CNS Lesions in Neonatal Isoimmune Thrombocytopenia

Naidu, Sakkubai; Messmore, Harry L.; Caserta, Vito; Fine, Michael

doi:10.1001/archneur.1983.04050080052009

Cited by 51 publications

(12 citation statements)

References 12 publications

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“…CT scan or transfontanellar US performed in the neo nate have revealed late sequelae, such as hy drocephalus and porencephaly. In the case published by Naidu et al [46], the vascular distribution of the porencephalic cyst diag nosed on CT scan in a 6-day-old infant is more difficult to explain. Fetal thrombocyto penia in viral infection such as rubella may also be associated with intracerebral bleeding and white matter softening [8].…”

Section: Blood Dyscrasiamentioning

confidence: 95%

Fetal Encephalopathies of Circulatory Origin

Larroche¹

1986

Neonatology

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Fetal brain damage may be due to a variety of pathological conditions resulting in circulatory impairments. With generalized ultrasonography of the fetus, the lesions can be detected in utero and subsequent neurological handicaps of the infants will no longer be attributed to difficult labor and birth. The type of the lesions may be anoxic-ischemic and/or hemorrhagic. The morphological appearance depends on the time of occurrence of the insult in utero and on the time elapsed between the insult and the examination of the brain. Although the pathogenesis of the lesions is not fully understood, they may be related either to maternal, fetal, or placental pathological situations. In a last group of cases no causes as yet have been found.

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Section: Blood Dyscrasiamentioning

confidence: 95%

Fetal Encephalopathies of Circulatory Origin

Larroche¹

1986

Neonatology

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“…Transient but severe thrombocytopenia occurs with an incidence of 1 in 25,000-40,000 vaccinations for measles, mumps, and rubella, [142][143][144] and less commonly after vaccination against pneumococcus, Haemiphilus influenzae B, varicella zoster virus (VZV), and hepatitis B. 145,146 More than 80% of patients recover within 2 months, typically within 2 to 3 weeks, 27,30,[147][148][149] with less than 10% evolving into chronic ITP 150 responsive to ITP-directed therapy. Thrombocytopenia occurs occasionally after naturally occurring infection with cytomegalovirus, rubella, Epstein-Barr virus, VZV, the severe acute respiratory syndrome coronavirus, and many others.…”

Section: Vaccination and Other Infectionsmentioning

confidence: 99%

Pathobiology of Secondary Immune Thrombocytopenia

Cines

Liebman

Stasi

2009

Seminars in Hematology

214

169

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“…Approximately 15% to 20% of infants with NAIT develop ICH during antenatal or perinatal periods [5], with as many as 50% of ICHs occurring antenatally [6]. To date, intracranial abnormalities associated with NAIT have primarily been detected and described by antenatal and postnatal radiographic findings [4,7,8]. These CNS abnormalities include intraventricular and intraparenchymal hemorrhage, porencephalic cysts, ventriculomegaly, and neuronal migrational disorders [7][8][9].…”

Section: Discussionmentioning

confidence: 99%

Cerebellar Loss and Brain-Stem Atrophy Associated with Neonatal Alloimmune Thrombocytopenia in a Discordant Twin

Mohila¹,

Kubicka

Ørnvold³

et al. 2010

Pediatr Dev Pathol

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Neonatal alloimmune thrombocytopenia (NAIT) is due to an immune-mediated maternal-fetal platelet antigen incompatibility. Central nervous system abnormalities have been reported in infants with NAIT and include intracranial hemorrhage, ventriculomegaly, porencephalic cysts, neuronal migrational disorders, and, rarely, cerebellar lesions. We present the clinical and neuropathological findings from a case of a 3-day-old diamniotic/dichorionic female twin with known bilateral ventriculomegaly born prematurely at 33-1/7 weeks in gestational age. The pregnancy was further complicated by discordant intrauterine growth, intraventricular hemorrhage in the co-twin, and NAIT. At birth, the infant was noted to have diffuse body ecchymoses and petechiae and arthrogryposis. She subsequently developed multisystem organ failure and disseminated intravascular coagulopathy and died on the 3rd day of life. Neuropathological findings at autopsy included a posterior fossa cyst with no gross anatomic evidence of a cerebellum, atrophic pons and medulla with prominent pyramidal tracts and absent olivary nuclei, thinned corpus callosum, and symmetrical dilation of bilateral lateral ventricles. Microscopic examination confirmed the gross findings and revealed no histological evidence of cerebellar tissue, absence of superior and inferior cerebellar peduncles, and acute and chronic germinal matrix hemorrhages. Immunohistochemical studies revealed a focus of reactive gliosis at the base of the posterior fossa cyst with no evidence of cerebellar Purkinje or granule cells. To our knowledge, this is the 1st report with well-characterized neuropathological examination detailing complete cerebellar loss and brain-stem atrophy in a neonate with NAIT.

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CNS Lesions in Neonatal Isoimmune Thrombocytopenia

Cited by 51 publications

References 12 publications

Fetal Encephalopathies of Circulatory Origin

Fetal Encephalopathies of Circulatory Origin

Pathobiology of Secondary Immune Thrombocytopenia

Cerebellar Loss and Brain-Stem Atrophy Associated with Neonatal Alloimmune Thrombocytopenia in a Discordant Twin

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