1/37. Quantitative MR diffusion mapping and cyclosporine-induced neurotoxicity.Apparent diffusion coefficient maps of two patients with cyclosporine-induced neurotoxicity showed areas of increased diffusion that corresponded to the characteristic regions of signal change on routine T2-weighted sequences. The majority of lesions subsequently resolved without residual T2 or diffusion signal alteration. These findings suggest that, in our patients, the neurotoxic effects of cyclosporine resulted in a partially reversible extravasation of fluid into the cerebral interstitium and were not associated with acute ischemia.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
2/37. Progressive multifocal leukoencephalitis (PML) in three patients treated with standard-dose fludarabine (FAMP).Since 1990 we have treated 60 patients with standard-dose fludarabine for chronic lymphocytic leukemia (B-CLL), on a compassionate basis. Three patients developed grade IV neurologic complications after treatment, with demyelination of white matter on magnetic resonance imaging (MRI) in patient # 1, diffuse demyelination, abnormal oligodendroglia and enlarged astrocytes at brain biopsy in patient no 2, and progressive multifocal leukoencephalitis (PML) with jc virus on brain biopsy in patient # 3. The neurotoxicity of fludarabine was often observed after administration of high doses (90-120 mg/m2). At standard doses (18-25 mg/m2) neurologic complications were observed in very few cases (0.2%). PML was observed in only 0.52% of patients with chronic lymphocytic leukemia (CLL), particularly those with advanced CLL. Our findings are consistent with the results of published studies and show an increase in neurologic complications in patients with advanced CLL treated with fludarabine. This increased vulnerability is probably multifactorial, but may be secondary to the immunodeficiency.- - - - - - - - - - ranking = 3.3223916806514keywords = brain (Clic here for more details about this article) |
3/37. Suspected ifosfamide-induced neurotoxicity.ifosfamide is an antineoplastic agent that requires hepatic activation to the cytotoxic active metabolite ifosforamide mustard. During metabolism, the byproduct, chloroacetaldehyde, which is structurally similar to both chloral hydrate and acetaldehyde, is produced. Secondary to its ability to cross the blood-brain barrier, this metabolite may be responsible for the neurotoxicity observed with ifosfamide. Any case of suspected ifosfamide-induced neurotoxicity, together with a decision to treat, must be determined on an individual patient basis. The differential diagnosis should include infection, laboratory abnormalities, and concomitant drugs. At this time, literature to support treatment modalities such as intravenous albumin and methylene blue is minimal.- - - - - - - - - - ranking = 2.7663949985465keywords = brain, cytotoxic (Clic here for more details about this article) |
4/37. diffusion-weighted MRI in cyclosporin A neurotoxicity for the classification of cerebral edema.Cyclosporin A, an immunosuppressive agent, is known to have neurotoxic effects, but until now, there has not been agreement on the underlying mechanism. Our report suggests, by using diffusion-weighted MRI, that the brain lesions caused by cyclosporin A, are probably related to vasogenic edema. This may explain the complete recovery of the lesions on imaging when cyclosporine therapy is stopped.- - - - - - - - - - ranking = 126.09803496125keywords = cerebral edema, edema, brain, cerebral (Clic here for more details about this article) |
5/37. Neurotoxicity associated with suspected southern Pacific rattlesnake (crotalus viridis helleri) envenomation.An 18-year-old man was bitten on the hand by a snake he believed to be a Southern Pacific rattlesnake (crotalus viridis helleri). Within minutes he developed generalized weakness, difficulty breathing, diplopia, dysphagia, and dysphonia. Neurological examination revealed ptosis and decreased motor strength. These symptoms partially improved after administration of Antivenin (Crotalidae) Polyvalent, but the patient continued to have difficulty walking for several days due to weakness. In addition to neurological symptoms, the patient also experienced pain immediately after the bite occurred and rapid swelling of the entire extremity, which extended beyond the shoulder. He complained of a metallic taste in his mouth and developed intense muscle fasciculations of the face, tongue, and upper extremities, which lasted for 2 days and did not improve with antivenin treatment. He exhibited laboratory evidence of coagulopathy and rhabdomyolysis. Although neurotoxins are known to occur in the venom of certain populations of rattlesnakes, only a few clinical reports describing severe neurological symptoms appear in the literature. To our knowledge, this is the first reported case of neurotoxicity associated with a suspected Southern Pacific rattlesnake envenomation.- - - - - - - - - - ranking = 0.012966157387195keywords = swelling (Clic here for more details about this article) |
6/37. fluorouracil-induced neurotoxicity.OBJECTIVE: To report a case of acute neurologic adverse effects related to fluorouracil administration and to review the neurotoxicity of this agent. CASE SUMMARY: A 73-year-old white man with a history of esophageal carcinoma was treated with fluorouracil 1,500 mg iv daily for four days. After completing treatment, he presented with sudden onset of confusion, cognitive disturbances, a cerebellar syndrome, and repeated seizures. A magnetic resonance image of the brain showed no structural abnormalities, and cerebrospinal fluid examination was normal; none of the other laboratory tests provided an explanation for his symptoms. The patient was treated with anticonvulsants, and the cognitive changes resolved in 72 hours. The cerebellar signs, however, did not resolve completely and persisted when the patient was examined two weeks after discharge. DISCUSSION: fluorouracil can cause both acute and delayed neurotoxicity. Acute neurotoxicity manifests as encephalopathy or as cerebellar syndrome; seizures, as seen in our patient, have rarely been reported. Acute neurotoxicity due to fluorouracil is dose related and generally self-limiting. Various mechanisms for such toxicity have been postulated, and treatment with thiamine has been recommended. Delayed neurotoxicity has been reported when fluorouracil was given in combination with levamisole; this form of subacute multifocal leukoencephalopathy is immune mediated and responds to treatment with corticosteroids. CONCLUSIONS: Clinicians should be aware of the adverse neurologic effects of fluorouracil and should include them in the differential diagnosis when patients receiving the drug present with neurologic problems.- - - - - - - - - - ranking = 1.6611958403257keywords = brain (Clic here for more details about this article) |
