Sleep, Epilepsies, and Cognitive Impairment

Peter Halasz, Anna Szucs

• Publisher: Academic Press
• Year: 2017
• Print ISBN: 9780128125793
• eBook ISBN: 9780128125809
• Topic: Biological Sciences
• Subtopic: Neurology
• Index: Biological Sciences

Translational research connects science and clinical medicine from "the bench to the bedside." In Sleep, Epilepsies and Cognitive Impairment, the authors look back from the bedside to the brain function underlying clinical symptoms and reveal mechanisms explored by contemporary neuroimaging and signal analysis in the overlapping fields of sleep and epilepsy. This book will help the reader to see epilepsy from a new viewpoint.The common pathophysiology binding together the diverse manifestations of epilepsies is the exaggeration of plastic functions of the brain involving the hippocampus, the non-specific thalamocortical system and the perisylvian cognitive network. Epileptic derailment seems to be the price for the latest achievements of the mammal and human brain; namely the highly developed ability to change and learn. The contemporary results of sleep research provide new viewpoints to explain why sleep and epilepsy are bedfellows. Converging evidence supports the concept that one of the most important biological roles of NREM sleep is the renewal of synaptic balance ensuring learning ability from one day to the next and consolidation of new memories. Epilepsy and NREM sleep use overlapping structures and functions, therefore epilepsy beginning in early childhood may interfere with sleep plastic functions. NREM sleep, which affects original learning and memory, may become the hidden source of chronic cognitive impairment when epilepsy occurs during sleep and blocks the plastic processes.Sleep, Epilepsies and Cognitive Impairment abandons the academic classification of epilepsy by following the system epilepsy concept, binding major epilepsies with structures and functions of physiological brain systems. It tries to show within this system the close interrelationship between sleep, epilepsy and cognition.Neuroscientists, clinical epileptologists and neurologists interested in brain processes underlying brain plasticity, sleep and epilepsy will find this book thought provoking. It offers good "brain-gymnastics" for reconsidering the ideas on epilepsy.- It provides contemporary knowledge about the neurophysiological and functional anatomical background of major epilepsies- Treats major epilepsies as system epilepsies of brain networks- Reveals the interrelationship of sleep, epilepsy and cognitive impairment showing how epileptic manifestations became facilitated in NREM sleep and interferes with sleep plastic functions

Chapter 1

Introductory Considerations

Abstract

Experimental research has proven that the spike-wake pattern of absence epilepsy and the NREM sleep-related burst-firing mode of the cortico-thalamic system share the same functional structures in the brain. Clinical research has shown that absences occur when the vigilance decreases, during transitions from waking to NREM sleep; whereas they are inhibited by full wakefulness and REM sleep. Those sensory stimuli which elicit slow wave responses during the transition states (reactive slow waves, i.e. CAP A1 phase) may activate spike wave responses, while those eliciting desynchronization-arousal responses, do not.

Therefore, in terms of states and functions, absence epilepsy seems to be linked to the periods of initiation and shifts towards NREM sleep.

Keywords

Epilepsy as derailment of brain plasticity; Epileptic networks; Link between sleep and epilepsy; Sleep plastic functions; Slow-wave sleep; System epilepsy

Outline

The Growing Knowledge About the Link Between Non–Rapid Eye Movement Sleep and Plastic Functions of the Brain

Changing Conceptual Frameworks in Epilepsy

Epilepsies as Disorders of Neural Plasticity

Epilepsies as Network Disorders

Epilepsies as Spectrum Disorders

New Biomarkers of Epilepsy

The Relationship Between Non–Rapid Eye Movement Sleep and Epileptic Events and the Underlying Physiologic Mechanisms

Some More Words About Our Frame of Approach

References

Owing to important progress in epilepsy and sleep research during the past decades, converging evidence has accumulated on new aspects of the interrelationship between sleep and epilepsy. Both fields have been enriched by the observations of intracranial recordings performed on epileptic patients under presurgical evaluation.

Sleep research has realized that the amount of sleep spindles and slow waves during non–rapid eye movement (NREM) sleep is associated with cognitive functions. It has become clear that slow-wave homeostatic regulation connects with synaptic homeostasis, determining the synaptic capacity of the brain for learning and memory (Tononi and Cirelli, 2003). Therefore, the link between sleep and epilepsy has been recognized as a key factor in the mechanism of cognitive impairment in epilepsy.

