1/13. 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) |
2/13. carbon disulfide vasculopathy: a small vessel disease.We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
3/13. Twenty-nine years after carbon monoxide intoxication.Carbon monoxide (CO) is a worldwide environmental toxin and a leading cause of deliberate or accidental poisoning. There is an extensive literature devoted to the clinical features and treatment of those victims who have survived acute CO poisoning for a short length of time. The long-term sequelae of non-fatal poisoning have received scanty references, and the prospects for the long-lasting survivors of acute CO intoxication are less clear. literature review uncovered reports of only three patients who were followed for a considerable period of time. We present a case of CO poisoning with progressive neurological and psychological deterioration that began 17 years after recovery from a severe, accidental CO asphyxia. The patient was examined in the neurology out patient clinic 29 years after the initial CO intoxication. We believe the unique status of this patient, her similarity to one other case in the literature and the circumstances allowing correlation of the clinical picture to the CO poisoning warrants emphasis.- - - - - - - - - - ranking = 6keywords = intoxication (Clic here for more details about this article) |
4/13. gerstmann syndrome in systemic lupus erythematosus: neuropsychological, neuroimaging and spectroscopic findings.gerstmann syndrome (GS) comprises four interlaced neuropsychological symptoms including finger agnosia, right-left confusion, agraphia, and acalculia. While GS is commonly associated with focal lesions to the region of the left angular gyrus, it has also been associated with numerous diffuse etiologies including atrophy, alcoholism, carbon monoxide poisoning, lead intoxication and anaphylactic shock. Thus, a vigorous debate has emerged as to whether GS represents a syndrome arising from general brain decline or a distinct and localizing lesion. We report a right-handed patient who developed neuropsychological dysfunction secondary to systemic lupus erythematosus (SLE). Neuropsychological evaluation found the patient to exhibit symptoms consistent with the GS tetrad, as well as general cognitive decline. magnetic resonance imaging revealed a distinct focal lesion of the left parieto-occipital white matter underlying the angular gyrus as well as diffuse atrophy. (1)H-magnetic resonance spectroscopy revealed substantial metabolic derangement in a voxel placed within the visible lesion, although substantial metabolic derangement was observed in regions remote from the focal pathology. Thus, GS in this first case in SLE would appear to comprise a focal neurological tetrad of disorders within a more general pattern of cognitive decline and metabolic derangement.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/13. Butane abuse associated Encephalopathy.Butane contained in household products is easily available for abuse and is not subject to legal prosecution in germany. The toxicological properties of butane mainly affect the heart and the CNS. A serious pathophysiological mechanism is asphyxia due to the replacement of oxygen by butane. We report an abusive butane inhalation in a 15-year old girl, resulting in cardiopulmonary resuscitation and subsequent development of severe brain damage. After reviewing the medical literature and questioning German toxicological information centres it became obvious, that abuse of butane is an increasing problem. We give an survey about the complications associated with butane intoxication.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
6/13. An autopsied case of dentatorubropallidoluysian atrophy with atypical pathological features.This is a report of an autopsied case of dentatorubropallidoluysian atrophy (DRPLA) with atypical neuropathological findings. The patients was a 31-year-old female. Her clinical symptoms were epileptic seizures, cerebellar ataxia, choreoathetosis and dementia. A neuropathological examination revealed the fibrillary gliosis in various areas of the CNS and severe degeneration in the cerebellar cortex and nucleus fasciculi dorsalis in addition to a marked degeneration of the dentatorubropallidoluysian systems. The present case is diagnosed neuropathologically as DRPLA associated with the findings of chronic diphenylhydantoin intoxication and epileptic brain damage.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
7/13. Transient tic disorder following carbon monoxide poisoning.We report a 12-year-old male patient who developed transient motor and vocal tics twelve days after carbon monoxide (CO) poisoning. Cranial magnetic resonance image (MRI) of the patient showed bilateral symmetric hyperintensity in the caudate nucleus and putamen. Tic disorder was successfully treated with haloperidol. Thirty-three months after CO poisoning, the patient was asymptomatic and MRI revealed atrophy in caudate nucleus and putamen. The mechanism of tic disorder in CO intoxication is discussed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
8/13. Clinical and CT scan findings in a case of cyanide intoxication.A 39-year-old man showed a combination of severe parkinsonism and progressive dystonia following attempted suicide with sodium cyanide. Computed tomography (CT) scan showed bilateral lucencies in the putamen and external globus pallidus. The topography of lesions on CT scan closely correlated with the pathological findings described in a previous report of cyanide-induced parkinsonism. This is the first reported case of cyanide intoxication with delayed-onset dystonia.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
9/13. Cerebellar atrophy following acute intoxication with phenytoin.A patient developed marked cerebellar atrophy after a single suicidal intoxication with 7 grams phenytoin. The clinical signs of cerebellar dysfunction subsided very slowly and incompletely within 18 months. We documented the cerebellar atrophy by CTs 4 weeks and 1 year after the intoxication, and we suggest that a single severe acute intoxication with phenytoin may directly cause cerebellar degeneration.- - - - - - - - - - ranking = 7keywords = intoxication (Clic here for more details about this article) |
10/13. Cerebellar atrophy following phenytoin intoxication.Cerebellar degeneration has been demonstrated in several patients receiving phenytoin therapy. In most cases it has been unclear, however, whether the degeneration was caused by the drug per se or by other mechanisms known to lead to cerebellar damage. We describe a patient who developed a marked cerebellar atrophy, demonstrated on computed tomographic scan, following an episode of acute, severe phenytoin intoxication. The patient received phenytoin prophylactically for 2 1/2 months after an uncomplicated subarachnoid hemorrhage and was in good health when the treatment was started. He has never had seizures, and no other possible cause of chronic cerebellar changes is known. The initially severe clinical signs of cerebellar dysfunction have subsided slowly. We conclude that phenytoin can directly cause cerebellar degeneration.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
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