[Is early treatment of infants at risk of spastic diplegia warranted?]. / La prise en charge précoce de l'enfant à risque de diplégie spastique est-elle utile? Est-elle opportune?

OBJECTIVE: To test the possible link between first investigation and development of spastic diplegia. METHOD: A long-term retrospective study was carried out in the Neonatal Medicine Department of Arras Hospital, the C.A.M.S.P. of that town and with corresponding therapists. RESULTS: The study undertaken from January 1, 1991, to December 31, 1997, involved 56 children suspected of developing spastic diplegia and requiring a specialized course of treatment during the evolution of disease. In 32, evolution of disease was favourable, and in 24 spastic diplegia developed. An unfavourable evolution was significantly associated with late intervention of rehabilitation. CONCLUSION: Although few pre- or neonatal factors differentiated the two groups of children in their opposite evolution, haemorrhage during pregnancy and early detection seem to be determining factors in spastic diplegia.

Prevalence, causes, and outcome at 2 years of age of newborn encephalopathy: population based study.

OBJECTIVES: To ascertain the prevalence of newborn encephalopathy in term live births, and also the underlying diagnoses, timing, and outcome at 2 years of surviving infants. DESIGN: Population based observational study. SETTING: North Pas-de-Calais area of France, January to December 2000. PATIENTS: All 90 neonates with moderate or severe newborn encephalopathy. RESULTS: The prevalence of moderate or severe newborn encephalopathy was 1.64 per 1000 term live births (95% confidence interval (CI) 1.30 to 1.98). The prevalence of birth asphyxia was 0.86 per 1000 term live births (95% CI 0.61 to 1.10). The main cause of newborn encephalopathy was birth asphyxia, diagnosed in 47 (52%) infants. It was associated with another diagnosis in 11/47 cases (23%). The timing was intrapartum in 56% of cases, antepartum in 13%, ante-intrapartum in 10%, and postpartum in 2%. In 19% of cases, no underlying cause was identified during the neonatal course. Twenty four infants died in the neonatal period, giving a fatality rate of 27% (95% CI 17% to 36%). Three infants died after the neonatal period. At 2 years of age, 38 infants had a poor outcome, defined by death or severe disability, a prevalence of 0.69 per 1000 term live births (95% CI 0.47 to 0.91). In infants with isolated birth asphyxia, this prevalence was 0.36 per 1000 term live births (95% CI 0.20 to 0.52). CONCLUSIONS: The causes of newborn encephalopathy were heterogeneous but the main one was birth asphyxia. The prevalence was low, but the outcome was poor, emphasising the need for prevention programmes and new therapeutic approaches.

The safety and efficacy of nitric oxide therapy in premature infants.

OBJECTIVES: To assess the safety-efficacy balance of low-dose inhaled nitric oxide (iNO) in hypoxemic premature infants because no sustained beneficial effect has been demonstrated clearly and there are concerns about side effects. STUDY DESIGN: Eight hundred and sixty infants <32 weeks were randomized at birth to receive 5 ppm iNO or placebo when they presented with hypoxemic respiratory failure (HRF) defined by a requirement for mechanical ventilation, fraction of inspired oxygen (FIO 2 ) >40%, and arterio-alveolar ratio in oxygen (aAO 2 ) <0.22. The primary end point was intact survival at 28 days of age. RESULTS: Sixty-one of 415 infants presented with HRF and were compared with 84 of 445 controls who presented with HRF. There was no difference in the primary end point (61.4% in infants [23% with HRF who were treated with iNO] vs 61.1% in controls [21.4% in controls with HRF]; P = .943). For the infants with HRF who were treated with iNO, there was no significant difference from controls for intraventricular hemorrhage (IVH) (6% vs 7%), necrotizing enterocolitis (8% vs 6 %), or patent ductus arteriosus (PDA) (34% vs 37%). Compared with nonhypoxemic infants, the risk of bronchopulmonary displasia (BPD) increased significantly in HRF controls (OR = 3.264 [CI 1.461-7.292]) but not in infants with HRF who were treated with iNO (OR = 1.626 [CI 0.633-4.178]). CONCLUSIONS: iNO appears to be safe in premature infants but did not lead to a significant improvement in intact survival on day 28.

