The Pathophysiology of Insomnia

From Models to Molecules (and Back)

Wilfred R. Pigeon; Matthew R. Cribbet

Disclosures

Curr Opin Pulm Med. 2012;18(6):546-553. 

In This Article

Abstract and Introduction

Abstract

Purpose of review: To provide an overview of foundational theories on the psychosocial and neurobiological mechanisms that underlie the pathophysiology of insomnia, a review of recent findings from across the spectrum of sleep sciences that are germane to conceptualizations of insomnia, and how such findings contribute to newer integrative models.
Recent findings: Recent findings come from a broad diversity of the sleep research spectrum including basic animal science, sleep neuroscience, especially sleep–wake regulation, psychoneuroimmunology, human genetics, epidemiology, psychology, and from the clinical research realm.
Summary: Our review focuses on the factors contributing to insomnia and to its maintenance over time as well as the theoretical models developed (and developing) to explain this pathophysiology. Early theoretical contributions have provided a backbone for insomnia research; the sleep sciences, in turn, have supported novel and increasingly complex theoretical models of insomnia. The overarching contention is that integrative models are needed that are fully comprehensive in scope.

Introduction

Insomnia that rises to the level of clinical meaningfulness affects approximately 5% of the general population. A number of models and hypotheses exist for conceptualizing the development and/or maintenance of insomnia. Nonetheless, a well-accepted unifying pathophysiologic model of insomnia is still awaited. This may previously have been due to divisions between psychological and biological perspectives, but now more likely reflects the complexity of the sleep–wake system, which is not fully delineated. As findings from sleep neuroscience often have implications for the pathophysiology of insomnia, integrative perspectives need to be continuously reformulated, vetted, and refined.

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