Visual evoked potentials in insulin-dependent diabetics

Summary The latency of pattern-reversal VEPs was studied in type I insulin-dependent diabetics without retinal and extraocular involvement. One hundred eyes of 50 diabetics (mean age 19.8±7.2 years) formed the study group; the duration of the disease ranged between 1 month and 15 years. The latencies of VEPs were progressively delayed in relation to the duration of the disease, becoming more and more evident and stabilizing after about 6 years from the onset of diabetes. The VEP alterations probably indicate alteration of membrane balance or demyelinization.     

Effects of hyperglycaemia on visual evoked potentials in insulin-dependent diabetic patients

Multimodality evoked potentials frequently reveal subclinical involvement of the central nervous system in patients with insulin-dependent diabetes mellitus. We devised this study to evaluate the possible effects of acute hyperglycaemia on visual evoked potential (VEP) parameters in type 1 diabetic patients. A hyperglycaemic clamp (250 mg/dl for 180 min) was performed in ten patients. Monocular pattern reversal VEPs (check size 15, contrast 50%) were recorded before, and every 30 min after the start of the clamp. Basal VEP latencies and amplitudes were normal bilaterally in nine patients. No significant changes in pattern reversal and flash VEP parameters were observed after the induction or during the clamp period. None of the neurophysiological parameters evaluated during the test was related to the duration of the disease, the basal VEP latency or amplitude or the presence of retinopathy. Our data suggest that the neurophysiological abnormalities detected in insulin-dependent diabetic patients are due to structural involvement of the central nervous pathways and not to functional damage induced by acute short-term hyperglycaemia.     

Somatosensory evoked potentials in hepatic encephalopathy

Median nerve somatosensory evoked potentials were recorded from 33 patients with various degrees of hepatic failure and from 10 age-matched controls. Within 20 ms poststimulation, one negative peak (N13) could be recorded from the middle of the back of the patient's neck at the C2 vertebral level. Within 150 ms, three negative and three positive peaks, sequentially designated as N1, P1, N2, P2, N3, and P3, could be recorded from the scalp over the contralateral sensory cortex. There was a progressive prolongation of peaks and interpeak latencies correlating with the severity of hepatic encephalopathy. In 10 patients with hepatic failure but no clinical evidence of hepatic encephalopathy, latencies of peak N3 and P3 were delayed and N1-N3 interpeak latencies were prolonged. Thirteen patients with grade 1 or 2 hepatic encephalopathy showed further delayed latencies of peaks P2, N3, and P3, further prolonged N1-N3, N1-P2 interpeak latencies, and distortion of waveforms. Peaks N2, P2, N3, and P3 were further delayed, and even disappeared in 10 patients with grade 3 or 4 hepatic encephalopathy. However, central conduction time (N13-N1 interpeak latency) was not prolonged in all stages of hepatic failure. In addition, serial somatosensory evoked potential studies correlated well with the clinical course. The present data suggest that somatosensory evoked potential recording is a reliable objective method in the early assessment and monitoring of hepatic encephalopathy.     

Somatosensory evoked potentials in moderate hyperthermia]

The effects of moderate whole-body hyperthermia on the cervical and cortical somatosensory evoked potentials (SEP) were studied in healthy male subjects, aged 22-32 years. They were immersed in hot water and heated to a median rectal temperature of 39.0 degrees C. Serial SEPs to median nerve stimulation were recorded during cooling at intervals of 0.1 degrees C. The general wave form and the amplitudes did not systematically change. For a 1 degrees C drop there was a median latency increase of 2.6-3.7% in cervical and 1.5-7.4% in cortical SEP components. In individual cases significant latency delays of cervical N13 and cortical N20 could already be observed at differences of 0.2 degrees and 0.5 degrees respectively. All other components showed significant latency changes at temperature intervals of 0.6 to 0.8 degrees C.     

Brainstem auditory and visual evoked potentials in Type 1 (insulin-dependent) diabetic patients

Summary Brainstem auditory evoked potentials and pattern shift visual evoked potentials were measured in 34 Type 1 (insulin-dependent) diabetic patients with long-standing disease and in 43 control subjects. Thirty-two percent of diabetic patients had abnormal brainstem auditory evoked potentials and 15% had abnormal visual evoked potentials. These abnormalities were not related to duration of diabetes, diabetic control or individual diabetic complications (retinopathy, nephropathy, peripheral or autonomic neuropathy). The aetiology of the abnormalities must remain a subject for speculation. The findings of this study are consistent with a central diabetic neuropathy involving the brainstem in long-standing diabetic patients.     

