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

Thirty-three workers, ages 24 to 63, developed clinical toxic encephalopathy after exposure to neurotoxins and were studied by SPECT brain scans. Five were exposed to pesticides, 13 were acutely exposed to mixtures of solvents, 8 were chronically exposed to mixtures of hazardous wastes that contained organic solvents, 2 were acutely exposed to phosgene and other toxins, and 5 had exposures to hydrogen sulfide. Twenty-nine had neuropsychological testing and all had a medical history and physical. Of the workers who had a clinical diagnosis of toxic encephalopathy, 31 (93.9%) had abnormal SPECT brain scans with the most frequent areas of abnormality being temporal lobes (67.7%), frontal lobes (61.3%), basal ganglia (45.2%), thalamus (29.0%), parietal lobes (12.9%), motorstrip (9.68%), cerebral hemisphere (6.45%), occipital lobes (3.23%), and caudate nucleus (3.23%). Twenty-three out of 29 (79.3%) neuropsychological evaluations were abnormal. Other modalities when performed included the following percentages of abnormals: NCV, 33.3%; CPT sensory nerve testing, 91.3%; vestibular function testing, 71.4%; olfactory testing, 89.2%; sleep EEG analysis, 85.7%; EEG, 8.33%; CT, 7.14%; and MRI brain scans, 28.6%. The complex of symptoms seen in toxic encephalopathy implies dysfunction involving several CNS regions. This series of patients adds to the previous experience of brain metabolic imaging and demonstrates that certain areas of the brain are typically affected despite differences in toxin structure, that these lesions can be globally defined by SPECT/PET brain scans, that these lesion correlate well with clinical and neuropsychological testing, and that such testing is a useful adjunct to previous methods. EEG and structural brain imaging such as CT and MRI are observed to have poor sensitivity in this type of patient. Additional metabolic imaging studies need to be done to explore dose, time, and specific toxin effects as well as mechanisms of toxicity and olfactory migration.
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PMID:Three-dimensional brain metabolic imaging in patients with toxic encephalopathy. 847 60

Hemimegalencephaly is associated with a poor clinical course characterized by intractable seizures and severe encephalopathy. We present a case report of a girl with hemimegalencephaly. At the age of 9 month hemispherectomy was undertaken to preserve function of the other hemisphere. MRI and histologic examinations showed characteristic dysplastic malformations. Follow-up and the complications are described.
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PMID:[Hemimegalencephaly. Therapy with hemispherectomy]. 848 91

Anthelmintic imidazoles induced delayed encephalopathy (AIIDE) is frequently encountered and has usually been misdiagnosed as sporadic encephalitis of unknown cause (SEU). This study was carried out to facilitate differentiation of the two diseases. The records of 202 cases of AIIDE were reviewed and the clinical features analyzed. As a results, 7 diagnostic criteria for AIIDE were proposed as follows: (1) history of exposure to anthelmintic before the onset; (2) presence of a latent period of of 2 to 5 weeks; (3) onset of the disease acute or subacute; (4) presence of neuropsychiatric symptoms and signs resulted from multifocal cerebral damage; (5) Fulfillment of two of the following conditions; (a) subinflammatory change in CSF with elevation of IgG; (b) diffuse slow waves in EEG during early stage; (c) characteristics of acute demyelinating encephalopathy in brain biopsy; (6) good therapeutic effect of adrenal corticosteroids; (7) exclusion of other neuropsychiatric disorders in a fallow-up period of one year. AIIDE is a new disease entity and its diagnosis is mainly based on the clinical features. EEG, CT or MRI are important diagnostic measures, but history of exposure to anthelmintic is the most important criterion. Multifocal hemorrhagic leukoencephalopathy is its main pathologic feature.
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PMID:[Differential diagnosis of delayed encephalopathy induced by anthelmintic imidazoles]. 855 29

