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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diseases of the central nervous system (CNS) occurring during treatment of acute lymphoblastic leukemia (ALL) may be of leukemic or nonleukemic origin. Well known examples for CNS disease of nonleukemic origin are somnolence following prophylactic CNS irradiation, methotrexate-induced encephalopathy and acute infections caused by bacteria, viruses and toxoplasma gondii. Less known is the fact that also subacute CNS infections may occur in patients undergoing cytostatic therapy. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis (SSPE) are examples of this category of disease. Up to now 11 well documented cases of SSPE were reported occurring during treatment of ALL. Main clinical features were disorders of behaviour, consciousness and speach, seizures, paresis and inappropriate secretion of ADH. Several authors were able to demonstrate a deficiency of cellular immunity in patients with SSPE. In some cases this deficiency was consistent with reduced reactivity of T-lymphocytes against measles antigen only. The presence of inhibiting factors may be responsible for this phenomenon. Other authors found a normal or increased function of cellular immunity in SSPE; In hamsters occurrence of SSPE is induced by the simultaneous injection of hamster-adapted SSPE virus and antihamster lymphocyte serum. We, therefore, conclude that also in humans SSPE appearing during treatment of ALL is due to immunosuppression.
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PMID:[Non-leukemic disease of the central nervous system in children with acute lymphoblastic leukemia. III. Subacute sclerosing panencephalitis (author's transl)]. 36 90

The cases presented with psychic troubles and repeated somnolence episodes accompanied by dysarthria in 5 cases, myoclonic jerks in 4 cases and epileptic seizures in 1 case. In all cases the EEG was disturbed. It showed symetrical, paroxystic, bilateral, monomorph slow activity with more or less frequent paroxysms. The average serum aluminium level was at 407 microgram/l in the acute phase, at 161 microgram/l in the remission phase and at 123 microgram/l three months later. After interruption of oral and dialytic aluminium intake the remission is maintained. However in 2 cases the transitory readministration of aluminium gel was followed by reversible recurrency. The role of both aluminium gel and dialysate aluminium as the origin of encephalopathy is discussed.
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PMID:[Reversible dialytic encephalopathy after interruption of aluminium intake. 6 cases (author's transl)]. 49 78

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

A case of encephalopathy with elevation of plasma aluminium level in a patient treated by maintenance hemodialysis is reported. Clinical symptoms were made of moderate impairment of intellectual functions and of intermittent drowsiness. EEG after 3 minutes of hyperpnea evidenced bisynchronous anteriorly dominant intermittent delta waves. Plasma aluminium level, determined by atomic absorption spectrophotometry, was initially at 300 microgram/l (normal range greater than 40 microgram/l). After interruption of aluminium gels, clinical and EEG symptoms slowly subsided in 9 months, plasma aluminium level came down to 145 microgram/l. This picture of encephalopathy could preceede irreversible dialysis dementia in chronic dialysis patients.
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PMID:[Prolonged and reversible encephalopathy in a chronic haemodialysis patient. Probable responsibility of aluminium salts (author's transl)]. 67 73

CNS symptoms ranging from mild to lethal have occurred following CNS radiotherapy and intrathecal chemotherapy. Cranial radiotherapy often produces signs of mild encephalopathy, with predominance of somnolence. In rare cases, it appears that CNS radiotherapy may be followed by progressive encephalopathy. Intrathecal methotrexate frequently causes symptoms of meningeal irritation. Occasionally cases of weakness and paralysis, and rare instances of severe encephalopathy, may occur. However, in leukemic children treated with intensive chemotherapy and CNS radiotherapy who develop neurological complications, it is often difficult to determine which of many possible factors may be causing the CNS symptoms. The pathogenesis of the various forms of methotrexate neurotoxicity is poorly understood. The best-established cause for these symptoms is high concentrations of methotrexate in the CSF or porlonged exposure of the brain to low CSF concentrations of methotrexate. These elevated concentrations of the drug may in turn be due to impaired elimination of the drug from the cerebrospinal fluid (usually due to overt CNS leukemia) or to increased dosage in relation to cerebrospinal fluid volume (due to adolescent age). Leukoencephalopathy is occasionally found at autopsy in children given intensive therapy with CNS radiotherapy and intrathecal methotrexate, together with intensive systemic chemotherapy. It was proposed that alteration of the blood-brain barrier by cranial radiotherapy allows systemically administered anti-leukemic drugs to enter the brain and to cause necrotic changes in the CNS white matter. Leukoencephalopathy also occurs following intraventricular administration of methotrexate. CNS-toxicity due to intrathecal cytosine arabinoside is clinically similar to the symptoms seen following intrathecal methotrexate.
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PMID:Neurotoxicity due to CNS therapy for leukemia. 84 Jan 59

Three cases (case 1, female, aged 30; case 2, male, aged 32; case 3, male, aged 34) of benign brainstem encephalopathy with truncal ataxia were reported. Two patients had prodromal symptoms Neurological examination revealed truncal ataxia in all cases. As additional neurological signs, anisocoria, mydriasis, nystagmus, ptosis, transient opsoclonus, and facial palsy were seen. There was neither drowsiness nor myoclonus in the three cases. On laboratory examinations, cold agglutination test revealed significant elevation in two cases. The examination of cerebrospinal fluid showed a moderate rise of proteins in one case, but did not revealed pleocytosis in any of the cases. Magnetic resonance imaging of one patient revealed an area of high intensity in the left pontine tegmentum by T2-weighed imaging. The prognosis for all these cases was good, and the reappearance of neurological signs was not present until now. Our cases were different from brainstem encephalitis (Bickerstaff's encephalitis) because of an absence of disturbed consciousness and no pleocytosis in the cerebrospinal fluid. Our cases were also different from "myoclonus-opsoclonus syndrome" because of an absence of myoclonus. We discussed a possibility of a new clinical syndrome which we call "benign brainstem encephalopathy with truncal ataxia".
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PMID:[Benign brainstem encephalopathy with truncal ataxia--a clinical study of 3 cases]. 128 89

