Coma With Diffuse White Matter Hemorrhages in Juvenile Diabetic Ketoacidosis

PEDIATRICS ◽  
2007 ◽  
Vol 120 (6) ◽  
pp. e1540-e1546 ◽  
Author(s):  
F. H. Mahmud ◽  
D. A. Ramsay ◽  
S. D. Levin ◽  
R. N. Singh ◽  
T. Kotylak ◽  
...  
2016 ◽  
Vol 24 (4) ◽  
pp. 266-271
Author(s):  
이훈상 ◽  
이윤진 ◽  
김영미 ◽  
Yeon Gyu Min ◽  
김경민 ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M De Carlo ◽  
R Liga ◽  
G.M Migaleddu ◽  
M Scatturin ◽  
C Spaccarotella ◽  
...  

Abstract Background Most patients undergoing transcatheter aortic valve implantation (TAVI) develop silent cerebral ischemic lesions (SCIL) detectable at magnetic resonance imaging (MRI). The natural history and clinical relevance of SCIL are not well established. We aimed to assess the characteristics, predictors, evolution, and neurocognitive effects of SCIL. Methods Cerebral MRI was performed within 7 days before TAVI to assess baseline status and age-related white matter changes (ARWMC) score. MRI was repeated postoperatively to assess the occurrence, location, number and dimensions of SCIL. Patients developing SCIL underwent a third MRI at 3–5 months follow-up. A neurocognitive evaluation was performed before TAVI, at discharge and at 3-month follow-up. Results Of the 117 patients enrolled, 96 underwent a postprocedural MRI; SCIL were observed in 76% of patients, distributed in all vascular territories, with a median number of 2 lesions, median diameter 4.5 mm, and median total volume 140 mm3. Independent predictors of SCIL occurrence were a higher baseline ARWMC score and the use of self-expanding or mechanically-expanded bioprostheses. Among 47 patients who underwent follow-up MRI, only 26.7% of postprocedural SCIL evolved into a gliotic scar. SCIL occurrence was associated with a more pronounced transient neurocognitive decline early after TAVI and with a lower recovery at follow-up. Conclusions SCIL occur in the vast majority of patients undergoing TAVR and are predicted by a more diffuse white matter damage at baseline and by the use of non-balloon-expandable prostheses. Although most SCIL disappear within months, their occurrence has a limited but significant impact on neurocognitive function. Figure 1 Funding Acknowledgement Type of funding source: Private company. Main funding source(s): unrestricted grants from Edwards Lifesciences SA, Nyon, Switzerland, and from Medtronic Italia SpA, Milan, Italy


1974 ◽  
Vol 84 (4) ◽  
pp. 510-514 ◽  
Author(s):  
Paul Munk ◽  
Melvin H. Freedman ◽  
Henry Levison ◽  
Robert M. Ehrlich

2009 ◽  
Vol 31 (1) ◽  
pp. 76-79 ◽  
Author(s):  
F. Aboul-Enein ◽  
M. Krššák ◽  
R. Höftberger ◽  
D. Prayer ◽  
W. Kristoferitsch

PEDIATRICS ◽  
2003 ◽  
Vol 112 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. J. Counsell ◽  
J. M. Allsop ◽  
M. C. Harrison ◽  
D. J. Larkman ◽  
N. L. Kennea ◽  
...  

2010 ◽  
Vol 6 (4) ◽  
pp. 209-211 ◽  
Author(s):  
R. Douglas Fields

Glutamate toxicity from hypoxia-ischaemia during the perinatal period causes white matter injury that can result in long-term motor and intellectual disability. Blocking ionotropic glutamate receptors (GluRs) has been shown to inhibit oligodendrocyte injury in vitro, but GluR antagonists have not yet proven helpful in clinical studies. The opposite approach of activating GluRs on developing oligodendrocytes shows promise in experimental studies on rodents as reported by Jartzie et al., in this issue. Group I metabotropic glutamate receptors (mGluRs) are expressed transiently on developing oligodendrocytes in humans during the perinatal period, and the blood–brain-barrier permeable agonist of group I mGluRs, 1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD), reduces white matter damage significantly in a rat model of perinatal hypoxia-ischaemia. The results suggest drugs activating this class of GluRs could provide a new therapeutic approach for preventing cerebral palsy and other neurological consequences of diffuse white matter injury in premature infants.


2019 ◽  
Vol 402 ◽  
pp. 40-47
Author(s):  
Mauro Morassi ◽  
Milena Cobelli ◽  
Elena Ghiselli ◽  
Paolo Costa ◽  
Daniele Bagatto ◽  
...  

1937 ◽  
Vol 83 (344) ◽  
pp. 258-267 ◽  
Author(s):  
A. Meyer ◽  
L. C. Cook

This paper is a preliminary report of some investigations we are now making into the pathology of mental deficiency, mainly from the histological point of view. We have so far examined 22 cases, comprising 7 low-grade defectives showing gross neurological lesions, chiefly of extrapyramidal character, 6 microcephalics with spastic diplegia and severe mental defect, 2 able-bodied microcephalics without gross neurological signs, 1 simple able-bodied idiot and 6 mongols. In this short paper it is impossible to give even the slightest indication of the wealth of pathological material found in such a variety of widely differing conditions. A full description of our findings, together with a more detailed discussion, must be left to further papers dealing with individual groups of cases. The purpose of making a short note at this stage is to draw attention to one particular finding which struck us by its surprising constancy, i.e., a proliferation of the fibrous glia, particularly pronounced within the cerebral and often also the cerebellar white matter. In many of the cases the cortical changes were slight compared with the intense lesions of the white matter. In none of them was demyelinization a well-marked feature, nor did its severity approach that of the glial proliferation; in many it was negligible, and there were none of the fatty breakdown products, characteristic of the demyelinizing disease of the white matter called after Schilder. The gliosis was either diffused or patchy, and was often markedly perivascular; even stripe-like scars, as described by Hallervorden (10), were to be seen, although, contrary to this author's observation, there was, as a rule, no corresponding myelin defect.


2020 ◽  
Vol 26 ◽  
pp. 102234
Author(s):  
Pavel Filip ◽  
Alena Svatkova ◽  
Adam F Carpenter ◽  
Lynn E Eberly ◽  
Igor Nestrasil ◽  
...  

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