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n. encefalomalacia, reblandecimiento del encéfalo.
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Brain MRI showed cystic encephalomalacia. Based on the clinical features, hypouricaemia and hypocystinaemia prompted the differential diagnosis of Molybdenum cofactor deficiency (MAdegCD), which was confirmed on the classical pattern of urine purine analysis (raised xanthine and hypoxanthine) with elevated urinary sulphocysteine.
described abnormal lactate peaks in 3 of the 7 patients (43%) and decreased N-acetylaspartate in the areas of encephalomalacia in 1 patient (14%).[29] Lee et al .[10] reported that all the 3 cases had a lactate peak on MRS (100%).[10] The sensitivity of increased lactate peak in the brain by MRS is higher than that of increased lactate levels in blood and/or CSF in some literature.[8],[34] We found increased lactate peak of brain lesions in only one recorded patient who underwent MRS, and the sensitivity could not be counted due to the small sample.
Necropsy revealed severe pancreatic atrophy and fibrosis with regionally extensive cerebellar encephalomalacia and generalized Purkinje cell degeneration and necrosis.
Most commonly documented lesions were generally encephalomalacia, hydrocephaly and brain atrophy with a percent of 5.90 (13 cases), 5.45 (12 cases) and 4.55 (10 cases) respectively.
The abnormalities of neuroimaging were as follows: encephalomalacia (11 patients), nonspecific ischemic gliotic region (9 patients), tumor (6 patients), hippocampal sclerosis (5 patients), brain atrophy (3 patients), encephalocele (1 patient).
At over 3 months postevent, brain MRI showed sequela of prior multifocal infarcts in the right cerebral hemisphere conforming to the R MCA vascular territory, with extensive multifocal encephalomalacia and gliosis.
Brain MRI on day of life 4 was consistent with cystic encephalomalacia of the bilateral frontal lobes and left parietal lobe.
MRI at the time of the second TBI showed evidence of a new subarachnoid hemorrhage in the left medial temporal sulcus, in addition to underlying encephalomalacia in the left frontal and left temporal lobes associated with the initial hematomas (see Figure 1).
A middle-aged man with a history of alcoholism and previous traumatic brain injury with surgical intervention resulting in right frontal encephalomalacia presented with recurrent focal seizures consisting of head and eye deviation to the left and left upper extremity clonic activity.
The hematoma was peripherally hyperintense and centrally hypointense on T1-weighted images, with surrounding areas of encephalomalacia. Patchy foci of T2 FLAIR hyperintensities are seen in the cortical and subcortical regions of the occipital and posterior parietal lobes bilaterally.
VITAMIN E: Important to avoid resorption of foetuses, muscle dystrophy, anaemia and encephalomalacia.