Obstructive sleep apnea and epilepsy: understanding the pathophysiology of the comorbidity.

Obstructive sleep apnea (OSA) is a sleep disorder of significant health concern with a high prevalence in the general population. It has been found to exhibit a high incidence of comorbidity with epilepsy, the exact underlying pathophysiology of which still remains poorly understood. OSA is characterized by apnea/hypopnea spells and arousals, leading to intermittent hypoxemia and sleep deprivation. Both sleep deprivation and hypoxemia adversely affect the cortical excitability and favor epileptogenesis and worsening of pre-existing epilepsy, if any. In patients with OSA, deprivation of rapid eye movement sleep (REMS) phase (known for its strong antiepileptic influence) is relatively more than that non rapid eye movement sleep phase leading to postulation of REMS deprivation as a significant factor in the development of epilepsy as a comorbidity in patients with OSA. Furthermore, OSA and epilepsy both have shown to exercise a bidirectional influence on one another and are also likely to exacerbate each other through a positive feedback mechanism. This is especially based on the reports of improved control of epilepsy upon treatment of comorbid OSA. This brief paper attempts to present an underlying pathophysiological basis of the comorbidity of OSA and epilepsy based upon sleep deprivation and hypoxemia that are characteristic features observed in patients with OSA.

Pedunculopontine Nucleus--Rapid Eye Movement Sleep--Electroencephalogram--Desynchronization (PRED) Axis in the Evolution of Epilepsy: A Novel Concept.

Epilepsy is one of the commonest and oldest neurological diseases in the history of mankind, the exact pathophysiology of the evolution of which still remains elusive. The intimate and intriguing relation between epilepsy and sleep has been known for a long time. Rapid eye movement sleep (REMS) is well documented to exert potent antiepileptic action in human epilepsies and the underlying mechanism of which is largely based on its property to induce widespread electroencephalogram (EEG)-desynchronization. The pedunculopontine nucleus (PPN) owing to its property to enhance REMS has recently been under study for its potential role in intractable epilepsy (IE) and has been proposed as a novel deep brain stimulation target in IE. This brief paper unfolds the existing role of PPN, REMS, and EEG-desynchronization (PRED) in the evolution of epilepsy in an axial manner, the realization and comprehension of which is likely to open new avenues for further understanding of epileptogenesis, improved treatment of epilepsy and reducing the risk of IE.

Pathophysiology of the comorbidity of glaucoma with obstructive sleep apnea: A postulation.

Glaucoma is a serious and progressive optic neuropathy, the exact pathophysiology of which is still poorly understood. Furthermore, glaucoma exhibits significant comorbidity with obstructive sleep apnea (OSA) that warrants an in-depth study in view of highly probable beneficial and far-reaching clinical implications. In this brief paper, the authors have studied the existing theories in an attempt to explain the comorbidity and its underlying pathophysiology. From the ensuing evidence, the role of connective tissue strength has emerged as a major factor and which appears to play a pivotal role not only in the development of glaucoma but also in the underlying pathophysiology of its enigmatic comorbidity with OSA. Understanding the pathophysiology of the comorbidity can stimulate newer therapeutic strategies targeted toward strengthening of connective tissues that may at least retard if not arrest the progression of glaucomatous changes and their complications.

A critical analysis of the purported role of hypoxaemia in the comorbidity of obstructive sleep apnoea and epilepsy.

Obstructive sleep apnoea (OSA) is a globally prevalent sleep disorder of significant health concern and confounded with several comorbidities resulting in adverse effect(s) on quality of life in patients afflicted with it. Of particular interest is the enigmatic high comorbidity of OSA with epilepsy, the exact underlying pathophysiology of which remains elusive despite a multitude of research performed in the last four decades. Hypoxaemia, which is an important characteristic feature found in OSA during apnoeic spells, has been implicated in the high comorbidity of OSA with epilepsy, the basis of which rests upon hypoxaemia-mediated brain damage, subcortical release phenomenon, oxidative stress and neuroinflammatory reactions. However, several studies present contradictory evidences that potentially refute the hypoxaemia-based mechanism. Additionally, the role of hypercapnia thatgenerally accompanies hypoxaemia during apnoeic spells, cannot be overlooked and is known to be potentially protective against neuronal hyperexcitability. Thus, hypoxaemia theory implicated in the high comorbidity of OSA and epilepsy appears weak and refutable. This brief paper studies and critically analyses the role of hypoxaemia in conjunction with hypercapnia in the underlying pathophysiology of the comorbidity.

Drug-Resistant Epilepsy and Obstructive Sleep Apnea: Exploring a Link Between the Two.

Drug-resistant epilepsy accounts for approximately one third of all epilepsy cases; yet its exact etiopathogenesis still remains under intense exploration. Several factors have been advocated for predicting drug resistance in patients with epilepsy. Obstructive sleep apnea (OSA) is a commonly prevalent sleep disorder that exhibits a bidirectional and strong comorbidity with epilepsy. The exact pathophysiology of this comorbidity is not yet clearly explained. This study analyzes the relationship between drug-resistant epilepsy and OSA, and the findings indicate a strong role of rapid eye movement sleep (REMS) in the pathogenesis of this relationship. It also emerges from the study that REMS reduction is a prominent feature of OSA, and drug resistance in patients with epilepsy and treatment of OSA has been shown to restore REMS in several studies with concomitant improvement in seizure control.