Tài liệu The Clinical Science of Neurologic Rehabilitation ppt

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xii Contents
MEASURES OF HEALTH-RELATED QUALITY OF LIFE 298
Instruments • Adjustment Scales • Style Of Questions
MEASURES OF HANDICAP 302
MEASURES OF COST-EFFECTIVENESS 303
STUDY DESIGNS FOR REHABILITATION RESEARCH 303
Ethical Considerations • Types of Clinical Trials • Confounding Issues in Research
Designs • Statistical Analyses
SUMMARY 314
8. ACUTE AND CHRONIC MEDICAL MANAGEMENT 323
DEEP VEIN THROMBOSIS 323
Prevention
ORTHOSTATIC HYPOTENSION 324
THE NEUROGENIC BLADDER 325
Pathophysiology • Management
BOWEL DYSFUNCTION 329
Pathophysiology • Management
NUTRITION AND DYSPHAGIA 330
Pathophysiology • Assessment • Treatment
PRESSURE SORES 334
Pathophysiology • Management
PAIN 336
Acute Pain
• Chronic Central Pain • Weakness-Associated Shoulder Pain • Neck,
Back, and Myofascial Pain
DISORDERS OF BONE METABOLISM 348
Heterotopic Ossification • Osteoporosis
SPASTICITY 348
Management
CONTRACTURES 357
MOOD DISORDERS 358
Posttraumatic Stress Disorder • Depression
SLEEP DISORDERS 363
SUMMARY 364
Part III. Rehabilitation of Specific Neurologic Disorders
9. STROKE 375
EPIDEMIOLOGY 375
Fiscal Impact • Stroke Syndromes
Contents xiii
MEDICAL INTERVENTIONS 377
Frequency of Complications • Secondary Prevention of Stroke
INPATIENT REHABILITATION 385
Eligibility for Rehabilitation • Trials of Locus of Treatment • Discharge
OUTPATIENT REHABILITATION 389
Locus of Treatment • Pulse Therapy • Sexual Function • Community Reintegration
OUTCOMES OF IMPAIRMENTS 392
Overview of Outcomes • The Unaffected Limbs • Impairment-Related Functional
Outcomes
OUTCOMES OF DISABILITIES 399
Overview of Outcomes • Upper Extremity Use • Ambulation • Predictors of
Functional Gains
CLINICAL TRIALS OF FUNCTIONAL INTERVENTIONS 404
Trials of Schools of Therapy • Task-Oriented Approaches • Concentrated Practice •
Assistive Trainers • Adjuvant Pharmacotherapy • Functional Electrical Stimulation •
Biofeedback • Acupuncture
TRIALS OF INTERVENTIONS FOR APHASIA 420
Rate of Gains • Prognosticators • Results of Interventions • Pharmacotherapy
TRIALS FOR COGNITIVE AND AFFECTIVE DISORDERS 425
Memory Disorders • Visuospatial and Attentional Disorders • Affective Disorders
SUMMARY 436
10. ACUTE AND CHRONIC MYELOPATHIES 451
EPIDEMIOLOGY 451
Traumatic Spinal Cord Injury • Nontraumatic Disorders
MEDICAL REHABILITATIVE MANAGEMENT 458
Time of Onset to Start of Rehabilitation • Specialty Units • Surgical Interventions •
Medical Interventions
SENSORIMOTOR CHANGES AFTER PARTIAL AND
COMPLETE INJURY 466
Neurologic Impairment Levels • Evolution of Strength and Sensation • Changes in
Patients with Paraplegia • Changes in Patients with Quadriplegia • Mechanisms of
Sensorimotor Recovery
FUNCTIONAL OUTCOMES 473
Self-Care Skills • Ambulation
TRIALS OF SPECIFIC INTERVENTIONS 477
Mobility • Strengthening and Conditioning • Upper Extremity Function • Neural
Prostheses • Spasticity
LONG-TERM CARE 485
Aging • Sexual Function • Employment • Marital Status • Adjustment and Quality
of Life
SUMMARY 489
xiv Contents
11. TRAUMATIC BRAIN INJURY 497
EPIDEMIOLOGY 498
Economic Impact • Prevention
PATHOPHYSIOLOGY 499
Diffuse Axonal Injury • Hypoxic-Ischemic Injury • Focal Injury • Neuroimaging
NEUROMEDICAL COMPLICATIONS 503
