Prenatal clastic encephalopathies.
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Abdominal Injuries↗
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Demonstration of a little known cause of infantile epilepsy, occipital porencephaly, by computerized tomography (CT).
Among 500 epileptic patients studied by Computerized Tomography, 11 patients presented an occipital porencephaly (or a dilation of the occipital horn with a "porencephalic" aspect) sometimes associated with a ventricular dilation. These 11 patients represented 2.2% of our patients and 5% of those less than 20 yr of age which is frequent in relation to lesions of the same type having a different topography. Clinical and EEG studies of these 11 patients revealed hemiplegia or hemiparesis in 8 cases, hemianopsia in 7 cases, a severe partial epilepsy in 6 cases which was temporal in 5 patients, a secondary generalized epilepsy in 3 cases, and an epilepsy unable to be classified in 2 cases. The "porencephalies" responsible for these clinical signs are most likely of encephalomalacic origin, secondary to circulatory troubles in the peri- or postnatal period. Remillard et al. maintain that perinatal occlusion of the posterior cerebral artery is responsible. However, in our personal series, the results obtained from CT, PEG and angiography do not permit us to be as affirmative as to the vascular etiology responsible.
Adolescent↗
Neurodevelopmental outcome of periventricular haemorrhage and leukomalacia in infants 1250 g or less at birth.
The brains of 50 consecutively admitted infants weighing 1250 g or less at birth were serially examined beyond the neonatal period for periventricular haemorrhage and for periventricular leukomalacia with real-time ultrasound. There was significant correlation between the presence or absence and the severity of haemorrhage with survival. A prospective neurodevelopmental assessment was completed at 2 years of age, corrected for prematurity, on all survivors. None of the 20 survivors with normal scans or germinal layer haemorrhages had evidence of major disability and all four survivors with intracerebral haemorrhage or periventricular leukomalacia had major disability. The mental performance on the Bayley scales of infant development was also significantly worse in the latter group. Six of the eight survivors with intraventricular haemorrhage had no major disability, including three who had post-haemorrhagic hydrocephalus. Our results showed that cerebral ultrasound detection of brain pathology is a good predictor of neurodevelopmental outcome in such extremely low birthweight infants. However, as the maximum extent of periventricular haemorrhage may develop beyond one week of age and cystic periventricular leukomalacia commonly develops after the neonatal period, serial scanning is mandatory to ensure diagnostic accuracy for both periventricular haemorrhage and leukomalacia.
Blindness↗
Evolution of periventricular leukomalacia during the neonatal period and infancy: correlation of imaging and postmortem findings.
Eighteen of 68 infants born over a 4-year period who had cranial ultrasound studies and later came to necropsy were found to have periventricular leukomalacia (PVL). Thirteen were diagnosed in life and there was one false positive diagnosis giving an accuracy of 91%, sensitivity of 72% and specificity of 98%. In 11 infants with sequential studies, who died at ages from 43 h to 3 years, the ultrasound findings were correlated with those at postmortem to establish the natural history of the condition. In infants who died within 7 days following the onset of the ultrasound changes, postmortem revealed early PVL without cysts: there were small haemorrhages into the affected areas in three of the four cases. In the five infants who died between 10 days and 9 weeks, cystic lesions were identified in life and at postmortem, but in two long-term survivors cysts resolved on ultrasound at 3-4 months of age. Correlation of ultrasound with postmortem findings demonstrated that, although the ultrasound lesions resolve, glial scarring and impaired myelination can still be demonstrated on careful pathological examination.
Brain↗
Head growth and neurodevelopmental outcome in neonates with intracranial haemorrhage and leukomalacia.
Head growth was correlated with outcome in 12 infants with major intracranial haemorrhages and in 9 with extensive cystic leukomalacia. Decreasing head growth was associated with a poor neurodevelopmental outcome whereas a normally growing head did not necessarily correlate with a normal outcome.
Cerebral Hemorrhage↗
Ultrasound evolution and later outcome of infants with periventricular densities.
The evolution of ultrasound findings in 59 infants with transient periventricular densities is described and the neurodevelopmental outcome of 53 of these infants was compared with 92 of 107 infants with normal ultrasound scans, born during the same 24-month period. Four of the 53 infants with transient periventricular densities developed spastic diplegia and 24 developed transient dystonia, whereas only 8 of the 92 children with normal ultrasound scans demonstrated this finding (P less than 0.001). Persistence of the densities for more than 10 days and the presence of densities in the trigone were especially related with subsequent problems. Postmortem findings in two infants and MRI studies in six infants also suggested that transient periventricular densities represent the milder end of the spectrum of periventricular leukomalacia.
Cerebral Palsy↗
Ventricular shapes, distortions, and deformities: mirrors of past cerebral insults. A study based on early sonographic follow-up studies.
Ventricular distortions and deformities often represent the endpoint of neuropathologic reactions that evolve early in life. Once fully developed, they may offer no clues as to preceding etiologic agents or pathogenesis. Serial sonography in the neonatal period of 14 patients with periventricular leukomalacia provided documentation of the evolution of certain ventricular patterns. When recognized early, these ventricular changes have prognostic significance because periventricular leukomalacia can produce serious neurologic sequelae. If found later in childhood, periventricular leukomalacia can be suggested as the original pathology. Ventricular deformities can be generalized (12 patients) or focal (11 patients); the various types of distortions are seen frequently in combination. The generalized form of ventricular expansion consisted of uniform expansion of the parieto-occipital components (hydroporencephaly), following extensive periventricular white matter necrosis. Hydroporencephaly is a new form of ex vacuo hydrocephalus in the pediatric age group. Focal changes are caused by more localized white matter cavitations with ventricularization of ensuing porencephalic cysts. These changes result in a footprint-shaped ventricular pattern (10 patients) or in frontal/occipital (polar) ventricular pointing (4 patients). White matter necrosis in other areas may lead to ventricles with bumpy contours (5 patients).
Brain Damage, Chronic↗
Infantile subcortical leukohypodensity demonstrated by computed tomography.
We reviewed the computed tomography scans of 126 term infants, ages 1-6 months; leukohypodensity was found just under the cerebral cortex (subcortical leukohypodensity [SLD]) in 3 infants (2.4%) at 1-3 months of age. On subsequent computed tomography at over 4 months of age, SLD had disappeared and anterior horn predominant dilatation of the lateral ventricles had appeared. Only 1 patient with a distinct SLD had a poor neurodevelopmental outcome: spastic diplegia. SLD in our patients is believed to be closely related to subcortical leukomalacia because of the similar location and age distribution. Transient SLD may be a mild form of cystic SLD which would require careful computed tomography follow-up examination in early infancy.
Birth Weight↗
MRI in motor delay: important adjunct to classification of cerebral palsy.
Cranial magnetic resonance imaging (MRI) was performed prospectively in 45 children (ages 3-27 months) with clinically documented motor delay to evaluate the ability of MRI to determine etiologic factors, to determine whether myelination correlated with motor delay, and whether the clinical category corresponded with the imaging findings. Of the 22 children diagnosed clinically as having major motor delay (i.e., cerebral palsy), 77% had magnetic resonance imaging abnormalities. In 23%, etiologic associations were established from MRI alone and in 32% a clinically suspected etiology was supported. No children had myelination delay as the sole abnormality. In 23 children with minor motor delay, only 17% had abnormal scans. Clearly, MRI provided useful information in the majority of children with cerebral palsy; therefore, a classification system is proposed in which MRI can be used in conjunction with clinical assessment to specify more precisely the etiologic factors in cerebral palsy.
Atrophy↗
Expression of beta-amyloid precursor protein in axons of periventricular leukomalacia brains.
Human beta-amyloid precursor protein immunoreactivity was demonstrated in axonal swellings (spheroids) around periventricular leukomalacia (PVL) of neonates. Immunoreactive axons were found at the early, but not late stage of PVL. beta-Amyloid precursor protein immunoreactivity was homogeneous in damaged axons at the early stage of PVL manifesting microglial activation, concentrated at the center of axonal swellings at the subsequent stage manifesting astrogliosis, and undetectable at the terminal stage of cavitation or neovasculation. Immunostaining for beta-amyloid precursor protein was useful in localizing PVL lesions at their early stages.
Amyloid beta-Protein Precursor↗
Altered mentation caused by polioencephalomalacia, hypernatremia, and lead poisoning.
Polioencephalomalacia in general and the specific disorders associated with lead toxicosis and sodium imbalances all have commonalities in risk groups and clinical presentations but can be differentiated based on herd history, subtle clinical differences, and diagnostic tests. Treatment also has some overlap, but determining the specific etiology enables more specific treatment and more effective prophylactic measures.
Animals↗
Encephalomalacic lesions in pigs dually infected with porcine reproductive and respiratory syndrome virus and pseudorabies virus.
Four pigs (group 1) were infected with an aerosol containing porcine reproductive and respiratory syndrome virus (PRRSV) followed 7 days later by pseudorabies virus (PRV). Three further pigs (group 2) received PRRSV alone, two (group 3) received PRV alone, and two (group 4) remained as uninfected controls. Despite the admittedly small numbers of animals, the experiment appeared to throw light on aspects of synergy. Thus, the group 1 pigs showed severe neurological signs characterized by ataxia and muscular tremors. Total cell numbers in the bronchoalveolar lavage fluid were increased in all PRRSV-infected pigs, and PRRSV antigen was detected in the alveolar macrophages. Total cell numbers in the cerebrospinal fluid of group 1 pigs were considerably greater than those demonstrated in group 3, but no PRV antigen was found. Pigs of groups 1 and 2 showed pulmonary lesions, characterized by interstitial pneumonia and PRRSV antigen immunolabelling. Non-suppurative encephalitis was found in five of the six pigs of groups 1 and 3. In particular, one group 1 animal had severe necrotizing encephalitis with intranuclear inclusion bodies and associated immunolabelling of PRV antigen. The other three group 1 pigs had prominent malacic lesions, with macrophages. These neuropathological findings strongly suggested that PRRSV infection in pigs enhances the severity of brain lesions caused PRV.
