Objective To elucidate significance of hyperintense vessel signs(HVS)on FLAIR MRI in patients with cerebral infarction. Methods Two hundred and sixty-two patients with cerebral infarction admitted in our hospital were included in this study. We retrospectively defined HVS on FLAIR MRI in these patients in comparison with time of flight(TOF)on MR angiograms(MRA), hyperintense lesions on diffusion-weighted images(DWI). Results HVS on FLAIR MR[were identified in 117 patients with cerebral infarction(45.4%), of which 47 patients(83.9%)were obtained within 24 hours of symptom onset. HVS on FLAIR MRI were detected in 74 patients at sylvian fissure(62.2%), 11 at cortical sulci (9.2% ,11/119),34 at the posterior circulation regions(28.6% ,34/119). HVS on FLAIR MRI coincided well with ischemia of TOF on MRA and lesion patterns on DWI (χ2 test,P<0.01, respectively). Conclusion HVS on FLAIR MRI is helpful to evaluate abnormal major cerebral arteries of patients with cerebral infarction.

Objective: Characteristics of clinical, MRI and electroencephalogram after trimethyltin chloride (TMT) poisoning. Methods: The clinical manifestations, MRI, EEG, treatment and prognosis of 16 patients with TMT poisoning were analyzed retrospectively. Results: Among the 16 cases of TMT poisoning, 6 cases were severe poisoning, 4 cases were moderate poisoning, and 6 cases were mild poisoning. All patients had dizziness, headache, general fatigue, loss of appetite, nausea, vomiting and other general clinical symptoms. Six patients with severe poisoning had psychobehavioral abnormalities, including 4 patients with mania, delirium, ataxia, epileptic seizures. Glasgow was 15 points in mild and moderate poisoning. Of the 6 cases of severe poisoning, 4 cases of Glasgow were 9~11 points, and 2 cases of Glasgow were 13 points. 2 patients with severe poisoning had abnormal MRI in head, and the total abnormal rate was 12.50%. Toxic encephalopathy was considered in 1 case with abnormal signal of corpus callosum pressure, and patchy ischemic foci of left cerebral foot and mild cerebral atrophy in 1 case. The total abnormal rate of EEG was 56.25%. The abnormal rate of electroencephalogram in severe poisoning was 83.33%. There were 2 cases of severe abnormal electroencephalogram, 2 cases of moderate abnormal electroencephalogram and 1 case of slight abnormal electroencephalogram. Twelve patients were recovered and discharged from hospital. 4 cases of severe poisoning are still getting better, and there are still cerebellar ataxia symptoms such as dizziness and unstable walking. Conclusion In clinical work, attention should be paid to the identification of patients with mild and moderate TMT poisoning, and attention should be paid to the patients with severe TMT poisoning manifested by disturbance of consciousness. The positive rate of MRI test in TMT poisoning is low, and the lesion is nonspecific. Electroencephalogram test has a high positive rate in TMT poisoning, which can well reflect the degree of illness. Attention should be paid to the prevention and treatment of neurodegeneration caused by TMT poisoning.

Objective: Clinical analysis of sequelae of 16 patients with trimethyltin chloride (TMT) poisoning after 2 years. Methods: Sixteen patients with TMT poisoning from a waste recycling company in Ganzhou City in August 2016 were enrolled. They were investigated by questionnaires and assessed by various scales after two years. 6 cases of severe poisoning were examined by head MRI. The scale includes Hamilton Anxiety Scale (HAMA) , Depression Scale (HAMD) , Simple Mental State Examination Scale (MMSE) , Activity of Daily Living (ADL) , International Cooperative Ataxia Rating Scale (ICARS) . Results: 16 cases of TMT poisoning still have headache, dizziness and other symptoms. Instability of walking in 4 patients with severe poisoning, and the brain MRI manifestations included obvious atrophy of temporal lobe, hippocampus, insula lobe, cerebellum and ventricle enlargement. Two patients were rated as severe mixed anxiety and depression, one as moderate mixed anxiety and depression, and one as mild anxiety. 3 cases were diagnosed as dementia and 1 case as mild cognitive impairment. Two cases were totally dependent on living ability. ICARS scores were 66 points and 63 points respectively. Two cases were mildly dependent on living ability. ICARS scores were 28 points and 6 points respectively. There were 2 cases of mild mixed anxiety and depression in mild and moderate poisoning patients, and 1 case of mild cognitive impairment in each patient. They could live independently. ICARS scores were 0. Conclusion After 2 years of TMT poisoning, some patients still have general clinical symptoms such as dizziness, headache and so on. There are also mental and intellectual symptoms such as anxiety, depression and cognitive impairment. Some of patients with severe poisoning presented with dementia and cerebellar ataxia, and even lost independent living ability.

