Fatal outcome following foetal cerebellar haemorrhage associated with placental thrombosis

Malinger, G.; Zahalka, Nariman; Kidron, Dvora; Ben-Sira, Liat; Lev, Dorit; Lerman‐Sagie, Tally

doi:10.1016/j.ejpn.2006.02.002

Cited by 27 publications

(17 citation statements)

References 13 publications

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“…Redline and Pappin highlighted the importance of even small foci of avascular villi in the absence of vascular thrombi and proposed the term of “fetal thrombotic vasculopathy” (FTV) [35]. This kind of placental lesions has been implicated in pathologies like cerebral palsy, fetal thromboembolic disease, intrauterine growth restriction, intrapartum monitoring abnormalities and discordant growth in twin pregnancies [19, 23, 36–41]. Severe fetal vascular lesions have been observed in over 50% of patients with hypoxic-ischemic encephalopathy or cerebral palsy at term [37].…”

Section: Discussionmentioning

confidence: 99%

Placental Vascular Obstructive Lesions: Risk Factor for Developing Necrotizing Enterocolitis

Dix

Roth‐Kleiner

Osterheld

2010

Pathology Research International

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Necrotizing enterocolitis (NEC) is a severe neonatal disease affecting particularly preterm infants. Its exact pathogenesis still remains unknown. In this study, we have compared the prevalence of vascular obstructive lesions in placentae of premature newborns which developed NEC and of a control group. We further compared separately the findings of placentae of infants of less than 30 weeks of gestation, the age group in which NEC occurs most frequently. We found signs of fetal vascular obstructive lesions in 65% of the placentae of preterm patients developing NEC, compared to only 17% of the placentae of preterm patients in the control group. In the age groups below 30 weeks of gestation, 58.5% of placentae of later NEC patients presented such lesions compared to 24.5% in the control group. The significant difference between NEC and control group suggests a strong association between fetal vascular obstructive lesions and NEC. Therefore, we propose that fetal vascular obstructive lesions might be considered as a risk factor for the development of NEC in premature infants.

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Section: Discussionmentioning

confidence: 99%

Placental Vascular Obstructive Lesions: Risk Factor for Developing Necrotizing Enterocolitis

Dix

Roth‐Kleiner

Osterheld

2010

Pathology Research International

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“…Follow-up examinations after fetal cerebellar haemorrhage have shown a gradual reduction in the size of the affected hemisphere. 5,7,24 Haemosiderin deposition was not seen on follow-up imaging in any of the patients. Indeed, in preterm infants with cerebellar haemorrhage haemosiderin is no longer detectable 6 weeks after its occurrence.…”

Section: Developmental Findingsmentioning

confidence: 96%

“…To our knowledge, only 18 non-neuropathological cases have been published previously. 3-13,20-22 UCH has been previously described prenatally from 21 weeks' gestation in five cases; [3][4][5][6][7] in one instance the pregnancy was terminated. In our series, UCH was detected incidentally by prenatal ultrasound and confirmed by MRI at 21 weeks' gestation in one case and in the early postnatal period in one case.…”

Section: Developmental Findingsmentioning

confidence: 99%

“…Cerebellar haemorrhage has been shown to occur pre-and perinatally. Increasing experience with prenatal ultrasound 3,23 and greater availability of fetal MRI 5,7,24 have demonstrated the prenatal occurrence of cerebellar haemorrhage. In these reports, cerebellar haemorrhages were detected at between 18 and 24 weeks' gestation.…”

Section: Developmental Findingsmentioning

confidence: 99%

“…1 In our experience, minor asymmetry of the cerebellar hemispheres is occasionally seen as an incidental finding without clinical significance whereas severe UCH is expected to be of clinical relevance. Previous descriptions of UCH have mostly been single case reports with a prenatal [3][4][5][6][7] or postnatal [8][9][10][11][12][13] diagnosis. The lack of outcome data available as a basis for well-founded prenatal counselling provided additional motivation for us to assess the prognosis of patients with UCH.…”

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confidence: 99%

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Outcome of severe unilateral cerebellar hypoplasia

Poretti

Limperopoulos

Roulet-Perez

et al. 2010

Develop Med Child Neuro

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AIM Complete or subtotal absence of one cerebellar hemisphere is exceptional; only single cases have been described. We aimed to assess the long-term outcome in children with severe unilateral cerebellar hypoplasia (UCH).METHOD As part of a retrospective study we describe neuroimaging features, clinical findings, and cognitive outcomes of seven children with UCH (five males, two females; age at first magnetic resonance imaging [MRI]: median 1y 3mo, range 9d-8y 10mo; age at latest follow-up: median 6y 6mo, range 2y 3mo-14y 11mo).RESULTS One child had abnormalities on prenatal MRI at 21 weeks' gestation. The left cerebellar hemisphere was affected in five children, and the right hemisphere in two children. The vermis was involved in five children. The volume of the posterior fossa was variable. At the latest followup, neurological findings included truncal ataxia and muscular hypotonia in five children, limb ataxia in three patients, and head nodding in two patients. Three children had learning disability*, five had speech and language disorders, and one had a severe behavioural disorder.

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Cerebellar hypoplasia: Differential diagnosis and diagnostic approach

Poretti¹,

Boltshauser

Doherty

2014

American J of Med Genetics Pt C

120

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Cerebellar hypoplasia (CH) refers to a cerebellum with a reduced volume, and is a common, but non-specific neuroimaging finding. The etiological spectrum of CH is wide and includes both primary (malformative) and secondary (disruptive) conditions. Primary conditions include chromosomal aberrations (e.g., trisomy 13 and 18), metabolic disorders (e.g., molybdenum cofactor deficiency, Smith-Lemli-Opitz syndrome, and adenylosuccinase deficiency), genetic syndromes (e.g., Ritscher-Schinzel, Joubert, and CHARGE syndromes), and brain malformations (primary posterior fossa malformations e.g., Dandy-Walker malformation, pontine tegmental cap dysplasia and rhombencephalosynapsis, or global brain malformations such as tubulinopathies and α-dystroglycanopathies). Secondary (disruptive) conditions include prenatal infections (e.g., cytomegalovirus), exposure to teratogens, and extreme prematurity. The distinction between malformations and disruptions is important for pathogenesis and genetic counseling. Neuroimaging provides key information to categorize CH based on the pattern of involvement: unilateral CH, CH with mainly vermis involvement, global CH with involvement of both vermis and hemispheres, and pontocerebellar hypoplasia. The category of CH, associated neuroimaging findings and clinical features may suggest a specific disorder or help plan further investigations and interpret their results. Over the past decade, advances in neuroimaging and genetic testing have greatly improved clinical diagnosis, diagnostic testing, recurrence risk counseling, and information about prognosis for patients and their families. In the next decade, these advances will be translated into deeper understanding of these disorders and more specific treatments.

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Fatal outcome following foetal cerebellar haemorrhage associated with placental thrombosis

Cited by 27 publications

References 13 publications

Placental Vascular Obstructive Lesions: Risk Factor for Developing Necrotizing Enterocolitis

Placental Vascular Obstructive Lesions: Risk Factor for Developing Necrotizing Enterocolitis

Outcome of severe unilateral cerebellar hypoplasia

Cerebellar hypoplasia: Differential diagnosis and diagnostic approach

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