Cases reported "Neurotoxicity Syndromes"

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1/11. Transient posterior encephalopathy induced by chemotherapy in children.

    The cases of three children, 16, 12, and 12 years of age, who suffered sudden confusional state and cortical blindness lasting 12 to 30 minutes while under treatment with high-dose methotrexate, cyclophosphamide, and dactinomycin for a lower limb osteosarcoma are reported. Transient neuropsychologic deficits arose after the acute phase of treatment: left hemispatial neglect and constructive apraxia (Patient 1); constructive apraxia (Patient 2); and constructive apraxia and alexia without aphasia (Patient 3). The three patients recovered completely from all their deficits within the time frame of 3 hours to 2 weeks. Arterial hypertension and hypomagnesemia were found during the acute phase in all patients. In patients 2 and 3, magnetic resonance imaging revealed increased parieto-occipital T(2) signal involving gray and white matter. In patients 1 and 2, HmPAO-SPECT revealed parieto-occipital hypoperfusion that resolved a few days later. The alterations detected by neuroimaging were concurrent with the appearance and disappearance of the clinical symptoms. Such transient acute episodes have been named occipital-parietal encephalopathy. On the basis of our clinical, laboratory, and neuroimaging findings, an explanation for the origin of this syndrome, a migrainelike mechanism, triggered by chemotherapy-induced hypomagnesemia, is proposed.
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2/11. 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.
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3/11. ifosfamide encephalopathy and nonconvulsive status epilepticus.

    BACKGROUND: ifosfamide (IFX), an alkylating agent and isomer of cyclophosphamide, is used as a single agent or a component of multi-agent chemotherapy in the treatment of ovarian, testicular, head and neck cancers, sarcomas and lymphomas. Encephalopathy is manifested by cerebellar ataxia, confusional state, complex visual hallucinations, extrapyramidal signs, seizures, and mutism. case reports: We report two patients with non-Hodgkin's lymphoma presenting with mutism and confusional state after IFX infusion. Nonconvulsive status epilepticus (NCSE) as the cause of confusion was diagnosed on the basis of EEG pattern and the apparent improvement following intravenous administration of diazepam. CONCLUSIONS: Electroencephalogram abnormalities during IFX treatment have been described but recordings are only available in six cases. In three of them, paroxysmal alterations warranted the diagnosis of NCSE; however, most cases of IFX encephalopathy might have associated NCSE.
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keywords = coma
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4/11. Don't throw in the towel! A case of reversible coma.

    A young woman with pre-eclampsia became unresponsive shortly after delivery. Examination revealed extensive brain stem dysfunction with absent pupillary light reflexes and decerebrate posturing. Computed tomography showed hypodensity throughout the brain stem, and it was initially thought that she had suffered catastrophic brain stem infarction. However, magnetic resonance diffusion imaging and apparent diffusion coefficient mapping showed that she had brain stem vasogenic oedema (posterior reversible encephalopathy syndrome, PRES), rather than cytotoxic oedema. With antihypertensive and supportive treatment, she recovered rapidly, and had no abnormalities on repeat imaging.
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ranking = 4
keywords = coma
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5/11. ammonia induced encephalopathy from valproic acid in a bipolar patient: case report.

    valproic acid is widely used as a mood stabilizer. We report a case of an adult with bipolar disorder taking therapeutic doses of valproic acid, who presented to the emergency department with coma related to hyperammonemia as a complication of valproic acid treatment. valproic acid was discontinued which resulted in rapid clinical recovery. valproic acid induced coma was likely related to a urea cycle enzymopathy. Clinicians should consider hyperammonemia in all patients who present with coma and other mental status changes while on valproic acid. In such patients, ammonia level should be obtained in addition to liver function tests.
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6/11. Prophylactic treatment of known ifosfamide-induced encephalopathy for chemotherapy with high-dose ifosfamide?

