1/49. Fatal poisoning from liquid dimethylmercury: a neuropathologic study.Since ancient times, mercury has been recognized as a toxic substance. Dimethylmercury, a volatile liquid organic mercury compound, is used by a small number of chemistry laboratories as a reference material in nuclear magnetic resonance spectroscopy. To our knowledge, dimethylmercury has been reported in only three cases of human poisoning, each proving fatal. Very small amounts of this highly toxic chemical can result in devastating neurological damage and death. We report the neuropathologic findings in a fatal case of dimethylmercury intoxication occurring in a laboratory researcher that resulted from a small accidental spill. We compare these findings to those reported in one previously reported fatal case of dimethylmercury poisoning, and to earlier reports of monomethylmercury poisoning, and discuss the clinicopathologic correlation.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/49. Myoclonic encephalopathy and diabetes mellitus in a boy.We describe an 18-month-old boy with insulin-dependent diabetes mellitus who developed idiopathic myoclonic encephalopathy (dancing eye syndrome) at 26 months of age. The neurological symptomatology (multifocal myoclonus, opsoclonus, ataxia, behavioural disturbance) developed within 10 to 14 days after presentation. Biological, neuroradiological, and scintigraphic examination excluded CNS infectious diseases, intoxication, or tumours. At onset of diabetes mellitus, anti-glutamic-acid decarboxylase (GAD) antibodies were observed, and markedly increased in titre when myoclonic encephalopathy occurred. Corticosteroid treatment resulted in a decrease in anti-GAD autoantibody titres and the disappearance of neurological disturbances. As GAD is expressed both in pancreatic beta-cells and cerebellar purkinje cells, it is possible that a common autoimmune disorder in this patient may account for both the diabetes and myoclonic encephalopathy.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
3/49. Hyperbaric oxygen for carbon monoxide poisoning-induced delayed neuropsychiatric sequelae.The clinical manifestations of delayed neuropsychiatric sequelae after carbon monoxide (CO) intoxication are variable. In addition, there is no specific therapy for these complications. Fortunately, these complications have occurred less frequently in recent years, probably due to the usage of hyperbaric oxygen (HBO) therapy. We report an 8-year-old boy who developed late psychiatric disturbances 2 days after full recovery of consciousness from initial CO intoxication. His neuropsychiatric symptoms included consciousness disturbance, motor dysfunction, chorea, aphasia and agnosias. He received HBO therapy at 2.0 barr for 60 minutes once a day for 7 consecutive days. Three weeks later, he was functioning normally with no neuropsychiatric symptoms. A literature review concluded that HBO may be effective in treating neuropsychiatric sequelae. Moreover, immediate administration of HBO during acute CO intoxication may prevent these complications.- - - - - - - - - - ranking = 3keywords = intoxication (Clic here for more details about this article) |
4/49. brain ultrastructure in Reye's syndrome.Cerebral biopsies were obtained for electron microscopy 48 and 72 hours after the onset of encephalopathy from a child with severe Reye's syndrome. Gravely ill at the time of craniectomy to relieve cerebral hypertension, the child survived and recovered good brain function; therefore, the biopsy findings appear to reflect the organelle pathology of the brain at a severe yet reversible stage in the disease process. The cardinal ultrastructural changes in the brain in Reye's syndrome are astrocyte swelling and partial deglycogenation, myelin bleb formation and universal injury of neuron mitochondria. The mitochondrial injury consists of matrix disruption with moderate but not massive swelling. dilatation of rough endoplasmic reticulum and nuclear changes occurred only in neurons with severely altered mitochondria. The organelle pathology of the brain in this case did not resemble the organelle pathology of the brain in human "hepatic encephalopathy" or in experimental ammonia intoxication in primates. The mitochondrial ultrastructure of the cerebral neurons resembled the unique mitochondrial ultrastructural changes seen in the liver parenchyma in Reye's syndrome.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/49. Acute intoxication with sodium valproate.Two epileptic patients developed an acute toxic encephalopathy consisting of altered behavior, deteriorating seizure control, and confusion while taking sodium valproate alone. serum valproate levels were greater than 100 microgram/ml in both. Toxic symptoms resolved when the dose of valproate was reduced, with a consequent fall in serum concentration of the drug.- - - - - - - - - - ranking = 4keywords = intoxication (Clic here for more details about this article) |