We describe the clinical, imaging, and pathologic findings in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). The patient experienced her first stroke-like episode at age forty-four. Brain MRI, obtained at symptom onset, at 3 weeks, and at 1 year, revealed migrating T2-weighted hyperintensities in the temporal/parietal and occipital cortices and later revealed atrophy. Abnormal cerebrovascular reserve was evident on xenon/CT four days after the first MRI. MR spectroscopy at 1 year revealed increased lactate in both the occipital and temporal lobes. Histologic sections demonstrated spongy degeneration of the cortex that was most prominent at the crests of the gyri. Electron microscopy of the blood vessels showed increased numbers of abnormal mitochondria within the vascular smooth muscle and in endothelial cells. We hypothesize that the stroke-like episodes in MELAS may be due to impaired autoregulation secondary to the impaired metabolic activity of mitochondria in the endothelial and smooth muscle cells of blood vessels.
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PMID:MELAS: Clinical and pathologic correlations with MRI, xenon/CT, and MR spectroscopy. 855 80

15 patients with predominantly alcoholtoxic liver cirrhosis (mean age 50 years; 8 men and 7 women) were treated by the technically successful implantation of a transjugular portosystemic stent-shunt (TIPS) within a period of 1 year. The indications for TIPS implantation were the following: gastroesophageal bleedings in 12 cases (10 patients with recurrent variceal bleeding including 2 emergency cases with severe bleeding resistant to conventional therapy and 2 patients with exclusively gastral bleeding due to severe hypertensive gastropathy) and ascites resistant to conventional therapy in 3 cases. Portovenous pressure could be effectively reduced by mean of 37%. Within a mean observation period of 8 months 13 patients including the emergency cases remained without recurrent bleeding. Duplexsonography showed patent stents. 1 patient suffered from an early recurrent bleeding due to occlusion of the stent-shunt. The estimation of liver function according to the Child-Pugh-classification showed only minor changes. Before TIPS 9 patients were in class A, 4 in B, 2 in C; after TIPS 8 patients in A, 5 in B and 2 in C. Ascites resolved completely. Following TIPS all patients appeared to abstain from alcohol. After TIPS 5 from 14 surviving patients (36%) developed clinically manifest encephalopathy within the first 4-8 weeks (2 patients with previous episodes of encephalopathy, 2 other patients after withdrawal of lactulose). By enhanced conservative treatment (lactulose, paromomycine and protein restriction) encephalopathy could be overcome. 8 from 11 surviving patients investigated displayed characteristic MRI changes with an increased signal intensity in the basal ganglia (T1 weighted images). According to our preliminary results TIPS represents a new successful interventional regimen for the treatment of portal hypertension in selected cases.
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PMID:[Initial clinical experiences with TIPS (transjugular intrahepatic portasystemic stent-shunt)]. 857 13

To identify brain lesions most often associated with cerebral visual i mpairment (CVI) after neonatal encephalopathy and to evaluate the prognostic value of MRI for visual outcome, the authors reviewed visual assessments and brain MRI of 80 infants and young children with documented perinatal hypoxic-ischaemic and/or haemorrhagic insults. MRIs were classified according to the severity of lesions at the optic radiations and at the visual cortex; visual acuity was tested with the acuity card procedure. Among the 48 children found to have a CVI, 42 had moderate to severe lesions of the optic radiations and 19 had lesions of the visual cortex. In both cases visual acuity was statically correlated with MRI grading, but the damage at the optic radiations was the better predictor. Early detection of abnormal MR findings in the visual cortex and especially, at the optic radiations may indicate which infants with neonatal encephalopthy should receive longitudinal visual assessment and specific rehabilitation and educational management.
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PMID:Correlation between cerebral visual impairment and magnetic resonance imaging in children with neonatal encephalopathy. 860 79

OBJECTIVES--(1) to evaluate regional cerebral blood flow (rCBF) with single photon emission computed tomography and 99mTc-hexamethylpropyleneamine oxime in patients with the idiopathic adult hydrocephalus syndrome (IAHS); (2) to examine regional cerebral blood flow (rCBF), gait, and psychometric functions before and after CSF removal (CSF tap test); (3) to assess abnormalities in subcortical white matter by MRI. METHODS--Thirty one patients fulfilling the criteria for IAHS (according to history and clinical and neuroradiological examination) were studied. Quantified gait measurements, psychometric testing, and rCBF before and after removal of CSF were obtained. Pressure of CSF and CSF outflow conductance were investigated with a constant pressure infusion method. Brain MRI was used to quantify the severity of white matter lesions and periventricular hyperintensities. In IAHS a widespread rCBF hypoperfusion pattern was depicted, with a caudal frontal and temporal grey matter and subcortical white matter reduction of rCBF as the dominant feature. Removal of CSF was not accompanied by a concomitant increase in rCBF. Significant white matter lesions were detected only in a minority of patients by MRI. An altered CSF hydrodynamic state with a higher CSF pressure and lower conductance was confirmed. IAHS is characterised by an abnormal CSF hydrodynamic state, associated with a widespread rCBF reduction with preference for subcortical white matter and frontal-temporal cortical regions. Furthermore in most patients MRI did not show white matter changes suggestive of a coexistent subcortical arteriosclerotic encephalopathy. At least in the idiopathic group of patients with AHS, measurements of rCBF before and after temporary relief of the CSF hydrodynamic disturbance will not provide additional information that would be helpful in the preoperative evaluation but is suggestive of a preserved autoregulation of rCBF.
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PMID:Regional cerebral blood flow, white matter abnormalities, and cerebrospinal fluid hydrodynamics in patients with idiopathic adult hydrocephalus syndrome. 860 4

