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

A case with acute disturbance of consciousness associated with calcium hopanthenate (HOPA) administration was reported. He was a 3-year-old boy with autistic developmental delay, had orally taken 1.5 g of HOPA daily for 3 months. Clinical manifestations consisted of fever, vomiting and coma. Laboratory examination revealed severe hypoglycemia and metabolic acidosis, but there were no hepatic enzyme abnormalities. Analysis of urinary organic acid profile showed that very large amounts of medium and long chain dicarboxylic acids and omega-1 hydroxy-fatty acids were excreted. In particular, 2-hydroxysebacic acid, the accumulation of which has only been reported in the urine of patients with Zellweger syndrome and neonatal adrenoleukodystrophy (NALD), was observed. Analysis of urinary acylcarnitines showed that acetylcarnitine was predominant and C6-C10 dicarboxylic acylcarnitines were also excreted. He was treated with and rapidly responded to intravenous glucose and bicarbonate. After withdrawal of the drug he has had no problems and dicarboxylic aciduria disappeared. A CT scan showed symmetric, low density areas in periventricular white matter, especially around the posterior horns of the lateral ventricles. A T2-weighted MRI scan revealed high-intensity signal in the white matter corresponding to areas of low density on CT scan. We conclude that that a large amount of HOPA administration may cause encephalopathy by the inhibition of both mitochondrial and peroxisomal beta-oxidation.
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PMID:[Clinical and biochemical studies in a case of acute encephalopathy associated with calcium hopanthenate administration]. 219 43

We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.
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PMID:MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy. 223 93

It is well known that professional boxers can develop chronic traumatic encephalopathy (dementia pugilistica) due to repeated head trauma. Beside CT findings indicating cerebral atrophy, the presence of a cavum septum pellucidum has been reported to indicate encephalopathy. CT findings in amateur boxers are not as well documented. The aim of this study was to find out if morphological changes could be demonstrated among former amateur boxers using CT and MRI. Two control groups of soccer players and track and field athletes in the same age-range were used for comparison. No significant differences in the width of the ventricular system, anterior horn index, width of cortical sulci, signs of vermian atrophy, or the occurrence of a cavum septum pellucidum were found between boxers and controls. A cavum septum pellucidum was found more often in the controls than in the boxers and is probably not a sign of earlier head trauma. MRI confirm no more findings than CT in this retrospective study.
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PMID:Does Swedish amateur boxing lead to chronic brain damage? 2. A retrospective study with CT and MRI. 228 46

The spectrum of cranial MRI findings was evaluated in 113 patients with the acquired immunodeficiency syndrome, assessing lesion number, size, location, and configuration in association with the autopsy and/or biopsy results. Correlation of cranial MRI and CT was performed in 32 patients. MRI was shown to be superior in sensitivity of lesion detection demonstrating more lesions than CT in 14 studies (44%) and equivalent information in 18 studies (56%). In no case did CT demonstrate lesions not detected on MRI. We conclude that MRI should be the study of choice in evaluating AIDS-related encephalopathy. Multiple lesions that involve both deep gray matter and white matter suggest the possibility of CNS lymphoma. The "target" appearance on MRI is not helpful in distinguishing toxoplasmosis from lymphoma.
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PMID:MRI evaluation of AIDS-related encephalopathy: toxoplasmosis vs. lymphoma. 232 18

We evaluated 85 patients with serologic evidence of Borrelia burgdorferi infection. Manifestations included encephalopathy (41), neuropathy (27), meningitis (2), multiple sclerosis (MS) (6), and psychiatric disorders (3). We performed lumbar punctures in 53, brain MRI in 33, and evoked potentials (EPs) in 33. Only patients with an MS-like illness had abnormal EPs, elevated IgG index, and oligoclonal bands in the cerebrospinal fluid. Twelve of 18 patients with encephalopathy, meningitis, or focal CNS disease had evidence of intrathecal synthesis of anti-B burgdorferi antibody, compared with no patients with either MS-like or psychiatric illnesses, and only 2/24 patients with neuropathy. MRIs were abnormal in 7/17 patients with encephalopathy, 5/6 patients with an MS-like illness, and no others. We conclude that (1) intrathecal concentration of specific antibody is a useful marker of CNS B burgdorferi infection; (2) Lyme disease causes an encephalopathy, probably due to infection of the CNS; (3) MS patients with serum immunoreactivity against B burgdorferi lack evidence of CNS infection with this organism.
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PMID:Lyme neuroborreliosis: central nervous system manifestations. 229 74

