ABSTRACT
CONTEXT: Foetal asphyxia, a frequent birth complication, detrimentally impacts the immature brain, resulting in neuronal damage, uncontrolled seizure activity and long-term neurological deficits. Oxytocin, a neurohormone mediating important materno-foetal interactions and parturition, has been previously suggested to modulate the immature brain's excitability, playing a neuroprotective role. Our aim was to investigate the effects of exogenous oxytocin administration on seizure burden and acute brain injury in a perinatal model of asphyxia in rats. ANIMALS AND METHODS: Asphyxia was modelled by exposing immature rats to a 90-minute episode of low oxygen (9% O2) and high CO2 (20% CO2). Control rats were kept in ambient room-air for the same time interval. In a third group of experiments, oxytocin (0.02 UI/g body weight) was nasally administered 30 minutes before the asphyxia episode. Seizure burden was assessed by the cumulative number of loss of righting reflex (LRR) over a two-hour postexposure period. Acute brain injury was assessed through hippocampal S-100 beta, a biomarker of cellular injury, 24-hours after exposure. RESULTS: Asphyxia increased both LRR and hippocampal S-100 beta protein compared to controls, and these effects were significantly reduced by oxytocin administration. CONCLUSION: Oxytocin treatment decreased both seizure burden and hippocampal injury, supporting a potential neuroprotective role for oxytocin in perinatal asphyxia.
ABSTRACT
BACKGROUND AND PURPOSE: High-resolution ultrasound is a valuable tool in supporting the diagnosis of multifocal motor neuropathy (MMN) but longitudinal data under therapy are lacking. METHODS: The change in peripheral nerve ultrasound pattern in patients with MMN was assessed over time. Patients with MMN received a thorough initial examination and follow-up over a period of 6-12 months using high-resolution ultrasound of the cervical roots and the nerves of the arms and legs, nerve conduction studies, Medical Research Council Sum Score (MRCSS) and Rotterdam Inflammatory Neuropathy Cause and Treatment Group (INCAT) score to evaluate changes under treatment. The Ultrasound Pattern Sum Score (UPSS) was used as standardized peripheral nerve ultrasound protocol. RESULTS: Seventeen patients with MMN received initial examinations of whom 12 were successfully followed up. All patients with MMN showed at least localized but often multifocal peripheral nerve enlargement. An enlarged overall cross-sectional area as well as enlarged single fascicles (>3 mm²) in clinically and electrophysiologically affected (>90%) and unaffected (>70%) nerves were found. The UPSS did not correlate with clinical disability at both visits. However, the change in clinical disability (evaluated as difference in MRCSS) and the change in UPSS correlated significantly inversely (P = 0.004). CONCLUSIONS: High-resolution sonography of peripheral nerves revealed multifocal nerve enlargement in MMN. Distinct enlargement patterns may support the diagnosis. Ultrasound findings did not correlate well with clinical severity or electrophysiological findings at initial presentation. As changes in UPSS correlated significantly with the clinical course in terms of muscle strength (MRCSS), sonographic assessment may represent a useful tool for therapeutic monitoring.