6/49. MR changes after acute cyanide intoxication.We describe MR changes that occurred 3 and 6 weeks after a suicide attempt with cyanide. The toxicity of cyanide causes damage, primarily to the basal ganglia, and those changes were visible as altered signal intensity on the first MR images. Extensive areas of hemorrhagic necrosis were seen 6 weeks later. Our case shows pseudolaminar necrosis along the central cerebral cortex 3 weeks after cyanide poisoning, showing that the sensorimotor cortex is also a site for toxic necrosis because of its high oxygen dependency.- - - - - - - - - - ranking = 4keywords = intoxication (Clic here for more details about this article) |
7/49. Subacute encephalopathy with seizures in alcoholism.Generalised seizures are a common manifestation of acute alcohol intoxication. Alcohol is known to precipitate generalised seizures in patients with focal brain pathology. A rare case of secondarily generalised seizures precipitated by alcohol in a patient without an underlying focal brain lesion is reported. Electroencephalopgraphy (EEG) showed periodic lateralised epileptiform discharges (PLEDs) on the side contralateral to the focal motor fits.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
8/49. Acute encephalopathy in siblings. reye syndrome vs salicylate intoxication.siblings, aged 9 and 7 years, had simultaneous onset of vomiting, disorientation, ataxia, and coma. Both children had prodromal symptoms of upper respiratory tract infections, and had been treated with large doses of aspirin. Laboratory data showed evidence of hepatocellular dysfunction, with an elevated serum ammonia level in one patient; salicylate levels were 50 and 44 mg/100 ml. The child who died had autopsy evidence of cerebral edema and fatty liver. The difficulty in clinically differentiating reye syndrome from salicylate intoxication is discussed.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
9/49. Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency.This report concerns two patients (female, 9 and 6 years) who were diagnosed with megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS). Although they exceeded the usual life expectancy of patients diagnosed with MMIHS because of total parenteral nutrition (TPN), they demonstrated progressive neurological deficits and showed histopathological features in the brain. Both patients were diagnosed with MMIHS in the neonatal period and were fed by TPN. The first patient developed visual and gait disturbances at the age of 7 years. Two months later, she developed dysarthria and muscular weakness, and could not maintain her posture. The level of serum selenium was extremely low. The second patient developed flexion and spasticity of the extremities followed by decorticate posture at the age of 3 years. Both patients died of sepsis. The brain weights of the two cases were 880 g and 715 g. In both cases, severe neuronal loss and gliosis were present in the medial convolutions of the occipital lobe, including the visual cortex. The postcentral gyrus and temporal transverse gyrus were also involved. In addition, extensive loss of purkinje cells and granular neurons, and gliosis were observed in the cerebellum. We measured the selenium content of the brains and livers using the graphite furnace atomic absorption spectrometry method. selenium was not detected in either brain, although the livers of both cases contained a low level of selenium. On immunohistochemical examination of the anti-oxidative enzymes, histiocyte-macrophage lineage cells in MMIHS cases, including microglia and kupffer cells, showed only a weak reaction for glutathione peroxidase, of which selenium is an essential component. However, the cells in the control cases were strongly positive. In cases of MMIHS and methylmercury intoxication, the brain features similar lesions, in both their topographical and histopathological aspects. We considered that the brain lesions of the MMIHS patients mainly resulted from oxidative damage of the brain related to the low levels of glutathione peroxidase and other selenoproteins due to selenium deficiency.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
10/49. Posterior encephalopathy with vasospasm: MRI and angiography.Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
| | Next -> |