OBJECTIVE: To investigate the clinical characteristics of acute toxic encephalopathy caused by trimethyltin chloride(TMT). METHODS: Literatures related to TMT acute poisoning accidents occurred in China from 1998 to 2018 were collected and analyzed using the CNKI, WEIPU Database and WANFANG Database. The clinical manifestations, neuroimaging images, electroencephalography(EEG), treatment and other data were collected and analyzed. RESULTS: A total of 15 literatures were included in the study. These studies involved 15 incidents with 1 339 patients with TMT acute poisoning. Among them, 325 patients(24.3%) presented toxic encephalopathy. They were moderate to severe poisoning.The clinical manifestations were headache, dizziness, limb weakness, abnormal mental behavior and memory loss. Magnetic resonance imaging(MRI) and computed tomography(CT) were performed in 105 and 86 patients, respectively, with 29.5% and 26.7% of abnormal rate. There was no significant difference in the abnormal rate between the above two methods(P>0.05). 294 cases were examined by electroencephalogram. The abnormal rate was 93.9%, which was higher than that of the MRI and CT examination(P<0.05). Patients with toxic encephalopathy were treated with glucocorticoid. Some patients were treated with hyperbaric oxygen, nerve cell nutritional drugs and rehabilitation exercise after the conditions were stable. CONCLUSION: The patients with TMT toxic encephalopathy were moderately and severely poisoned by TMT. EEG examination is helpful for the diagnosis and treatment of TMT toxic encephalopathy.

OBJECTIVE: To explore the characteristics of peripheral nerve injury caused by occupational acute trimethyltin chloride(TMT) poisoning. METHODS: The clinical manifestations and test data of neurotic electrophysiology, pure tone hearing threshold and acoustic immittance in 16 patients with occupational acute TMT poisoning were retrospectively analyzed. The patients were followed up after 6 months of discharge. RESULTS: Among the 16 cases of occupational acute TMT poisoning, 6, 4 and 6 cases were with mild, moderate and severe poisoning, respectively. For the firstly appeared symptoms, 7 cases had abnormal mental behavior and memory loss, 5 cases had tinnitus and hearing loss, 5 cases had decreased visual acuity, 2 cases had diplopia and 2 cases had binocular pain. The main clinical manifestations included 8 cases of disturbance of consciousness, and 6 cases of abnormal orientation and aggressive behavior. After correction of hypokalemia, 7 cases of patients had limb muscle weakness, hypomyotonia and weakened tendinous reflect, 9 cases had decreased tactile sensation below the groin in the lower limbs, and 6 cases had instability of walking. The main manifestations of neuroelectrophysiological detection were: 9 patients(accounting for 56.3%) showed abnormal neuroelectromyography, 4 cases of severe poisoning had damaged motor nerve, sensory nerve axon and myelin sheath, and the proximal nerve was also partially damaged. There were 2 cases of moderate poisoning showing abnormal symptoms, the axon and myelin sheath of sensory nerve were damaged, one common peroneal nerve was demyelinated. Three cases of mild poisoning had one common peroneal nerve axon damaged, one proximal tibial nerve damaged, and the axon and myelin sheath of sensory nerve were damaged. Brainstem auditory evoked potential I wave and visual evoked potential P100 latency prolonged and amplitude decreased in some of the patients with mild, moderate and severe poisoning. The sensorineural hearing loss occurred in 81.3% of patients. CONCLUSION: Occupational acute TMT poisoning can cause damage to motor nerve, sensory nerve axon and myelin sheath of extremities. Both distal and proximal nerves might be involved. It can also damage cochlear hair cells and optic nerve. Attention should be paid to the early treatment of peripheral nerve damage, cochlear hair cell and optic nerve damage caused by TMT.