Residual latency is the difference between the expected and measured terminal latencies in nerve conduction study. The main contributors to the residual latency are the nerve tapering in the hand and fingers and the neuromuscular delay. We measured median motor and sensory residual latencies in the controls and in patients with diabetes mellitus(DM) to establish the normal values, to evaluate the diagnostic value of the residual latency in diabetic polyneuropathy. we studied 50 healthy controls and 100 diabetic patients with or without polyneuropathy. The normal residual latency values were 1.42+/-0.41 msec(mean+/-SD) in motor part and 0.44+/-0.20 msec in sensory part of median nerve. The standard deviation of residual latency in median motor nerve was decreased by 12% as compared with that of distal latency in the patient with diabetic polyneuropathy. Duration of DM and age were not related to the residual latency of median nerve. The results suggest that the residual latency of median motor nerve provides a narrower normal range in the diagnosis of diabetic polyneuropathy irrespective of duration of DM or age.
Diabetes Mellitus* ; Diabetic Neuropathies ; Diagnosis ; Fingers ; Hand ; Humans ; Median Nerve* ; Neural Conduction ; Polyneuropathies ; Reference Values

This study was performed to develop a useful nerve conduit which provides favorable environment for Schwann cell viability and proliferation. Milipore membrane of 0.45um pore size was selected because it permits nutritional inflow from the outside of the conduit and prevents from invading the fibrotic tissue into the conduit. The membrane was rolled and sealed to form a conduit of 2mm diameter and 20mm length. To improve the axonal regeneration and to render better environment for endogenous and exogenous Schwann cell behaviour, the microgeometry and surface of conduit was modified by coating with thin film of calcium phosphate. Cellular viability within the conduit and attachment to its wall were assessed with MTT assay and SEM study. Milipore filter conduit showed significantly higher rate of Schwann cell attachment and viability than the culture dish. However, the reverse was true in case of fibroblast. Coating with thin film of low crystalline calcium phosphate made more favorable environment for both cells with minimal change of pore size. These findings means the porous calcium phosphate coated milipore nerve conduit can provide much favorable environment for endogenous Schwann cell proliferation and exogenous ones, which are filled within the conduit for the more advanced strategy of peripheral nerve regeneration, with potential of reducing fibrotic tissue production.
Axons ; Calcium* ; Cell Proliferation ; Cell Survival ; Crystallins ; Fibroblasts ; Membranes ; Nerve Regeneration ; Peripheral Nerves* ; Regeneration ; Schwann Cells

PURPOSE OF STUDY: Peripheral nerve regeneration depends on neurotrophism of distal nerve stump, recovery potential of neuron, supporting cell like Schwann cell and neurotrophic factors such as BDNF. Peripheral nerve regeneration can be enhanced by the conduit which connects the both sides of transected nerve. The conduit maintains the effects of neurotrophism and BDNF produced by Schwann cells which can be made by gene therapy. In this study, we tried to enhance the peripheral nerve regeneration by using calcium phosphate coated porous conduit and BDNF-Adenovirus infected Schwann cells in sciatic nerve of rats. MATERIALS AND METHODS: Microporous filter which permits the tissue fluid essential for nerve regeneration and does not permit infiltration of fibroblasts, was made into 2mm diameter and 17mm length conduit. Then it was coated with calcium phosphate to improve the Schwann cell adhesion and survival. The coated filter was evaluated by SEM examination and MTT assay. For effective allogenic Schwann cell culture, dorsal root ganglia of 1-day old rat were extracted and treated with enzyme and antimitotic Ara-C. Human BDNF cDNA was obtained from cDNA library and amplified using PCR. BDNF gene was inserted into adenovirus shuttle vector pAACCMVpARS in which E1 was deleted. We infected the BDNF-Ad into 293 human mammary kidney cell-line and obtained the virus plaque 2 days later. RT-PCR was performed to evaluate the secretion of BDNF in infected Schwann cells. To determine the most optimal m.o.i of BDNF-Ad, we infected the Schwann cells with LacZ adenovirus in 1, 20, 50, 75, 100, 250 m.o.i for 2 hours and stained with beta-galactosidase. Rats(n=24) weighing around 300g were used. Total 14mm sciatic nerve defect was made and connected with calcium phosphate coated conduits. Schwann cells(1x10(6)) or BDNF-Ad infected Schwann cells(1x10(6)) were injected in conduit and only media(MEM) was injected in control group. Twelve weeks after surgery, degree of nerve regeneration was evaluated with gait analysis, electrophysiologic measurements and histomorphometric analysis. RESULTS: 1. Microporous Millipore filter was effective conduit which permitted the adhesion of Schwann cells and inhibited the adhesion of fibroblast. We could enhance the Schwann cell adhesion and survival by coating Millipore filter with calcium phosphate. 2. Schwann cell culture technique using repeated treatment of Ara-C and GDNF was established. The mean number of Schwann cells obtained 1 and 2 weeks after the culture were 1.54+/-4.0*10(6) and 9.66+/-9.6*10(6). 3. The mRNA of BDNF in BDNF-Ad infected Schwann cells was detected using RT-PCR. In Schwann cell 0.69 microgram/microliter of DNA was detected and in BDNF-Adenovirus transfected Schwann cell 0.795 microgram/microliter of DNA was detected. The most effective infection concentration was determined by LacZ Adenovirus and 75 m.o.i was found the most optimal. CONCLUSION: BDNF-Ad transfected Schwann cells successfully regenerated the 14mm nerve gap which was connected with calcium phosphate coated Millipore filter. The BDNF-Ad group showed better results compared with Schwann cells only group and control group in aspect to sciatic function index, electrophysiologic measurements and histomorphometric analysis.
Adenoviridae ; Animals ; beta-Galactosidase ; Brain-Derived Neurotrophic Factor* ; Calcium* ; Cell Adhesion ; Cell Culture Techniques ; Cytarabine ; DNA ; DNA, Complementary ; Fibroblasts ; Gait ; Ganglia, Spinal ; Gene Library ; Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Kidney ; Micropore Filters ; Nerve Growth Factors ; Nerve Regeneration ; Neurons ; Peripheral Nerves ; Polymerase Chain Reaction ; Rats* ; Regeneration* ; RNA, Messenger ; Schwann Cells ; Sciatic Nerve*

Animals ; Axons ; Brain-Derived Neurotrophic Factor ; Cell Separation ; Ganglia, Spinal ; Intercellular Signaling Peptides and Proteins ; Neurons ; Peripheral Nerves ; Peripheral Nervous System ; Rats ; Regeneration ; Spinal Nerve Roots