically an extremity.1 Typical Magnetic Resonance Imaging (MRI) findings in hyperglycemia-induced seizures include focal subcortical T2 hypointensity, gyral swelling, meningeal enhancement, and diffusion restriction, primarily in the posterior cerebral hemisphere.2 The nonketotic hyperglycemic hyperosmolar state (NKHH) is marked by severe hyperglycemia (>600 mg/dL) and hyperosmolarity (>330 mOsm/L).3 Nonketotic hyperglycemia (NKH) refers to conditions that do not fully meet NKHH criteria.3 In NKH, neurological symptoms, particularly seizures, may be the initial clinical signs.4 Reflex seizures linked to NKH, characterized by distinct clinical features, have been recognized as a specific neuroendocrine syndrome.1 Recent publications have documented cases where reflex visual focal seizures from the occipital lobe are associated with hyperglycemia and elevated HbA1C levels.3, 5-7 This report presents a case of focal visual reflex seizures triggered by gaze and chronic hyperglycemia, supported by clinical data, MRI, electroencephalography (EEG), laboratory findings, and video footage. A 66-year-old man, with no history of epilepsy, presented with seizure-like episodes in the last days. He reported seeing flashes of light and flickering colors only when gazing to the right, which subsided when focusing elsewhere, lasting only as long as he gazed right. During examination in the emergency room, he also experienced these visual symptoms triggered by right gaze (Video S1). His neurological examination was otherwise normal. He also experienced a clinical episode during the EEG recording, characterized by visual symptoms with the same semiology as previously mentioned. His EEG confirmed the seizure originating from the posterior regions of the left hemisphere (Figure 1). The patient's medical history included diabetes mellitus for 13 years, with no history of coma or ketoacidosis. Upon presentation, his blood sugar level was 180 mg/dL (N: 70–100 mg/dL) and HbA1c level was 11.6 mmol/mol (N: 3.5–5.6 mmol/mol). Other tests revealed no significant abnormalities, and ketones were absent in urine. Serum osmolarity was 288 mOsm/kg (N: 285–296 mOsm/kg). The patient had not been using oral antidiabetic medications and insulin regularly and had not been attending regular follow-ups. MRI of the brain showed T2-FLAIR cortical hyperintensity and subcortical hypointensities in the left parieto-occipital region (Figure 2). All these findings confirmed reflex visual focal seizures triggered by right gaze due to nonketotic hyperglycemia. The patient's increased blood glucose was regulated with insulin. His focal seizures did not disappear; therefore, intravenous 2000 mg of Levetiracetam (LEV) was given and followed by a maintenance dose of 1000 mg/day orally. His daily brief focal seizures persisted; LEV was increased to 2000 mg/day. At that time, EEG revealed reduced epileptiform activity, with no ictal findings. However, lacosamide (LCM) was added at 200 mg/day at the end of the first week of admission due to further seizures. After a week, the seizures were controlled, and the patient was discharged with antiseizure drugs. At the six-month follow-up, he has no reflex seizures, characterized by flashing lights seen when gazing to the right, and his EEG was normal. Seizures are common complications of hyperglycemia with or without NKHH.8 But reflex occipital visual seizures due to hyperglycemia are rarely reported.1, 3 The patient's complaint of flashing lights (reflex seizures) was not attributed to the current hyperglycemia but rather to the chronic nature of long-standing diabetes mellitus and poor management. GABA is an inhibitory neurotransmitter, and issues in its pathways in prolonged hyperglycemia may lower the seizure threshold, increasing susceptibility to seizures.4 Occipital lobe strokes can cause visual seizures, but the rapid resolution of lesions and subcortical T2 hypointensity suggests no infarct. Subcortical T2 hypointensity present in 94% of NKH patients may serve as a sensitive diagnostic marker.9 The exact cause of subcortical T2/FLAIR hypointensity is unclear, but it may be linked to excitotoxic damage.10 Treatment of hyperglycemia was essential to control the acute seizures in most of the cases.3 But in our patient, we had to use antiseizure drugs due to intractable focal seizures from hyperglycemia treatment. We suggest that prolonged exposure to uncontrolled hyperglycemia, as indicated by HbA1C, rather than an acute NKHH or NKH state, is an important finding to consider early treatment with antiseizure drugs. The authors thank the patient who took part in the study. There was no financial support for this case report. No conflict of interest was declared by the authors. Consent obtained from the patient. The data that support the findings of this study are available from the corresponding author upon reasonable request. Video S1. Data S1. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.