Encefalopatia reversível induzida por contraste após embolização com espiras por epistaxe / Reversible contrast-induced encephalopathy after coil embolization of epistaxis

RESUMO Uma mulher com 37 anos de idade, gestante de 35 semanas, foi admitida em um hospital local em razão de epistaxe grave, que resultou em choque e em necessidade de realização de cesárea emergencial. Após falha do tamponamento para controlar a hemorragia, decidiu-se por tratamento angiográfico. Após o procedimento, ela foi admitida à unidade de terapia intensiva neurocrítica, encontrando-se confusa e agitada, com necessidade de sedação e intubação orotraqueal. Na unidade de terapia intensiva, as investigações incluíram exames de ressonância magnética, punção lombar com painel viral, eletroencefalograma, testes para autoimunidade e avaliações hidroeletrolítica e metabólica. O exame de ressonância magnética mostrou área puntiforme restrita na corona radiata esquerda nas sequências de imagens pesadas em difusão, além de leve edema cortical posterior (sem restrição à difusão), e o eletroencefalograma mostrou atividade lenta difusa moderada, atividade frontoparietal lenta e escassos componentes paroxísticos associados no hemisfério esquerdo. Outros exames não mostraram alterações relevantes. Por causa da relação temporal e da história clínica, assim como imagens de ressonância magnética, formulou-se o diagnóstico de encefalopatia induzida por contraste. A sedação foi retirada após 2 dias na unidade de terapia intensiva, e a paciente foi extubada, verificando-se completa recuperação neurológica dentro das 24 horas seguintes.

ABSTRACT A 37-year-old woman (35 weeks pregnant) was admitted to a local hospital due to severe epistaxis resulting in shock and the need for emergency cesarean section. After failure to tamponade the bleeding, angiographic treatment was provided. After the procedure, she was admitted to the neurocritical intensive care unit and was confused and agitated, requiring sedation and endotracheal intubation. In the intensive care unit, diagnostic investigations included brain magnetic resonance imaging, lumbar puncture with viral panel, electroencephalogram, tests for autoimmunity, and hydroelectrolytic and metabolic evaluations. Magnetic resonance imaging showed a puntiform restricted diffusion area on the left corona radiata on diffusion weighted imaging and mild cortical posterior edema (without restricted diffusion), and an electroencephalogram showed moderate diffuse slow activity and fronto-temporal slow activity of the left hemisphere with associated scarce paroxysmal components. The other exams did not show any relevant alterations. Due to the temporal relationship, the clinical history and the magnetic resonance imaging results, a diagnosis of contrast-induced encephalopathy was made. After 2 days in the intensive care unit, sedation was withdrawn, the patient was extubated, and total neurological recovery was verified within the next 24 hours.

Complicaciones neurológicas tras intervencionismo cardíaco percutáneo / Neurological complications following percutaneous coronary intervention

Resumen Introducción: Las complicaciones neurológicas agudas del intervencionismo cardiaco percutáneo (ICP) son variadas e infrecuentes, pero pueden resultar fatales. Casos: Presentamos un ictus isquémico -II- (caso 1), y dos casos de encefalopatía por contraste -EC- (2 y 3). Dos varones (1 y 2) y una mujer (3), con FRCV y edad media de 76 años. Los tres pacientes debutaron con focalidad neurológica aguda (FNA) al finalizar el procedimiento, lo que motivó la activación de código ictus intrahospitalario desde cardiología. 2 y 3 asociaron además agitación. El TC multimodalfue normal en 2y 3, y mostró oclusión de M1 izquierda en 1. Se desestimó tratamiento de reperfusión cerebral en 1 por anticoagulación. El EEG fue normal en 2 y mostró paroxismos focales en hemisferio izquierdo de baja persistencia en 3.2 y 3 fueron tratados con sueroterapia y anticomiciales (3), quedando asintomáticos en las primeras doce horas. 1 falleció a los diez días por infección respiratoria. Conclusiones: En presencia de FNA tras ICP, la sospecha clínica resulta vital para establecer un diagnóstico diferencial precoz entre II y EC, y considerar tratamiento específico urgente, ya que puede modificar el pronóstico del paciente.

