To investigate the relationship between glycosylated hemoglobin A (HbA1c) and complex regional pain syndrome (CRPS) in stroke patients with type 2 diabetes mellitus (T2DM).
A retrospective chart review was performed of stroke patients from January 2012 to December 2013. We reviewed 331 patients and included 200 in the analysis. We divided them into CRPS and non-CRPS groups and compared them by age, gender, stroke lesion, cause of stroke, duration of T2DM, HbA1c (%), National Institutes of Health Stroke Scale score, affected shoulder flexor muscle strength, Fugl-Meyer Assessment score, motricity index, Functional Independence Measure, Korean version of Modified Barthel Index, blood glucose level on admission day, duration from stroke onset to HbA1c check, and duration from stroke onset to three-phase bone scan for CRPS diagnosis. Thereafter, we classified the patients into five groups by HbA1c level (group 1, 5.0%–5.9%; group 2, 6.0%–6.9%; group 3, 7.0%–7.9%; group 4, 8.0%–8.9%; and group 5, 9.0%–9.9%) and we investigated the difference in CRPS prevalence between the two groups.
Of the 200 patients, 108 were in the CRPS group and 92 were in the non-CRPS group. There were significant differences in HbA1c (p<0.05) between the two groups but no significant differences in any other factors. Across the five HbA1c groups, there were significant differences in CRPS prevalence (p<0.01); specifically, it increased as HbA1c increased.
This study suggests that higher HbA1c relates to higher CRPS prevalence and thus that uncontrolled blood glucose can affect CRPS occurrence in stroke patients with diabetes.
Citations
To investigate risk factors for diabetic peripheral polyneuropathy and their correlation with the quantified severity of nerve dysfunction in patients with diabetes mellitus (DM).
A total of 187 diabetic patients with clinically suspected polyneuropathy (PN) were subclassified into 2 groups according to electrodiagnostic testing: a DM-PN group of 153 diabetic patients without electrophysiological abnormality and a DM+PN group of 34 diabetic patients with polyneuropathy. For all patients, age, sex, height, weight, duration of DM, and plasma glycosylated hemoglobin (HbA1c) level were comparatively investigated. A composite score was introduced to quantitatively analyze the results of the nerve conduction studies. Logistic regression analysis and multiple regression analysis were used to evaluate correlations between significant risk factors and severity of diabetic polyneuropathy.
The DM+PN group showed a significantly higher HbA1c level and composite score, as compared with the DM-PN group. Increased HbA1c level and old age were significant predictive factors for polyneuropathy in diabetic patients (odds ratio=5.233 and 4.745, respectively). In the multiple linear regression model, HbA1c and age showed a significant positive association with composite score, in order (β=1.560 and 0.253, respectively).
Increased HbA1c level indicative of a state of chronic hyperglycemia was a risk factor for polyneuropathy in diabetic patients and a quantitative measure of its severity.
Citations
Objective: To determinate the reference values of residual latencies of motor nerves and to evaluate the early diagnostic value of residual latency.
Method: The subjects were 129 diabetes mellitus patients and 60 controls with no known neurological disorders. The patients were divided into two groups based on the conventional nerve conduction study: Group 1, 75 patients without neuropathy; Group 2, 54 patients with neuropathy. The group 2 patients were subdivided into 4 sub- groups on the basis of conduction velocity and residual latency of the median nerve. Residual latencies were measured in all subjects and glycosylated hemoglobin percentages (HbA1c) were measured in the diabetes patients. In group 2, each nerve conduction parameter was correlated with the duration of diabetes and HbA1c. The duration of diabetes, HbA1c, and amplitude of median nerve response were compared between the subgroups of group 2 patients.
Results: Motor residual latencies obtained from the controls were 1.93⁑0.28 msec, 1.53⁑0.24 msec, 2.46⁑0.43 msec, 2.21⁑0.53 msec in median, ulnar, deep peroneal and posterior tibial nerves, respectively. In group 1, motor residual latencies of median & deep peroneal nerves were significantly delayed compared with those of the controls. In group 2, motor residual latencies of median, ulnar, deep peroneal and posterior tibial nerves were significantly delayed more than those of the controls and group 1.
In group 2, increased HbA1c correlated to the decreased conduction velocities of median, deep peroneal, posterior tibial nerves but not to the residual latencies.
In the subgroup of group 2 (2-D), the nerve involved more distally showing lower compound muscle action potential and higher HbA1c.
Conclusion: Residual latency measurement can be a useful diagnostic method for the early detection of diabetic neuropathy.
Method: Prospectively, total 40 patients with non-insulin dependent diabetes mellitus were included in the study. NCS was performed on median, ulnar, posterior tibial, deep peroneal, superficial peroneal, and sural nerves. Distal latency and conduction velocity (CV) of compound muscle action potential (CMAP), distal latency and amplitude of sensory nerve action potential (SNAP) were used as parameters of NCS. Multiple linear regression analysis were used to analyze the relations of HbA1c and parameters of NCS, after adjustment for age, height, weight, and disease duration of diabetes mellitus.
Results: HbA1c level had an inverse relation to CV of median motor nerve (β=1.272, p＜0.01), ulnar motor nerve (β=1.287, p＜0.01), posterior tibial nerve (β=0.982, p＜0.05), and deep peroneal nerve (β=1.449, p＜0.05).
Conclusion: This study indicates that HbA1c level was inversely related to motor nerve CV, and that sustained hyperglycemia may be involved in demyelination of motor nerves. Analysis of motor nerve CV related to HbA1c is expected to be useful in the follow-up or efficacy study of diabetes mellitus neuropathy as baseline data. (J Korean Acad Rehab Med 2003; 27: 80-84)
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