Paclitaxel (Taxol) is a novel antineoplastic agent that acts by promoting microtubule polymerization. Although myelosuppression and peripheral neurotoxicity are well known and dose limiting, there have been no reports of CNS toxicity apart from two patients with seizures. This may reflect that paclitaxel has little or no blood-brain barrier penetration. We report two women treated with paclitaxel who developed a clinical state characterized by confusion, word-finding difficulty, and behavioral changes. One had bilateral extensor plantar responses. These symptoms appeared 1 week after paclitaxel infusion and resolved spontaneously. Subsequent infusions were associated with a similar self-resolving encephalopathy in one patient and recurrent headache and ataxia in the other. Neuroimaging (including enhanced MRI), LP, and laboratory investigations did not reveal other causes. Electroencephalography showed diffuse nonspecific slowing. One MRI had prominent but nonspecific high signal intensity abnormalities in the deep white matter of the cerebral hemispheres. Based on temporal association, diagnostic exclusion, and repeated episodes with subsequent challenges, we believe these patients may have experienced CNS toxicity from paclitaxel. The mechanism for this self-resolving encephalopathic process is unclear.
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PMID:Transient encephalopathy after paclitaxel (Taxol) infusion. 933 33

White matter change occurs in human immunodeficiency virus (HIV) encephalopathy, which may be difficult to assess subjectively especially in the early stages of disease. This study applies a quantitative approach to the assessment of this finding. Sixty-three HIV seropositive subjects, 47 seronegative blood donors and 17 seronegative homosexual men underwent axial T2 weighted MRI of the brain at 1.5T. Quantitative analysis was performed by obtaining the pixel contrast between parieto-occipital white matter and head of caudate grey matter (Cwg). Highest values of Cwg were found in a subgroup of subjects with AIDS who had diffuse/patchy white matter abnormalities and atrophy on qualitative image assessment. Statistically significant differences were found in Cwg between subjects with high (> or = 200 x 10(6)/I) and low (< 200 x 10(6)/I) CD4 lymphocyte counts (P < 0.05) and between subjects with and without HIV-1 associated cognitive/motor complex (P < 0.05). This technique provides an objective measure of diffuse HIV-related parenchymal abnormality seen on T2 weighted MRI.
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PMID:Sub-cortical white-grey matter contrast on MRI as a quantitative marker of diffuse HIV-related parenchymal abnormality. 868 21

Three unusual cases of focal continuous myoclonus with onset during the first months of life, lasting from dozens of minutes to hours, are reported. During disease evolution, prolonged bilateral myoclonic seizures and generalized tonic-clonic seizures occur. Subsequently, a progressive encephalopathy with hypotonia and ataxia appears. A net worsening of the neurological condition is observed after the age of 4-5 years. Cortical atrophy is shown by CCT and MRI. Neurometabolic screening is not contributory. Repeated polygraphic recordings show continuous and segmental myoclonic jerks, localized in different muscles, at frequencies ranging between 0.5-1 c/s and 6-8 c/s. Moreover action myoclonus is recorded. During the first period of disease the EEG does not show any paroxysmal activity. As to the classification, this syndrome corresponds to an early onset progressive encephalopathy of unknown origin, similar in some aspects to Alper's disease. Another problem is the interpretation of the myoclonic phenomena. Some important aspects suggest a cortical origin of the diverse myoclonic phenomena observed in these cases.
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PMID:Early-onset progressive encephalopathy with migrant, continuous myoclonus. 873 1


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