Cerebral autoregulation is compromised in type 2 diabetic patients at an early stage of the disease

Background: In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation. Due to cardiac autonomic neuropathy, standard procedures often fail to quantify cerebral autoregulation in diabetic patients. We evaluated whether the technique of metronomic breathing at 0.1Hz might be suited to quantify cerebral autoregulation in diabetic patients.

Objective: To assess dynamic cerebral autoregulation in patients with type 2 diabetes.

Methods: In 10 patients with early-stage type 2 diabetes and 10 healthy volunteers, we continuously monitored cerebral blood flow velocity (CBFV) and mean arterial pressure (MAP) during 5 minutes metronomic deep breathing with 6 cycles per minute (0.1Hz). We assessed the response of cerebral blood flow velocity (CBFV) to oscillations in mean arterial pressure (MAP) induced by deep breathing. We determined spectral powers at 0.1Hz and calculated the transfer function gain and phase shift between 0.1Hz MAP and CBFV oscillations as parameters of cerebral autoregulation.

Results: 0.1Hz spectral powers of MAP were slightly lower in the patients than in the healthy volunteers (4.1±2.3 vs. 9.1±8.1mmHg2). 0.1Hz spectral powers of CBFV were similar in the patients and the healthy volunteers (4.3±4.8 vs. 6.1±5.2 cm2/s2). The MAP-CBFV gain was similar in both groups (0.9±0.5 vs. 0.9±0.3cm/s/mmHg), while the phase shift was significantly lower in the patients than the healthy volunteers (0.832±0.505 vs. 1.394±0.709rad).

Conclusion: The slightly decreased power of 0.1Hz blood pressure oscillations suggests mild autonomic neuropathy in the diabetic patients. Gain analysis did not show compromised cerebral autoregulation. The decreased phase shift in the patients, however, indicates a more passive transmission of blood pressure fluctuations onto the cerebrovascular circulation, i.e. altered cerebral autoregulation, in the patients and therefore identifies subtle impairment of cerebral regulation even at a mild stage of the disease.