1/15. Acute dilated cardiomyopathy and central nervous system toxicity following propranolol intoxication.OBJECTIVE: We report a case of a 16-year-old boy who developed central nervous system (CNS) depression and acute dilated cardiomyopathy following ingestion of 3200 mg of propranolol in a suicide attempt. Early echocardiographic findings were the only sign of cardiac toxicity. DESIGN: A case report. SETTING: Pediatric intensive care unit of a teaching hospital. RESULTS: This child developed significant acute dilated cardiomyopathy and severe CNS depression 2 hours after ingesting 3200 mg of propranolol. The child was treated with gastric lavage, activated charcoal, and mechanical ventilation. Following the echocardiographic findings, treatment with isoprenaline hydrochloride and glucagon were given intravenously. Echocardiographic examination 12 hours following treatment showed normal left ventricular size and function. No change in pulse rate or blood pressure was reported on admission and during his hospitalization. DISCUSSION: In the early stages of propranolol and other lipophilic beta-blocker intoxication, severe CNS depression can develop in the absence of clinical signs of cardiac toxicity. Early echocardiographic evaluation is important and may prevent delay in diagnosis and treatment of cardiac toxicity.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/15. Superficial siderosis of the central nervous system: report of three cases and review of the literature.We present 3 cases and a review of the literature to demonstrate the current state of clinical diagnosis and therapy of superficial siderosis of the central nervous system. Typical symptoms were progressive cerebellar ataxia, spasticity and hearing loss. Repeated subarachnoid hemorrhage was indicated by persistent xanthochromia of the cerebrospinal fluid and confirmed by the presence of erythrophages, siderophages and iron-containing pigments. Deposition of free iron and hemosiderin in pial and subpial structures leads to intoxication of the central nervous system and represents the pathophysiological mechanism of superficial siderosis. Hypointensity of the marginal zones of the central nervous system on T2 weighted MR images indicates an iron-induced susceptibility effect and seems pathognomonic for superficial siderosis. In 39 of the 43 previously described cases superficial siderosis was verified by biopsy or autopsy. Today magnetic resonance imaging enables diagnosis at an early stage of the disease. Therapeutic management requires the elimination of any potential source of bleeding. In patients with unknown etiology no proofed therapy is yet available.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
3/15. central nervous system effects in acute thallium poisoning.We report the central nervous system manifestations, neuropsychological studies and brain magnetic resonance image (MRI) findings of two patients with acute thallium intoxication. Neurologically the patients suffered from confusion, disorientation, and hallucination in the acute stage, followed by anxiety, depression, lack of attention, and memory impairment, in addition to peripheral neuropathy. neuropsychological tests revealed an impairment of memory function, including reversed digital span, memory registration, memory recall, memory recognition, similarity, proverb reasoning, and verbal fluency. High concentrations of thallium were found in the urine, blood, and drinking water of these two patients. brain MRI showed lesions in the corpus striatum in one patient. During the follow-up periods, the clinical manifestations and neuropsychological studies showed a slowly progressive improvement, and a follow-up brain MRI 1.5 months later demonstrated a resolution of the lesions. We conclude that thallium intoxication might induce encephalopathy, and brain MRI studies demonstrated the acute-stage brain lesions in a severe intoxicated patient. In addition, neuropsychological tests also confirmed memory deficits, although the brain lesions in the corpus striatum might resolve.- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
4/15. evoked potentials in chronic n-hexane intoxication.Somatosensory, brainstem auditory and pattern-reversal visual evoked potentials (SEP, BAEP and PVEP) were studied in 5 patients with n-hexane polyneuropathy to determine if the CNS was affected. In SEPs, the median central conduction (N13-to-N20) was normal but the tibial central conduction (N22-to-P40) was delayed. The central conduction time (I-to-V interval) of the BAEP was also prolonged. However, the P100 latency of the PVEP was normal. The present data indicate that the spinal cord and the brainstem are primarily affected in chronic n-hexane intoxication.