Introduction: Percutaneous coronary intervention (PCI) related neurological complications are wide and rare, but may be fatal. Cases: We present an ischaemic stroke -IS- (case 1), and two cases of contrast induced encephalopathy -CIE- (2 and 3). Two males (1 and 2) and one woman (3), with vascular risk factors and an average age of 76. All of them presented with acute focal neurological symptoms at the end of the procedure and Stroke Code was activated inmediately. 2 and 3 also associated psychomotor agitation. Multimodal CT head was normal in 2 and 3, whereas it showed a left Ml occlusion in 1. Reperfusion treatment was contraindicated 1 due to anticoagulation. EEG was normal in 2 and showed focal paroxisms in left hemisphere in 3.2 and 3 were successfully treated with fluids and antiepileptics (3). 1 died due to respiratory infection. Conclusions: Acute focal neurological symptoms following PCI should make us consider IS and CIE and provide the patient with urgent specific treatment.

Beneficial effects of glucan against cisplatin side effects on the nervous system in rats 1

ABSTRACT PURPOSE: To investigate the protective effect of Bg on cisplatin (CP)-induced neurotoxicity in rats. METHODS: Twenty eight rats were randomly distributed into four groups. The first group was kept as a control. In the second group, CP was given at the single dose of 7 mg/kg intraperitoneally. In the third group, βg was orally administered at the dose of 50 mg/kg/day for 14 days. In the fourth group, CP and βg were given together at the same doses. RESULTS: CP treatment caused significant oxidative damage via induction of lipid peroxidation and reductions antioxidant defense system potency in the brain tissue. In addition, histopathological damage increased with CP treatment. On the other hand, βg treatment largely prevented oxidative and histopathological negative effects of CP. CONCLUSIONS: Cisplatin has severe neurotoxic effects in rats and βg supplementation has significant beneficial effects against CP toxicity depending on its antioxidant properties. Thus, it appears that βg might be useful against CP toxicity in patients with cancer in terms of nervous system.

Tacrolimus induced reversible encephalopathy: a case report

Tacrolimus is a novel immunosuppressant used to prevent graft rejection after allogenic organ transplantation. Serious neurological complications of tacrolimus are rare. We present a lady who developed confusion, paresthesiae and visual hallucinations while on tacrolimus following a renal transplant. Her tacrolimus level was high and she improved on stopping the drug. This case highlights the reversible encephalopathy induced by tacrolimus

Cefepime encephalopathy and normal renal function / Encefalopatia induzida por cefepime em um paciente com função renal normal

BACKGROUND: Several cases of cefepime neurotoxicity have been reported. Herein reported is a case of cephalosporin-associated neurotoxicity in apatient with normal renal function. CASE REPORT: A 64-year-old woman with a history of post-transplantation chronic myeloid leukemia was admittedto hospital due to hyporexia, fever, productive cough and mild dyspnea. Initial blood screen revealed pancytopenia and a normal renal function.Intravenous cefepime was empirically started and after 40 hours the patient developed sudden mental confusion. Neurological examination was normal. Cranial computed tomography and brain magnetic resonance scans were normal. Electroencephalography showed triphasic waves of diffuse slowness without ongoing epileptic activity. Lumbar puncture was normal. Cefepime neurotoxicity was promptly considered and antibiotics were switched to piperacillin and tazobactam. After five days, the patient recovered completely with remission of myoclonus. CONCLUSIONS: Awareness should be given to possible central nervous system complications induced by cefepime, especially in the elderly, even without renal failure