7/37. Reversible tacrolimus-induced neurotoxicity isolated to the brain stem.diplopia, nystagmus, visual hallucinations, and internuclear ophthalmoplegia developed in a 30-year-old woman 84 days after she received a matched, unrelated bone marrow transplant for chronic myeloid leukemia. A regimen of tacrolimus had been administered since the transplantation was performed. MR imaging revealed bilaterally symmetric regions of signal abnormality with abnormal contrast enhancement in the brain stem. No supratentorial abnormality was present. tacrolimus therapy was discontinued, and the symptoms resolved. MR imaging that was performed 10 days after tacrolimus was discontinued showed resolution of the abnormalities.- - - - - - - - - - ranking = 8.3059792016284keywords = brain (Clic here for more details about this article) |
8/37. Transient contrast encephalopathy after carotid artery stenting.PURPOSE: To report an unusual case of transient contrast encephalopathy arising after carotid artery stenting. CASE REPORT: An 82-year-old right-handed man with a recent history of transient ischemic events was admitted to the hospital for evaluation of carotid artery disease. During cerebral angiography, which identified a 90% right internal carotid artery stenosis, the patient received 25 mL of an ionic, low-osmolar contrast agent (ioxaglate) in each carotid artery. The following day he underwent successful carotid stenting, during which 180 mL of ioxaglate were used. He developed rapidly worsening confusion and left hemiparesis on the table. Noncontrast computed tomography showed marked cortical enhancement and edema of the right cerebral hemisphere in the distribution of the right anterior and middle cerebral arteries. The patient improved rapidly and by day 2 was completely recovered; magnetic resonance imaging documented no cortical edema and normal sulci. One month after the procedure, he was well, with patent carotid arteries. CONCLUSIONS: Transient neurotoxicity after carotid interventions must be differentiated from massive cerebral infarction and hyperperfusion syndrome, but the prognosis is excellent. However, subsequent contrast studies in a patient with this complication should be undertaken with extreme caution.- - - - - - - - - - ranking = 7.5972282568525keywords = edema, cerebral (Clic here for more details about this article) |
9/37. Ping-pong gaze in combined intoxication with tranylcypromine, thioridazine, and clomipramine.OBJECTIVE: This paper reports the occurrence of ping-pong gaze, a neuro-ophthalmological syndrome usually related to severe structural brain damage, in a patient intoxicated with tranylcypromine, thioridazine, and clomipramine. BACKGROUND: Although there have been some reports about the occurence of Ping-pong gaze after intoxications, it is usually related to severe bilateral hemispheric brain damage following stroke or traumatic injuries. METHOD: We report the case of a 56-year old woman who developed a neurotoxic syndrome with coma, hyperthermia, muscular rigidity, myoclonic jerks and tachycardia following an intoxication. Additionally rhythmic and pendular conjugate horizontal eye movements could be observed for three days, so that the diagnosis of ping-pong gaze was made. RESULTS: A treatment with dantrolene lead to complete remission of the neurotoxic syndrome with no signs of neurological or physical deficits. At the stage of regaining consciousness the eye movements became normal. CONCLUSION: In our case the combined intoxication with an monoamine oxidase inhibitor, a neuroleptic and a tricyclic agent lead to a neurotoxic syndrome and the occurrence of a rare neuro-ophthalmological syndrome usually related to bilateral hemispheric brain dysfunction.- - - - - - - - - - ranking = 4.983587520977keywords = brain (Clic here for more details about this article) |
10/37. muromonab-cd3-induced neurotoxicity: report of two siblings, one of whom had subsequent cyclosporin-induced neurotoxicity.muromonab-cd3 is widely used for immunosuppression in patients undergoing solid organ transplant. We report two siblings with oligomeganephronia and end-stage renal disease who developed encephalopathy and seizures from muromonab-cd3 following renal transplant. The first case is a 13-year-old girl who developed encephalopathy, seizure, and triparesis following renal transplant while muromonab-cd3 was used for immunosuppression. The second case was the 6-year-old sister of the first case, who also developed recurrent focal seizures while she was on muromonab-cd3 for renal transplant immunosuppression. In both cases, a sequential brain magnetic resonance image (MRI) showed progression of abnormalities from the cerebral cortex to the white matter. In the first case, the MRI normalized after muromonab-cd3 was discontinued. In the second case, the patient developed a leukoencephalopathy following cyclosporin administration. The pathophysiology of muromonab-cd3 encephalopathy is believed to be a disturbance to the blood-brain barrier mediated by cytokine release from lymphocyte stimulation by muromonab-cd3. Because the major histocompatibility complex genes are known to regulate cytokine responses, it is possible that the excessive production of cytokines that causes encephalopathy may occur in patients who share close major histocompatibility complex genes. muromonab-cd3 in a patient whose sibling has developed cerebral complications from its use should be administered with caution. The second case suggests that muromonab-cd3 encephalopathy predisposes patients to develop cyclosporin neurotoxicity. Because the pathogenesis of muromonab-cd3 encephalopathy and cyclosporin-related cerebral complications are both potentially mediated through a disturbance of the blood-brain barrier, it is possible that one agent may predispose a patient to the complication of the other.- - - - - - - - - - ranking = 7.983587520977keywords = brain, cerebral (Clic here for more details about this article) |
| | Next -> |