Nutrition • Hypothalamic-Pituitary Dysfunction • Pain • Seizures • Delayed-Onset
Hydrocephalus • Acquired Movement Disorders • Persistent Vegetative State
ASSESSMENTS AND OUTCOME MEASURES 510
Stages of Recovery • Disability
PREDICTORS OF FUNCTIONAL OUTCOME 513
Level of Consciousness • Duration of Coma and Amnesia • Neuropsychologic Tests •
Population Outcomes
LEVELS OF REHABILITATIVE CARE 515
Locus of Rehabilitation • Efficacy of Programs
REHABILITATION INTERVENTIONS AND THEIR EFFICACY 519
Overview of Functional Outcomes • Physical Impairment and Disability • Psychosocial
Disability • Cognitive Impairments • Neurobehavioral Disorders • Neuropsychiatric
Disorders
SPECIAL POPULATIONS 535
Pediatric Patients • Geriatric Patients • Mild Head Injury
ETHICAL ISSUES 537
SUMMARY 538
12. OTHER CENTRAL AND PERIPHERAL DISORDERS 547
DISORDERS OF THE MOTOR UNIT 548
Muscle Strengthening • Respiratory Function • Motor Neuron Diseases •
Neuropathies • Myopathies
PARKINSON’S DISEASE 557
Interventions
MULTIPLE SCLEROSIS 559
Epidemiology of Disability • Pathophysiology • Rehabilitative Interventions • Clinical Trials
PEDIATRIC DISEASES 565
Cerebral Palsy • Myelomeningocele
BALANCE DISORDERS 567
Frailty and Falls in the Elderly • Vestibular Dysfunction
ALZHEIMER’S DISEASE 570
EPILEPSY 570
CONVERSION DISORDERS WITH NEUROLOGIC SYMPTOMS 570
Contents xv
CHRONIC FATIGUE SYNDROME 571
ACQUIRED IMMUNODEFICIENCY SYNDROME 571
SUMMARY 571
INDEX 579
PART I
NEUROSCIENTIFIC
FOUNDATIONS
FOR REHABILITATION
Chapter 1
Organizational Plasticity
in Sensorimotor and
Cognitive Networks
SENSORIMOTOR NETWORKS
Overview of Motor Control
Cortical Motor Networks
Somatosensory Cortical Networks
Pyramidal Tract Projections
Subcortical Systems
Brain Stem Pathways
Spinal Sensorimotor Activity
STUDIES OF REPRESENTATIONAL
PLASTICITY
Motor Maps
Sensory Maps
BASIC MECHANISMS OF SYNAPTIC
PLASTICITY
Hebbian Plasticity
Cortical Ensemble Activity
Long-Term Potentiation and Depression
Molecular Mechanisms
Growth of Dendritic Spines
Neurotrophins
Neuromodulators
COGNITIVE NETWORKS
Overview of the Organization
of Cognition
Explicit and Implicit Memory
Network
Working Memory and Executive Function
Network
Emotional Regulatory Network
Spatial Awareness Network
Language Network
SUMMARY
Function follows structure. The central (CNS)
and peripheral (PNS) nervous system matrix is
a rich resource for learning and for retraining.
This chapter begins with the structural frame-
work of interconnected neural components
that contribute to motor control for walking,
reaching, and grasping, and to cognition and
mood. I then review what we know about cel-
lular mechanisms that may be manipulated by
physical, cognitive, and pharmacologic therapies
to lessen impairments and disabilities. These
discussions of functional neuroanatomy provide
a map for mechanisms relevant to neural repair,
functional neuroimaging, and theory-based
practices for neurologic rehabilitation.
Injuries and diseases of the brain and spinal
cord damage clusters of neurons and discon-
nect their feedforward and feedback pro-
jections. The victims of neurologic disorders
often improve, however. Mechanisms of
activity-dependent learning within spared mod-
ules of like-acting neurons are a fundamental
property of the neurobiology of functional gains.
