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PubMed2002

Subtle developmental abnormalities in the inferior olive: an indicator of prenatal brainstem injury in the sudden infant death syndrome.

Subtle quantitative abnormalities in neuronal populations derived from the rhombic lip (i.e. arcuate nucleus at the ventral medullary surface, external granular layer of the cerebellum) have been reported in victims of the sudden infant death syndrome (SIDS). In this study, we examined the inferior olive, a major rhombic lip derivative, to determine if subtle rhombic lip abnormalities also involve this nucleus in SIDS. We analyzed the number and density of neurons and reactive astrocytes in the inferior olive in 29 SIDS cases and 29 controls. Computer-assisted cell counting procedures were used in sections stained with hematoxylin and eosin/Luxol fast blue. There was a significant difference in the postconceptionally age-adjusted mean for neuronal density between SIDS cases (7,687 +/- 255 neurons/mm(3)) and controls (8,889 +/- 255 neurons/mm(3)) (p = 0.002). The difference in age-adjusted mean neuronal number between SIDS cases (1,932 +/- 89 neurons/2 sections) and controls (2,172 +/- 89 neurons/2 sections) was marginally significant (p = 0.063). Reactive astrocytes were present in the inferior olive in SIDS cases, but their number, density, and developmental profile were not significantly different from that of control infants dying of diverse known causes. SIDS victims found dead in cribs, beds, and sofas, prone or supine had subtle olivary abnormalities, suggesting that affected infants are at risk in various sleeping situations. We propose that at least some SIDS victims experience intrauterine brainstem injury including the olivo-arcuato-cerebellar circuitry derived from the rhombic lip. These observations provide future directions for SIDS research concerning the role of early insults in pregnancy, the rhombic lip, and the interactions of the ventral medulla and cerebellum in cardioventilatory control.

Age Factors↗
PubMed1996

Role of the clinical toxicologist in court.

The clinical toxicologist may play a role in court when issues arise concerning therapeutic drug monitoring, drug abuse, environmental chemicals, or toxic torts, where the traditional forensic toxicologist may not have expertise. Beyond being credible in court, the toxicologist's testimony must be based on good scientific evidence. The ruler for measuring good scientific evidence had previously been the Frye Test, or the general acceptance test. In 1993, however, the US Supreme Court established four balancing tests that should be used for the admissibility of scientific evidence. Although the ruling is binding only in federal courts, state courts are expected to follow. When testifying, the clinical toxicologist should be aware of other court rules and expectations. As with all testimony, objections from opposing counsel can be raised to disallow the presentation of evidence by a toxicologist. The toxicologist is usually used to establish causation of injury, whether from negligence, prenatal injury, or environmental chemicals. Several examples are presented.

Chemistry, Clinical↗
PubMed1991

Effects of prenatal exposure to methylazoxymethanol (MAM) on brain weight, hypothalamic cell number, pituitary structure, and postnatal growth in the rat.

Congenital brain damage syndromes typically are described in terms of behavioral symptoms. Many brain functions are not reflected in behavior, however, and prenatal injury to the developing nervous system could alter these functions, as well. To test the hypothesis that prenatal brain injury can result in postnatal endocrine malfunction, rats were exposed in utero to 20 mg/kg of methylazoxymethanol acetate, a potent neuroteratogen, at two stages of gestation when different sets of growth-controlling neurons of the hypothalamus are forming. The growth hormone releasing factor (GRF) neurons stimulate release of growth hormone from the somatotropes of the anterior pituitary, contributing to rapid growth in the period between weaning and puberty. The somatotropin release inhibiting factor (SRIF) neurons have the opposite effect on the pituitary and can inhibit the GRF cells directly. Growth of treated animals was monitored daily from birth to 40 days and compared to that of controls. Treatment on the 14th day of gestation produced a small number of dwarf animals characterized by normal weight at birth and a sudden decrease in growth rate at the beginning of the fourth postnatal week that led to a body weight about 50% of normal. Treatment on day 16 yielded an acceleration of postnatal growth (significant in males). In each group, most treated animals were like controls in adult size and pattern of growth. As adults, both treatment groups demonstrated massive reductions in brain weight which characterized all the subjects, whether or not they exhibited growth anomalies. The animals treated on day 14 were confirmed to have a significant, selective reduction in growth hormone releasing factor neurons. Reductions were greatest in the middle and posterior levels of the GRF cell distribution, the regions forming most actively at the time of exposure. Unexpectedly, the same group also had increased numbers of periventricular SRIF neurons. Neither type of neurons was significantly altered in the later treatment group. Examination of pituitary structure indicated that dwarfs had very small pituitaries, with an immature pattern of somatotrope distribution, and giants had very large pituitaries, with some hypertrophy of somatotropes. The results suggest that endocrine anomalies which manifest themselves long after birth may originate as birth defects of the nervous system.

