Chiari malformation type I and obstructive sleep Apnea

Abstract

Chiari Malformation Type I (CMI) is a structural anomaly of the craniocervical junction, characterized by herniation of the cerebellar tonsils through the foramen magnum. This neural compression results in Sleep-Disordered Breathing (SDB), historically associated with Central Sleep Apnea (CSA). CSA stems from direct dysfunction of the respiratory centers in the brainstem, compromising neurological drive and causing the brain to fail to send the command for breathing. However, recent evidence highlights a complex prevalence of Obstructive Sleep Apnea (OSA) in patients with CMI. OSA is a disorder of recurrent collapse of the upper airways, and in this context, it is attributed to a secondary mechanism: compression at the craniocervical junction can damage the lower cranial nerves (Glossopharyngeal IX, Vagus X, and Hypoglossal XII). Dysfunction of these nerves results in loss of tone in the dilator muscles of the pharynx and larynx, culminating in airway obstruction and, frequently, in the manifestation of mixed respiratory distress syndrome (RDS). The need to synthesize the true prevalence and mechanisms of obstructive obstructive syndrome (OSA) versus central obstructive syndrome (ACS) is crucial for optimizing therapeutic management. Polysomnography (PSG) is the gold standard for this differentiation, evaluating respiratory effort to distinguish obstructive from central obstructive events. Accurate diagnosis guides treatment, which may begin with surgical decompression of the posterior fossa (SFD). In cases of persistent residual OSA after surgery, adjuvant therapies such as CPAP become essential.