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  • 1
    ISSN: 1433-0350
    Keywords: Stillborn ; Acute cerebral damage ; Hypoxic/ischemic injuries
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The occurrence of germinal matrix hemorrhage (GMH), pontosubicular necrosis (PSN), and periventricular leukomalacia (PVL) was evaluated in 58 stillborn, among whom 23 (40%) showed one or more lesions. A comparative study of neuropathological findings and obstetrical histories in stillborn beyond 26 weeks of gestation showed a greater frequency of damage when the pregnancies had been complicated. The pathogenesis of PSN is disputed. As PSN was found in stillborn (13 cases), hyperoxia is not an essential pathogenetic factor. PSN may represent a form of anoxic encephalopathy. However, PSN was found as an isolated lesion in an infant of a diabetic mother and in most cases of intrauterine growth retardation; hypoglycemia may therefore be involved in the pathogenesis. Ultrasound examinations of living neonates have indicated the prenatal occurrence of GMH in some cases, and our study opens the possibility that there is intrauterine involvement of PVL and PSN as well. Consequently, cerebral lesions diagnosed in newborn may have occurred in utero.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Perinatal hypoxic brain damage ; Pontosubicular necrosis ; Dentate fascia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The dentate fascia of the hippocampus was studied in 25 infants with pontosubicular necrosis and in 21 control cases without hypoxic cerebral lesions. Of the control cases 19 were completely normal and 2 showed one single necrotic cell in the granule cell layer. In contrast 15 of the cases with pontosubicular necrosis showed varying degrees of neuronal karyorrhexis in the dentate fascia. The severity of these changes largely parallelled those in the subiculum but there were exceptions to this rule. It is concluded that the dentate fascia is frequently involved in pontosubicular necrosis.
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  • 3
    ISSN: 1432-0533
    Keywords: Preterm neonates ; Germinal matrix hemorrhage ; Periventricular leukomalacia ; Pontosubicular necrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The occurrence of germinal matrix hemorrhage (GMH), periventricular leukomalacia (PVL), and pontosubicular necrosis (PSN) was evaluated in a material of 96 preterm infants. All cases were born at less than 38 weeks of gestation, and died within 30 days after birth. The frequency of GMH (50%) and PVL (24%) was within the range of previous observations, but the 59% occurrence of PSN argues against the assertion that intraventricular hemorrhage is the most common neuropathological finding in preterm neonates. However, different combinations of these injuries were found in more than half the cases affected. Of the 48 infants with GMH, 36 (75%) showed either PSN (19 cases), PVL (2 cases), or both lesions (15 cases), and the frequency of additional damage was related to the severity of hemorrhage. Thus, neonatal mortality may be more related to additional hypoxic/ischemic lesions than to the severity of hemorrhage per se. Clinical follow-up studies on subpopulations of preterm infants with and without GMH have shown no difference in frequency of mild and moderate psychomotoric deficiences. The 35% occurrence of PSN as a solitary lesion in the 48 cases without GMH was similar to the frequency of PSN as a single additional lesion in 48 cases with GMH (40%). This finding makes PSN and not GMH the most likely cause of at least less severe handicaps.
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  • 4
    ISSN: 1432-0533
    Keywords: Metabolic Encephalopathy ; Cerebral Degeneration ; Alpers' Disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical and pathological features of a case with primary progressive degeneration of the cerebral cortex are presented. Two siblings had nearly identical clinical histories. All three children were born microcephalic and they died at the age of 7, 10 and 18 months, respectively. All showed progressive mental and motor deterioration. Myoclonus and attacks of opisthotonus were prominent features. Postmortem examination was performed in the third child, who died at the age of 10 months. The brain weight was 310 g. The cerebral cortex was severely atrophic, with extensive laminar neuronal loss. The cerebellum was normal. The optic tracts were atrophic. Neuronal loss was observed also in a few other systems but their relation to the primary disease is uncertain. The basal ganglia were normal and the hippocampus showed only slight nerve cell loss. The case is considered to belong to a small group of cases with primary progressive cortical degeneration described by Laurence and Cavanagh (1968). This group should be distinguished from cases with secondary cortical degeneration caused by anoxic damage from recurrent epileptic attacks. The primary cortical degeneration may start shortly before birth, or after a brief periood of normal postnatal development. A positive family history has been reported in most cases, suggesting an inherited metabolic defect as cause of the disease.
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  • 5
    ISSN: 1432-0533
    Keywords: Pyroglutamic aciduria ; 5-Oxoprolinuria ; Glutathione deficiency ; Encephalopathy ; Cerebellar atrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical and pathologic features of a male patient with generalized glutathione deficiency and pyroglutamic aciduria are presented. The patient died at the age of 28 years. He was mentally retarded from infancy and developed progressive tremor, retardation of movement, and ataxia as from the age of 16. Neuropathologic examination of the brain disclosed a selective atrophy of the granule cell layer of the cerebellum and focal lesions in the right frontoparietal cortex and bilaterally in the visual cortex and the thalamus. The type and distribution of the lesions resembled those seen after mercury intoxication. However, in our patient the damage was probably caused by the lack of protection by glutathione against oxidative damage in the brain. Possible treatment of this rare metabolic disorder might include external supply of an antioxidant, e.g., a thiol capable of penetrating the blood brain barrier.
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  • 6
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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