Animals↗
PubMed1988

Neuropathologic documentation of prenatal brain damage.

Neuropathologic evidence of prenatal brain damage, chiefly in cerebral white matter, was found in 25% of infants who died at 7 days of age or less, with a total of ten preterm (16%) and 12 term (48%) infants among the 89 subjects studied. Few clinical features distinguished infants with prenatal injury from those without such injuries. Apgar scores were low, seizures were rare, and acute intracranial hemorrhage occurred equally often in both groups. Few pregnancies were entirely normal, but hydramnios was the only factor that occurred more often in prenatally injured infants, a statistically significant difference only among term infants. Oligohydramnios was not associated with prenatal brain injury. Unless fetal/maternal abnormalities in late gestation are identified and corrected, improved neonatal care will increase survival for prenatally damaged infants and the incidence of cerebral palsy may rise.

Brain↗
PubMed2002

The triple risk hypotheses in sudden infant death syndrome.

Sudden infant death syndrome (SIDS) victims were regarded as normal as a matter of definition (Beckwith 1970) until 1952 when Kinney and colleagues argued for elimination of the clause, "unexpected by history." They argued that "not all SIDS victims were normal," and referred to their hypothesis that SIDS results from brain abnormalities, which they postulated "to originate in utero and lead to sudden death during a vulnerable postnatal period." Bergman (1970) argued that SIDS did not depend on any "single characteristic that ordains a infant for death," but on an interaction of risk factors with variable probabilities. Wedgwood (1972) agreed and grouped risk factors into the first "triple risk hypothesis" consisting of general vulnerability, age-specific risks, and precipitating factors. Raring (1975), based on a bell-shaped curve of age of death (log-transformed), concluded that SIDS was a random process with multifactorial causation. Rognum and Saugstad (1993) developed a "fatal triangle" in 1993, with groupings similar to those of Wedgwood, but included mucosal immunity under a vulnerable developmental stage of the infant. Filiano and Kinney (1994) presented the best known triple risk hypothesis and emphasized prenatal injury of the brainstem. They added a qualifier, "in at least a subset of SIDS," but, the National Institute of Child Health and Development SIDS Strategic Plan 2000, quoting Kinney's work, states unequivocally that "SIDS is a developmental disorder. Its origins are during fetal development." Except for the emphasis on prenatal origin, all 3 triple risk hypotheses are similar. Interest in the brainstem of SIDS victims began with Naeye's 1976 report of astrogliosis in 50% of all victims. He concluded that these changes were caused by hypoxia and were not the cause of SIDS. He noted an absence of astrogliosis in some older SIDS victims, compatible with a single, terminal episode of hypoxia without previous hypoxic episodes, prenatal or postnatal. Kinney and colleagues (1983) reported gliosis in 22% of their SIDS victims. Subsequently, they instituted studies of neurotransmitter systems in the brainstem, particularly the muscarinic (1995) and serotenergic systems (2001). The major issue is when did the brainstem abnormalities, astrogliosis, or neurotransmitter changes occur and whether either is specific to SIDS. There is no published method known to us of determining the time of origin of these markers except that the injury causing astrogliosis must have occurred at least 4 days before death (Del Bigio and Becker, 1994). Because the changes in neurotransmitter systems found in the arcuate nucleus in SIDS victims were also found in the chronic controls with known hypoxia, specificity of these markers for SIDS has not been established. It seems likely that the "acute control" group of Kinney et al (1995) died too quickly to develop gliosis or severe depletion of the neurotransmitter systems. We can conclude that the acute controls had no previous episodes of severe hypoxia, unlike SIDS or their "chronic controls." Although the average muscarinic cholinergic receptor level in the SIDS victim was significantly less than in the acute controls, the difference was only 27%, and only 21 of 41 SIDS victims had values below the mean of the acute controls. The study of the medullary serotonergic network by Kinney et al (2001) revealed greater reductions in the SIDS victims than in acute controls, but the questions of cause versus effect of the abnormalities, and whether they occurred prenatally or postnatally, remain unanswered. Hypoplasia of the arcuate nucleus was stated to occur in 5% of their SIDS cases by Kinney et al (2001), but this is a "primary developmental defect" according to Matturri et al (2002) with a larger series, many of whom were stillbirths. These cases should not be included under the rubric of SIDS, by definition. There are difficulties with Filiano and Kinney's (1994) explanation of the age at death distribution of SIDS. They postulate that the period between 1 and 6 months represents an unstable time for virtually all physiologic systems. However, this period demonstrates much less instability than does the neonatal period, when most deaths from congenital defects and severe maternal anemia occur. We present data for infants born to mothers who were likely to have suffered severe anemia as a consequence of placenta previa, abruptio placentae, and excessive bleeding during pregnancy; these infants presumably are at increased risk of hypoxia and brainstem injury. The total neonatal mortality rate in these 3 groups of infants is 4 times greater than the respective postneonatal mortality, and in the postneonatal period the non-SIDS mortality rate is between 14 and 22 times greater than the postneonatal SIDS rate in these 3 groups. A preponderance of deaths in the neonatal period is also found for congenital anomalies, a category that logically should include infants who experienced prenatal hypoxia or ischemia; this distribution of age of death is very different from that for SIDS, which mostly spares the first month and peaks between 2 and 3 months of age. Finally, evidence inconsistent with prenatal injury as a frequent cause of SIDS comes from prospective studies of ventilatory control in neonates who subsequently died of SIDS; no significant respiratory abnormalities in these infants have been found (Waggener et al 1990; Schectman et al 1991). We conclude that none of the triple risk hypotheses presented so far have significantly improved our understanding of the cause of SIDS. Bergman's and Raring's concepts of multifactorial causation with interaction of risk factors with variable probabilities is less restrictive and more in keeping with the large number of demonstrated risk factors and their varying prevalence. If prenatal hypoxic damage of the brainstem occurred, it seems likely that the infant so afflicted would be at risk for SIDS, but it is even more likely that their death would occur in the neonatal period, as we have demonstrated in infants who have known maternal risk factors that involve severe anemia. This is in contrast to the delay until the postneonatal period of most SIDS deaths. A categorical statement that the origin of SIDS is prenatal is unwarranted by the evidence. Brainstem abnormalities have not been shown to cause SIDS, but are more likely a nonspecific effect of hypoxia.

Age Factors↗
PubMed1997

Glucose metabolism in the human cerebellum: an analysis of crossed cerebellar diaschisis in children with unilateral cerebral injury.

