Related Experiment Videos
Persistent increases in cerebral lactate concentration after birth asphyxia
J D Hanrahan1, I J Cox, A D Edwards
1Section of Paediatrics, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
Insights
Persistent cerebral lactate detected via proton magnetic resonance spectroscopy (1H MRS) after one month in infants with abnormal neurodevelopmental outcomes suggests a prolonged post-injury process following perinatal hypoxia-ischemia.
Area of Science:
- Neuroscience
- Biochemistry
- Pediatrics
Background:
- Perinatal hypoxia-ischemia (HI) can lead to severe neurodevelopmental impairment.
- The temporal window for detecting brain injury markers after HI is crucial for understanding long-term outcomes.
Purpose of the Study:
- To investigate if lactate, a marker of brain injury, can be detected beyond one month in infants with neurodevelopmental impairment after perinatal HI.
- To correlate persistent cerebral lactate levels with neurodevelopmental outcomes at one year of age.
Main Methods:
- Prospective study using proton magnetic resonance spectroscopy (1H MRS) on three infant groups: abnormal neurodevelopment, normal neurodevelopment after HI, and controls.
- Cerebral lactate to creatine plus phosphocreatine (Cr) concentration ratios were measured between 4 and 68 weeks post-birth.
Main Results:
- Lactate was detected later than one month in 7 of 8 infants with abnormal neurodevelopmental outcomes.
- No lactate was detected after one month in infants with normal neurodevelopmental outcomes or most controls.
- One control infant showed a minimal lactate level (lactate/Cr=0.04).
Conclusions:
- Persistent cerebral lactate detected by 1H MRS after the first month post-birth is associated with abnormal neurodevelopmental outcomes.
- This suggests the pathologic process following perinatal HI may extend beyond the acute injury phase.
Abstract:
In this prospective study proton magnetic resonance spectroscopy (1H MRS) was used to test the hypothesis that lactate can be detected later than 1 mo after birth in the brains of infants who display severe neurodevelopmental impairment 1 y after transient perinatal hypoxia-ischemia. Data were obtained from three groups of infants: 1) eight infants suffering birth asphyxia followed by perinatal encephalopathy and abnormal neurodevelopmental outcome at 1 y of age (defined as major neurologic impairment, Griffiths quotient <85%, and low optimality score); 2) 10 infants with signs of perinatal hypoxia-ischemia but normal neurodevelopmental outcome at 1 y; and 3) six control infants with uneventful perinatal courses and normal neurodevelopment at 1 y. Between one and four examinations (median 1) were performed at median (range) 11 (4-68) wk after birth, and the cerebral concentration ratio of lactate to creatine plus phosphocreatine (Cr) calculated from each spectrum. Lactate was detected later than the 1st mo after birth in seven of eight infants with abnormal neurodevelopmental outcome [maximum detected lactate/Cr was median (range) 0.44 (0.24-0.67)]. No lactate was detected later than the 1st mo after birth in infants with normal neurodevelopmental outcome, nor in five of six control subjects, although a small amount of lactate was detected in one control infant (lactate/Cr=0.04). These results suggest that the pathologic postasphyxial process, indicated by persistent cerebral lactate, may not be confined to the period immediately after injury.