Key result
Proliferative diabetic retinopathy in type 1 diabetes was associated with less deactivation in the anterior cingulate and orbital frontal gyrus during hypoglycemia compared with euglycemia (P<0.05).
Why the study?
The mechanisms underlying cognitive deterioration in type 1 diabetes, potentially related to microvascular brain changes, are poorly understood.
Does the presence of proliferative diabetic retinopathy alter brain activation during standardized hypoglycemia in patients with type 1 diabetes?
Observational (n=24)
Does the presence of proliferative diabetic retinopathy alter brain activation during standardized hypoglycemia in patients with type 1 diabetes?
p-value: p=<0.05
Microvascular disease in type 1 diabetes, marked by retinopathy, alters brain activation patterns during hypoglycemia, likely as a compensatory mechanism for functional loss.
Retinopathy-associated microvascular changes may alter hypoglycemia brain responses in type 1 diabetes without performance impact; leaves open causal role in cognitive decline.
Individuals with type 1 diabetes have mild performance deficits on a range of neuropsychological tests compared with nondiabetic control subjects. The mechanisms underlying this cognitive deterioration are still poorly understood, but chronic hyperglycemia is now emerging as a potential determinant, possibly through microvascular changes in the brain. In 24 type 1 diabetic patients, we tested at euglycemia and at acute hypoglycemia whether the presence of proliferative diabetic retinopathy, as a marker of microvascular disease, adversely affects the ability of the brain to respond to standardized hypoglycemia, using functional magnetic resonance imaging with a cognitive task. Patients with retinopathy, compared with patients without, showed less deactivation (hence, an increased response) in the anterior cingulate and the orbital frontal gyrus during hypoglycemia compared with euglycemia (P < 0.05). Task performance and reaction time were not significantly different for either group. We conclude that microvascular damage in the brain of patients with retinopathy caused this increased brain response to compensate for functional loss.
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Wessels et al. (2006) conducted an observational in Type 1 diabetes (n=24). Proliferative diabetic retinopathy vs. Patients without retinopathy was evaluated on Brain response (deactivation) in the anterior cingulate and orbital frontal gyrus during hypoglycemia compared with euglycemia (p=<0.05). Proliferative diabetic retinopathy in type 1 diabetes was associated with less deactivation in the anterior cingulate and orbital frontal gyrus during hypoglycemia compared with euglycemia (P<0.05).
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