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)

A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait ataxia and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
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PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49

A seven-month-old girl with atypical West syndrome with pedaling automatism was reported. She started to have early infantile epileptic encephalopathy with suppression-burst (EIEE) at age 14 days followed by infantile spasms at 3 months of age. She began to have spasms with automatism at 4 month, mainly consisting of pedaling movements of both feet associated with tonic spasms of upper extremities and writhing of trunk. Ictal EEG showed irregular slow waves with occasional spikes predominantly over the right hemisphere mixed with artifacts. Interictal EEG during sleep showed suppression-burst patterns. Cerebral atrophy and microcephaly were revealed on brain CT, immature myelination on MRI and decreased blood flow in the frontal, temporal, and parietal lobes on the right on PET scan. Pedaling automatism is rare in infancy and its clinical significance was discussed in relation to West syndrome and complex partial seizures.
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PMID:[Pedaling automatism in atypical West syndrome: a case report]. 176 Feb 11

In this 35-year-old woman with chronic glomerulonephritis and uremic encephalopathy, the basal ganglia bilaterally, internal capsules and periventricular white matter showed hypodensity on CT, low signal intensity on T1-weighted MRI and high signal intensity on T2-weighted MRI. Following a series of dialyses, her clinical symptoms and blood chemistry improved. The CT and MRI returned to normal. These reversible abnormalities may be caused by reversible ischemic change, but disorders of cerebral metabolism and uremic toxins may contribute.
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PMID:Reversible MRI and CT findings in uremic encephalopathy. 178 56

A case of toxic encephalopathy due to podophyllin poisoning was presented. It is documented for the first time by MRI that diffuse cerebral atrophy occurred as a result of podophyllin toxicity.
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PMID:Magnetic resonance imaging in toxic encephalopathy due to podophyllin poisoning. 192 61

Two 30-year old twins, one male, the other female, were followed up for 20 years for predominantly proximal muscular deficit without increase of muscle enzymes. The lactic acid level was elevated at rest and further increased during exercise. Muscle biopsy revealed mitochondrial abnormalities. Encephalopathy was also present. The female patient had been treated, at the age of 10 years, for myoclonic attacks which regressed when she was over 18 years. None of the two patients had dementia. CT and MRI showed very extensive and symmetrical lesions of the white matter which did not involve the basal ganglia. These two cases are interesting on three scores: (1) clinically, the woman exhibited symptoms of the MELAS syndrome (without cerebral vascular accidents) and symptoms of the MERRF syndrome, which suggests the existence of borderline cases; (2) genetically, our cases were in favour of a so-called "maternal" heredity (boys are affected in all cases): here both sexes were involved but the phenotype varied; (3) biochemically, we found no enzyme activity deficit likely to explain the clinical features. The significance of a selective increase of cytochrome c oxidase in both mother and daughter is unclear.
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PMID:[Mitochondrial myopathy and leukoencephalopathy in twins of different sexes]. 196 56

Three children, one pair of siblings and a sporadic case, with "infantile (familial) encephalopathy with cerebral calcification and leukodystrophy" are reported. Neuroimaging studies demonstrated extensive bilateral calcifications particularly in paraventricular location and within the cerebral white matter. MRI, performed in two infants, confirmed marked white matter involvement with diffuse delay of myelination. This condition can be added to the growing list of leukodystrophies.
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PMID:Magnetic resonance imaging in infantile encephalopathy with cerebral calcification and leukodystrophy. 328 8

Two children, an eight-year-old girl and a seven-month-old boy, recovered from herpes simplex encephalitis with minimal neurological residua following acyclovir treatment. Subsequently, they experienced marked deterioration, interpreted as either recrudescent infection or a post-infectious phenomenon. Features of the deterioration included encephalopathy and hyperkinetic movement disorder. MRI studies showed extensive neocortical damage, without involvement of the basal ganglia, thalamus or subthalamic nuclei. With aggressive supportive care, both children made a slow, steady recovery over several months. This supportive care is best provided in a closely supervised interdisciplinary setting.
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PMID:Movement disorder following herpes simplex encephalitis. 204 55

The MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) can be difficult to identify. We report MRI abnormalities that we believe are specific to this disorder in three patients with complete or partial MELAS syndrome. The patients all showed an unusual pattern on T2-weighted MRI with multifocal areas of hyperintense signal confined to the cortex of the cerebrum, cerebellum, and adjacent white matter. Some images suggested selective cortical involvement of deeper layers only. Deep white matter was relatively spared, distinguishing this from usual cerebrovascular disease or the edema after status epilepticus. Specificity of these findings is further suggested by a good correlation of these findings with the previously described unique postmortem brain pathology of MELAS.
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PMID:Magnetic resonance imaging shows specific abnormalities in the MELAS syndrome. 206 32

A 13-year-old boy was the victim of a strangulation attempt. His behavior was normal by the 6th day after the assault. However, from the 7th day, he developed choreoathetosis, dystonia and marked pseudobulbar palsy. CT and T2-weighted MRI at this time revealed a low density and high signal intensity in the region of the bilateral putamen and caudate respectively for the first time. Thereafter, these symptoms and changes in CTs and MRIs subsided gradually over two months. Sequential analysis of CSF for GABA and dopamine during illness revealed reciprocal changes each other with normal recovery. Because of delayed onset of neurological changes, and findings of CSF with reversible symptoms the delayed encephalopathy after strangulation is probably related to biochemical alteration secondary to anoxia in vulnerable basal ganglia.
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PMID:[Delayed postanoxic encephalopathy after strangulation--the serial neuroradiological and neurochemical studies]. 210 26

Doppler ultrasound has become a powerful diagnostic tool in evaluating the portal system. It can provide a great deal of information about the morphology and hemodynamics of portal hypertension. Together with CT and MRI, it has partly relegated the role of angiography from diagnostic towards preoperative evaluation. The diagnosis of portal hypertension can be made and the cause of the elevated pressure can be located before, in, or after the liver parenchyma. Spontaneous shunts can be identified. On the basis of their location and direction of flow, portohepatic collaterals can be differentiated from portosystemic collaterals. The presence of portohepatic collaterals may be the first indication of portal thrombosis or stenosis. Portosystemic collaterals can be either collaterals towards the SVC, with consequent risk of bleeding, or collaterals draining into the IVC, which do not carry such risk. The latter may mimic surgically created shunts in their large volume-flow capacity. The hemodynamic conditions leading to encephalopathy are identifiable by looking at the size of the collaterals in conjunction with the direction of flow in the major portal vessels. Patency of surgically created shunts can be established. Flow patterns may be quantified by performing volume flow estimations, and the presence of a hyperdynamic circulation can thus be identified. By providing insight into portal hemodynamics, Doppler ultrasound can help to select optimal individualized treatment and is well suited for follow-up of medical and surgical therapy.
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PMID:Doppler ultrasound in the evaluation of portal hypertension. 218 92


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