Using high-resolution positron emission tomography (PET), we have recently described the normal pattern of glucose utilization in 11 anatomical regions of the human cerebellum. In the present study, we evaluated the phenomenon of crossed cerebellar diaschisis in 40 patients (mostly children) with unilateral cerebral injury sustained at various periods of brain development. Diaschisis refers to a functional impairment at a remote site following injury to an anatomically connected area of brain and, presumably due to a loss of afferent input to the remote site. Of the 40 patients, 11 had sustained their cerebral injury prenatally, 7 in the perinatal period (+/- 24 hours of birth), and 22 postnatally (1 day to 15 years). Crossed cerebellar hypometabolism was seen in 22 patients; symmetric cerebellar metabolism was found in 16 subjects. The presence of crossed cerebellar hypometabolism was typically associated (75% of cases) with a postnatal injury, while symmetric cerebellar metabolism was seen only in patients with injury occurring prior to 4 weeks of age (13 of the 16 had prenatal or perinatal insults). A third pattern of cerebellar metabolism, consisting of paradoxical crossed cerebellar hypermetabolism, was seen in two patients; both had sustained their cerebral injury at 4 months of age. These findings suggest the presence of considerable plasticity, which is dependent on age at injury, in the cerebrocerebellar pathway of developing brain.

Adolescent↗
PubMed1999

Proton MR spectroscopy for the evaluation of brain injury in asphyxiated, term neonates.

BACKGROUND AND PURPOSE: Neurologic and developmental outcomes of asphyxiated, term neonates are difficult to predict applying clinical or laboratory criteria. In this study, we investigated the association of MR spectroscopy (MRS) results with neurodevelopmental status at age 12 months. METHOD: Thirty-one term neonates, who were enrolled in a prospective study of the utility of MR imaging for the determination of neurologic and developmental status, underwent single-voxel proton MRS of the basal nuclei and intervascular boundary zones. Ratios of lactate, choline, creatine, and N-acetylaspartate (NAA) peaks were calculated and tested for association with neuromotor scores and Mental Development Index of the Bayley Scores of Infant Development obtained at age 12 months. RESULTS: Elevated lactate and diminished NAA were the most common findings in infants with neurologic and developmental abnormalities at age 12 months. Although many ratios had statistically significant associations with outcome (P<.05), the highest significance was obtained with lactate/choline ratios in the basal nuclei. A false-positive finding was seen in a patient who was born after a 36-week gestation period (high lactate/choline but normal neurodevelopmental status at 12 months) and in three patients with apparent watershed injury (high watershed lactate/choline but normal neurodevelopmental status at 12 months). A false-negative MRS finding (normal lactate/choline but abnormal outcome) was seen in a patient who had an apparent prenatal injury. CONCLUSION: Proton MRS appears to be a useful tool for assessing brain injury in neonates who have suffered hypoxia or ischemia. Correlation with gestational age and imaging findings are essential for proper interpretation of the spectra. Patients with apparent watershed injuries may have normal neurodevelopmental status at age 12 months.

Aspartic Acid↗
PubMed2001

Bilateral posterior parietal polymicrogyria: a mild form of congenital bilateral perisylvian syndrome?

PURPOSE: The main features of congenital bilateral perisylvian syndrome (CBPS) are pseudobulbar palsy, cognitive deficits, epilepsy, and perisylvian abnormalities on imaging studies, however, the clinical spectrum of this syndrome is much wider than previously believed and may vary from minor speech difficulties to severely disabled patients. The objective of this study was to present the different imaging and clinical findings of 17 patients with CBPS, their genetic background, and the occurrence of prenatal injury during their pregnancies. METHODS: We evaluated 17 consecutive patients with CBPS and divided them into two groups according to the imaging findings: (a) diffuse polymicrogyria around the sylvian fissure and (b) posterior polymicrogyria at the posterior parietal regions. They were systematically interviewed regarding history of prenatal events during their pregnancies, family history of speech difficulties, epilepsy, or other neurologic abnormality. RESULTS: There were seven women, ages ranging from 3 to 41 years (mean, 11.5; median, 7 years). Seven patients had bilateral posterior parietal polymicrogyria (BPPP), and 10 had diffuse bilateral perisylvian polymicrogyria. All seven patients with BPPP had only minor speech difficulties, none had epilepsy, and all but one had a family history of epilepsy or cortical dysgenesis. In contrast, 10 patients with diffuse bilateral perisylvian polymicrogyria had pseudobulbar palsy, four had epilepsy, eight had a history of a major prenatal event, and only four had a family history of epilepsy or developmental delay. CONCLUSIONS: These findings suggest that diffuse bilateral perisylvian polymicrogyria appears to be more related to injuries caused by environmental factors, whereas BPPP has a stronger genetic predisposition. In addition, BPPP appears to have a wider clinical spectrum than previously believed, and may represent a milder extreme within the spectrum of CBPS.

