No abstract available.
Neurotoxicity Syndromes* ; Solvents*

Humans ; Neurotoxicity Syndromes ; Paraquat ; toxicity

Humans ; Neurotoxicity Syndromes ; etiology ; Xylenes ; toxicity

Animals ; Biomarkers ; Hexanes ; poisoning ; toxicity ; Humans ; Neurotoxicity Syndromes ; etiology

Oculogyric crisis is an acute dystonia involving ocular muscles characterized by sustained conjugate upward or lateral deviation of the eyes. Metronidazole is a commonly used antimicrobial agent in treatment of anaerobic infections. However, its long-term use can cause toxic encephalopathy particularly in patients with hepatic dysfunction. Here, we describe a case of oculogyric crisis as a presenting manifestation of metronidazole-induced encephalopathy.
Brain Diseases ; Dystonia ; Humans ; Metronidazole ; Muscles ; Neurotoxicity Syndromes

Viagra has been prescribed worldwide to treat men with erectile dysfunction. Clinical trials have shown that Viagra may cause various kinds of adverse effects include some central nervous system (CNS) adverse effects. Although extremely rare, toxic encephalopathy also can be one of those effects. This report presents a case of encephalopathy caused by Viagra in correlation with its radiologic findings. Its pharmacologic mechanism and potential effects on the biochemistry of the CNS are reviewed.
Biochemistry ; Brain Diseases ; Central Nervous System ; Erectile Dysfunction ; Humans ; Male ; Neurotoxicity Syndromes* ; Sildenafil Citrate*

Metronidazole is commonly used for brain abscess but is not well known for its neurotoxic complications. Metronidazole-induced encephalopathy (MIEP) is toxic encephalopathy associated with the use of metronidazole. We experienced a case of brain abscess which developed reversible severe MIEP during treatment period. Although MIEP occurs in typical locations, it is not easy to differentiate from other conditions such as cerebral infarction, demyelinating diseases and metabolic diseases. Neurosurgeons should be aware that severe MIEP can occur during the use of metronidazole though it is not common.
Brain ; Brain Abscess ; Cerebral Infarction ; Demyelinating Diseases ; Humans ; Metabolic Diseases ; Metronidazole ; Neurotoxicity Syndromes

OBJECTIVETo investigate the clinical features, cranial MRI and treatment of toxic encephalopathy induced by 1, 2-dichloroethane (1, 2-DCE).

METHODSThe clinical, MRI features and treatment of 5 patients with toxic encephalopathy induced by 1,2-DCE were observed and analyzed.

RESULTSFive patients all presented with subacute onset with a history of direct exposure to 1,2-DCE. Lumbar cerebrospinal fluid pressures were all increased in 5 patients. All 5 patients had obvious intracranial hypertension. Liver and kidney function had no obvious abnormalities; Cranial MRI showed T1WI low signal and T2WI high signal in bilateral hemispheric white matter, cerebellar dentate nucleus and globus pallidus. After the treatment of dehydrating agent, glucocorticoid and supportive treatment, four patients were clearly improved, and one patient had cerebral hernia formation.

CONCLUSIONThe main neurological clinical features in patients with 1,2-DEC poisoning is obvious intracranial hypertension. The prognosis is usually good with early and long term use of glucocorticoids and dehydrating agent in poisoning patients.

Adult ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Neurotoxicity Syndromes ; diagnosis ; therapy ; Young Adult

OBJECTIVETo establish a rat model of 1,2-dichloroethane (DCE)-induced subacute toxic encephalopathy.

METHODSSixty Sprague-Dawley rats were randomly divided into five groups: negative control, positive control, low-dose DCE (1 472 mg/m(3)), middle-dose DCE (2 550 mg/m(3)), and high-dose DCE (4 418 mg/m(3)). The three DCE groups received static inhalation of DCE 6 hours a day for 6 consecutive days. The positive control group received intraperitoneal injection of lipopolysaccharide (5 mg/kg) and were sacrificed 8 hours after injection. Blood and brain tissue were collected, followed by determination of brain water content and HE staining for pathological examination of brain tissue.

RESULTSThe rats in DCE groups suffered decreased body weight with increasing DCE dose (P < 0.01), and brain water content rose with increasing DCEdose. The brain water content of middle-dose DCE group (80.09 ± 0.14%) and high-dose DCE group (80.28±0.10%) increased significantly as compared with that of the negative control group (79.46±0.23%) (P < 0.001). Optical microscopy discovered loose structure and vasodilation in the brain tissue of middle-dose DCE group, indicating obvious brain edema; the high-dose DCE group and positive control group had spongiform and vacuolated brain tissues with severe vascular dilation, indicating severe brain edema.

CONCLUSIONA rat model of subacute toxic encephalopathy induced by 1, 2-dichloroethane has been successfully established.

Animals ; Disease Models, Animal ; Ethylene Dichlorides ; toxicity ; Male ; Neurotoxicity Syndromes ; Rats ; Rats, Sprague-Dawley

Acute Disease ; Adult ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Male ; Neurotoxicity Syndromes ; therapy