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/15. Chronic exposure to the fungicide maneb may produce symptoms and signs of CNS manganese intoxication.manganese (Mn) poisoning, a well-known hazard in miners and industrial workers, shares many features with Parkinson's disease. Two young agricultural workers with a parkinsonian syndrome, who mentioned exposure to the fungicide maneb (manganese ethylene-bis-dithiocarbamate), led us to investigate a new possible source of Mn intoxication. Fifty male rural workers with occupational exposure to maneb were compared with 19 rural workers without fungicide exposure. We noted significantly higher prevalence of plastic rigidity with cogwheel phenomenon, headache, fatigue, nervousness, memory complaints, and sleepiness in the exposed group. In addition, we saw other neurologic signs, such as postural tremor, cerebellar signs, and bradykinesia, although without statistical significance. The data suggest that occupational exposure to pesticides containing Mn is a possible source of Mn intoxication of the CNS.- - - - - - - - - - ranking = 1.2keywords = intoxication (Clic here for more details about this article) |
6/15. Neurological sequelae after intoxication with sodium valproate.A case of valproic acid poisoning with coma and neurological sequelae is presented. The course of the intoxication was severe with affection of the brain, heart and liver. The patient remained in coma for thirteen days. After this he recovered slowly although reduction in vision still persisted after two months. The toxicity of valproate is discussed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
7/15. Downbeat nystagmus with phenytoin.Downbeat nystagmus is generally the result of a structural lesion at the craniocervical junction. It has rarely been reported as a manifestation of metabolic disease or drug intoxication. We observed two patients with downbeat nystagmus secondary to phenytoin (Dilantin) intoxication. Both individuals had other features of phenytoin-induced central nervous system dysfunction with toxic blood levels of the drug (greater than 20 micrograms/ml). Complete resolution of the downbeat nystagmus followed the return of phenytoin levels to the therapeutic range.- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
8/15. Acute isoniazid intoxication: reversal of CNS symptoms with large doses of pyridoxine.Acute toxicity from ingestion of isoniazid (INH) is manifested by coma and seizures unresponsive to conventional therapy. Though small doses of pyridoxine can reverse the seizure activity of acute isoniazid toxicity, large doses of pyridoxine (B6) are needed to completely reverse the symptoms. A case report is presented demonstrating the need for large doses of pyridoxine to reverse the symptoms of isoniazid intoxication and the literature of isoniazid toxicity in the pediatric age group is reviewed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
9/15. Clinical and neuropathological aspects of long-term damage to the central nervous system after lithium medication.A female patient, who died at the age of 61 and had suffered from several manic-depressive psychoses for more than 30 years, developed three phases of intoxication under lithium therapy. There was a 15-year history of electro- and Pentetrazol-induced convulsive therapy prior to lithium medication; neuroleptics were still administered during lithium therapy. The last lithium intoxication, 3 years prior to death was during a low-dosage therapy with normal lithium levels followed by severe lasting impairment: akinesia, rigidity, dysarthria, ataxia, and an organic alteration in character. For the first time, neuropathological findings could be established in such a case: extensive damage to granule and purkinje cells in the cerebellum; gliosis in the dentate nucleus, the inferior olives, and the nucleus ruber; cytoplasmic inclusions in various nerve cells of the cranial nerve nuclei; cytoplasmic vacuoles, especially in the cells of the supra-optic nucleus. Surprisingly little damage could be found in the substantia nigra and in the neostriatum. The clinical course as well as the pattern and intensity of the brain damage oppose an interpretation as a consequence of preceding convulsive shock therapy.- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
10/15. hemoperfusion in theophylline neurotoxicity.Four patients with severe theophylline toxicity (theophylline levels of 60 to 180 micrograms/ml) are reported. Three patients with neurotoxicity were treated with hemoperfusion. Two of these were hemoperfused early after the onset of seizures; they recovered with no neurologic deficit. In the third patient hemoperfusion was delayed for 16 hours after uncontrolled seizures; severe brain damage resulted. The fourth patient, who had the highest peak theophylline level but no seizures, was successfully treated with conservative management and peritoneal dialysis. The role of hemoperfusion in severe theophylline intoxication is discussed.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
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