Magnetic resonance (MR) has begun to play an important role in neonatal neurology. Several MRI techniques have been applied to the diagnosis of hypoxic ischemic encephalopathy. Cerebral perfusion examined by intravoxel incoherent motion, a non-invasive tool, seems to be opening new inroads for detecting variations (neurophysiological modifications) in cerebral flows during hypoxic ischemic encephalopathy. MR spectroscopy allows identification of specific biochemical alteration of spectra patterns at various moments of hypoxic ischemic distress, including: (1) primary expression of metabolic disorders induced by the lack of blood and O2, revealed by a peak of the water-suppressed H1 spectrum, the earliest and most persistent-marker; (2) a secondary marker for the establishment of permanent lesions of anoxic-ischemic origin revealed that variations of the phosphocreatine/inorganic phosphorous index in the P31 spectrum are of diagnostic and prognostic significance in this phase. In relation to different neuropathological, structural lesions, MRI becomes particularly important in diagnosing the acute phase of cerebral edema and the different types of infarct. MRI is especially fruitful in monitoring the evolution of the lesion, providing an evaluation of myelinization, and defining the neuropathological outlook. Spectroscopic studies on human neonates have helped establish the therapeutic effects of mannitol in cerebral metabolism. MR studies on neonate animals seem to open new therapeutic prospect for CA antagonists.
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PMID:State of the art of magnetic resonance (MR) in neonatal hypoxic-ischemic encephalopathy. 269 12

Tuberculous encephalic infection is commonly reported as confined to Asians or Africans or people living in poor hygienic conditions; very often it follows meningitis in patients with lung TB infection. We describe three western patients coming from good social environment and suffering from multifocal tuberculous encephalopathy. Two of them showed neither meningitis or lung TB when CNS involvement appeared. Complete recovery after therapy is described, together with the evolution of brain CT and, in 1 case, MRI features. The instrumental findings accompanying the complete recovery suggest that the lesions described in these cases are a localized form of encephalitis responsive to medical treatment, unlike tuberculomas, which often need surgical treatment. The occurrence of tuberculous encephalic infection in western, middle-class patients with or without meningitis emphasizes that tuberculous encephalopathy must be considered in the differential diagnosis of multifocal brain lesions.
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PMID:Reversible multifocal encephalopathy following tuberculous infection. 273 62

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.
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PMID:Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study. 278 40

A case of a survivor who showed alpha coma after an attempted suicide by hanging was reported. A 19 years old woman was admitted to the hospital because of respiratory arrest following a hanging attempt on October 10, 1987. She was found pendent completely. On admission she was comatose and the pupils were not reactive to light. The systolic blood pressure was 60 mmHg and immediately an endotracheal intubation was instituted. After six hours from the onset, the spontaneous respiration was restored and the pupils reacted briskly to light. At 48 hours later she was still comatose, presenting flaccid quadriplegia with no responses to stimulations. An EEG showed a moderate amount of regular, 8 approximately 10 Hz, 10 approximately 50 microV potentials distributed predominantly on the centro-parieto-occipital regions. This alpha rhythm had persisted until 72 hours from the onset, and subsequently diffuse 5 approximately 7Hz, 10 approximately 40 microV slow activity replaced the alpha frequency at 120 hours after the attempt. On the 5th hospital day the hyperbaric oxygen therapy was given and on the 7th day she had become conscious, but showed the apallic syndrome. The both auditory and somatosensory evoked potentials were normal. On the 45th day the brain MRI revealed diffuse cerebral cortical atrophy, although no lesions were visualized in the brain stem. She showed gradual progress towards neurologic recovery. This is the first presentation of a survivor from alpha coma caused by anoxic encephalopathy following a hanging attempt.
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PMID:[Hanging survivor showing alpha coma--a case report]. 279 12

Since the initial report of Beyers & Moll (1948), numerous cases of seizures and encephalopathy after pertussis immunization or DPT immunization have been reported. However, acute cerebellar ataxia and/or facial palsy after DPT immunization is unusual, although there have been several reports from Japan. We report a 1-year-11-month-old girl with acute cerebellar ataxia and facial palsy after DPT immunization. On admission, she was alert. She was active and had a 6-day history of an ataxic gait and asymmetric facial movement which had begun 5 hours after DPT immunization. Neurological examination revealed an ataxic gait, horizontal nystagmus and right facial palsy. A CT scan showed low density on the right side of the pons with marked contrast enhancement. A MRI scan indicated the involvement of not only the right side of the pons, but also of the bilateral cerebellar peduncles. The child did well subsequently and was neurologically normal 20 days after the initial symptoms. To our knowledge, the present case is probably the first reported one of acute cerebellar ataxia after DPT immunization with CT and/or MRI correlation.
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PMID:[Acute cerebellar ataxia and facial palsy after DPT immunization]. 280 99


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