Rehabilitation strategies can aim to manipulate
the molecules, cells, and synapses of networks
that learn to represent some of what has been
lost. This plasticity may be no different than
what occurs during early development, when a
new physiologic organization emerges from in-
trinsic drives on the properties of neurons and
their synapses. Similar mechanisms drive how
living creatures learn new skills and abilities.
3
4 Neuroscientific Foundations for Rehabilitation
Activity-dependent plasticity after a CNS or
PNS lesion, however, may produce mutability
that aids patients or mutagenic physiology that
impedes functional gains.
Our understanding of functional neu-
roanatomy is a humbling work in progress. Al-
though neuroanatomy and neuropathology
may seem like old arts, studies of nonhuman
primates and of man continue to reveal the
connections and interactions of neurons. The
brain’s macrostructure is better understood
than the microstructure of the connections be-
tween neurons. It is just possible to imagine
that we will grasp the design principles of the
100,000 neurons and their glial supports within
1 mm
3
of cortex, but almost impossible to look
forward to explaining the activities of the 10
billion cortical neurons that make some 60 tril-
lion synapses.
1
Aside from the glia that play an
important role in synaptic function, each cubic
millimeter of gray matter contains 3 km of axon
and each cubic millimeter of white matter in-
cludes 9 meters of axon. The tedious work of
understanding the dynamic interplay of this
matrix is driven by new histochemical ap-
proaches that can label cells and their projec-
tions, by electrical microstimulation of small
ensembles of neurons, by physiological record-
ings from single cells and small groups of neu-
rons, by molecular analyses that localize and
quantify neurotransmitters, receptors and gene
products, and by comparisons with the archi-
tecture of human and nonhuman cortical neu-
rons and fiber arrangements.
Functional neuroimaging techniques, such
as positron emission tomography (PET), func-
tional magnetic resonance imaging (fMRI),
and transcranial magnetic stimulation (TMS)
allow comparisons between the findings from
animal research and the functional neu-
roanatomy of people with and without CNS le-
sions. These computerized techniques offer in-
sights into where the coactive assemblies of
neurons lie as they simultaneously, in parallel
and in series, process information that allows
thought and behavior. Neuroimaging has both
promise and limitations (see Chapter 3).
What neuroscientists have established about
the molecular and morphologic bases for learn-
ing motor and cognitive skills has become more
critical for rehabilitationists to understand.
Neuroscientific insights relevant to the restitu-
tion of function can be appreciated at all the
main levels of organization of the nervous sys-
tem, from behavioral systems to interregional
and local circuits, to neurons and their den-
dritic trees and spines, to microcircuits on ax-
ons and dendrites, and most importantly, to
synapses and their molecules and ions. Expe-
rience and practice lead to adaptations at
all levels. Knowledge of mechanisms of this
activity-dependent plasticity may lead to the
design of better sensorimotor, cognitive, phar-
macologic, and biologic interventions to en-
hance gains after stroke, traumatic brain and
spinal cord injury, multiple sclerosis, and other
diseases.
SENSORIMOTOR NETWORKS
Motor control is tied, especially in the rehabil-
itation setting, to learning skills. Motor skills
are gained primarily through the cerebral or-
ganization for procedural memory. The other
large classification of memory, declarative
knowledge, depends upon hippocampal activ-
ity. The first is about how to, the latter is the
what of facts and events. Procedural knowl-
edge, compared to learning facts, usually takes
considerable practice over time. Skills learning
is also associated with experience-specific or-
ganizational changes within the sensorimotor
network for motor control. A model of motor
control, then, needs to account for skills learn-
ing. To successfully manipulate the controllers
of movement, the clinician needs a multilevel,
3-dimensional point of view. The vista includes
a reductionist analysis, examining the proper-
ties of motor patterns generated by networks,
neurons, synapses, and molecules. Our sight-
line also includes a synthesis that takes a sys-
tems approach to the relationships between
networks and behaviors, including how motor
patterns generate movements modulated by ac-
tion-related sensory feedback and by cognition.
The following theories, all of which bear some
truth, focus on elements of motor control.