Somatosensory evoked potentials following tactile skin stimulation

Somatosensory evoked potentials were recorded for tactile stimuli applied to the fingers II and V as well as paravertebrally. The advantage of the painless mechanical stimuli is their specificity and the well defined stimulus localization. The question was therefore if the evoked responses are clearly demarcated. Nack potentials (N22: 22.5 and 22.3 ms) as well as cortical SEP's (P1: 33.2 and 32.8 ms) were easily to derive. It was also possible to get SEP's for segmental paravertebral tactile stimuli. For the finger stimulation an Erb's potential could not be recorded reliably.     

The value of visual evoked potentials in optic neuropathy of Graves' disease.

Visual evoked potentials (VEP) were tested in patients with ophthalmopathy (OP) of Graves' disease (GD) before treatment and half-a-year and 5-7 yr after orbital decompression (7 patients) or retrobulbar irradiation (3 patients). Five patients not requiring treatment for OP and 16 healthy subjects served as controls. Treatment of OP was given on clinical grounds including decreased visual acuity (VA) indicating optic neuropathy. Before treatment VA was decreased in 5 out of 19 eyes whereas VEP were abnormal in all. The mean latency at N60 both in the operated (83.1 +/- 21.6 ms) and in the irradiated groups (80.9 +/- 7.0 ms) was significantly different from that in the untreated group (62.6 +/- 8.2 ms; p < 0.001) and the healthy subjects (58.9 +/- 6.3; p < 0.001). At P120 only the latency of the operated group differed significantly from that of the other groups (p < 0.001). There was a relationship between the eye muscle changes seen on CT scans and the ophthalmopathy score (according to the classification of the American Thyroid Association) and the latency both at N60 and P120. A change from a V-shape to a W-shape of the waves occurred more often in the treated patients before therapy than in the other groups. Two patients had multiphase VEP in both eyes which improved after treatment. After adequate clinical response the visual acuity improved in one of the 5 patients with initially depressed VA. VEP, initially abnormal in all, improved in 7 of the 19 eyes (37%) but further deterioration was observed in 8 (42%).(ABSTRACT TRUNCATED AT 250 WORDS)     

事件相关电位与视觉诱发电位诊断帕金森病的价值

目的　探讨事件相关电位 (ERPs)和视觉诱发电位 (VEP)在帕金森病中 (PD)的诊断作用。方法　对 6 0例正常对照组和 5 8例无认知障碍的 PD患者组进行了 ERPs和 VEP检测。结果　 PD组 ERPs的 P30 0 波潜伏期较对照组的明显延长 (P<0 .0 5 ) ,波幅则较对照组明显降低 (P<0 .0 5 ) ;PD组 VEP的 P1 0 0 波潜伏期较对照组明显延长 (P<0 .0 5 ) ,而波幅则无显著性差异 (P>0 .0 5 )。结论　 ERPs的 P30 0 和 VEP对帕金森病的亚临床认知功能障碍及视觉传导通路功能的检测具有独特的诊断价值     

Impaired exocrine pancreatic function in diabetics with diarrhea and peripheral neuropathy

Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.Dr. Staples was a USC Medical Student during this protocol.     

Somatosensory evoked potentials (SSEPs) in rheumatoid cervical subluxation

Somatosensory evoked potentials (SSEPs) were recorded in 34 patients with severe rheumatoid arthritis. Eighteen had atlanto-axial subluxation and 16 had no roentgenological evidence of cervical subluxation. Four patients in the group with cervical subluxation showed pathological SSEP values from both median and tibial nerves indicating conduction block in the upper cervical medulla. In the group with no cervical subluxation, 6 patients had prolonged SSEP latency, 5 of these on recordings from the tibial nerves with normal median nerve latencies and one with only bilaterally prolonged median nerve latencies. The pathological SSEP findings in the former group of patients we attribute to the cervical subluxation, while the findings in the latter group might be related to spinal cord vasculitis or extradural granulation tissue. The SSEP method can be useful in providing objective evidence for spinal cord lesions in patients with rheumatoid cervical subluxation.     