INTRODUÇÃO: Existem vários relatos de casos de toxicidade do sistema nervoso central induzida pelo cefepime. Relata-se um caso de toxicidade do sistema nervoso central associada ao uso de uma cefalosporina em um paciente com função renal normal. RELATO DE CASO: Uma mulher de 64 anos com história de transplante de medula óssea devido a leucemia mielóide crônica foi admitida ao hospital devido a hiporexia, febre, tosse produtiva e dispnéia leve. Os exames laboratoriais de rotina demonstraram pancitopenia e função renal normal. O cefepime intravenoso foi empiricamente iniciado e, após 40 horas da administração, o paciente apresentou quadro súbito de confusão mental. Exame neurológico foi normal, assim como a tomografia computadorizada craniana e a ressonância magnética encefálica. O eletroencefalograma demonstrou ondas trifásicas de lentificação difusa sem evidência de atividade epileptiforme. O líquor estava normal. A toxicidade do sistema nervoso central pelo cefepime foi rapidamente considerada e o antibiótico foi trocado para piperacilina e tazobactan. Após cinco dias, o paciente apresentou recuperação completa com remissão da mioclonia. CONCLUSÃO: Deve-se dar atenção às possíveis complicações do sistema nervoso central induzidas pelo cefepime, especialmente em idosos, mesmo sem insuficiência renal.

Metronidazole-induced encephalopathy in a patient with liver cirrhosis / 대한간학회지

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.

Encefalopatía inducida por ácido valproico: serie de siete casos / Valproic acid-induced encephalopathy: series of seven cases

Introducción: La encefalopatía inducida por ácido valproico (AV) es una complicación infrecuente caracterizada por disminución del nivel de conciencia, déficits neurológicos focales, enlentecimiento cognitivo, vómitos, somnolencia y letargia, con o sin hiperamonemia. El electroencefalograma (EEG) muestra enlentecimiento difuso. Los hallazgos EEG, las manifestaciones clínicas y la hiperamonemia tienden a normalizarse con la suspensión del AV. Pacientes y Métodos: Se presenta una serie de 7 pacientes que desarrollaron encefalopatía por AV, en el Servicio de Neurología del Hospital del Salvador, entre 2003 y 2010. Se detallan dos casos clínicos ilustrativos. Resultados: La serie está compuesta por 5 mujeres y 2 hombres. Cinco pacientes desarrollaron hiperamonemia (amonemia sobre 50 ug/dl). El promedio de edad fue de 55 años (37 a 82 años). Las dosis de AV fueron de 375 a 2.000 mg (promedio = 903). La latencia entre el inicio o ajuste significativo del AVfue de 3 días hasta 16 años y un mes. Todos los pacientes presentaban daño orgánico cerebral. La politerapia con fenobarbital, fenitoína y carbamazepina fue significativa. El patrón de EEG más frecuente fue el enlentecimiento difuso. Una paciente de 82 años desarrolló actividad pseudoperiódica sugerente de un status epilepticus no convulsivo. En todos los pacientes hubo normalización clínica, de laboratorio y del EEG con la suspensión del AV. Conclusiones: La encefalopatía inducida por ácido valproico es una reacción adversa reversible pero potencialmente fatal que requiere un alto índice de sospecha. El daño orgánico cerebral y la politerapia parecen ser importantes factores de riesgo para su producción.

Introduction: Valproic acid (VA) induced encephalopathy is an unusual complication characterized by decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy, with or without hyperammonemia. Electroencephalography (EEG) is characterized by continuous generalized slowing. The EEG findings, as well as clinical manifestations and hyperammonemia, tend to normalize after VA withdrawal. Patients and Methods: We present a series of seven patients who developed VA-induced encephalopathy at the Neurology Department of Hospital Salvador between 2003 and 2010. We report two illustrative cases in extenso. Results: Our series is composed by five women and two men. Five patients developed hyperammonemia (ammonemia above 50 ug/dl). 55years was the average of patients (range: 37 to 82 years). VA dose was between 375 and 2.000 mg (average 903 mg). Latency between start or important change in VA dose was 3 days to 16 years and a month. All patients had brain damage. Polytherapy with phenobarbital, phenytoin and carbamazepine was significant. The most frequent EEG pattern was diffuse slowing. A 82-year-old female developed a seudo-periodic activity suggesting a non-convulsive status epilepticus. The clinical manifestations, EEG findings and laboratory normalized after VA withdrawal. Conclusions: Acid valproic-induced encephalopathy is a reversible but potentially fatal adverse reaction that requires a high index of suspicion. Brain damage and polytherapy seem to be important risk factors.

