Arterial spin labeling hyperperfusion in seizures associated with non-ketotic hyperglycaemia: is it merely a post-ictal
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Arterial spin labeling hyperperfusion in seizures associated with non-ketotic hyperglycaemia: is it merely a post-ictal phenomenon? Sabarish Sekar 1
&
Selvadasan Vinayagamani 1 & Bejoy Thomas 1 & Chandrasekharan Kesavadas 1
Received: 22 May 2020 / Accepted: 8 October 2020 # Fondazione Società Italiana di Neurologia 2020
Abstract A 53-year-old chronic uncontrolled diabetic patient presented with one episode of generalized seizures followed by drowsiness and post-ictal confusion. MR imaging at admission revealed left temporal subcortical T2/FLAIR hypointensities with overlying cortical T2/FLAIR hyperintensities and increased perfusion on arterial spin labeling (ASL). Follow-up imaging at 4- and 8-week interval revealed persistent ASL hyperperfusion with significant resolution of conventional MR imaging findings. Delayed persistent ASL hyperperfusion suggests that hyperglycemia-induced increased blood-brain barrier permeability rather than a mere post-ictal phenomenon in non-ketotic hyperglycemia (NKH) and may result in long-term cognitive disturbances. Keywords Arterial spin labeling . Hyperperfusion . Non-ketotic hyperglycemia . Blood-brain barrier
Background
Clinical presentation
Non-ketotic hyperglycemia (NKH) is the most common complication of type 2 DM with age more than 50 years, characterized by a triad of severe hyperglycemia, hyperosmolarity, and intracellular dehydration without ketoacidosis [1, 2]. Neurological manifestations in NKH are diverse, which include hyperglycemic hyperosmolar nonketotic coma (HONK), focal seizures, hyperkinetic movement disorderhemiballismus hemichorea syndrome, and hemianopsia [3]. About 15–40% of patients with NKH can present with seizures [2]. Reversible subcortical hypointensity on T2 and fluid-attenuated inversion recovery (FLAIR) images are more frequently reported imaging findings in seizures associated with NKH [2, 4]. This report focuses on hitherto unreported ASL findings in seizures associated with NKH and also provides possible pathogenesis for persistent ASL findings.
A 53-year-old chronic uncontrolled diabetic patient on oral hypoglycaemic agents presented with a history of vomiting and reduced appetite for 3 days. He developed one episode of generalized seizures followed by drowsiness and irrelevant talk. He had post-ictal confusion and no history of fever. Clinical examination was within normal limits. No focal neurological deficit. Serum glucose at the time of admission was 600 mg/dl, without ketonuria and serum acidosis. HbA1c was 11.8%, and serum osmolality was 301 mOsm/l. The serum creatinine was 1.6 mg/dl. The rest of the biochemical investigations were unremarkable. In view of clinical and biochemical findings, seizures associated with non-ketotic hyperglycemia kept as the first possibility. Other differentials like vascular and autoimmune/paraneoplastic lesions were worked up and turned out to be negative. Electro-encephalography (EEG) on day 1 showed frequent left frontotemporal epileptic discharges. Intensive insulin therapy i
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