Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methotrexate (MTX) is a major cause of treatment-related acute neurotoxicity. We report on clinical and imaging findings of reversibly restricted diffusion in a patient with transient encephalopathy after high dose MTX therapy for osteosarcoma. During the chemotherapy, a 19-year-old man was introduced for the evaluation of consciousness disturbance. Neurological examination revealed confusion, inability of speak at the onset On next day, there were still difficulties in swallowing and phonation, and furthermore deep tendon reflexes were hyperactive in bilateral lower limbs with positive Babinski responses bilaterally. By the 6th day, findings at neurological examination were completely normal. Initial imaging on presentation was performed using MRI. Diffusion weighted MRI clearly indicated areas of restricted diffusion within both centrum semiovale. These abnormalities were confirmed by the diffusion tensor (DT) technique (ADC and FA map). The follow-up MRI examinations using same protocol showed resolution of the ADC and FA abnormalities but increasing T2-signal changes. Neither contrast enhancement nor atrophy was encountered. Early detection of MTX white matter injury by DT image has the potential to alert the oncologist and neurologist to this event and provide a technique by which treatment of neurotoxicity can be monitored.
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PMID:[Case of methotrexate encephalopathy: findings on diffusion tensor image and correlation with clinical outcome]. 1751 Dec 73

It is known that rotavirus gastroenteritis can accompany some neurological manifestations, including encephalitis/encephalopathy or seizures. However, the detailed pathogenesis involved has not been fully understood. To date, acute cerebellitis associated rotavirus gastroenteritis has not been previously reported, except for one case. Herein, we describe two cases of acute encephalitis/encephalopathy and concurrent cerebellitis, associated rotavirus gastroenteritis. Following vomiting and diarrhea, case 1 experienced convulsions and consciousness disturbance and case 2, transient loss of consciousness with eye deviation. After these symptoms subsided, cerebellar signs became evident and a brain MRI showed cerebellar involvement in both cases. Both cases showed speech disturbances, such as mutism, slow speech and dysarthria. In this report, we will discuss the possible pathogenesis of rotavirus associated acute encephalitis/encephalopathy and concurrent cerebellitis.
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PMID:Rotavirus associated acute encephalitis/encephalopathy and concurrent cerebellitis: report of two cases. 1753 86

We report an 84-year-old woman who suffered from acute fentanyl intoxication followed by delayed encephalopathy. She used fentanyl patch at her ached knee joint and stayed in the covered table with a heat source underneath. Serum concentration of fentanyl suddenly elevated and she developed coma due to acute fentanyl intoxication. She gradually recovered, however, she showed consciousness disturbance again at 15th day and developed neurological symptoms including mutism, pyramidal tract signs, frontal lobe signs and parkinsonism. These symptoms also steadily improved without specific treatment, and became able to talk with colleagues and walk with assistance at 90th day. We considered that delayed encephalopathy due to periodic anoxia caused by fentanyl intoxication occurred in the present patient; however, the neurological sequelae were relatively mild as compared with reported cases of carbon monoxide intoxication. Neuroprotective effect of fentanyl may have contributed to the better prognosis in the present patient.
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PMID:[Delayed encephalopathy following acute fentanyl intoxicication]. 1758 4

Reversible posterior encephalopathy syndrome (RPES) is a clinical entity characterized with headache, nausea, vomiting, seizures, consciousness disturbance, and frequently visual disorders associated with neuroradiological findings, predominantly white matter abnormalities of the parieto-occipital lobes. The central nervous system manifestations of systemic lupus erythematosus (SLE) are highly diverse. However, SLE-associated RPES has been seldom reported. Here, we report a case with RPES in SLE and lupus nephritis with exclusive involvement of parietal and occipital cortices. A systematic review of the literature on the pathogenesis and treatment of SLE-associated RPES is included.
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PMID:Reversible posterior encephalopathy syndrome in systemic lupus erythematosus and lupus nephritis. 1845 82

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that can occur in people with normal liver-associated enzyme levels, and despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl suffering from absence seizures, who complained of progressive dizziness and general malaise several days after restarting valproate. She developed vomiting and decreased consciousness after 3 weeks of valproate use. She had a serum ammonia level five times higher than the upper normal limit, normal liver-associated enzymes, and a supra-therapeutic valproate level. Electroencephalography (EEG) showed continuous generalized slowing. Tandem mass spectrometry analysis revealed carnitine deficiency. Her consciousness improved after emergent hemodialysis. Her ammonia level and EEG also became normal. Possible mechanisms, risk factors and treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1913 74

We present a 7-year-old boy diagnosed as having salmonella encephalopathy. He developed severe consciousness disturbance following enterocolitis. Electroencephalography showed diffuse and high-voltage slow activity but MR images of the brain were normal. Examination of inflammatory cytokines in serum and cerebrospinal fluid revealed high levels of interleukin-6, -8, and -10, and interferon gamma. Salmonella typhimurium was detected in a stool specimen. He was diagnosed as having salmonella-associated encephalopathy that had features of septic encephalopathy and quickly responded to high-dose methylpredonisolone therapy. High-dose methylpredonisolone was considered to be an effective treatment for hypercytokine-mediated S. encephalopathy.
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PMID:Salmonella encephalopathy successfully treated with high-dose methylpredonisolone therapy. 1921 41

