Chronic toxic neuropathy after organophosphorus poisoning in quails (Coturnix coturnix japponica).

Peripheral neuropathy was induced by the long-term administration of organo-phosphorus compounds (phtalimid/phosmet) in quails (Coturnix coturnix japponica). After 4 weeks, the first symptoms of organophosphorus (OPC) poisoning (apathy, diarrhea) were present. During the second month of a daily administration of the toxic substance using the probe, an apparent clinical autonomic and peripheral neuropathy with ataxia had developed. Toxic disturbance of the nervous system was confirmed by the examination of spinal and cortical somatosensory evoked potentials (SEP) after tibial nerve stimulation. The prolongation of the peripheral conduction time (wave P6 and N9 represent the response from the ischiadic nerve and the entry of the stimulus to spinal cord, respectively) confirmed a peripheral nerve lesion. We suggest that these clinical and electrophysiological changes, displayed by the disturbed nervous system, are caused by either slowing or stoppage of the axonal flow, transport of proteins and other substances, as well as by axon demyelination (Tab. 1, Fig. 1, Ref. 22).

An acute toxic neuropathy caused by organo-phosphate poisoning in hens.

OBJECTIVE: Organophosphorus compounds can induce an acute toxic peripheral neuropathy. In hens, the acute peripheral neuropathy was induced by poisoning with organo-phosphorus compound (OPC)--tri-ortho-cresyl phosphate (TOCP). METHODS: In the course of an acute TOCP-induced toxic neuropathy in hens the activity of following enzymes was analysed: asparaginase, glutaminase, glutamat-dehydrogenase, AMP and adenosine deaminases and 5'nucleotidase; ALT (SGPT), AST (SGOT) and proteins levels were estimated. RESULTS: A decrease in activity of all analysed enzymes was observed; the amount of proteins was increased. CONCLUSION: The biochemical changes display the slowing or stoppage in axonal transport of proteins. The disturbance of axoplasmic flow and the axonal demyelination may be considered as an attribute of peripheral neuropathy. (Tab. 1, Fig. 1, Ref. 32.).

Is the spinal cord lesion rare in diabetes mellitus? Somatosensory evoked potentials and central conduction time in diabetes mellitus.

BACKGROUND: Diabetic neuropathy and autonomic nervous system neuropathy are recognized as the most common clinical pictures of nervous system disorders caused by DM, while the damage to the brain and the spinal cord is considered to be rare. The aim of this work is to indicate the importance of somatosensory evoked potentials (SEP) for the early diagnosis of nerve system damage related to diabetes mellitus. MATERIAL AND METHODS: We studied 20 patients (aged 35-50 years), with type 2 diabetes mellitus lasting for 5-10 years. The control group population comprised of 30 healthy individuals of the same median age. The spinal and cortical somatosensory evoked potentials (SEP) after stimulation of median and fibular nerves were examined in both groups of patients. We measured the latencies and amplitudes of individual wave deflections, peripheral and central conduction time (PCT and CCT) of spinal and cortical SEP. RESULTS: The examination proved and confirmed the elongation not only of peripheral conduction time but also of the central conduction time - especially in spinal cord structures. The spinal cord changes connected with decrease of myelinated fibers which are able of conduction from periphery have to be accepted. The comparison of CCT1 and CCT2 conduction times showed that in group of diabetic patients the spinal cord structures are responsible for prolongation CCT. CONCLUSIONS: We confirm that the use of somatosensory evoked potentials examination and conduction times measurement has the significance in the confirmation of inapparent lesion of the spinal cord in diabetics.