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Despite the clinical and medicolegal significance attached to perinatal asphyx ia, the neuropathological basis of this condition remains obscure. There are ver y few studies in the literature which correlate the pathological findings in neo natal brains with detailed epidemiological data, and none which are population b ased. In a Scotland-wide study of neonatal deaths, 70 brains have been examined . On the basis of glial and macrophage reactions, we previously identified infan ts with putative antepartum brain damage in this cohort and have related these r eactions to signs of birth asphyxia. The present study explores the extent of ne uronal/axonal injury in these infants since this is likely to be the basis for n eurological deficits in surviving infants. We have also investigated these brain s for β-amyloid precursor protein (βAPP) positivity to determine whether this is a useful marker of neuronal injury in neonates. Neuronal eosinophilia and ka ryorrhexes were detected in 43%and 27%of the cohort, respectively; maximally i n the subiculum and ventral pons, but often present elsewhere. White matter dama ge was detected in 24%of cases but without classic cystic lesions of periventri cular leucomalacia. βAPP positivity was present in neuronal soma in 52%of case s and, in axons, in 27%of cases, and was seen from as early as 25-weeks gestat ion. Axonal bulbs were clearly delineated by βAPP positivity and were usually l ocated in the cerebral white matter and internal capsule, and infrequently in th e brain stem. Although white matter damage and βAPP axonal positivity were ofte n detected in the same cases (P=0.034), these features also occurred independent ly of each other. Both neuronal karyorrhexes and white matter βAPP positivity w ere significantly correlated with the features of birth asphyxia, particularly a history of seizures. Immunocytochemistry for both βAPP and glial fibrillary ac idic protein proved useful in detecting neuropathological features which escaped detection on routine examination, particularly in preterm infants. The presence together of recent and older damage in individual brains suggests that there is an ongoing neuronal response to cerebral insults. We find that βAPP is a usefu l marker of white matter damage in the neonatal brain. Immunopositivity for βAP P in these circumstances is not attributable to inflicted or accidental trauma. While birth-related trauma cannot be ruled out, hypoxia/ischaemia is a likely c ause in these infants. However, the exact pathogenesis of neuro-nal/axonal inju ry in the neonatal brain remains unclear.
Despite the clinical and medicolegal significance attached to perinatal asphyx ia, the neuropathological basis of this condition remains obscure. There are few studies in the literature which correlate the pathological findings in neo natal brains with detailed epidemiological data, and none which are population b ased. In a Scotland-wide study of neonatal deaths, 70 brains have been examined. On the basis of glial and macrophage reactions, we who identified infan ts with putative antepartum brain damage in this cohort and have related these r eactions to signs of birth. asphyxia. The present study explores the extent of ne uronal / axonal injury in these infants since this is likely to be the basis for n eurological deficits in surviving infants. We have also laboratory these brains for β-amyloid precursor protein (βAPP) positivity to determine whether this is a useful marker of neuronal injury in neonates. Neuronal eosinophilia and ka ryorrhexes were detected in 43% an d 27% of the cohort, respectively; maximally in the subiculum and ventral pons, but often present elsewhere. White matter dama ge was detected in 24% of cases but without classic cystic lesions of periventri cular leucomalacia. βAPP positivity was present in neuronal soma in 52% of cases s and, in axons, in 27% of cases, and was seen from as early as 25-weeks gestat ion. Axonal bulbs were clearly delineated by βAPP positivity and were usually l ocated in the cerebral white matter and internal capsule, and infrequently in th e brain stem. Both white matter damage and βAPP axonal positivity were detected in the same cases (P = 0.034), these features also showed independent ly of each other. Both neuronal karyorrhexes and white matter βAPP positivity w ere significantly correlated with the features of birth asphyxia, particularly a history of seizures. Immunocytochemistry for both βAPP and glial fibrillary ac idic protein proved useful in detecting neuropathological features w hich escaped detection on routine examination, particularly in preterm infants. The presence together of recent and older damage in individual brains suggests that there is an ongoing neuronal response to cerebral insults. We find that βAPP is a usefu l marker of white matter damage in the neonatal brain. Immunopositivity for βAP P in these circumstances is not allowed to inflicted or accidental trauma. While birth-related trauma can not be ruled out, hypoxia / ischaemia is a likely c ause in these infants. However, the exact pathogenesis of neuro-nal / axonal inju ry in the neonatal brain remains unclear.