Overview of Motor Control
Mountcastle wrote, “The brain is a complex of
widely and reciprocally interconnected sys-
tems,” and “The dynamic interplay of neural
activity within and between these systems is the
very essence of brain function.” He proposed:
“The remarkable capacity for improvement of
Plasticity in Sensorimotor and Cognitive Networks 5
function after partial brain lesions is viewed as
evidence for the adaptive capacity of such dis-
tributed systems to achieve a goal, albeit slowly
and with error, with the remaining neural
apparatus.”
2
A distributed system represents a collection
of separate dynamic assemblies of neurons with
anatomical connections and similar functional
properties.
3
The operations of these assemblies
are linked by their afferent and efferent mes-
sages. Signals may flow along a variety of path-
ways within the network. Any locus connected
within the network may initiate activity, as both
externally generated and internally generated
signals may reenter the system. Partial lesions
within the system may degrade signaling, but
will not eliminate functional communication so
long as dynamic reorganization is possible.
What are some of the “essences” of brain and
spinal cord interplay relevant to understanding
how patients reacquire the ability to move with
purpose and skill?
No single theory explains the details of the
controls for normal motor behavior, let alone
the abnormal patterns and synergies that
emerge after a lesion at any level of the neu-
raxis. Many models successfully predict aspects
of motor performance. Some models offer both
biologically plausible and behaviorally relevant
handles on sensorimotor integration and mo-
tor learning. Among the difficulties faced by
theorists and experimentalists is that no simple
ordinary movement has only one motor control
solution. Every step over ground and every
reach for an item can be accomplished by many
different combinations of muscle activations,
joint angles, limb trajectories, velocities, accel-
erations, and forces. Thus, many kinematically
redundant biological scripts are written into
the networks for motor control. The nervous
system computates within a tremendous num-
ber of degrees of freedom for any successful
movement. In addition, every movement
changes features of our physical relationship to
our surrounds. Change requires operations in
other neural networks, such as frontal lobe con-
nections for divided attention, planning, and
working memory.
Models of motor behavior have explored the
properties of neurons and their connections to
explain how a network of neurons generates
persistent activity in response to an input of
brief duration, such as seeing a baseball hit out
of the batter’s box, and how networks respond
to changes in input to update a view of the en-
vironment for goal-directed behaviors, such as
catching the baseball 400 feet away while on
the run.
4
A wiring diagram for hauling in a fly
ball, especially with rapidly changing weights
and directions of synaptic activity, seems im-
possibly complex. Researchers have begun,
however, to describe some clever solutions for
rapid and accurate responses that evolve within
interacting, dynamic systems such as the CNS.
5
Each theory contains elements that describe,
physiologically or metaphorically, some of the
processes of motor control. These theories lead
to experimentally backed notions that help ex-
plain why rehabilitative therapies help patients.
GENERAL THEORIES OF
MOTOR CONTROL
Sherrington proposed one of the first physio-
logically based models of motor control. Sen-
sory information about the position and veloc-
ity of a limb moving in space rapidly feeds back
information into the spinal cord about the cur-
rent position and desired position, until all
computed errors are corrected. Until the past
decade or two, much of what physical and oc-
cupational therapists practiced was described
in terms of chains of reflexes. Later, the the-
ory expanded to include reflexes nested within
Hughling Jackson’s hierarchic higher, middle,
and lower levels of control. Some schools of
physical therapy took this model to mean that
motor control derives in steps from voluntary
cortical, intermediate brain stem, and reflexive
spinal levels.
6
Abnormal postures and tone
evolve, in the schools of Bobath and
Brunnstrom (see Chapter 5), from the release
of control by higher centers. These theories for
physical and for occupational therapy imply
that the nervous system is an elegantly wired
machine that performs stereotyped computa-
tions on sensory inputs. Lower levels are sub-
sumed under higher ones. This notion, how-
ever, is too simple. All levels of the CNS are
highly integrated with feedforward and feed-
back interactions. Sensory inputs are critical,
however.
