title: Previous episodes of hypoglycemic coma are not associated with permanent cognitive brain dysfunction in IDDM patients on intensive insulin treatment.
abstract: Intensive insulin treatment of IDDM is associated with increased frequency of hypoglycemic coma. The extent of possible cerebral sequelae after recovery is still unknown. We studied the impact of previous hypoglycemic coma on neurophysiological measures of cognitive brain function in 108 patients with adult-onset IDDM receiving intensive insulin treatment. In the study, 55 IDDM patients (age 38 +/- 14 years, mean +/- SD) who had a history of > or =1 (median 3, range 1-35) comatose hypoglycemic event were compared with 53 IDDM patients (age 34 +/- 12 years) with no history of hypoglycemic events using P300 event-related potentials and psychometric tests (the Mini-Mental State Exam and trailmaking test, part A). Findings on these patients were compared with those from 108 matched healthy control subjects. No difference was observed in P300 latencies and psychometric tests between patients with and without a history of hypoglycemic coma (P300 latency, 346 vs. 342 ms; trailmaking test, 31 vs. 30 s; Mini-Mental State Exam, 29.5 vs. 29.6; NS). In diabetic patients, however, P300 latencies were delayed compared with those of healthy control subjects (344 vs. 332 ms; P < 0.001) and were correlated to diabetes duration but not to total hypoglycemic episodes. Scores on the Mini-Mental State Exam (29.5 vs. 29.6; P = 0.59) and trailmaking test (31 vs. 28 s; P = 0.10) were not different between patients and control subjects. In conclusion, previous episodes of hypoglycemic coma are not associated with permanent impairment of cognitive brain function in patients with adult-onset IDDM receiving intensive insulin treatment compared with patients without such episodes. Cognitive brain function, however, is subclinically impaired in relation to duration of diabetes.
authors.affiliation: Department of Medicine, University of Vienna, Austria. ludwig.kramer@akh-wien.ac.at
authors.forename: L
authors.initials: L
authors.lastname: Kramer
authors.forename: P
authors.initials: P
authors.lastname: Fasching
authors.forename: C
authors.initials: C
authors.lastname: Madl
authors.forename: B
authors.initials: B
authors.lastname: Schneider
authors.forename: P
authors.initials: P
authors.lastname: Damjancic
authors.forename: W
authors.initials: W
authors.lastname: Waldhäusl
authors.forename: K
authors.initials: K
authors.lastname: Irsigler
authors.forename: G
authors.initials: G
authors.lastname: Grimm
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000097:blood; D001921:Brain / Q000187:drug effects* / Q000503:physiopathology; D003072:Cognition Disorders / Q000139:chemically induced* / Q000503:physiopathology; D003430:Cross-Sectional Studies; D003627:Data Interpretation, Statistical; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy*; D003929:Diabetic Neuropathies / Q000097:blood; D003930:Diabetic Retinopathy / Q000097:blood; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia / Q000097:blood / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D007328:Insulin / Q000009:adverse effects / Q000627:therapeutic use*; D007331:Insulin Coma / Q000097:blood / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011594:Psychometrics
chemical_list: D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin