Neurological Rehabilitation

Michael P. Barnes, David C. Good

• Publisher: Elsevier
• Year: 2013
• ISBN:
  9780444595843
• Topic: Biological Sciences
• Subtopic: Neuroscience
• Index: Biological Sciences

Neurological Rehabilitation is the latest volume in the definitive Handbook of Clinical Neurology series. It is the first time that this increasing important subject has been included in the series and this reflects the growing interest and quality of scientific data on topics around neural recovery and the practical applications of new research. The volume will appeal to clinicians from both neurological and rehabilitation backgrounds and contains topics of interest to all members of the multidisciplinary clinical team as well as the neuroscience community. The volume is divided into five key sections. The first is a summary of current research on neural repair, recovery and plasticity. The authors have kept the topics readable for a non-scientific audience and focused on the aspects of basic neuroscience that should be most relevant to clinical practice. The next section covers the basic principles of neurorehabilitation, including excellent chapters on learning and skill acquisition, outcome measurement and functional neuroimaging. The key clinical section comes next and includes updates and reviews on the management of the main neurological disabling physical problems, such as spasticity, pain, sexual functioning and dysphagia. Cognitive, emotional and behavioural problems are just as important and are covered in the next section, with excellent chapters, for example, on memory and management of executive dysfunction. The final part draws the sections on symptom management together by discussing the individual diseases that are most commonly seen in neurorehabilitation and providing an overview of the management of the disability associated with those disorders. The volume is a definitive review of current neurorehabilitation practice and will be valuable to a wide range of clinicians and scientists working in this rapidly developing field.

• A volume in the Handbook of Clinical Neurology series, which has an unparalleled reputation as the world's most comprehensive source of information in neurology
• International list of contributors including the leading workers in the field
• Describes the advances which have occurred in clinical neurology and the neurosciences, their impact on the understanding of neurological disorders and on patient care

Chapter 1

Neural plasticity and its contribution to functional recovery

Nikhil Sharma¹, Joseph Classen² and Leonardo G. Cohen^1*

¹Human Cortical Physiology and Stroke Neurorehabilitation Section, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA

²Department of Neurology, University of Leipzig, Leipzig, Germany

*Correspondence to: Leonardo G. Cohen, M.D., Chief, Human Cortical Physiology Section and Stroke Neurorehabilitation Clinic, National Institute of Neurological Disorders and Stroke NIH, Building 10, Room 7D54 Bethesda, MD 20892, USA. Tel: [phone], Fax:[phone], E-mail: [email protected]

Abstract

In this chapter we address the phenomena of neural plasticity, operationally defined as the ability of the central nervous system to adapt in response to changes in the environment or lesions. At the cellular level, we discuss basic changes in membrane excitability, synaptic plasticity as well as structural changes in dendritic and axonal anatomy that support behavioral expressions of plasticity and functional recovery. We consider the different levels at which these changes can occur and possible links with modification of cognitive strategies, recruitment of new/different neural networks, or changes in strength of such connections or specific brain areas in charge of carrying out a particular task (i.e., movement, language, vision, hearing). The study of neuroplasticity has wide-reaching implications for understanding reorganization of action and cognition in the healthy and lesioned brain.

Definition

The idea that the cerebral cortex is dynamically organized was proposed in 1912, when Brown and Sherrington stimulated the motor cortex of chimpanzees and found that “a point which began by yielding primary extension may come to yield primary flexion in the latter part of the stimulation series” (Brown and Sherrington, 1912). In many investigations since then these phenomena have been referred to as neural plasticity. Neural plasticity can be defined as the ability of the central nervous system (CNS) to adapt in response to changes in the environment or lesions. This property of the CNS may involve modifications in overall cognitive strategies to successfully cope with new challenges (i.e., attention, behavioral compensation) (Bury and Jones, 2002), recruitment of new/different neural networks (Johansen-Berg et al., 2002; Fridman et al., 2004; Lotze et al., 2006; Heuninckx et al., 2008), or changes in strength of such connections or specific brain areas in charge of carrying out a particular task (i.e., movement, language, vision, hearing) (Cohen et al., 1997; Grefkes et al., 2008). At the cellular level, changes in membrane excitability, synaptic plasticity, as well as structural changes in dendritic and axonal anatomy as measured in vivo and in vitro may be demonstrated in animals and humans (Clarkson et al., 2010; Li et al., 2010). The study of neuroplasticity engages scientists from many different disciplines because of the profound implications it has for understanding the functional underpinnings of action and cognition in the healthy and lesioned brain (Dimyan and Cohen, 2010). Mechanistic understanding of neuroplastic changes in the process of functional recovery following brain lesions, one of the focuses of this volume, is already starting to lead to the development of more rational strategies to facilitate neurorehabilitation (Taub et al., 2002; Cheeran et al., 2009).

At a cellular level, neuronal circuits consist of synaptic connections between axons and dendrites. As these circuits extend over the brain there is the potential for a large number of possible interactive combinations allowing for great flexibility. Modification of sensory input may induce rapid changes in cortical representations through various mechanisms including unmasking of connections that are silent in the native state (Calford and Tweedale, 1991a, b). For example, blocking inhibition pharmacologically within a small region of the primary motor cortex (M1) immediately unveils new representational patterns (Jacobs and Donoghue, 1991), through unmasking horizontal excitatory connections previously hidden by inhibitory neurons. The strength of these horizontal connections and the balance of excitation and inhibition appear to shape cortical representations. Corticofugal connections make extensive long-range (± 1 mm) links with other pyramidal tract neurons, and with local inhibitory interneurons (Landry et al., 1990; McGuire et al., 1991). It is now known that long-term potentiation (LTP) can be induced in these horizontal connections of adult M1, contributing to long-lasting associations among neurons within a motor cortical area (Hess and Donoghue, 1994). Moreover, vertical synaptic pathways in M1 can experience short-term depression, short-term facilitation, long-term depression and, under conditions of disinhibition, also LTP (Castro-Alamancos et al., 1995). In addition, slower, progressive plastic changes can be driven by learning (Robertson and Irvine, 1989; Chino et al., 1997), competition with other inputs (Merzenich et al., 1983), and use (Nudo et al., 1996b).

Basic science investigations have substantially advanced our understanding of the mechanisms of plasticity and metaplasticity, important in multiple areas of human cognition such as learning and memory, and in functional recovery from lesions in the CNS, as in stroke (Buonomano and Merzenich, 1998; Floel and Cohen, 2006). The term “metaplasticity” is often, but incorrectly, used interchangeably with “homeostatic” plasticity (see below) (Abraham and Bear, 1996; Fischer et al., 1997; Gentner et al., 2008; Jung and Ziemann, 2009). In the past few years it has become evident that these findings have direct implications for the way in which human disease is treated, and new efforts have been invested in research that translates these advances in the basic science domain to the formulation of new, rational strategies for promoting recovery of function in humans. To accomplish this goal, it is important to demonstrate that similar principles to those described in animal models apply to the human cerebral cortex in relevant behavioral settings.

Sites of plasticity

In most cases, the cerebral cortex has been the target of studies of human plasticity (Wolpaw and Tennissen, 2001). However, reorganization requires fine-tuning of activity at cortical as well as subcortical sites. In the motor domain, for example, spinal processes play a role in modulating locomotor learning (Bizzi et al., 2000) and plasticity after amputations and nerve transections (Wu and Kaas, 1999). Plastic changes following deafferentation can be identified at cortical (Kaas et al., 1983) and subcortical (Devor and Wall, 1981) sites. The extent to which plastic changes detected at cortical levels reflect reorganization in subcortical structures is incompletely understood and still underinvestigated (Wu and Kaas, 2000). Therefore, it is important to keep in mind that the neural substrates of recovery of function are likely distributed over multiple sites at different levels of the neuroaxis and not restricted to one specific location. It still represents a challenge to understand how these different levels interact with one another to accomplish a particular behavioral goal.

Window of opportunity

Neural plasticity occurs throughout the life span (Elias and Wagster, 2007). During normal human development the CNS must continue to optimize performance and learn and adapt in the presence of changes in anatomical constraints (such as, for example, changes in limb length or muscle mass or strength) and experience (Gaillard et al., 2000). Additionally, neuroplastic changes identified following CNS abnormalities during development have been particularly impressive given their ability to re-establish almost normal behavior (Chen et al., 2002). One such example is the substantial recovery of motor function or language in children posthemispherectomy, implemented to ameliorate intractable seizures (Vargha-Khadem et al., 1997). The potential of neuroplastic changes to influence behavior and recovery of function was first widely accepted in relation to the developing brain. Only more recently was it understood that neuroplastic changes of substantial clinical relevance could occur in the adult CNS and in the elderly (Merzenich et al., 1996). It has now been proposed, for example, that recruitment of wider brain networks in the elderly and after stroke may play a beneficial role in maintaining the ability of individuals to carry out specific tasks or even in facilitating relearning (Heuninckx et al., 2008; Hummel et al., 2010).

Functional relevance

Plasticity of cortical representations within and across different brain regions is thought to represent the neural basis underlying sensory substitution, for example in blind and deaf humans (Rauschecker, 1995), as well as in the recovery of motor function after cortical lesions like stroke (Nudo et al., 1996a). Although neuroplasticity, as defined above, is a ubiquitous phenomenon (our brain is constantly changing), it may have different impact on different behaviors. It may be beneficial (often referred to as adaptive plasticity, the most common forms of plasticity studied; Cohen et al., 1997; Lee, 2009), have no influence (representing only epiphenomena of the modified behavior), or even result in deleterious consequences (i.e., maladaptive; Flor et al., 2006) on performance of particular tasks or sensory experiences. This concept has been referred to as functional relevance of neuroplasticity. Conceptually, it would not be surprising that plastic changes in, for example neuronal networks, may have beneficial implications on a particular behavior but at a cost to other behavior (Chklovskii et al., 2004). This concept of cost of neuroplastic changes, which has been to some extent overlooked, is starting to receive attention. Understanding these changes and how they can be influenced is pivotal in developing better treatments and therapies for patients (Hodics et al., 2006; Hummel and Cohen, 2006; Cramer, 2008).

Plasticity, metaplasticity, and homeostatic plasticity

Plasticity likely depends on multiple mechanisms evolving on different temporal scales – minutes to months, even years. Rapid onset-mechanisms, which may operate over a limited period of time, are believed to represent initial steps of more slowly evolving processes of reorganization through which functional gains (or losses) may be sustained (Classen et al., 1998; Kleim and Jones, 2008). At the level of neuronal synapses, multiple transformations may occur from relatively short-lasting LTP, which appears to be largely independent of protein synthesis, to long-lasting LTP, which may persist along the life span. These synaptic changes are complemented by changes in neuronal excitability and struc...

Table of contents

• Cover image
• Title page
• Table of Contents
• Series Page
• Copyright
• Handbook of Clinical Neurology 3rd Series
• Foreword
• Preface
• Contributors
• Chapter 1. Neural plasticity and its contribution to functional recovery
• Chapter 2. Plasticity of cerebral functions
• Chapter 3. Neuroplasticity in the spinal cord
• Chapter 4. Neural tissue transplantation, repair, and rehabilitation
• Chapter 5. Clinical trials in neurorehabilitation
• Chapter 6. Brain–computer interfaces
• Chapter 7. Epidemiology of neurologically disabling disorders
• Chapter 8. Motor learning principles for neurorehabilitation
• Chapter 9. Outcome measures in stroke rehabilitation
• Chapter 10. Organization of rehabilitation services
• Chapter 11. Functional neuroimaging
• Chapter 12. Gait disorders
• Chapter 13. The diagnosis and management of adults with spasticity
• Chapter 14. Neurorehabilitation approaches to facilitate motor recovery
• Chapter 15. Neuropathic pain
• Chapter 16. Balance
• Chapter 17. Neurogenic lower urinary tract dysfunction
• Chapter 18. Neurogenic bowel
• Chapter 19. Neurological rehabilitation
• Chapter 20. Autonomic dysfunction
• Chapter 21. Dysphagia
• Chapter 22. Disorders of communication
• Chapter 23. Rehabilitation Robotics
• Chapter 24. Neurogenic respiratory failure
• Chapter 25. Chronic fatigue syndrome
• Chapter 26. Other physical consequences of disability
• Chapter 27. Rehabilitation of aphasia
• Chapter 28. Apraxia
• Chapter 29. Rehabilitation of spatial neglect
• Chapter 30. Memory deficits
• Chapter 31. Rehabilitation and management of executive function disorders
• Chapter 32. Neurobehavioral disorders
• Chapter 33. Emotional disorders in neurological rehabilitation
• Chapter 34. Traumatic and nontraumatic brain injury
• Chapter 35. Traumatic spinal cord injury
• Chapter 36. Stroke
• Chapter 37. Neurorehabilitation in Parkinson disease
• Chapter 38. Cerebral palsy
• Chapter 39. Multiple sclerosis
• Chapter 40. Rehabilitation of the muscular dystrophies
• Chapter 41. Rehabilitation of motor neuron disease
• Chapter 42. Rehabilitation of brachial plexus and peripheral nerve disorders
• Index