[Very preterm infant (< 32 weeks) vs very low birth weight newborns (1500 grammes): comparison of two cohorts]. / Grands prématurés infant (< 32 semaines) vs nouveau-nés de très faible poids de naissance (< 1500 grammes): comparison de deux cohortes.

UNLABELLED: Studies concerning very preterm newborns are either defined by birth weight (<1500 g) or gestational age (<32 weeks). The aim of our study was to underline limits of cohort definitions by birth weight. METHODS: Data come from the Nord Pas de Calais EPIPAGE cohort. Every birth occurring in 1997 before 32 weeks or with a birth weight less than 1500 g and transferred in a neonatal unit was included. Two cohorts were defined, one by gestational age (<32 weeks), the other by birth weight (<1500 g). Two subgroups could be defined from these to cohorts: group A (<32 weeks and > or =1500 g), from cohort (<32 weeks), group B (> or =32 weeks and <1500 g) from cohort (<1500 g). RESULTS: Five hundred nine newborns were included. Perinatal characteristics of both cohorts seemed comparable. The analysis by subgroups A and B revealed an excess of pulmonary and neurological morbidity in very preterm infant compared to very low birth weight newborn. This was linked to an excess of growth restricted newborns in this cohort with more advanced gestational ages. CONCLUSION: Cohorts of very preterm newborns should rather be defined by gestational age. If not possible, results in very low birth weight cohorts should also be given by gestational age and rate of growth restriction should be described.

Chronic oxygen dependency in infants born at less than 32 weeks' gestation: incidence and risk factors.

OBJECTIVE: To assess incidence and clinical risk factors of chronic oxygen dependency (COD) among survivors who were born at or before 31 weeks' gestation. METHODS: This prospective, multicenter study enrolled 802 infants who were born at or before 31 weeks' gestation and admitted to 8 level III neonatal intensive care units in northern and eastern France from January 1 through December 31, 1997. Need for oxygen to maintain oxygen saturation between 92% and 96% was assessed at 28 days of life and at 36 and 42 weeks' postconceptional age (PCA). Stepwise logistic regression analysis was used to identify the incidence of COD and the risk factors related to its occurrence. RESULTS: The mortality rate was 14%. Antenatal corticotherapy was administered to 51% of patients, surfactant therapy to 76% of the ventilated patients, and high-frequency oscillatory ventilation at day 1 to 32%. At 28 days and 36 and 42 weeks' PCA, respectively, 25%, 15%, and 6% of survivors had COD. After adjustment for intercenter variations, we identified the significant risk factors for COD at these dates: a low gestational age, a high score on the Clinical Risk Index for Infants, intrauterine growth restriction, and surfactant treatment. CONCLUSION: COD incidence was high at 28 days of life but decreased dramatically by 42 weeks' PCA. This study confirmed previously reported risk factors and underlined the importance of intrauterine growth restriction and the Clinical Risk Index for Infants as significant risk factors.

[The value of electroneurography in recognition of peripheral ischaemic polyneuropathy in patients suffering from critical leg ischaemia]. / Wartosc badan EMG w rozpoznaniu polineuropatii niedokrwiennej u chorych z krytycznym niedokrwieniem konczyn dolnych.

Peripheral arteries disorders cause not only leg ischaemia, but also peripheral polyneuropathy. Polyneuropathy increases ischaemic pain. The aim of this study was to estimate how many patients suffering from critical leg ischaemia have symptoms of peripheral polyneuropathy. 40 patients were investigated: 37 men and 3 women; mean age was 57 years. All patients underwent electroneurographic examination. It consisted of measurements of motor conduction in tibial and peroneal nerves, wave F, sensory conduction in sural nerve. Polyneuropathy was observed in 95% of patients. The frequency of polyneuropathy was also significantly enlarged in leg with non critical ischaemia. We did not observe the greater risk of polyneuropathy in diabetic patients. The work is an introduction to the following clinical studies.

