Assessment of brain tissue injury after moderate hypothermia in neonates with hypoxic-ischaemic encephalopathy: a nested substudy of a randomised controlled trial (original) (raw)

Abstract

Background Moderate hypothermia in neonates with hypoxic-ischaemic encephalopathy might improve survival and neurological outcomes at up to 18 months of age, although complete neurological assessment at this age is diffi cult. To ascertain more precisely the eff ect of therapeutic hypothermia on neonatal cerebral injury, we assessed cerebral lesions on MRI scans of infants who participated in the Total Body Hypothermia for Neonatal Encephalopathy (TOBY) trial.

Figures (6)

Figure 1: MkI appearances In neonatal hypoxic-ischaemic encephalopathy (A-C) T1-weighted images in the transverse plane. (A) Normal neonatal brain with linear high signal intensity representing myelin in the posterior limb of the internal capsule (arrow). (B) Moderate basal ganglia and thalamic lesions with abnormal increased signal intensity in the globus (top arrow), putamen (middle arrow), and thalamus (bottom arrow). There is no normal linear high signal intensity from the intervening posterior limb of the internal capsule. (C) Cortical lesions. There is abnormal increased signal intensity in the cortex around the central sulcus (arrow head) and along the interhemispheric fissure. Abnormal low signal intensity is seen in the adjacent subcortical white matter (arrow). (D-F) T2-weighted images in the transverse plane. (D) Mild lesions in the basal ganglia. There are small bilateral foci of abnormal low signal intensity in the lentiform nuclei (arrow). (E) Mild white matter lesions. There is diffuse and slightly increased signal intensity in the periventricular white matter (arrow). (F) Severe basal ganglia and thalamic and white matter lesions. There is mixed abnormal signal intensity throughout the basal ganglia and thalami. The intervening posterior limb of the internal capsule shows abnormal high signal intensity with no evidence of low signal intensity from myelin (arrow). The hemispheric white matter has diffuse abnormal high signal intensity throughout.

Figure 1: MkI appearances In neonatal hypoxic-ischaemic encephalopathy (A-C) T1-weighted images in the transverse plane. (A) Normal neonatal brain with linear high signal intensity representing myelin in the posterior limb of the internal capsule (arrow). (B) Moderate basal ganglia and thalamic lesions with abnormal increased signal intensity in the globus (top arrow), putamen (middle arrow), and thalamus (bottom arrow). There is no normal linear high signal intensity from the intervening posterior limb of the internal capsule. (C) Cortical lesions. There is abnormal increased signal intensity in the cortex around the central sulcus (arrow head) and along the interhemispheric fissure. Abnormal low signal intensity is seen in the adjacent subcortical white matter (arrow). (D-F) T2-weighted images in the transverse plane. (D) Mild lesions in the basal ganglia. There are small bilateral foci of abnormal low signal intensity in the lentiform nuclei (arrow). (E) Mild white matter lesions. There is diffuse and slightly increased signal intensity in the periventricular white matter (arrow). (F) Severe basal ganglia and thalamic and white matter lesions. There is mixed abnormal signal intensity throughout the basal ganglia and thalami. The intervening posterior limb of the internal capsule shows abnormal high signal intensity with no evidence of low signal intensity from myelin (arrow). The hemispheric white matter has diffuse abnormal high signal intensity throughout.

Data are median (IQR) or n (%). Amplitude integrated EEG was not available for two infants in each group. *y’ test for the proportion of moderately abnormal to severely abnormal amplitude integrated EEG in cooled (27:35) and non-cooled (34:31) groups.

Data are median (IQR) or n (%). Amplitude integrated EEG was not available for two infants in each group. *y’ test for the proportion of moderately abnormal to severely abnormal amplitude integrated EEG in cooled (27:35) and non-cooled (34:31) groups.

Data are number or OR (95% Cl).*Odds ratio for presence or absence of MRI abnormalities in cooled and non-cooled infants, with and without adjustment for severity of amplitude integrated EEG and postnatal age. OR=odds ratio. +Cortex could not be assessed in one infant in the non-cooled group.

Data are number or OR (95% Cl).*Odds ratio for presence or absence of MRI abnormalities in cooled and non-cooled infants, with and without adjustment for severity of amplitude integrated EEG and postnatal age. OR=odds ratio. +Cortex could not be assessed in one infant in the non-cooled group.

Data are number of infants. Major MRI abnormalities were defined as moderate or severe basal ganglia or thalamic lesions, severe white matter lesions, or abnormal posterior limb of the internal capsule. Severe disability was defined as at least one of the following: mental development index (MDI) score less than 70 (=2 SD below the mean) on the Bayley Infant Scales (BSID II); score of 3-5 on the gross motor function classification system (GMFCS), which ranges from 1 to 5, with 1 being the mildest impairment; or bilateral cortical visual impairment with no useful vision. “Outcome at 18 months was not available for one infant in the group allocated to cooling.

Data are number of infants. Major MRI abnormalities were defined as moderate or severe basal ganglia or thalamic lesions, severe white matter lesions, or abnormal posterior limb of the internal capsule. Severe disability was defined as at least one of the following: mental development index (MDI) score less than 70 (=2 SD below the mean) on the Bayley Infant Scales (BSID II); score of 3-5 on the gross motor function classification system (GMFCS), which ranges from 1 to 5, with 1 being the mildest impairment; or bilateral cortical visual impairment with no useful vision. “Outcome at 18 months was not available for one infant in the group allocated to cooling.

Data are proportions (95% Cl). Major MRI abnormalities were defined as moderate or severe basal ganglia or thalamic lesions, severe white matter lesions or an abnormal posterior limb of the internal capsule. Table 3: Postnatal age at scan, MRI abnormalities, and outcome up to 18 months of age in cooled and non-cooled infants

Data are proportions (95% Cl). Major MRI abnormalities were defined as moderate or severe basal ganglia or thalamic lesions, severe white matter lesions or an abnormal posterior limb of the internal capsule. Table 3: Postnatal age at scan, MRI abnormalities, and outcome up to 18 months of age in cooled and non-cooled infants

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