Adolescent↗
PubMed1998

Uniform abnormalities in the hippocampus of five chronic schizophrenic men compared with age-matched controls.

In a post-mortem study five chronic schizophrenic men were matched with respect to age and sex to five control subjects without a known history of psychiatric illness, and were compared in pairs with regard to neurone number and pyramidal cell orientation in the left hippocampus. All five schizophrenics had significantly more disoriented pyramidal cells in the Cornu Ammonis subregions CA1-CA3 than their matched controls. They also had significantly fewer pyramidal cells in the observed areas of CA1 and CA3, but not in CA2 and CA4. There was no difference in the number of granular cells of the dentate gyrus. In pairwise comparisons the pattern was never reversed with respect to these two parameters, except in a single case where one schizophrenic proband had more cells in subregion CA2. In the absence of gliosis the findings were interpreted as sequelae of an early, presumably prenatal, injury.

Aged↗
PubMed1984

Congenital trigeminal anaesthesia. A review and classification.

Forty-three patients with the syndrome of congenital trigeminal anaesthesia (CTA) have been reported to date. The cases have been divided into three groups based on the presence and nature of any associated clinical problems. Three additional cases are presented as characteristic of each of the groups. A different aetiology is proposed for each group. Group I consists of patients with CTA as an isolated finding. It is almost always bilateral, and typically involves the distribution of only the first division of the fifth nerve. There is no evidence of other neurological abnormalities or associated mesoectodermal congenital anomalies. The aetiology is suspected to be a primary neural hypoplasia. Patients with associated congenital mesenchymal anomalies were placed in the second group. CTA was often a minor part of another well defined, more extensive clinical syndrome, such as Möbius or oculoauriculovertebral dysplasia (OAVD). The sensory abnormality was either unilateral or bilateral. The skin of the face was almost always involved, as well as the cornea and conjunctiva. This may be a heterogenous group with multiple aetiologies having in common an injury early in embryogenesis. The third group is defined as patients with CTA without evidence of mesenchymal dysplasia. These cases differ from the first group primarily because of the presence of associated focal brainstem signs. The aetiology is thought to be due to focal neural dysgenesis secondary to a prenatal injury, possibly vascular in nature.

Child, Preschool↗
PubMed2005

The morality of screening for disability.

Many people object to preimplantation or prenatal screening for disability on the grounds that it is discriminatory, has pernicious effects on the lives of existing disabled people, expresses a hurtful view of disabled people, and reduces human diversity. I argue that if these objections are held to be strong enough to show that screening is wrong, they must also imply the permissibility of causing oneself to have a disabled rather than a non-disabled child. Indeed, those who object to screening on these grounds and also claim that it is not worse to be disabled than not to be, seem to be committed to accepting the permissibility of deliberately causing disabling prenatal injury, even for frivolous reasons. If we cannot accept these implications, we cannot accept that the objections to screening show that it is wrong.

Persons with Disabilities↗
PubMedDate not supplied

Nonreplication of the association between ab-ridge count and cerebral structural measures in schizophrenia.

