[LS7-2C-2] BRAINSTEM RESPIRATORY CENTRES IN THE FETUS AND NEONATE: APNOEA OF PREMATURITY; CENTRAL HYPOVENTILATION; SIDS
The nucleus/tractus solitarius is the principal pneumotaxic centre in the brainstem. Anatomically it is a pair of ascending and descending axons in the tegmentum of the medulla oblongata extending from the pons, surrounded by a neuronal layer constituting its nucleus, a primitive arrangement. Its rostral cap is the unrelated principal gustatory nucleus. The nucleus/tractus solitarius receives afferent ascending axons from the carotid body and other peripheral chemoreceptors and from stretch receptors in respiratory muscles and in the lungs themselves; it projects efferent descending axons to the cervical phrenic nucleus for the diaphragm and to motor neurons of supplementary respiratory muscles. It also has many other synaptic relations with other brainstem nuclei, including the vagal nucleus ambiguus to coordinate with swallowing, the pre-Botzinger complex, reticular formation, vestibular nuclei and periaqueductal grey matter. Synaptogenesis in the nucleus solitarius begins at 12wks and is completed by 15wks gestation; it subserves fetal respiratory movements that help circulate amniotic fluid. Myelination is initiated at 33wks and not completed until postnatally. Delayed synapse formation or myelination may occur in some genetic inborn metabolic diseases, in chromosomopathies, in some brain malformations such as holoprosencephaly, or secondary to acquired insults such as fetal alcohol spectrum disorder or fetal exposure to teratogenic maternal drugs and toxins. The nucleus solitarius lies within the tegmental watershed zone and may be impaired by ischaemia during episodes of prenatal or perinatal systemic hypotension and may become infarcted bilaterally because the blood supply of both sides is provided by the single basilar artery. Asymmetrical or unilateral ischaemia/infaction may occur with vascular anomalies of posterior fossa circulation. Any of these conditions may lead to apnoeic spells, central hypoventilation or even SIDS in early infancy. Immaturity of synapse formation or myelination can be a basis of transitory apnoea of prematurity. Limited neuroimaging may provide some clues to diagnosis, but at present post-mortem examination remains the definitive confirmation; special neuropathological techniques are required to demonstrate maturational delays not revealed by standard histological stains. Normal development and examples of causes of central respiratory failure will be demonstrated.