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[Trouble within compassion: psychological guidance during prenatal diagnosis, from indication to decision].

This paper outlines the importance of psychological guidance throughout the process of prenatal diagnosis, according to the author's everyday experience in a multidisciplinary fetal medicine department. Consequences of the indication of a fetal disease are described for both sides (doctor and patient). The psychological mechanisms involved lead to the discomfort in the obstetrician's compassion and explain the intensity of the mother-to-be's reaction in the devastating situation. Being guided from the indication of a fetal malformation to her final decision aims to allow the mother to think through her first often impulsive and spontaneous decision and to consider different possibilities concerning the outcome of her pregnancy. A protocol is proposed. Guidance throughout the process of medical termination of pregnancy is developed. The psychiatrist's role should complement and follow through the psychological medical guidance. Its aim is to back up the technical and medical teams, to work on the psychoanalytic understanding of what the mother and the couple go through and have experienced, and also the consequences and the significance for the family. This is a preventive approach which deals with the feeling of guilt.

Counseling↗

The present status of prenatal detection of neural tube defects.

In experimentally induced myelocele in rats, efforts to find neural cells in amniotic fluid (AF) were unsuccessful. Creatine phosphokinase (CPK) and aldolase concentrations studied in serum of 118 and cerebrospinal fluid (CSF) in 9 patients with myelomeningocele showed serum CPK to be significantly elevated and more responsive to additional muscle injury than aldolase, but both enzymes appeared in lower concentrations in patients with myelomeningocele than those with infantile atrophy or cerebral palsy. In CSF, CPK, and aldolase concentrations averaged 4.2 I.U. and 2.7 S.L.U. per milliliter, respectively. Significant CPK elevation (p less than 0.001) was also found in AF from myeloschitic fetuses and maternal rat serum. Although these findings suggest that increased CPK concentration is an indicator of myelocele in rats, the technique is impractical for prenatal detection of human fetus occurs too late in gestation. This does not, however, preclude the value of CPK for detecting onset of paraparesis. In all myeloschitic human fetuses, the CSF communicates directly with AF for at least 3 to 4 weeks. This implies that CSF is probably the principal source of increased alpha-fetoprotein concentration encountered in AF of all pregnancies with NTD. When biological variables are recognized, it is evident that increased concentration of amniotic fluid alpha fetoprotein is a reliable indicator of fetuses with open myelocele and/or anenciphalus.

Adolescent↗

Asphyxia.

The prevention of fetal asphyxia or hypoxia starts with prepregnancy counseling and continues with careful antenatal care and intrapartum fetal surveillance. Further progress in eliminating antepartum and intrapartum deaths will only be made when it is accepted that, even with intense investigation by detailed autopsy, the cause of many deaths remains unknown. Many of these deaths may be ascribed to hypoxia. In the future, with more detailed non-invasive probing with CAT scanning and magnetic resonance imaging, other causes may be determined. The mother at risk of hypoxia requires specialized attention. Such mothers will include those with severe cardiac, pulmonary or circulatory problems. Others will be those with endocrine problems, such as diabetes or thyroid dysfunction. At present, failure of fetal growth is generally ascribed to hypoxia, but undoubtedly, in solution to such problems of possible hypoxia is elective delivery at the appropriate time. What Hensleig said in 1986 (Hensleig et al, 1986) is equally true today: 'Preventative programmes will remain unsuccessful until the causation of cerebral palsy is more understood. What we are presently lacking is an understanding of the underlying conditions responsible for brain injury when asphyxia occurs despite our best efforts. While we have learned much about the causation and prevention of perinatal mortality very little has been established about the causation and prevention of cerebral palsy'. Finally, Hall (1989), in a review of birth asphyxia and cerebral palsy, concludes the following five points. 1. The incidence of cerebral palsy is not falling despite improved obstetrics. 2. The cause of more than 90% of cases of cerebral palsy remains unknown. 3. Asphyxia is hard to define and measure and is rarely the cause of cerebral palsy. 4. Hypoxic ischaemic encephalopathy is the most reliable indicator of asphyxia. 5. Neither traditional clinical signs nor electronic monitoring allow reliable recognition of asphyxia.

Cerebral Palsy↗

Obstetric risk factors for early-onset schizophrenia in a Finnish birth cohort.

OBJECTIVE: Although case-control investigations have shown an association between obstetric complications and schizophrenia, particularly among patients with early onsets, cohort studies have mostly failed to confirm this effect. The authors examined whether a history of fetal hypoxia and other obstetric complications elevated risk for early-onset schizophrenia in a 1955 Helsinki birth cohort. METHOD: The subjects were 80 randomly selected patients with schizophrenia (36 with early and 44 with later onsets) representative of all available probands in the cohort, 61 of their nonschizophrenic siblings, and 56 demographically matched nonpsychiatric comparison subjects. Psychiatric diagnoses were obtained from structured clinical interviews, and obstetric data were taken from standardized, prospectively ascertained obstetric records. A score for hypoxia-associated obstetric complications was entered into logistic regression models, along with measures of prenatal infection and fetal growth retardation. RESULTS: Hypoxia-associated obstetric complications significantly increased the odds of early-onset schizophrenia but not of later-onset schizophrenia or unaffected sibling status, after prenatal infection and fetal growth retardation were taken into account. CONCLUSIONS: These findings support an association between obstetric complications and increased risk for early-onset schizophrenia. The authors advance a model whereby the neurotoxic effects of fetal hypoxia may lead to an early onset of schizophrenia due to premature cortical synaptic pruning.

Adult↗

[Analysis of selected parameters of maternal and fetal status during stimulation of fetal lung maturation].

At patients threatened with premature childbirth the influence of glicocorticoids on short and tong-term fetal heart rate variability and the occurrence of respiratory arrhythmia was evaluated. It has been ascertained statistical significant lowering of the incidence of fetal respiratory arrhythmia and short-term variability. Described changes had a temporary character and surrendered of normalization in the course 72 of hours after last use of glicocorticoids. The influence of glicocorticoids on select biochemical and biophysical parameters of state pregnant women was also studied. One specified occurrence of incidental symptoms in road drove of therapy. Pregnant women in road of treatment glicocorticoids have also observed a temporary weakness of feeling of fetal movements.

Betamethasone↗