The origins of cerebral abnormalities in psychotic patients remain unknown. Dermatoglyphics are suitable markers of prenatal injury due to their fetal ontogenesis and their susceptibility to some of the factors that also affect cerebral development. In a previous study, positive associations between brain volumetric measures and a dermatoglyphic marker, the ab-ridge count, were reported. The present study is an attempt to replicate that finding in an independent sample. Magnetic resonance imaging (MRI) scans and dermatoglyphic measures were available for 29 schizophrenia patients (Research Diagnostic Criteria [RDC] criteria) and 26 unrelated healthy controls. The images were processed using an automated procedure, yielding volumes of total grey matter, white matter, cerebrospinal fluid (CSF), and total brain volume. The ab-ridge count was not positively associated with brain volumes in either patients or controls. The present findings do not support the hypothesis that the changes in brain volume seen in patients with schizophrenia are of prenatal origin.

Adolescent↗
PubMed1993

Skeletal growth lines seen on radiographs of newborn infants: prevalence and possible association with obstetric abnormalities.

OBJECTIVE: Skeletal transverse metaphyseal and vertebral lines, seen frequently on radiographs of infants and children, are usually believed to result from interrupted bone growth. Such lines have not been systematically studied in neonates. Accordingly, I determined the prevalence of growth lines on chest radiographs of newborn infants and assayed the gestational and obstetric abnormalities that occurred with these infants. MATERIALS AND METHODS: Chest radiographs were obtained (over a 4-year period) in 3687 neonates within the first 48 hr after birth for clinical indications. A single observer prospectively examined the radiographs for the presence of skeletal lines. When skeletal lines were seen on chest radiographs, lines in the pelvis were also sought when this region was imaged during the first 48 hr after birth. The medical records of affected neonates were reviewed to determine the presence and nature of potential in utero injuries. RESULTS: Skeletal lines were noted on chest radiographs of 200 neonates (5%) and appeared most commonly as "bone-within-bone" vertebral bodies and as transverse metaphyseal lines in the proximal humeri. Of affected neonates, 176 (88%) were born prematurely (< 38 weeks' gestation) and 59 (30%) had significant intrauterine growth retardation. Obstetric risk factors, which were varied and often multiple, were noted in 177 neonates (89%). The most common of these factors were pregnancy-induced hypertension (58 patients), multiple gestations (48 patients), drug abuse (30 patients), magnesium therapy (30 patients), prescribed maternal medications (27 patients), preterm labor before final labor (23 patients), and oligohydramnios (20 patients). In 23 neonates, no gestational complications were identified. CONCLUSION: Skeletal lines in the population of neonates who require chest radiography are relatively common, and often but not invariably appear to occur in the setting of potentially significant prenatal injury. It is speculated that these lines represent a tool for identifying and exploring causes of intrauterine growth disturbance.

Bone and Bones↗
PubMed2006

Treatment from birth of nonketotic hyperglycinemia due to a novel GLDC mutation.

OBJECTIVE: To determine whether the devastating outcome of neonatal-onset glycine encephalopathy (NKH) could be improved by instituting treatment immediately at birth rather than after symptoms are already well established. METHODS: A newborn with NKH diagnosed prenatally following the neonatal death of a previous affected sibling was treated from birth with oral sodium benzoate (250 mg/kg/day) and the NMDA receptor antagonist ketamine (15 mg/kg/day) immediately after sampling cord blood and cerebrospinal fluid (CSF) for glycine determination. Glycine cleavage system (CGS) activity was determined in placental tissue. Mutation analysis was performed by sequencing all GLDC, GCSH and AMT exons. RESULTS: CSF glycine (99 micromol/L, reference 3.8-8.0) was already markedly elevated at birth. GCS activity in placental tissue was severely reduced (2.6% of controls). A novel homozygous GLDC c.482A-->G(Y161C) missense mutation was identified. Neonatal hypotonia and apnea did not occur but the long-term outcome was poor, with intractable seizures and severe psychomotor retardation. This contrasts with the favorable outcome with early treatment in variant NKH with mild GCS deficiency (Ann Neuol 2004;56:139-143). INTERPRETATION: Prospective treatment with this regimen can favorably modify the early neonatal course of severe NKH but does not prevent the poor long-term outcome, suggesting glycine-induced prenatal injury and/or ongoing postnatal damage.

Aldehydes↗
PubMed1991

Subtle signs of prenatal maldevelopment of the hand ectoderm in schizophrenia: a preliminary monozygotic twin study.

Genes that predispose to psychosis may act by making individuals more vulnerable to the disruptive effects of various prenatal insults. Fetal organogenesis is mostly completed in the first prenatal trimester. The second trimester is a critical period of massive neuronal migration from the periventricular germinal matrix to the cortex. A peripheral appendage developing simultaneously with this neural migration to the cortex is the distal upper limb. The ectodermal cells of the fetal upper limb migrate to form the hand skin during the fourth and fifth months of gestation (first two-thirds of the second prenatal trimester). Discrepancies in hand morphology between two identical (monozygotic [MZ]) co-twins may be temporal markers, that is, the "fossilized" evidence of various ischemic and other nongenetic insults that may have affected one fetus more than his MZ co-twin during that early part of the second trimester. In twins, prenatal insults (e.g., ischemia) frequently do not affect both co-twins to the same extent, so we examined seven putative markers of prenatal injury to the hand in 24 MZ twin pairs discordant for schizophrenia or delusional disorder. Compared with well co-twins, the affected co-twins had significantly higher total scores of fourth- and fifth-month dysmorphological hand anomalies.

Delusions↗
PubMed1978

Multicystic encephalomalacia of infancy: clinico-pathological report of 7 cases.

Clinical follow up and complete neuropathological examination was made on seven cases of multicystic encephalomalacia of infancy. Etiological factors were carefully studied in all the cases. They consisted of prenatal injuries presenting as a cord prolapse, in 3 cases; prolonged labour with marked cyanosis; abdominal trauma during gestation, and various maternal infections at different stages of pregnancy. Pathological interest is centred on the variable involvement of different areas of the brain, generally sparing the cerebellum and brain stem, and being minimal or absent in the occipito-temporal areas. This distribution may be explained by a different effect of the "causal agency" on these different areas, or by a different capacity of these regions to react against injury. Among the etiological factors reviewed in the literature, the anoxic theory appears the most probable, as there was a close parallelism between lesions and vascular areas, mainly the carotid and vertebro-basilar systems.

Asphyxia Neonatorum↗
PubMed2000

Congenital bilateral perisylvian syndrome (CBPS): do concomitant esophageal malformations indicate a poor prognosis?

Congenital bilateral perisylvian syndrome (CBPS) is a syndrome of cortical malformation characterized by faciopharyngoglossomasticatory diplegia. We report on two cases of CBPS with associated esophageal malformations and a poor mental and motor development. The association of CBPS and esophageal malformations may indicate a subgroup of patients with a very early prenatal injury, characterised by a bad prognosis due to severe cortical disorganization. However, it can not be excluded that the association of CBPS and esophageal malformation is purely coincidental.

Abnormalities, Multiple↗
PubMed1989

Minor physical anomalies in schizophrenia.

This study was conducted to investigate the value of using physical anomalies (PAs) to evaluate early prenatal injury in schizophrenia. PAs are minor abnormalities in development of the head, hands, and feet that are presumably associated with insult during the first trimester. Sixty-seven schizophrenic inpatients and 88 normal controls were evaluated for PAs. The schizophrenic patients showed significantly more anomalies than the controls. The difference remained significant even when patients were compared to controls of low socioeconomic status. Both male and female patients showed a high incidence of mouth abnormalities, and female patients showed a high incidence of abnormalities in head circumference. Patients with early age of onset (less than or equal to 18 years) had more physical anomalies than did later onset patients. This relationship was most noticeable for males. Physical anomalies were not associated with deficits on measures of vigilance, selective attention, or orientation.

Adult↗