Animals↗
Brain lesions in pigs dually infected with porcine reproductive and respiratory syndrome virus and pseudorabies virus.
Four pigs were inoculated with an aerosol containing porcine reproductive and respiratory syndrome virus (PRRSV) followed 14 days later by inoculation with pseudorabies virus (PRV). The four dually infected pigs showed severe clinical signs, and one died on day 6 after infection with PRV. As demonstrated previously, the clinical disease was much more severe than that produced by either virus alone. All four dually infected pigs developed severe non-suppurative encephalitis, two had tonsillitis, two had necrotizing bronchiolitis, and one had lymphadenitis. The distribution of lesions corresponded closely with the detection of intranuclear inclusion bodies and PRV antigen. High numbers of TUNEL-positive cells detected in the thymus were associated with thymic atrophy.
Animals↗
Motor and cognitive development of infants with intraventricular hemorrhage, ventriculomegaly, or periventricular parenchymal lesions.
Two hundred twenty-six moderate- or high-risk newborn infants were studied to examine the relationship between ultrasound findings in the newborn period and at 6 months and motor and cognitive deficits at 1 year. A three-part classification of abnormal ultrasound findings was used to grade intraventricular hemorrhage, ventriculomegaly, and parenchymal lesions. Abnormal ultrasound findings were observed in 48 infants, of whom 21 had intraventricular hemorrhage, 18 persistent ventriculomegaly, and nine parenchymal lesions. The incidence of deficits was as follows: normal ultrasound examination, 20%; intraventricular hemorrhage, 33%; persistent ventriculomegaly, 67%; and parenchymal lesions, 89%. The present study indicates that serial ultrasound examinations are indicated in preterm newborn infants less than 1500 gm and in selected newborn infants at risk and greater than 1500 gm at birth. The three-part classification of abnormal ultrasound findings should be used because of the predictive significance of persistent ventriculomegaly and parenchymal lesions for motor and cognitive deficits at 1 year of age.
Cerebral Hemorrhage↗
Antenatal origin of neurologic damage in newborn infants. I. Preterm infants.
Currently, the diagnosis of white matter necrosis may be performed with echoencephalography when cysts are observed in the white matter adjacent to the lateral ventricles. One hundred twenty-seven infants with a gestational age less than 36 weeks (mean [+/- SE] gestational age = 31 +/- 3.2 weeks) were studied in the neonatal period with echoencephalography to determine the incidence of white matter necrosis and the perinatal variables associated with this complication. Twenty-three infants (18.3%) had white matter necrosis. Thirteen (10.3%) had cysts by day 3 (11 on day 1), indicating that the onset of white matter necrosis occurred antenatally. The incidence of antenatal white matter necrosis was inversely related to birth weight and was more frequent in infants weighing less than 1000 gm (19%). Stepwise logistic regression analysis of 31 antenatal variables showed that placental vascular anastomoses in multiple pregnancies, funisitis, and purulent amniotic fluid were the only complications associated with antenatal white matter necrosis. Follow-up neurologic evaluations were abnormal in four of six patients with antenatal white matter necrosis. The findings in this study focus attention on prenatal, rather than intrapartum and postnatal, factors as causative agents of neurologic morbidity and emphasize the importance of early and sequential evaluation of neonatal brain structures.
Cerebral Hemorrhage↗
The aetiology of cerebrocortical necrosis: the role of thiamine deficiency and of deltapyrrolinium.
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Animals↗
Biochemical aspects of cobalt deficiency in sheep with special reference to vitamin status and a possible involvement in the aetiology of cerebrocortical necrosis.
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Animals↗
Extensive cystic leucomalacia: correlation of cranial ultrasound, magnetic resonance imaging and clinical findings in sequential studies.
Cranial ultrasound (US) was used in 14 neonates to define three categories of extensive cystic leucomalacia, namely periventricular, mixed, and subcortical. The initial US findings were compared with serial magnetic resonance imaging (MRI) and the neurodevelopmental outcome of the children. In the infants with periventricular leucomalacia, MRI showed a decrease in the size of the cystic areas with age. Six of these seven children showed an increase in the level of myelination upon follow-up examination, although white matter development was slower in the vicinity of the cysts. The lateral ventricles of these children were slightly enlarged and the occipital horns showed an irregular angular outline. In the infants with mixed leucomalacia, MRI showed cystic areas which remained obvious at the final examination. Myelination was grossly delayed in these patients. The lateral ventricles were enlarged and remained unchanged, with the exception of one infant whose ventricles collapsed after shunt revision. In the three children with subcortical leucomalacia, MRI confirmed shrinkage of the cysts in two of the three infants upon the first follow-up examination but thereafter the cysts remained unchanged. No supratentorial myelination was demonstrated in these patients. The ventricles were enlarged and the cortical sulci were prominent in all these infants. A strong correlation was shown between the MRI appearances and the clinical outcome in these children. MRI may be most useful for making the diagnosis of cystic leucomalacia in children not submitted to US examination as neonates or in whom only some of the classical US features have been identified.
Brain↗