1/7. 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) |
2/7. Late onset polyneuropathy due to organophosphate (DDVP) intoxication.BACKGROUND: Organophosphate intoxication can cause some well-known life threatening acute neurological complications such as seizures, paralysis, neuromuscular and cardiac conduction disorders. Less often, a predominantly motor and delayed axonal neuropathy can occur. This syndrome is due to inhibition of neuropathy target esterase. CASE REPORT: A 30-year-old woman attempted suicide by drinking approximately 1,000mg/kg dimethyl-2,2-dichloro vinyl phosphate (DDVP). After a muscarinic and cholinergic syndrome lasting four days, she developed a purely motor distal axonal polyneuropathy on the fifth week after ingestion confirmed by electroneuromyography and sural nerve biopsy. Neurological examination and electroneuromyography revealed a slight recovery at the end of the 21st month. CONCLUSION: This case of late onset polyneuropathy caused by organophosphate intoxication had unusual features such as intact sensory nerves and worse prognosis when compared to previously reported cases.- - - - - - - - - - ranking = 6keywords = intoxication (Clic here for more details about this article) |
3/7. Late-onset distal polyneuropathy due to acute organophosphate intoxication case report.Intoxications due to organophosphate insecticides are common in our country, since agriculture has an important place. Besides the well known acute cholinergic toxicity, these compounds may cause late-onset distal polyneuropathy occurring two to three weeks after the acute exposure. An eight-year-old boy and a 13-year-old girl admitted to the hospital with gait disturbances. Beginning 15 and 20 days, respectively, after organophosphate ingestion. neurologic examination revealed bilateral dropped foot, absent achilles tendon reflexes and peripheral sensory loss. electromyography demonstrated motor weighed sensory-motor polyneuropathy with axonal degeneration significant in the distal parts of bilateral lower extremities. Biochemical, radiological findings and magnetic resonance imagings were normal. The two cases were taken under a physiotherapy program. The two cases are presented here since organophosphate poisonings are common in our country, and since late-onset polyneuropathy is not a well known clinical presentation as acute toxicity.- - - - - - - - - - ranking = 4keywords = intoxication (Clic here for more details about this article) |
4/7. Reversible motor and sensory peripheral neuropathy in a patient following acute carbon monoxide intoxication.central nervous system complications following carbon monoxide (CO) poisoning are well reported in the literature but peripheral neuropathy is under-recognized. We report the clinical and electrophysiological studies of the transient peripheral neuropathy developed in a patient following acute CO intoxication. A 27-year-old woman was found unconscious with severe hypoxia and 34.5% serum level of carboxyhemoglobin. She progressed favourably after hyperbaric oxygen therapy. Neurological examination revealed bilateral pyramidal signs. The patient referred weakness and sensory abnormalities in her right foot. An electroencephalogram did not show focal abnormalities and brain magnetic resonance was normal. Needle electromyography of weak right tibialis anterior muscle showed a reduced recruitment pattern but no spontaneous activity. Electroneurographic evaluation revealed findings compatible with a motor and sensory peripheral neuropathy in nerves of both lower limbs. In few months complete clinical recovery was reached, and the electroneurography showed normality a year later Reversible peripheral neuropathy should be considered as a possible neurological complication following acute CO poisoning. The electrophysiological studies were essential for its diagnosis and follow up.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
5/7. Axonal polyneuropathy after acute dimethylamine borane intoxication.OBJECTIVE: To study a patient with axonal polyneuropathy due to acute dimethylamine borane (DMAB) intoxication. PATIENT: confusion and drowsiness in the acute stage, followed by cognitive impairments and polyneuropathy, are reported in a chemical factory worker after acute exposure to DMAB. RESULTS: Nerve conduction studies indicated axonal polyneuropathy, particularly in the motor nerves. sural nerve biopsy studies 3 months later revealed an axonal degeneration with a mild decrease of fiber density in the large myelinated fibers. Quantitative sensory testing also disclosed an impairment of pinprick, temperature, and touch sensations. Cutaneous nerve biopsy studies 9 months later demonstrated a moderate loss of epidermal nerves. During the follow-up period of 1.5 years, the clinical features and serial nerve conduction studies showed a steady improvement. CONCLUSIONS: Since DMAB is a new product and has been widely used recently in the manufacturing of semiconductors and electronics, we conclude that DMAB intoxication may produce motor-predominant axonal polyneuropathy and that the establishment of a threshold limit value is warranted.- - - - - - - - - - ranking = 6keywords = intoxication (Clic here for more details about this article) |
6/7. Severe generalized polyneuropathy in lithium intoxication.A woman developed a severe generalized polyneuropathy in acute lithium intoxication. Nerve conduction studies suggested an axonal neuropathy. Her peripheral nerve problem became manifest after treatment had already started; therefore, a high serum lithium level is not considered to be the only factor for the development of a severe polyneuropathy in lithium intoxication.- - - - - - - - - - ranking = 6keywords = intoxication (Clic here for more details about this article) |
7/7. Effect of temperature on motor responses in organophosphate intoxication.We studied the effect of temperature on median motor responses in a 41-year-old man with organophosphate intoxication. At 32 degrees C, a normal amplitude compound motor action potential (CMAP) and a smaller spontaneous repetitive discharge (SRMAP) were present. With warming to 39 degrees C, the CMAP amplitude decreased 20%, while the SRMAP amplitude decreased 33%. With cooling to 14 degrees C, the CMAP amplitude decreased 9%, while the SRMAP became unobtainable. Possible mechanisms for these findings are discussed.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |