A rebuttal against the set of well-contended arguments by Gozal (2012), the majority of which we essentially agree with, does not come easy. However, differences between our viewpoints exist (Rosenzweig et al. 2012), and are perhaps best accounted for by reviving the ‘reductionism versus holism’ debate.
Loosely, reductionism in science is the concept that a complex system can be explained by reduction to its fundamental parts (Mazzocchi, 2012). Gozal (2012) reviews most of the contemporary, largely ‘reductionist’ obstructive sleep apnoea (OSA) research in his account. Putting aside the inconsistencies in the neurocognitive testing and the discrepancies in the neuroimaging methods (e.g. see Morrell & Glasser, 2011) in the body of current literature the neuropsychiatric sequelae of OSA are overwhelmingly viewed as an amalgamation of end-effect neural injury via oxidative stress and inflammation, the genesis and severity of which is set off by the chronic exposure to intermittent hypoxia (IH), and further defined by the genetically and environmentally determined modifiers of susceptibility (Sforza & Roche, 2012). Gozal (2012) appears to be in agreement with this contemporary view and whilst he acknowledges the additional contribution of the major co-morbidities of OSA, along with the potential synergistic (or additive) role of sleep fragmentation, his analysis nonetheless openly favours the main role for the IH.
In contrast to the above viewpoint, the scientific holism would suggest that complex systems behaviour cannot be reliably and consistently deduced from the properties of its elements alone (Mazzocchi, 2012). In a similar fashion, we argue for a reconceptualisation of the neurocognitive sequelae of OSA (Rosenzweig et al. 2012) with the lowest common detrimental denominator defined as the elementary dynamic interplay of the IH and the (cerebello)-thalamocortical oscillator, calibrated at various stages of sleep (Rosenzweig et al. 2012; Timofeev et al. 2012; Vukadinovic & Rosenzweig, 2012). Notably, despite the recent advances in the fields of sleep-related neuroplasticity (Frank, 2012) and functional neuroconnectivity, it is surprising how little of that opus of work has inspired recent OSA research. Furthermore, as far as we are aware, there are no animal or clinical studies which authoritatively answer whether neuroregional susceptibility to hypoxia during the awake states is the same, similar or significantly different to that occurring during the sleep entrainment. Moreover, sleep staging and its contributory role to the effects of IH is equally far from clear (Mukhlesi & Punjabi, 2012). Collectively, it could be argued that the current body of research largely overlooks the role of ‘sleep’ in patients with sleep apnoea, most of whom as a minimum are also deprived of slow wave sleep. We believe this is pertinent for the holistic understanding of the involved neurocircuitry in these patients, and for any future therapeutical interventions in OSA.