Another theory of motor control suggests
that stored central motor programs allow sen-
sory stimuli or central commands to generate
movements. Examples of stored programs in-
clude the lumbar spinal cord’s central pattern
generators for stepping and the cortical “rules”
6 Neuroscientific Foundations for Rehabilitation
that allow cursive writing to be carried out
equally well by one’s hand, shoulder, or foot.
This approach, however, needs some elabora-
tion to explain how contingencies raised by the
environment and the biomechanical character-
istics of the limbs interact with stored programs
or with chains of reflexes. A more elegant the-
ory of motor control, perhaps first suggested
by Bernstein in the 1960s, tried to account for
how the nervous system manages the many de-
grees of freedom of movement at each joint.
7
He hypothesized that lower levels of the CNS
control the synergistic movements of muscles.
Higher levels of the brain activate these syn-
ergies in combinations for specific actions.
Other theorists added a dynamical systems
model to this approach. Preferred patterns of
movement emerge in part from the interaction
of many elements, such as the physical prop-
erties of muscles, joints, and neural connec-
tions. These elements self-organize according
to their dynamic properties. This model says
little about other aspects of actions, including
how the environment, the properties of objects
such as their shape and weight, and the de-
mands of the task all interact with movement,
perception, and experience.
Most experimental studies support the ob-
servations of Mountcastle and others that the
sensorimotor system learns and performs with
the overriding objective of achieving move-
ment goals. All but the simplest motor activi-
ties are managed by neuronal clusters distrib-
uted in networks throughout the brain. The
regions that contribute are not so much func-
tionally localized as they are functionally spe-
cialized. Higher cortical levels integrate sub-
components like spinal reflexes and oscillating
brain stem and spinal neural networks called
pattern generators. The interaction of a dy-
namic cortical architecture with more auto-
matic oscillators allows the cortex to run sen-
sorimotor functions without directly needing to
designate the moment-to-moment details of
parameters such as the timing, intensity, and
duration of the sequences of muscle activity
among synergist, antagonist, and stabilizing
muscle groups.
For certain motor acts, the motor cortex
needs only to set a goal. Preset neural routines
in the brain stem and spinal cord carry out the
details of movements. This system accounts for
how an equivalent motor act can be accom-
plished by differing movements, depending on
the demands of the environment, prior learn-
ing, and rewarded experience. Having achieved
a behavioral goal, the reinforced sensory and
movement experience is learned by the motor
network. Learning results from increased
synaptic activity that assembles neurons into
functional groups with preferred lines of com-
munication.
8
Thus, goal-oriented learning, as
opposed to mass practice of a simple and repet-
itive behavior, ought to find an essential place
in rehabilitation strategies.
Several experimentally based models sug-
gest how the brain may construct movements.
Target-directed movements can be generated
by motor commands that modulate an equilib-
rium point for the agonist and antagonist mus-
cles of a joint.
9
During reaching movements,
for example, the brain constructs motor com-
mands based on its prediction of the forces the
arm will experience. Some forces are external
loads and need to be learned. Other forces de-
pend on the physical properties of muscle, such
as its elasticity. The computations used by neu-
rons to compose the motor command may be
broadly tuned to the velocity of movements.
10
Using microstimulation of closely related re-
gions of the lumbar spinal cord, Bizzi and col-
leagues have also defined fields of neurons in
the anterior horns that store and represent spe-
cific movements within the usual workspace of
a limb, called primitives.
11
Combinations of
these simple flexor and extensor actions may
be fashioned by supraspinal inputs into the vast
variety of movements needed for reaching and
walking. The motor cortex, then, determines
which spinal modules to activate, along with
the necessary coefficient of activation, pre-
sumably working off an internal, previously
learned model of the desired movement. The
representations for the movement, described
later, are stored in sensorimotor and associa-
tion cortex. Thus, some simplifying rules gen-
erate good approximations to the goal of the
reaching or stepping movement. Systems for
error detection, especially within connections
to the cerebellum, simultaneously make fine
adjustments to reach the object.
A variety of related concepts about neural
network modeling for the generation of a
reaching movement have been offered.
12,13
Much work has gone into what small groups of
cortical cells in the primary motor cortex (M1)
encode. The activity of these neurons may en-
code the direction or velocity of the hand as it