Symmetry of cerebral blood flow and cognitive responses to hypoglycaemia in humans

• Published in: Diabetologia 1993, Vol.36 (1), p.73-78
• Main Authors: KERR, D, STANLEY, J. C, BARRON, M, THOMAS, R, LEATHERDALE, B. A, PICKARD, J
• Format: Article
• Language: English
• Subjects: Adult; Analysis of Variance; Anatomical correlates of behavior; Behavioral psychophysiology; Biological and medical sciences; Blood Flow Velocity; Blood Pressure; Brain - blood supply; Cardiac Output; Catecholamines - blood; Cerebral Arteries - physiology; Cerebral Arteries - physiopathology; Cognition; Dominance, Cerebral; Fundamental and applied biological sciences. Psychology; Glucose Clamp Technique; Humans; Hypoglycemia - physiopathology; Hypoglycemia - psychology; Insulin - pharmacology; Male; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Regional Blood Flow
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/BF00399097

A low blood glucose level is associated with impairment of higher cerebral function and an increase in cerebral blood flow. This study examined whether there are differences in the physiological responses to hypoglycaemia between the cerebral hemispheres. Eight healthy men participated in two hyperinsulinaemic glucose clamp studies: after 60 min at 4.5 mmol/l, blood glucose was either lowered to 2.0 mmol/l and "clamped" there for 60 min (hypoglycaemia) or continuously maintained at 4.5 mmol/l (euglycaemia). Cardiac output, middle cerebral artery velocity (transcranial Doppler) and cerebral blood flow (133-xenon inhalation) were measured during the studies. Neuropsychological tests were used to determine whether hypoglycaemia caused differential impairment of hemispheric cognitive function. Hypoglycaemia was associated with symmetrical impairment of cognitive function in both cerebral hemispheres and a rise in cardiac output (from 5.5 [0.2] to 8.7 [0.2] l.min-1, p < 0.0001, mean [standard error]), middle cerebral artery velocity (from 55 [2.6] to 64 [2.8] cm.s-1, p < 0.002), and global cerebral blood flow (from 56 [2.6] to 69 [2.9] ml.100 g-1.min-1, p < 0.005 compared to pre-insulin values). There were no differences in the blood flow response during hypoglycaemia between hemispheres and the increase in blood flow did not correlate with either the change in cardiac output or rise in plasma catecholamine levels. After 120 min of hyperinsulinaemic, euglycaemia, global cerebral blood flow rose significantly above baseline (from 58 [2.4] to 63 [2.2] ml.100 g-1.min-1, p < 0.05). In conclusion, using the techniques described, the physiological and cognitive responses of each cerebral hemisphere to hypoglycaemia were symmetrical.