Evaluation of central nervous conduction by visual evoked potentials in insulin-dependent diabetic children. metabolic and clinical correlations

Summary Peripheral neuropathy is a well-known complication of diabetes, but few data are available on central lesions. Visual evoked potentials (VEPs) seem a reliable and feasible technique for detecting a conduction delay in the central nervous, system. Seventy-one insulin-dependent type 1 diabetic children (mean age 15±3 years) and 33 controls were investigated for central neuropathy. We used a pattern of reversal stimulation with television display of a checker board pattern (15 min and 30 min check size). The latencies of the positive peak (P100 wave) were significantly lengthened in 17 patients (27%) but no correlation was found between VEPs and age, duration of diabetes, insulin requirement and HbA₁ level. A negative correlation was found between VEPs and peripheral nervous conduction velocity. VEPs measurement seems a simple and reliable technique for detecting early alterations in CNS function in diabetics. Our data suggest that central and peripheral nervous alterations progress simultaneously.     

Pattern reversal visual evoked potentials in phenylketonuria

Summary The pathogenesis of brain dysfunction in phenylketonuria (PKU) is still under investigation. Hyperphenylalaninaemia results in increased turnover of myelin. In order to demonstrate the derangement of myelinization in PKU we studied the visual evoked potentials (VEP) in 14 PKU patients and in 20 normal subjects. VEP findings were correlated with the metabolic control of the disease and with the electroencephalographic findings. VEP were more sensitive than the EEG in detecting a neurological dysfunction. VEP are influenced by dietary control and are normal only in children with good metabolic control.     

Pattern-reversal visual evoked potentials in hepatic cirrhosis

Whole-field pattern-reversal VEPs (VEP) were examined in fifteen patients screened for hepatic cirrhosis. Twelve age- and sex-matched normal individuals and twenty-four psychotic patients on maintenance neuroleptic medication served as controls. There were no differences in latency or amplitude of the major positive component VEP (P100) to binocularly or monocularly presented reversing patterns between hepatic and control groups. Pre-exposure to flicker (the "photostress test") caused no abnormalities of VEP. Only in one patient with hepatic cirrhosis did monocular stimulation in the photostress condition cause a marked delay of P100. It is possible that this was an idiosyncratic response and that visual abnormalities detectable with the VEP technique can be attributed to other factors such as poor attention or accompanying disorders of the visual system.     

Somatosensory evoked potentials in comatose patients: comparison with clinical findings, EEG and prognosis

21 comatose patients were examined by somatosensory evoked potentials (SSEP). The findings were correlated with the stage of brainstem herniation, the EEG and the outcome. We evaluated the early components of the SSEP (N10, N13, N14, P15, N20) in view of presence, latency and interpeak-latency of the potentials. In most cases the percentage of abnormal SSEP increased from caudal to rostral registration sites, but the potential P15 and N20 were equally abnormal. The progression of herniation correlated with increasing abnormality of the potentials. SSEP over the scalp (P15, N20) could not be registered in patients without any EEG-activity (isoelectric). Mean values of latencies and the interpeak-latencies were significantly prolonged in all cases with fatal outcome. Our findings suggest SSEP as a useful tool in the evaluation of brain-dysfunction in comatose patients.     

Subpopulations of peripheral lymphocytes in insulin-dependent diabetics (author's transl)]

There is an increasing evidence that autoimmune mechanisms may have a role in the pathogenesis in insulin-dependent diabetics. The numerical and functional study of peripheral blood lymphocytes in diabetes mellitus might indirectly contribute to the understanding of its pathogenesis. In this study, detection of peripheral blood T lymphocytes was measured by rosettes with sheep red blood cells (SRBC), and B lymphocytes were measured by immunofluorescence with specific antiserum to immunoglobulins. The mean (+/- SD) percentage of SRBC was 67.6 +/- 7.2 in 21 normal subjects, 71.5 +/- 7.0 in 15 insulin-dependent diabetics, and 68.6 +/- 6.7 in 30 insulin-independent diabetics. There was no difference in the absolute T-lymphocyte number per mm3 in these three groups. Insulin-dependent diabetics showed a normal percentage and absolute number of B lymphocytes when compared with normal subjects.     

Isolated symptomatic peripheral neuropathy in type 1 insulin-dependent diabetes mellitus

Diabetic neuropathy is probably the most frequent of the chronic complications of diabetes, and is usually found in association with diabetic retinopathy and/or nephropathy. We report seven patients with long-standing insulin-dependent diabetes mellitus in whom symptomatic peripheral neuropathy was the first and only documented complication. The diagnosis of peripheral symmetrical neuropathy was based on the presence of symptoms and abnormal physical findings, confirmed with abnormal electrophysiological and/or vibratory and thermal threshold measurements. Diabetic retinopathy and nephropathy were absent. We conclude that in some type 1 insulin-dependent diabetic patients, similar to what has been reported in type 2 non-insulin-dependent diabetes, peripheral neuropathy may be the first chronic complication to become manifest. This observation provides additional evidence to suggest that each of the diabetic complications may have a different pathogenic mechanism.     