    We report about a case of advanced Ewing sarcoma in a 30-year-old woman. Initial treatment was started according to the Euro-Ewing 99 protocol. During the initial therapy, an ifosfamide-induced encephalopathy occurred as status epilepticus. Because of cerebral toxicity, the following chemotherapies went without ifosfamide. During final radiotherapy multiple lung metastasis were diagnosed. After two cycles of chemotherapy with cyclophosphamide and topotecan (no response), left thoracotomy, and palliative pneumectomy, the patient was transferred to our ward for further treatment. Undergoing two cycles of chemotherapy with ifosfamide 4 g/m(2) intravenously for 3 consecutive days followed by high-dose chemotherapy (HDCT) according to the ice-regimen (ifosfamide 2 g/m(2), carboplatin 200 mg/m(2), and etoposide 2 x 100 mg/m(2) intravenously for 6 consecutive days), and peripheral blood stem cell transplantation (PBSCT), complete remission was achieved. Under preventive therapy with methylene blue, thiamin, and glucose 5% infusions, no encephalopathy occurred.
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7/11. Reversible coma secondary to cefepime neurotoxicity.

    OBJECTIVE: To describe a case of cefepime neurotoxicity associated with acute renal failure that resulted in nonconvulsive status epilepticus. CASE SUMMARY: A 66-year-old woman with acute myeloid leukemia had fever on the third day of the initial chemotherapy cycle. Empiric antibiotic treatment with cefepime 2 g every 8 hours was started; fluconazole and vancomycin were subsequently added due to the persistence of fever. Ten days after initiation of cefepime, the patient developed acute renal failure followed by altered consciousness (glasgow coma scale 6) associated with nonconvulsive status epilepticus. Cefepime was discontinued. Epileptiform activity in the electroencephalogram disappeared with clonazepam, and the patient regained consciousness 48 hours after cefepime withdrawal. DISCUSSION: Acute renal impairment combined with the use of cefepime may account for nonconvulsive status epilepticus. An objective causality assessment revealed that the adverse event was probably due to cefepime. Cefepime's neurotoxic effects derive from high serum concentrations resulting from decreased renal clearance, increased unbound antibiotic, and blood-brain barrier dysfunction during uremia. CONCLUSIONS: The combination of cefepime treatment and acute renal failure may induce drug-related neurotoxicity. Nonconvulsive status epilepticus frequently passes unnoticed in severely ill patients without a history of epilepsy. This disorder should be included in the list of potential causes of coma. In this patient, early detection of nonconvulsive status epilepticus and withdrawal of the antibiotic resulted in full recovery.
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ranking = 6
keywords = coma
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8/11. Acute transient cerebral toxicity associated with administration of high-dose methotrexate.

    OBJECTIVE: To report the first case of transient central nervous system toxicity after administration of high-dose methotrexate (HDMTX) in the middle east. CLINICAL PRESENTATION: A 10-year-old boy was diagnosed with osteosarcoma of the proximal end of the left tibia. He underwent primary amputation and was started on adjuvant chemotherapy, which included administration of HDMTX. He developed acute cerebral toxicity after the 5th dose of HDMTX in the form of diplopia, seizures and disorientation. He recovered completely without any complication or neurological sequelae. CONCLUSION: The acute cerebral toxicity associated with HDMTX was completely reversible and without any sequelae.
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keywords = coma
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9/11. Recurrent seizure and sustained encephalopathy associated with dimethylsulfoxide-preserved stem cell infusion.

    We report the case of a patient who received two infusions of dimethylsulfoxide (DMSO) cryopreserved autologous peripheral blood progenitor cells (PBPCs) after myeloablative chemotherapy for a relapsing lymphoma. A 49-year-old man presented an episode of tonic-clonic seizure over a few minutes after the start of each infusion and developed a profound and sustained but reversible encephalopathy with coma after the second infusion. The patient's neurological condition correlated well with the electrophysiological findings (electroencephalogram and multimodality evoked potentials) and, to a lesser extent, with the radiological abnormalities (magnetic resonance imaging). Severe but reversible neurological complications may occur with the infusion of PBPCs cryopreserved with DMSO.
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10/11. pica with paradichlorobenzene mothball ingestion associated with toxic leukoencephalopathy.

    This is a case report of central nervous system toxicity associated with paradichlorobenzene (PDCB) ingestion. The patient had ingested mothballs composed of 99.99% PDCB for a period of 7 months. She was admitted for depression and had no neurologic symptoms. Later she developed an acute cerebellar syndrome followed by stupor and coma. An extensive workup was negative except for decreasing levels of PDCB in her serum. Imaging revealed a diffuse leukoencephalopathy. Her clinical picture was attributed to PDCB toxicity.
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