Diagnostika casných fází difuzního axonálního poranĕní s vyuzitím imunohistochemických metod
[Diagnosis of early phase diffuse axonal injury using immunohistochemical methods]
Jazyk čeština Země Česko Médium print
Typ dokumentu anglický abstrakt, časopisecké články
PubMed
9931570
- MeSH
- amyloidový prekurzorový protein beta analýza MeSH
- axony chemie patologie MeSH
- dospělí MeSH
- fosfopyruváthydratasa analýza MeSH
- imunohistochemie MeSH
- kojenec MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- molekulová hmotnost MeSH
- mozek - chemie * MeSH
- mozek patologie MeSH
- náhlá smrt kojenců patologie MeSH
- neurofilamentové proteiny analýza MeSH
- poranění mozku metabolismus patologie MeSH
- senioři MeSH
- soudní lékařství MeSH
- ubikvitiny analýza MeSH
- Check Tag
- dospělí MeSH
- kojenec MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- senioři MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- Názvy látek
- amyloidový prekurzorový protein beta MeSH
- fosfopyruváthydratasa MeSH
- neurofilamentové proteiny MeSH
- ubikvitiny MeSH
Histologic and immunohistochemical investigation of the brain aimed at diagnosis of diffuse axonal injury (DAI) was performed in a group of 12 persons deceased of craniocerebral injury. Traumatic axonal change was visualized by immunohistochemical positivity of ubiquitin, low-molecular neurofilaments, beta-amyloid precursor protein and neuron-specific enolase. In addition, H-E stain and silver impregnation of axons according to Palmgren were performed. Diffuse axonal injury was found in 7 cases (58%). In persons surviving more than 12 hours, morphological diagnosis of DAI was based on the finding of so called retraction balls. In person deceased in the first hours after injury, the retraction balls had not been formed yet and DAI was diagnosed according to histochemistry of axonal lesion. The earliest diagnosis of DAI was established 2 hours after injury when axonal lesion showed an immunohistochemical positivity with anti-neuron-specific enolase. In a control group of 6 sudden death cases, axonal oedema was also found but lacking immunohistochemical positivity. Immunohistochemical proof, specially of neuron-specific enolase, seems to be inevitable for diagnosis of early phase DAI when the traumatic etiology of axonal deformities is to be distinguished from possible artificial lesions.