Encefalopatía asociada a Valproato / Val proate-associated hyperammonemic encephalopathy. Report of one case

Valproate can be associated to hyperammonemic encephalopathy, characterized by fluctuating sudden-onset alterations of sensorium, focal symptoms and an increase in the frequency of seizures. We report a 78 year-old female using valproate 1,000 mg/ day for 10 months for the treatment to tonic-clonic seizures. She was admitted on three occasions in the last fourth months for self limited clouding of sensorium. Laboratory, imaging and electroencephalografic studies were non-contributory Blood ammonia levels were 123 fig/dl (normal: 15-50 fig/dl). Due to the possibility of a hyperammonemic encephalopathy secondary to valproate, the drug was discontinued and she was treated with lactulose and intravenous L-carnitine, 1 g/day The patient showed a complete recovery within 48 hours. This drug-associated encephalopathy is a reversible but potentially fatal cause, probably underdiagnosed, that requires a high index of suspicion.

Cassia occidentalis poisoning as the probable cause of hepatomyoencephalopathy in children in western Uttar Pradesh.

BACKGROUND & OBJECTIVE: Recurrent annual outbreaks of acute encephalopathy illness affecting young children have been reported for several years in many districts of western Uttar Pradesh (UP). Our earlier investigations over three consecutive years (2002-2005) proved that these outbreaks were due to a fatal multi-system disease (hepatomyoencephalopathy syndrome) probably caused by some phytotoxin and not due to viral encephalitis as believed so far. We conducted a case-control study to investigate the risk, if any, from various environmental factors and also to identify the putative toxic plant responsible for development of this syndrome. METHODS: Eighteen cases with acute hepatomyoencephalopathy syndrome admitted in 2005 in a secondary care paediatric hospital of Bijnor district of western UP were included in the study. Three age-matched controls were selected for each case. A semi-structured questionnaire was developed and applied to all 18 cases and 54 controls. All interviews were conducted within one week of discharge or death of each case. Quantitative data were analyzed using the relevant established statistical tests. RESULTS: Parents of 8 (44.4%) cases gave a definite history of their children eating beans of Cassia occidentalis weed before falling ill, compared with 3 (5.6% controls), the odds ratio being 12.9 (95% CI 2.6-88.8, P<0.001). History of pica was the other associated factor with the disease, odds ratio 5.20 (95% CI 1.4-19.5, P<0.01). No other factor was found significantly associated with the disease. INTERPRETATION & CONCLUSION: Consumption of C. occidentalis beans probably caused these outbreaks, described earlier as hepatomyoencephalopathy syndrome. Public education has the potential to prevent future outbreaks.

Transient cortical blindness during chemotherapy (PVB) for ovarian germ cell tumor.

A 17 year-old female with stage IIIc endodermal sinus tumor of the ovary developed transient cortical blindness and severe hypertension after 5 cycles of PVB regimen consisting of cisplatin, vinblastine and bleomycin. Clinical and radiological findings were compatible with Posterior LeukoEncephalopathy (PLE). Her visual acuity and blood pressure completely recovered within a few days after supportive treatment with antihypertensive drug. This condition is unpredictable but it can be reversible without long term sequelae. Most reports suggested that this rare toxicity was from cisplatin therapy. However, the exact pathophysiogenesis of this condition was not known precisely. Prompt reduction in blood pressure and withdrawal of immunosuppressive agents might lead to rapid reversal of this syndrome and prevent permanent brain damage.

Reversible posterior leukoencephalopathy caused by azathioprine in systemic lupus erythematosus.

