Cystic Brain Lesion in Utero

Nakamura, Yasuhiro; Fujiyoshi, Yoshinori; Fukuda, Seiichi; Matsunaga, Takamoto; Hasegawa, T.; Manabe, Akihiro; Nakashima, Teruyuki

doi:10.1111/j.1440-1827.1986.tb01051.x

Cited by 4 publications

(5 citation statements)

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“…The authors concluded that multicystic encephalomalacia and chronic PVL were caused by persistent circulatory disturbance in utero . 6 In the present patient, although mild fetal ventriculomegaly was noted from 22 weeks of gestation, PVE and cystic PVL were not observed during pregnancy. We speculate that some persistent circulatory disturbance, perhaps induced by a traumatic event, may have occurred before 22 weeks of gestation and fetal PVE may have developed at that time, but we were unable to obtain information about traumatic events that may have affected the mother.…”

Section: Discussioncontrasting

confidence: 46%

“…The second infant was stillborn at 30 weeks of gestation at a birthweight of 1030 g. An autopsy showed thanatophoric dysplasia with associated chronic PVL. The authors concluded that multicystic encephalomalacia and chronic PVL were caused by persistent circulatory disturbance in utero 6 …”

Section: Discussionmentioning

confidence: 99%

“…4 Murata et al described early changes associated with cystic PVL that may be apparent histologically within hours of insult, but at least 2 -6 weeks are required before lesions can be visualized on US. 1 Therefore, if cystic PVL is observed within 7 days after birth, the origins must be intrauterine, 1 and we suggest that the cause of cystic PVL in fetal onset is different from that in postnatal onset, based on the reports of Yamamoto et al 5 and Nakamura et al 6 Yamamoto et al investigated the fetal brain on transvaginal US and examined the relationship between fetal periventricular echodensity (PVE) and neonatal PVL. In PVE the quantifi ed echogenicity Patient Report…”

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confidence: 94%

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Congenital cystic periventricular leukomalacia in a small‐for‐gestational age full‐term infant

Nitta¹,

Suzumura²,

Kano³

et al. 2008

Pediatrics International

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The mother was 36 years old with a birth history of gravida two para 2. Fetal ultrasonography indicated mild ventriculomegaly from 22 weeks of gestation and intrauterine growth retardation from 28 weeks of gestation ( Fig. 1 ), with unexplained causes. The mother had gestational diabetes, which was being monitored without medication, and pre-natal infections including toxoplasma, rubella, herpes and cytomegalovirus infection during pregnancy, but these were ruled out as causes. Case reportA small-for-gestational age (SGA) infant was born at 40 weeks of gestation, with birthweight 1806 g; height 44 cm, and head circumference 30.7 cm. Apgar scores were 9 and 10 at 1 and 5 min, respectively, and no abnormal pathological fi ndings were found in the placenta and umbilical cord. The infant appeared alert and looked healthy without spasms. Primitive refl exes including palmar grasp, rooting, and a Moro refl ex were present, and no hypotonia and spasticity were noted on physical examination. Laboratory data at birth were pH 7.402, PCO 2 33.7 mmHg, HCO 3 20.9 mmHg, white blood cells 11 600/ L, hemoglobin 18.5g/dL, platelet count 163 000/ L, aspartate aminotransferase 32 IU/L, alanine aminotransferase 3 IU/L, total/direct bilirubin 2.7/0.5 mg/dL, lactate dehydrogenase 970 IU/L, blood urea nitrogen 10 mg/dL, creatinine 0.8 mg/dL, glucose 62 mg/dL, Na 141 mEq/L, K 5.0 mEq/L, Cl 105 mEq/L, Ca 9.6 mg/dL, C-reactive protein <0.01 mg/dL, IgM 8 mg/dL and karyotypic analysis 46, XY.Brain computed tomography (CT) at birth showed irregular ventricular dilatation and cystic periventricular leukomalacia (PVL) near the left ventricular anterior horn ( Fig. 2a ), and brain ultrasonography (US) showed the same fi ndings. Brain magnetic resonance imaging (MRI) at 7 days of age showed cystic PVL and irregular ventricular dilatation ( Fig. 2b,c ). Auditory brainstem response audiometry at 13 days of age showed no abnormal fi ndings, and an electroencephalogram (EEG) at 14 days of age showed slightly low activity but no epileptic waves.After discharge from the neonatal intensive care unit the patient had a generalized spasm at 2 months of age. EEG showed a spike and wave complex in the left hemisphere. At 4 months of age the patient had a tonic spasm and an EEG showed hypsarrhythmia. Brain MRI at 6 months of age showed irregular ventricular dilatation and loss of white matter ( Fig. 3 ). Thus, we diagnosed West syndrome and subsequently the patient developed spastic quadriplegia. DiscussionIn this report we describe an SGA full-term infant with cystic PVL at birth. Although cystic PVL in premature infants is the major neuropathology for spastic motor defi cits in cerebral palsy or epilepsy, 1 cystic PVL in full-term infants is a rare neurological disorder of which the characteristics remain unknown.Most cases of PVL in full-term infants are diagnosed after 4 months of age based on clinical manifestations, including developmental delay, motor abnormalities, and a history of seizures. Miller et al. described 12 full-term children with PVL, inc...

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Section: Discussioncontrasting

confidence: 46%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 94%

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Congenital cystic periventricular leukomalacia in a small‐for‐gestational age full‐term infant

Nitta¹,

Suzumura²,

Kano³

et al. 2008

Pediatrics International

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“…Nakamura et al . [ 52 ] have confirmed cystic brain lesions in two autopsy cases. One was a donor fetus in twin-to-twin transfusion syndrome, and the other was a case of thanatophoric dwarfism.…”

Section: Radiologic Findings Of White Matter Injury Of Prematuritymentioning

confidence: 83%

“…Chronic PVL was found in the second case. The findings observed in these cases imply that cerebral circulatory disturbance is a pathogenetic mechanism of in utero brain injuries [ 52 ].…”

Section: Radiologic Findings Of White Matter Injury Of Prematuritymentioning

confidence: 99%

White Matter Injury of Prematurity: Its Mechanisms and Clinical Features

Lee¹

2017

J Pathol Transl Med

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A developing central nervous system is vulnerable to various insults such as infection and ischemia. While increased understanding of the dynamic nature of brain development allows a deeper insight into the pathophysiology of perinatal brain injury, the precise nature of specific fetal and neonatal brain injuries and their short- and long-term clinical consequences need special attention and further elucidation. The current review will describe the pathophysiological aspects and clinical significance of white matter injury of prematurity, a main form of perinatal brain injury in premature newborns, with a particular emphasis on its potential antenatal components.

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Clinicopathological study of germinal matrix hemorrhage, pontosubicular necrosis, and periventricular leukomalacia in stillborn

Skullerud

Skjaeraasen

1988

Child's Nerv Syst

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Cystic Brain Lesion in Utero

Cited by 4 publications

References 0 publications

Congenital cystic periventricular leukomalacia in a small‐for‐gestational age full‐term infant

Congenital cystic periventricular leukomalacia in a small‐for‐gestational age full‐term infant

White Matter Injury of Prematurity: Its Mechanisms and Clinical Features

Clinicopathological study of germinal matrix hemorrhage, pontosubicular necrosis, and periventricular leukomalacia in stillborn

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