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Within amygdala: Basolateral parts are selectively impaired in premature-born adults
NeuroImage: Clinical  (IF4.881),  Pub Date : 2021-08-09, DOI: 10.1016/j.nicl.2021.102780
Benita Schmitz-Koep, Juliana Zimmermann, Aurore Menegaux, Rachel Nuttall, Josef G. Bäuml, Sebastian C. Schneider, Marcel Daamen, Henning Boecker, Claus Zimmer, Dieter Wolke, Peter Bartmann, Dennis M. Hedderich, Christian Sorg

While it is known that whole amygdala volume is lastingly reduced after premature birth, it is unknown whether different amygdala nuclei are distinctively affected by prematurity. This question is motivated by two points: First, the observation that developmental trajectories of superficial, centromedial and basolateral amygdala nuclei are different. And second, the expectation that these different developmental pathways are distinctively affected by prematurity. Furthermore, we stated the question whether alterations in amygdala nuclei are associated with increased adults’ anxiety traits after premature birth.

We investigated 101 very premature-born adults (<32 weeks of gestation and/or birth weight below 1500 g) and 108 full-term controls of a prospectively and longitudinally collected cohort at 26 years of age using automated amygdala nuclei segmentation based on structural MRI.

We found selectively reduced volumes of bilateral accessory basal nuclei (pertaining to the basolateral amygdala of claustral developmental trajectory) adjusted for whole amygdala volume. Volumes of bilateral accessory basal nuclei were positively associated with gestational age and negatively associated with duration of ventilation. Furthermore, structural covariance within the basolateral amygdala was increased in premature-born adults. We did not find an association between reduced volumes of basolateral amygdala and increased social anxiety in the prematurity group.

These results demonstrate specifically altered basolateral amygdala structure in premature-born adults. Data suggest that prematurity has distinct effects on amygdala nuclei.