The authors report a case of systemic lupus erythematosus with posterior leukoencephalopathy who presented with headache, tonic-clonic seizure, loss of consciousness and bilateral loss of vision, after taking azathioprine for three weeks. The patient had hypertension with normal eye grounds. The brain CT showed a hypodensity lesion at both bilateral occipital lobes, mainly in the white matter The symptoms and follow-up MRI were improved after the control of hypertension and discontinuation of azathioprine.

Two Cases of Metronidazole-induced Encephalopathy / 대한소화기학회지

Metronidazole is a 5-nitroimidazole compound known as an antimicrobial agent widely used for the treatment of protozoal infection, anaerobic infection, Helicobacter pylori infection and hepatic encephalopathy. It may produce a number of neurologic side effects including peripheral neuropathy, seizure, encephalopathy, ataxic gait and dysarthritic speech. There have been ten or more reports of metronidazole-induced encephalopathy in the literatures including a few reports of brain imaging changes by magnetic resonance images (MRI). However, none of the case of metronidazole-induced encephalopathy in patients with hepatic encephalopathy has been reported yet. Recently, we experienced two cases of metronidazole-induced encephalopathy in patients with liver cirrhosis caused by chronic hepatitis B, which were diagnosed by brain MRI and MR spectroscopy. In this report, we present 2 cases of metronidazole-induced encephalopathy with MR imaging and MR spectroscopic changes including follow- up imaging performed after the discontinuation of the metronidazole with a review of the literatures.

Valproate-induced encephalopathy

Valproate-induced encephalopathy is a rare syndrome that may manifest in otherwise normal epileptic individuals. It may even present in patients who have tolerated this medicine well in the past. It is usually but not necessarily associated with hyperammonemia. The EEG shows characteristic triphasic waves in most patients with this complication. A case of valproate-induced encephalopathy is presented. The problems in diagnosing this condition are subsequently discussed

Reversible posterior leukoencephalopathy due to oral cyclosporine in severe ulcerative colitis.

We report a rare neurological complication, posterior leukoencephalopathy, occurring with oral cyclosporine use in a 44-year-old woman with severe ulcerative colitis. The condition reversed on discontinuation of the drug and correction of associated factors.

Encephalopathy induced by antihelminthic use of levamisole. A report of two patients

The antihelminthic Levamisole [LVM] is actually used as an immunomodulator in colon cancer. Its neurological toxicity is well known when used concomitantly with 5-Fluorouracil [5 FU] and, rarely when used solely at high doses. Antihelminthic imidazoles induced encephalopathy [AIIE], has been reported only in China. methods: We report two Lebanese patients with AIIE, with literature review concerning the pathophysiology, clinical presentation, laboratory, imaging and prognosis of this entity. AIIE supervenes after sensitization and re-exposure to the drug. It resembles the acute disseminated encephalomyelitis [ADEM] and the differentiation from multiple sclerosis is primarily based on the monophasic clinical and radiological [MRI] pattern of the disease. The treatment consists of steroids, and it has a good prognosis. The immunomodulatory role of Levamisole is evident but the pharmacokinetics remain unknown. This disease entity has to be considered anytime a patient, in an endemic area for helminthiasis, develops an encephalopathy, especially after a documented exposure to imidazoles, even at low doses and particularly after re-exposure to the drug that has to be prudent

Aluminium related changes in brain histology: protection by calcium and nifedipine.

Aluminium (Al; 50 mg AlCl3/kg body wt/day) treatment caused a marked change in histological picture of normal brain as indicated by an increased number of vacuolated spaces. These changes returned to normal partially by simultaneous treatment with nifedipine (0.7 mg/kg body wt/day) and completely by similar treatment with 50 ppm calcium (CaCl2; 12.5 mg/kg body wt./day). Neither nifedipine nor calcium treatment alone altered the normal histological condition. The histological changes could not be correlated with the decrease in calcineurin activities in brain as nifedipine decreases calcineurin activity without any histological changes. Hence the histological changes may be considered as specific for Al and not due to a general decrease in calcineurin activity.