This peculiar 11-14 Hz spindle activity appears predominantly in the frontal area, and was observed in eight patients with impaired consciousness caused by nontraumatic diffuse encephalopathy. Characteristic of this frontal spindle activity is its transience and accordance with changes in the arousal level of the patient. When the degree of impaired consciousness in the patient was minimal and clinically not very apparent, this spindle activity appeared during light drowsiness. In lethargic patients, it was observed when the patient's level of consciousness rose (e.g. immediately after opening and closing the eyes). These frontal spindles disappeared at the onset of Stage 2 sleep, when normal physiologic spindle waves that are dominant in the vertex area appeared. A paroxysmal discharge was sometimes recorded in association with the frontal spindle activity and it disappeared at about the same time as these spindles. The prognosis was satisfactory for all patients in whom frontal spindle activity was observed; its correlation to spindle coma is also studied.
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PMID:Frontal spindle activity that appears in conjunction with nontraumatic diffuse encephalopathy. 139 58

Two children with osteosarcoma are presented in whom Wernicke encephalopathy with vomiting occurred during the chemotherapy. One of the children died with symptoms of toxic cardiomyopathy. Autopsy revealed Wernicke encephalopathy. The other child had similar symptoms (ocular signs, ataxia, somnolence). Parenteral thiamine had been given and after this therapy the child recovered from the encephalopathy. The authors emphasize the importance of the recognition of this neurological disorder occurring rarely in childhood: it can be cured with parenteral thiamine. Without thiamine treatment this condition is lethal.
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PMID:[Wernicke encephalopathy in childhood osteosarcoma]. 140 86

Ifosfamide is an oxazaphosphorine alkylating agent with a broad spectrum of antineoplastic activity. It is a prodrug metabolised in the liver by cytochrome P450 mixed-function oxidase enzymes to isofosforamide mustard, the active alkylating compound. Mesna, a uroprotective thiol agent, is routinely administered concomitantly with ifosfamide, and has almost eliminated ifosfamide-induced haemorrhagic cystitis and has reduced nephron toxicity. Therapeutic studies, mostly noncomparative in nature, have demonstrated the efficacy of ifosfamide/mesna alone, or more commonly as a component of combination regimens, in a variety of cancers. In patients with relapsed or refractory disseminated nonseminomatous testicular cancer, a salvage regimen of ifosfamide/mesna, cisplatin and either etoposide or vinblastine produced complete response in approximately one-quarter of patients. As a component of both induction and salvage chemotherapeutic regimens, ifosfamide/mesna has produced favourable response rates in small cell lung cancer, paediatric solid tumours, non-Hodgkin's and Hodgkin's lymphoma, and ovarian cancer. Induction therapy with ifosfamide/mesna-containing chemotherapeutic regimens has been encouraging in non-small cell lung cancer, adult soft-tissue sarcomas, and as neoadjuvant therapy in advanced cervical cancer. As salvage therapy, ifosfamide/mesna-containing combinations have a palliative role in advanced breast cancer and advanced cervical cancer. Ifosfamide/mesna can elicit responses in patients refractory to numerous other antineoplastic drugs, including cyclophosphamide. With administration of concomitant mesna to protect against ifosfamide-induced urotoxicity, the principal dose-limiting toxicity of ifosfamide is myelosuppression; leucopenia is generally more severe than thrombocytopenia. Reversible CNS adverse effects ranging from mild somnolence and confusion to severe encephalopathy and coma can occur in approximately 10 to 20% of patients after intravenous infusion, and the incidence of neurotoxicity may be increased to 50% after oral administration because of differences in the preferential route of metabolism between the 2 routes of administration. Other adverse effects of ifosfamide include nephrotoxicity, alopecia, and nausea/vomiting. In general, intravenously administered mesna is associated with a low incidence of adverse effects; however, gastrointestinal disturbances are common following oral administration. Thus, ifosfamide/mesna is an important and worthwhile addition to the currently available range of chemotherapeutic agents. It has a broad spectrum of antineoplastic activity and causes less marked myelosuppression than many other cytotoxic agents. At present, the role of ifosfamide/mesna in refractory germ cell testicular cancer is clearly defined; however, its overall place in the treatment of other forms of cancer awaits delineation in future well-controlled comparative studies.
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PMID:Ifosfamide/mesna. A review of its antineoplastic activity, pharmacokinetic properties and therapeutic efficacy in cancer. 172 Mar 82

We report a case of acute transient encephalopathy with confusion, drowsiness, myoclonic jerks, periodic triphasic sharp wave EEG patterns induced by low doses of baclofen. We discuss the pathogenesis and the differential diagnosis from the subacute spongiform encephalopathy of sudden onset.
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PMID:Acute transient cerebral intoxication induced by low doses of baclofen. 187 11


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