Epilepsy has an unknown face hidden in sleep. It is impossible to conceive the pathophysiology of several epilepsies without incorporating up-to-date knowledge about slow-wave sleep (SWS). Our book is devoted to this aim: exploring and reinterpreting the role of sleep in epilepsy.

For introduction, we briefly summarize the changes in and new aspects of both sleep and epilepsy and their relationship.

The Growing Knowledge About the Link Between Non–Rapid Eye Movement Sleep and Plastic Functions of the Brain

There are convincing data supporting that one of the main biological functions of SWS is fueling plasticity, of which epilepsy may be considered a severe derailment (exaggeration) (Vyazovskiy et al., 2000; Huber et al., 2006; Buzsáki, 2015).

From the sleep side, our view of SWS has importantly changed. We consider sleep as a self-regulating open system in an organic interrelationship with both environmental stimuli and epileptic events, gating them by the elements of sleep microstructure. Understanding how different sleep constituents participate in cognitive functioning may shed light on the interference caused by epileptic events.

Since the 1970s a new, finer-graded sleep EEG analysis has developed beyond the broader frame of sleep states, established by Dement and Kleitman and elaborated in the form of a standardized scoring system by Rechtschaffen and Kales (1968).

The recognition of the finer-grade sleep structure and its dynamic nature started with the identification of recurring transient (phasic) events within the sleep EEG. The universal recurrence of phasic events in NREM sleep and the fact that they could be elicited by different stimuli highlighted that even seemingly spontaneous episodes might be evoked by unnoticed internal (within the body or brain) or environmental stimuli (Halász et al., 1979) not awakening the sleeper. Although the potential to elicit a phasic event proved to be variable by different stimulus modalities (acoustic stimuli prevail), the essential observation was the modality independence of these events. Another basic feature is the association with a variable degree of autonomic activation as heart rate and motor augmentation evidenced by EMG.

Whatever the input is, the reactive events belong to two types (Fig. 1.1). The first type behaves as a classical arousal response: an increase in the EEG frequency and a decrease in the amplitude. It is the “phases d’activation transitoire” (PAT) (Schieber et al., 1971) prototype. The second type is more sleep- than arousal-like, associated with no or lower intensity autonomic and motor changes. The EEG morphology is consistent with this sleep-like character: K complexes and slow-wave groups. During the 1970s and 1980s, it became clear that there is a continuous sleep level oscillation in each stage of NREM sleep, related to phasic events. We started to call them microarousals (Halász et al., 1979).

Figure 1.1 Working mode schemes of reflex epilepsies (top), system epilepsies of arousal (nocturnal frontal lobe epilepsy; bottom), and sleep induction (absence epilepsy; middle). System epilepsies are triggered by the operation of a system ignited by the specific sensory input. The intrinsic activation of the network of a physiologic system (such as the sleep or arousal system) also may result in system-specific epileptic manifestations if the given system has an increased susceptibility to epilepsy (see more details in Chapters 2 and 3).

After the recognition of the “cyclic alternating pattern” (CAP) by the Parma Sleep Research Group (Terzano et al., 1985) a new microstructure broadened our dynamic view of NREM sleep (Fig. 1.2). The CAP is a microcyclicity: present during all NREM sleep stages and constituted by alternations of activated (A phase) ...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Acknowledgments
• Author Profiles
• Glossary
• Preface
• Chapter 1. Introductory Considerations
• Chapter 2. Absence Epilepsy as the System Epilepsy of the Non–Rapid Eye Movement Sleep-Promoting System
• Chapter 3. Autosomal Dominant Nocturnal Frontal Lobe and Nocturnal Frontal Lobe Epilepsy as System Epilepsies of the Ascending Cholinergic Arousal System
• Chapter 4. Juvenile Idiopathic Myoclonic Epilepsy (Janz Syndrome) as a System Epilepsy Affecting the Corticothalamic System and the Frontal Motor and Cognitive Frontal Subsystems
• Chapter 5. Medial Temporal Lobe Epilepsy (MTLE): The Epilepsy of the Hippocampal Declarative Memory System
• Chapter 6. Idiopathic Polyfocal Hyperexcitability Conditions (HIEC) of Childhood and Their Transition to Electrical Status Epilepticus in Sleep
• Chapter 7. Epileptic Encephalopathies
• Chapter 8. Summary
• Index