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July2007 Vol.44 Issue:        2        Table of Contents
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Clinically Unapparent Central Nervous System Impairment in Diabetic Patients

Lobna M El-Nabil1, Inas Sabry2

Departments of Neuropsychiatry1, Internal Medicine2, Ain Shams University


Background: Diabetes mellitus is the result of absolute or relative hypoinsulinemia, and is currently described as an endocrine disease that causes damage to many organs and systems. The consequences of chronic diabetes mellitus in the central nervous system (CNS) are less known than diabetic peripheral neuropathy and autonomic nervous system neuropathy. Damage to the brain and the spinal cord is less common. The aim of this study is to show the importance of motor and somatosensory evoked potentials (MEP and SEP) for the early diagnosis of unapparent CNS damage related to diabetes mellitus. Methodology: Thirty diabetic patients (type 1 and type 2) and twenty healthy volunteers who match patient group for age and sex, both groups with no clinical symptoms or signs of central or peripheral nervous system lesion were evaluated. MEPs were recorded from upper and lower extremities bilaterally and central motor conduction time (CMCT) was calculated according to formula: CMCT=MEP-[0.5x (F-M-1) +M]. Similarly, we examined spinal and cortical SEP after median nerve stimulation in diabetics and control group. We measured the peak latencies of individual wave deflections and peripheral and central conduction time of spinal and cortical SEP. Results: The examination of MEPs and SEPs proved and confirmed the prolongation not only of peripheral conduction time, but also of the central conduction time especially in the lower limbs in the diabetic patients compared to the control group.  There was no correlation between central conduction time delay and the degree of metabolic control, type of diabetes (type 1 or type 2 diabetes mellitus), patient age, disease duration, presence or absence of retinopathy or nephropathy. Conclusion: In spite of an absence of clinical signs of central nervous system lesion in diabetic patients, a significant prolongation of central conduction time compared to control group was recorded. We assume a presence of diffuse subclinical CNS lesion induced by many factors.  Measurement of central conduction time using transcranial magnetic stimulation and somatosensory evoked potentials could be a complementary electrophysiological method for assessment of subclincal cerebral and spinal cord involvement in diabetic patient.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 723-735)


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