Event
related P300 potential in NIDDM patients without cognitive
impairment and its relationship with previous hypoglycemic
episodes
Miguel
N. Hissa, José Artur C. D'Almeida, Fernanda Cremasco & Veralice
M. S. de Bruin
Department of Clinical Medicine, Federal University of Ceará,
Fortaleza, BRASIL
Keywords:
P300, diabetes, NIDDM, retinopathy, hypoglycemia, nervous
system
Abstract
OBJECTIVES:
The purpose of this study was to evaluate the ERP P300 in
non insulin dependent diabetes mellitus (NIDDM) patients without
cognitive impairment and the relationship with clinical variables,
the presence of retinopathy and previous hypoglycemic episodes.
METHODS:
NIDDM patients (N=44) without evidence of cognitive impairment
and controls (N=17) were studied clinically and with ancillary
exams and the ERPs P300 were recorded. Patients were examined
clinically and with the Folstein Mini-Mental Examination (MMSE)
for cognitive function and all patients showed a score higher
than 26 (maximal value=30). Previous hypoglycemia was evaluated
through a questionnaire establishing the number of episodes
and the symptoms of hypoglycemia in a scale scoring from zero
to 15.
RESULTS:
ERP P300 latencies were significantly higher in NIDDM patients
than in controls (p<0.03). ERP P300 measures were significantly
related to age (Pearson, p<0.01) and not to metabolic variables,
disease duration or the presence of retinopathy. Severity
of hypoglycemia was not associated to ERP P300 latency.
CONCLUSIONS:
Our study supports the evidence that NIDDM patients, without
signs of nervous system involvement, have ERP P300 alterations
and this is not related to retinopathy, metabolic variables
or previous hypoglycemic episodes. Chronic hyperglycemia may
alter brain glucose transport and increase tolerance to hypoglycemia
effects in the nervous system.
Introduction
The
chronic course of diabetes is frequently associated to severe
nervous system (NS) complications such as brain hemorrhages,
ischemia associated to vascular pathology, peripheral and autonomic
neuropathy [1,2,3]. More subtle changes in the central NS can
frequently move forward without perception [4]. Chronic hypertension,
high cholesterol level, cardiac dysfunction and toxic effects
of hyperglycemia are some factors contributing to central NS
alterations [5,6,7]. Other factors as disease duration, age,
exercise and co-morbid conditions may influence cerebral complications
and cognitive function [8,9,10].
The optimum control of diabetes has been recommended in an attempt
to prevent or delay microvascular and neuropathic complications
[11]. Hyperglycemia has been associated to increased cerebral
damage in stroke [12] and on the other extreme, it is well established
that states of hypoglycemia can induce severe brain damage [13,14,15].
Adding further controversy to the subject, evidences indicate
that chronic hyperglycemia can alter brain glucose transport
and tolerance to hypoglycemia [16,17,18]. Previously, studies
indicate that episodes of hypoglycemic coma have not always
been associated to permanent impairment of cognitive function
in IDDM patients [19,20,21]. Cognitive function can be slowly
and unrecognizably impaired in assymptomatic adults and recently,
with increasing more strict controls of glucose levels, it is
important to understand if deterioration of cortical function
will prevail over time.
Event-related potential (ERP) P300 auditory evoked potential
measure reflects the speed of neural events related to attention
and short term memory [22,23,24]. Increase in ERP P300 latency
has been associated to abnormalities in psychometric tests in
diabetic patients [23,24]. Recognizing assymptomatic cerebral
dysfunction and the modifiable risk factors influencing cognitive
changes can put forward preventive treatment in diabetes. To
verify undetected NS involvement in diabetic patients, we studied
the measure of ERP P300 latency and its relationship to clinical
and metabolic variables.
Material and methods
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