Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of patients with chronic renal failure managed conservatively, the rise in the plasma-myo-inositol (myoinositol) concentration has been found to be related to depression of sural-nerve conduction velocity. There was no correlation with motor-nerve conduction velocity in the peroneal nerve, or with either of these variables in a series of patients receiving chronic haemodialysis. Despite the negative correlation with sural-nerve conduction velocity, there was no correlation between the plasma-myoinositol concentration and the presence of peripheral neuropathy as assessed clinically. It is concluded that hypermyoinositolaemia may depress nerve conduction velocity, but there is no evidence that it is responsible for the development of uraemic polyneuropathy.
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PMID:Plasma-myoinositol concentrations in uraemic neuropathy. 6 75

Eight sailors on board the Asiafreighter were exposed to arsine that had escaped from a cylinder in the cargo hold. Four suffered severe toxicity and within a few hours had developed fever, weakness, nausea, vomiting, diarrhoea, abdominal pain, and haemoglobinuria. These patients had pronounced intravascular haemolysis, which in one patient was complete. This patient was also stuporose and anoxic, a condition attributed to failure of oxygen transport and sludging of red cell debris in the cerebral and pulmonary circulations, but he regained a normal level of consciousness after exchange transfusion. Evidence of marrow depression was present: the reticulocyte response to the haemolysis was poor and there was a thrombocytopenia. All four patients developed renal failure, one being totally anuric for five weeks. Two patients developed peripheral neuropathy, and one was still severely disabled six months after the incident. The other four patients had a similar, though less severe, illness.
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PMID:Arsine toxicity aboard the Asiafreighter. 16 42

Five patients received overdoses of vincristine ranging from 3.5 to 32 mg. Neurotoxicity accounted for most of the complications observed. Peripheral neuropathies, cranial nerve palsies, paralytic ileus, atony of the bladder, hypertension, hypotension, seizures, inappropriate ADH secretion, and severe bone marrow depression were all encountered. Two patients died within 72 hours of the overdose. Another patient died of sepsis 22 days after the overdose. Two patients recovered and were discharged. The three patients who survived longer than a few days showed improvement in the vincristine-induced neuropathy, and the two long-term survivors had essentially complete recovery. It appears that if a patient can be supported through the critical period following an overdose, he can be expected to recover normal neurologic function.
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PMID:Overdosage with vincristine. 18 48

A quantitative assessment of post-ischaemic paraesthesiae has been made in 50 pellagrins and 20 healthy identical controls. The results show a higly significant diminution of the paraesthetic response in pellagrins. In pellagrins having peripheral neuropathy the depression of paraesthesiae was more marked than in those without peripheral neuropathy. There was no consistent relationship between severity of peripheral neuropathy and degree of depression of paraesthetic response.
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PMID:Post-ischaemic paraesthesia in pellagrins. 19 50

Surface, needle and micro-electrode recordings were obtained from sensory nerves of patients with various types of peripheral neuropathy. Changes in amplitude and conduction velocity of nerve action potentials were measured after a single conditioning stimulus and after tetanic stimulation for 2 min. In patients with hereditary forms of axonal degeneration (AD), recovery processes of nerve fibres of all conduction velocities were normal; in acquired forms of AD fibres with conduction velocity less than 30 m/sec had greater and more prolonged post-tetanic depression than control nerves of similar conduction velocity. Where neuropathy was associated with segmental demyelination (SD), fibres of all conduction velocities had prolonged recovery processes after both single and tetanic stimulation. The changes were especially marked at higher skin temperature, and were greater than the changes seen in nerves with acquired forms of AD. Finally, 2 sural nerves were studied during the process of Wallerian degeneration after a biopsy had been obtained proximally, and recovery processes did not change during the period of degeneration. Perceptual abnormalities were similar in AD and SD. It is suggested that changes in recovery processes of nerve fibres with segmental demyelination or regeneration after injury contribute to the perceptual abnormalities which occur in clinically encountered peripheral neuropathies.
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PMID:A micro-electrode study of peripheral neuropathy in man. Part 2. Responses to conditioning stimuli. 20 Jul 18

In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.
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PMID:Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia. 20 86

Leg paralysis and wallerian degeneration of sciatic nerve fibres have been produced in rats by intraneural injection of 0.5, 1 or 5 microgram of vincristine (VCR) or formyl leurosine (FLR) dissolved in 5 microliter of saline. Nerve lesions were dose-related, and were similar for equal concentrations of the two drugs. Six patients received one to three 5-day courses of FLR. The total dose of FLR administered ranged from 15 to 131 mg (mean 83 mg). Clinical signs of peripheral neuropathy were absent in four patients, and limited to orthostatic hypotension in one case and transient depression of reflexes in another. Motor conduction velocities measured in four peripheral nerves, and muscle evoked potentials remained unchanged throughout the treatment in all patients.
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PMID:[Neurotoxicity of formyl leurosine. An experimental and clinical study (author's transl)]. 23 62

Marked weight loss with cachexia together with severe depression and pain from symmetrical peripheral neuropathy were noted in a 66-year-old man, known to have had diabetes for six years, which required insulin on admission to hospital. The patient died of bronchopneumonia after one year. The severe neuropathy was proven both neurophysiologically and at necropsy. There was no diabetic retinopathy and no histological evidence of renal glomerulosclerosis. There was no evidence of a malignant tumour either clinically or at necropsy.
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PMID:[Diabetic neuropathic cachexia (author's transl)]. 44 96

Initial observations in adults revealed that peripheral neuropathy, as documented by reduced conduction velocity is common in chronic renal failure. Critical analysis of this problem in children on long-term dialysis is scarce, consisting of a simgle report which demonstrated that the motor nerve conduction velocities were decreased early and frequently with more severe depression in peroneal nerve velocities. This is in distinct contrast to data from adults, in whom uniform rates of deterioration are encountered. In addition, a direct correlation of the degree of nerve conduction defect with the severity of the renal failure is found in adult patients. The present study showed a relative lack of nerve conduction defects in 11 children on long-term hemodialysis. With rare exceptions, the conduction velocities were normal. To date, no clinical symptoms of neuropathy were evident in our patients. It would seem that, with the short-dialysis schedule of 12--14 h/wk over a period of up to 5 yr, there is no progressive neuropathy as quantitated by nerve conduction measurements.
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PMID:Long-term hemodialysis and nerve conduction in children. 47 89

Leg paralysis and wallerian degeneration of sciatic nerve fibres have been produced in rats by intraneural injection of 0.5, 1 or 5 micrograms of vincristine (VCR) or formyl leurosine (FLR) dissolved in 5 microliters of saline. Nerve lesions were dose-related, and were similar for equal concentrations of the two drugs. Six patients received one to three 5-day courses of FLR. The total dose of FLR administered ranged from 15 to 131 mg (mean 83 mg). Clinical signs of peripheral neuropathy were absent in four patients, and limited to orthostatic hypotension in one case and transient depression of reflexes in another. Motor conduction velocities measured in four peripheral nerves, and muscle evoked potentials remained unchanged throughout the treatment in all patients.
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PMID:[Neurotoxicity of formyl leurosine. An experimental and clinical study (author's transl)]. 53 76


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