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Researches On Peripheral Nerve Injury Caused By Mercury Poisoning

Posted on:2018-08-04Degree:DoctorType:Dissertation
Country:ChinaCandidate:B B SunFull Text:PDF
GTID:1314330518951850Subject:Neurology
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Background and Objectives:Mercury and its compounds are neurotoxic. Previous studies on the effects of mercury and their compounds on the nervous system were more focused on the central nervous system, and there were few studies on mercury-induced peripheral nerve damage. The purpose of this study is to comprehensively assess the impact of mercury exposure on peripheral nerves by combination of clinical and experimental animal researches.Methods:1. Mercury poisoning patients admitted to our hospital from 1994 to 2015 were reviewed.The clinical data of all patients were collected and analysed.2. 29 cases of newly diagnosed as chronic mercury poisoning patients were included continuously in the case group from June 2015 to April 2016, and 29 healthy subjects were included as the control group. The clinical data of all the subjects were analyzed statistically.3. To establish the rat model of subacute mercury chloride poisoning, to evaluate the neurobehavioral, and to observe the morphological changes of motor neurons of spinal cord anterior horn and sensory neurons of dorsal root ganglion. To assess the the effects of mercury on the density of IENF and SGNF in the pad skin of rats and to assess the possible relationship between IENFD and sensory disturbances.Results:Part I: A total of 740 cases of hospitalized patients with mercury poisoning during the period from 1994 to 2015 were included. The average age of the patients was 37.5 years old, female: male = 2.15: 1. The top three regions were Hebei Province, Beijing, Inner Mongolia Autonomous Region. 582 cases (78.6%) were non-occupational exposure and 623 cases (84.2%) were chronic poisoning. Pain, edema and malaise were the most common clinical symptoms. Mercury poisoning can cause multiple system damage, 250 patients (33.8%) had suspected peripheral nervous system damage. Urine mercury level in acute group was higher than that in chronic group (P <0.05). The urinary mercury level in the non-occupational group was significantly higher than that in the occupational exposure group (P <0.05).Part II: The main clinical manifestations of peripheral nerve damage in 29 patients with chronic mercury poisoning were palpitations, dizziness, pain, limb weakness, limb tremor,numbness etc. Electrophysiological abnormalities were detected in 9 patients. MCV examination showed mercury poisoning patients had prolonged distal motor latency of the median nerve and peroneal nerve than the control group (P<0.05). SCV examination showed that the conduction velocity of the ulnar nerve was slower than that of the control group and the latent period of the radial nerve was longer than that of the control group(P<0.05).Combined clinical examination, scale assessment and neurophysiological examination, we found possible peripheral neuropathy in 17 paitent, and possible small fiber neuropathy in 10 cases.Part III: Rats in all three HgCl2 groups exhibited varying degrees of weight and hair loss.Additionally, although thermal hypersensitivity was evident in the low-and middle-dose groups (medium-2w subgroup, P < 0.05). Mechanical sensitivity tests revealed hyposensitivity in the low- and middle-dose groups (especially in the low-2w subgroup,P <0.05) , but hypersensitivity in the high-1w subgroup. The number of motor neurons in the anterior horn of spinal cord in poisoning rats decreased and there were morphological changes in these cells. Significant decreases in IENFD and significant increases in the density of PGP9.5-positive cells (all P < 0.05, except the low-lw and high-2w subgroups) were found in all groups after HgCl2 exposure. Additionally, an association analysis revealed a significant correlation between the decrease in IENFD and the increase in PC density (R2 = 0.329, P < 0.05). In all poisoned rats, the sweat gland nerve fibers were lower in the control group than in the control group (P <0.05, except for the middle-1w subgroup).Conclusion:1. Mercury and its compounds can cause multiple system damage and multiple clinical manifestations. The proportion of peripheral nervous system damage was about 33.8%.Strengthening public risk awareness education is beneficial to the prevention of the disease.2. The main clinical manifestations of peripheral nerve damage of chronic mercury poisoning were dizziness, pain, limb weakness, limb tremor, numbness etc. Some patients with clinical symptoms and normal nerve electrophysiological examination, might have damage of small nerve fibers.3. Mercuric chloride poisoning can lead to small nerve damage, which were related to sensory disturbances.
Keywords/Search Tags:mercury poisoning, peripheral nerve injury, small fibre neuropathy, epidermal nerve fiber density, sweat gland nerve fiber density
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