Acute hyperglycaemia leads to altered frontal lobe brain activity and reduced working memory in type 2 diabetes

How acute hyperglycaemia affects memory functions and functional brain responses in individuals with and without type 2 diabetes is unclear. Our aim was to study the association between acute hyperglycaemia and working, semantic, and episodic memory in participants with type 2 diabetes compared to a sex- and age-matched control group. We also assessed the effect of hyperglycaemia on working memory–related brain activity. A total of 36 participants with type 2 diabetes and 34 controls (mean age, 66 years) underwent hyperglycaemic clamp or placebo clamp in a blinded and randomised order. Working, episodic, and semantic memory were tested. Overall, the control group had higher working memory (mean z-score 33.15 ± 0.45) than the group with type 2 diabetes (mean z-score 31.8 ± 0.44, p = 0.042) considering both the placebo and hyperglycaemic clamps. Acute hyperglycaemia did not influence episodic, semantic, or working memory performance in either group. Twenty-two of the participants (10 cases, 12 controls, mean age 69 years) were randomly invited to undergo the same clamp procedures to challenge working memory, using 1-, 2-, and 3-back, while monitoring brain activity by blood oxygen level–dependent functional magnetic resonance imaging (fMRI). The participants with type 2 diabetes had reduced working memory during the 1- and 2-back tests. fMRI during placebo clamp revealed increased BOLD signal in the left lateral frontal cortex and the anterior cingulate cortex as a function of working memory load in both groups (3>2>1). During hyperglycaemia, controls showed a similar load-dependent fMRI response, whereas the type 2 diabetes group showed decreased BOLD response from 2- to 3-back. These results suggest that impaired glucose metabolism in the brain affects working memory, possibly by reducing activity in important frontal brain areas in persons with type 2 diabetes.

DIABETIC STRIATOPATHY: A RARE PRESENTATION OF NONKETOTIC HYPERGLYCEMIA

Type II Diabetes Mellitus is one of the most common non-communicable diseases with innumerable & potentially life threatening complications. In 2017, approximately 462 million individuals were affected by type 2 diabetes corresponding to 6.28% of the world's population (4.4% of those aged 15-49 years, 15% of those aged 50-69, and 22% of those aged 70+), or a prevalence rate of 6059 cases per 100,000. Over 1 million deaths per year can be attributed to diabetes alone, making it the ninth leading cause of mortality. The burden of diabetes mellitus is rising globally, and at a much faster rate in developed regions, such as Western Europe. The gender distribution is equal, and the incidence peaks at around 55 years of age. Global prevalence of type 2 diabetes is projected to increase to 7079 individuals per 100,000 by 2030, reecting a continued rise across all regions of the world.[¹] . Two of the common complications due to acute hyperglycaemia are Diabetic Ketocidosis & Non ketotic hyperosmolar coma which are considered a spectrum of the same complication due to low circulating levels of insulin leading to impaired glucose metabolism by insulin dependant tissues with rising levels of anti-insulin hormones like glucagon, cortisol & catecholamines due to intracellular starvation resulting in hypergylcemia & fatty acid breakdown & ketonemia. Amongst the numerous complications of Type II Diabetes Mellitus, here we present a rare complication of acute hyperglycaemia and its radiological picture in the central nervous system. A 56 year old female patient with a history of Type II Diabetes Mellitus with Hypertension under long term medication came for a private consultation with a complaint of Right sided involuntary, random, irregular, inging and ailing, rapid, non-patterned movements for past 7 days. The patient was advised for an urgent MRI of Brain which demonstrated high T1 signal & low T2/FLAIR intensity with no diffusion restriction of DWI & ADC map in left sided putamen & head of caudate nucleus. We illustrated a rare classical nding of acute hyperglycemic effect on brain in a case of long standing Type II Diabetes Mellitus despite being on medications