Correlation of visual evoked potentials with dementia in Parkinson's disease]

There has been some debate regarding abnormalities in visual evoked potentials (VEP) in Parkinson's disease (PD). To elucidate the mechanism causing abnormal VEP, we investigated the relationship between VEP and mental function in PD patients. Pattern reversal VEP was recorded in PD patients (n = 27) and age-matched control subjects (n = 14). PD patients consisted of two subgroups; PD without dementia (nD-PD; n = 17) and PD with dementia (D-PD; n = 10). Dementia was evaluated according to the criteria for dementia assigned in DSM III-R, and mental faculties were estimated by using the mini-mental state examination (MMSE). In pattern VEP recordings, P100 latency and amplitude were measured for each eye stimulated. No patient or control subject had impairment of corrected visual acuity or ophthalmological disease. There was no significant difference in age among the three groups (D-PD, nD-PD and control subjects). D-PD patients showed significantly prolonged P100 latency compared to nD-PD patients and control subjects (p less than 0.05). With respect to P100 amplitude, no significant difference was shown among the three groups. In PD patients, there was a rough correlation between P100 latency and MMSE score. No correlation was found between P100 amplitude and MMSE score. In control subjects, P100 latency did not correlate with advancing age. In PD patients, nD-PD patients showed a significant correlation between P100 latency and age, whereas D-PD patients presented no correlation. Abnormal VEP in PD has been mostly ascribed to dopaminergic deficiency in the retina.(ABSTRACT TRUNCATED AT 250 WORDS)     

糖尿病性神经病变的运动诱发电位研究

目的 探讨糖尿病运动神经中枢及神经根,周围神经功能。方法 应用经皮层,脊髓电刺激运动诱发电位对５０例ＤＭ进行观察。结果 异常率８２％,表现皮层,脊髓刺激ＭＥＰ潜伏期延迟,波形分化欠佳。部分伴有ＣＭＥＴ异常,ＭＥＰ异常率与病程长短呈正相关;空腹血糖水平对ＭＥＰ结果无明显影响。     

Somatosensory evoked potentials and number connection test in the detection of subclinical hepatic encephalopathy

To compare the diagnostic ability of somatosensory evoked potentials and the number connection test in the detection of subclinical hepatic encephalopathy, 44 decompensated cirrhotic patients with no overt encephalopathy were admitted to the study and followed up for 6 months. Twenty-two patients developed overt encephalopathy during follow-up, and were retrospectively considered as patients with subclinical encephalopathy at entry. Of the 15 patients with abnormal somatosensory evoked potentials, 14 (93%) experienced at least one episode of hepatic encephalopathy in the following 6 months, while 16 (70%) of the 23 patients with abnormal number connection test did so. The data suggested that somatosensory evoked potential measurement was less sensitive, but more specific than number connection test in the detection of subclinical encephalopathy, although the differences were not statistically significant. Besides, the number connection test is much simpler, convenient and cheap, and it specificity could be improved if the learning effect and age, education and visual factors were carefully considered. We therefore recommend using the number connection test routinely in patients with decompensated liver diseases for the detection of subclinical hepatic encephalopathy, and reserving somatosensory evoked potential measurement as a complementary examination, when appropriate, or for assessment of overt hepatic encephalopathy.     

血清胰岛素样生长因子-Ⅱ与2型糖尿病外周神经病变的关系研究

目的 探讨胰岛素样生长因子-Ⅱ(IGF-Ⅱ)与2型糖尿病外周神经病变的关系.方法 将2005年6月至2006年1月浙江大学医学院附属第一医院内分泌科收治的71例2型糖尿病非外周神经病变患者(A组)、77例2型糖尿病外周神经病变患者(B组)及30名健康对照者(C组)纳入研究,测定3组血清IGF-Ⅱ.A、B组加测静脉空腹血糖、胰岛素等相关临床指标及神经电生理检查.结果 B组血清IGF-Ⅱ低于A组和C组,差异有显著性意义(P＜0.05),C组和A组间血清IGF-Ⅱ差异无显著性意义(P＞0.05);血清IGF-Ⅱ与神经传导速度呈正相关(P＜0.05);血清IGF-Ⅱ是2型糖尿病外周神经病变的主要相关因素(P＜0.05).结论 2型糖尿病外周神经病变患者血清IGF-Ⅱ明显下降,且IGF-Ⅱ降低与2型糖尿病外周神经病变的发生有关.