Brain activation was increased and deactivation was decreased in type 1 diabetic versus control subjects during hypoglycemia.…
The study was done to investigate the effects of acute hypoglycemia on working memory and brain function in patients with type 1 diabetes.
Using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging during euglycemic (5.0 mmol/L) and hypoglycemic (2.8 mmol/L) hyperinsulinemic clamps, researchers compared brain activation response to a working-memory task (WMT) in type 1 diabetic subjects (n = 16) with that in age-matched nondiabetic control subjects (n = 16). Behavioral performance was assessed by percent correct responses.
The results showed that during euglycemia, the WMT activated the bilateral frontal and parietal cortices, insula, thalamus, and cerebellum in both groups. During hypoglycemia, activation decreased in both groups but remained 80% larger in type 1 diabetic versus control subjects (P < 0.05). In type 1 diabetic subjects, higher HbA1c was associated with lower activation in the right parahippocampal gyrus and amygdale. Deactivation of the default-mode network (DMN) also was seen in both groups during euglycemia. However, during hypoglycemia, type 1 diabetic patients deactivated the DMN 70% less than control subjects (P < 0.05). Behavioral performance did not differ between glycemic conditions or groups.
From the results it was concluded that, BOLD activation was increased and deactivation was decreased in type 1 diabetic versus control subjects during hypoglycemia. This higher level of brain activation required by type 1 diabetic subjects to attain the same level of cognitive performance as control subjects suggests reduced cerebral efficiency in type 1 diabetes.
In summary, patients with type 1 diabetes activate more brain regions than control subjects during hypoglycemia by maintaining activity from euglycemia to hypoglycemia in task-relevant regions and by failing to suppress activation in the DMN. This suggests that type 1 diabetic patients may need to recruit more brain resources to preserve cognitive performance. The pattern of hyperactivation of both the DMN and task-relevant regions is consistent with findings in disease states with impaired cognition, such as mild cognitive impairment and Alzheimer’s disease. There has been persistent concern about the consequences of recurrent hypoglycemia on brain structure and cognitive function. There are minimal long-term effects of recurrent hypoglycemia on cognition into middle age, but it is not clear whether this resiliency will last throughout the aging process. Future research should evaluate our findings as an early manifestation and warning of future clinically relevant cognitive decline.
This research may guide the development of treatment regimens to enhance symptom recognition or to stabilize the neurochemical response to hypoglycemia to reduce the impact of glucodeprivation on cognitive function.