Two newly proposed infectious encephalitis/encephalopathy syndromes, in which magnetic resonance imaging (MRI) is essential for the diagnosis, have been reviewed. Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is reported only in East Asian infants, characterized by a febrile seizure (usually >30 min) as the initial neurological symptom on day 1, followed by secondary seizures at day 4 to 6; affected children display variable levels of neurological sequelae. MRI shows no acute abnormality during the first two days; reduced diffusion appears in the frontal or fronto-parietal subcortical white matter during days 3 to 9, then disappears between days 9 and 25. Excitotoxic injury with delayed neuronal death is hypothesized as a possible mechanism based on MR spectroscopic findings. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is characterized by a reversible lesion with homogeneously reduced diffusion in the corpus callosum (at least involving the splenium), sometimes associated with symmetrical white matter lesions. The most common neurological symptom is delirious behavior, followed by consciousness disturbance, and seizures, all of which completely recover within a month. The reason for the transiently reduced diffusion within the lesions is unknown; possibilities that have been postulated include intramyelinic edema, interstitial edema in tightly packed fibers, and a transient inflammatory infiltrate.
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PMID:Two newly proposed infectious encephalitis/encephalopathy syndromes. 1933 28

Hashimoto's thyroiditis (HT) is the most common disorder affecting the thyroid gland. Encephalopathy associated with abnormal thyroid functions, such as myxedema encephalopathy, is treatable. Hashimoto's encephalopathy (HE) was recognized as a new clinical disease based on an autoimmune mechanism associated with HT, and steroid treatment has been successfully administrated. Recently, we discovered serum autoantibodies against the NH2-terminal of a-enolase (NAE) as a specific diagnostic marker for HE. We analyzed these serum anti-NAE autoantibodies and the clinical features in 84 cases of HE. The 84 patients consisted of 26 men and 58 women, from many institutions throughout Japan and other countries. A total of 37 patients carried anti-NAE antibodies (44%). The age was widely distributed between 19 and 87 years old, with two peaks (around 20-30 and 50-70 years old). Most patients were in euthyroid states, and all patients had anti-thyroid (TG) and/or anti-thyroid peroxidase (TPO) antibodies, and anti-TSH receptor (TSHR) antibodies in some cases. Only 20% of patients had past histories of HT. The acute encephalopathy form was the most common clinical feature, and subacute or chronic psychiatric forms and other forms such as pure ataxia, limbic encephalopathy, and Creutzfeldt Jakob-like forms followed. The patients with anti NAE antibodies tended to exhibit acute encephalopathy. The most common neuropsychiatric features were consciousness disturbance, psychiatric symptoms, and seizures. Involuntary movements (tremor, myoclonus, or choreoathetosis) or ataxia occasionally occurred. Abnormalities, especially the slowing of background activities, on EEG and elevated levels of protein/IgG in cerebrospinal fluid (CSF) were common and useful laboratory findings for the diagnosis, while abnormalities on brain MRI were rare and non-specific in HE. Immunotherapies such as glucocorticoid, immunosuppressants, immunoglobulin, and plasma exchange, were recommended and effective for HE treatment. HE belongs to a part of a clinical spectrum consisting of individuals with anti-thyroid antibodies, overlapping the clinical spectrum of HT. Anti-NAE autoantibodies were positive in 44% of patients with HE. Considering the overall findings, we should be aware of the possibility of autoimmune encephalopathy associated with thyroid disorders (HE) in patients with an unknown etiology of neuronpsychiatric symptoms with/without a past history of HT.
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PMID:[Anti-NAE autoantibodies and clinical spectrum in Hashimoto's encephalopathy]. 1936 98

We present an 11-year-old boy diagnosed as having acute encephalopathy and liver failure with the underlying condition of a metabolic dysfunction. He developed convulsions and severe consciousness disturbance following gastroenteritis after the ingestion of some fried rice. He showed excessive elevation of transaminases, non-ketotic hypoglycemia and hyperammonemia, which were presumed to reflect a metabolic dysfunction of the mitochondrial beta-oxidation, and he exhibited severe brain edema throughout the 5th hospital day. He was subjected to mild hypothermia therapy for encephalopathy, and treated with high-dose methylprednisolone, cyclosporine and continuous hemodiafiltration for liver failure, systemic organ damage and hyperammonemia. The patient recovered with the sequela of just mild intelligence impairment. In this case, Bacillus cereus, producing emetic toxin cereulide, was detected in a gastric fluid specimen, a stool specimen and the fried rice. It was suggested that the cereulide had toxicity to mitochondria and induced a dysfunction of the beta-oxidation process. The patient was considered as having an acute encephalopathy mimicking Reye syndrome due to food poisoning caused by cereulide produced by B. cereus.
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PMID:Acute encephalopathy of Bacillus cereus mimicking Reye syndrome. 1979 86


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