[Multimodal evoked potentials in the early period after cranio-cerebral trauma]. / Multimodalne potencjaly wywolane we wczesnym okresie po urazie czaszkowo-mózgowym.

In 83 patients aged 17-68 years somatosensory evoked potentials by median nerve stimulation, and visual and auditory evoked potentials were studied 5-28 days after craniocerebral trauma. Brain concussion was diagnoses in 43 cases on the basis of neurological examination, CT and duration of unconsciousness. In the remaining 40 cases brain contusion was diagnosed. In SSEP the latency was calculated of waves N9, N13, P16, N20, P22, N35 and P40: in the visual evoked potentials the latency of the P100 component, and in auditory evoked potential the latency of waves I, III and V, and interpeak latency I-III, III-V and I-V SSEP changes were found in 39% of cases of brain concussion and 52.9% of brain contusion cases. The abnormalities in both groups involved mainly the component of latency and deviation P100 of visual evoked potential P40 and N35. Prolongation of the latency of P100 of the visual evoked potential was recorded in 20% of patients with brain concussion and 16.7% with brain contusion. Auditory evoked potentials were abnormal in 10.3% of brain concussion and 26.5% of brain contusion cases. In 64 cases all three types of evoked potentials were studied and pathological changes in at least one of these types were found in 56.4% of brain concussion and 72% of brain contusion cases. The results show that as least in a part of cases diagnosed as brain concussion according to generally accepted criteria, central nervous system injury is present.

[Prospective studies of multimodal evoked potentials in patients after cranio-cerebral injury]. / Prospektywne badania multimodalnych potencjalów wywolanych u chorych po urazie czaszkowo-mózgowym.

In 42 patients aged 18-68 years somatosensory, visual and brainstem auditory evoked potentials were studied in the first month after trauma and after 6-8 months after craniocerebral trauma for evaluation of their diagnostic importance in less severe craniocerebral trauma. On the basis of the results of neurological examination, CT of the head, and duration of unconsciousness in 22 cases brain concussion and in 20 cases brain contusion was diagnosed. In patients after brain concussion the frequency of early and late abnormalities after head trauma was as follows: for SSEP 36.4% and 27.3% respectively, for visual evoked potentials 21.1% and 5.3%, for auditory potentials 9.5% and 4.8%. In cases of brain contusion abnormalities were found in the 1st month and 6-8 months after trauma in SSEP in 60% and 20% respectively, in visual EP in 11.1% and 22.2%, and in auditory EP in 30% and 40%. In the group of concussion the greatest and most persistent changes developed in the later components od SSEP. Among certain patients with brain contusion deterioration of the results of visual and auditory evoked potentials were noted late after trauma.

[Value of multimodal evoked potentials in the assessment of the neurotoxic effects of carbon disulphide]. / Przydatnosc badan multimodalnych potencjalów wywolanych w ocenie neurotoksycznego wplywu dwusiarczku wegla.

Central nervous system dysfunction among CS2-exposed workers was studied by measuring short latency SSEPs and VEPs. The examinations were done in 40 men. Chronic CS2 intoxication was diagnosed in 21 of them. Latency of N19, N11, N20 of somatosensory evoked potentials and latency of P100 wave of visual evoked potentials were statistically significant longer in CS2 exposed group in comparison with controls. The amplitude of N20 SSEPs was also significantly higher. Increase of N20 amplitude (33 persons) and elongation of its latency (25 persons) were frequent abnormalities of SSEps. In individual assessment of VEPs, most frequent were: abnormal difference in interocular latency of P100 (26 persons) and elongation of P100 latency (25 persons). In the analysed SSEPs and VEPs parameters there was no significant difference between two clinical groups. The authors conclude that the CS2--neurotoxic effect leads to impairment of the peripheral and central part of the somatosensory pathway, as well as to central dysfunction of the visual pathway.