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TitleNeurological Rehabilitation: Spasticity and Contractures in Clinical Practice and Research
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Total Pages312
Table of Contents
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Title Page
Copyright Page
Table of Contents
Chapter 1: Definition and Measurement of Spasticity and Contracture
	1.1 Introduction
	1.2 Definition of Spasticity
		1.2.1 Can the Words Increased Tone/Hypertonia and Spasticity Be Used Interchangeably?
		1.2.2 Developing the Framework for Defining Spasticity Increased (Hyper-Excitable/Exaggerated) Reflexes Spasms and Clonus Altered Tone or the Response of a Relaxed Muscle to an Externally Imposed Stretch Abnormal Movement Patterns and Co-Contraction
		1.2.3 The Classification and Definition of Spasticity in Upper Motoneuron Syndrome
		1.2.4 Contractures in Patients with Upper Motoneuron Syndrome
		1.2.5 The Measurement of Spasticity and Contracture
		1.2.6 Concluding Thoughts
Chapter 2: Pathophysiology of Spasticity
	2.1 How to Measure Spasticity – From Clinical Evaluation to Biomechanical Techniques
	2.2 The Nature of the Muscle Response to Stretch
	2.3 Is Spasticity Caused by Lesion of the Pyramidal Tract?
	2.4 Spasticity Does Not Appear Immediately after Lesion but Is Caused by Adaptive Changes in Spinal Networks
	2.5 Pathophysiology of Exaggerated Stretch Reflex Activity: Adaptive Changes in Spinal Neural Networks
		2.5.1 Pathophysiological Role of Motoneuronal Changes
		2.5.2 Sprouting, New Synapses
		2.5.3 Regulation at Presynaptic Sites: Increasing the Input from Surviving Fibres Presynaptic Inhibition Post-Activation Depression
		2.5.4 Transmission in Group II Pathways
		2.5.5 Pathophysiological Role of Changes in Postsynaptic Inhibition of Motoneurons Disynaptic Reciprocal Ia Inhibition Recurrent Inhibition Autogenetic Ib Inhibition Fusimotor Drive, Gamma-Spasticity
	2.6 How Is Clonus Related to Spasticity?
	2.7 What Causes a Spasm?
	2.8 Spastic Dystonia Is Not Caused by Increased Stretch Reflex Activity
	2.9 Concluding Remarks
Chapter 3: Functional Problems in Spastic Patients Are Not Caused by Spasticity but by Disordered Motor Control
	3.1 Reflexes Are an Integrated Part of Voluntary Movement
	3.2 Stretch Reflex Modulation in Spastic Subjects
		3.2.1 Reflex Modulation during Simple Contraction of Agonist Muscle
		3.2.2 Hyperexcitable Stretch Reflexes in the Stance Phase of Gait
		3.2.3 Control of Reflexes in the Antagonist
		3.2.4 Suppression of Reflexes in Swing Phase
	3.3 Sensory Feedback Contribution to Movement
	3.4 Long-Latency Stretch Reflexes and Coordination of Movement
	3.5 Interjoint Coordination
	3.6 Interlimb Coordination
	3.7 Co-Contraction as a Strategy to Maintain Joint Stiffness
	3.8 Over-Activity as a General Adaptation to Central Lesion Causing Disordered Motor Control
	3.9 Training to Learn New Strategies and Thereby Make Use of Spasticity
Chapter 4: The Clinical Management of Spasticity and Contractures in Cerebral Palsy
	4.1 Introduction
	4.2 Cerebral Palsy
	4.3 Treatment Objectives
	4.4 Medical Treatment
		4.4.1 Oral Medication Benzodiazepines Oral Baclofen Gabapentin and Pregabalin
		4.4.2 Injection Therapies Botulinum Toxin Phenol
	4.5 Therapy
		4.5.1 Stretching
		4.5.2 Strengthening
	4.6 Surgical Treatment
		4.6.1 Neurotomy
		4.6.2 Intrathecal Baclofen
		4.6.3 Selective Dorsal Rhizotomy Case Study
	4.7 Conclusion
Chapter 5: Clinical Management of Spasticity and Contractures in Stroke
	5.1 Introduction
	5.2 Pathophysiology of Spasticity after Stroke
	5.3 Motor Recovery and Motor Control after Stroke
	5.4 The Role of Spasticity in the Control of Posture and Gait
		5.4.1 Muscle Overactivity during the Stance Phase
		5.4.2 Muscle Overactivity during the Swing Phase
	5.5 The Role of Spasticity in Arm and Hand Function
		5.5.1 Spasticity in Patients with a Severely Affected Upper Limb (UAT 0–1)
		5.5.2 Spasticity in Patients with a Moderately Affected Upper Limb (UAT 2–3)
		5.5.3 Spasticity in Patients with a Mildly Affected Upper Limb (UAT 4–7)
	5.6 Assessment of Spasticity in Stroke Patients
		5.6.1 Assessment of Spasticity: Body Function and Structure
		5.6.2 Assessment of Spasticity: Activity and Participation
	5.7 Management of Spasticity after Stroke
		5.7.1 Noninvasive Methods
		5.7.2 Invasive, Reversible Methods
		5.7.3 Invasive, Permanent Methods
		5.7.4 Management Strategy for Stroke Patients with Spasticity
Chapter 6: Clinical Management of Spasticity and Contractures in Spinal Cord Injury
	6.1 Introduction
		6.1.1 Epidemiology and Specific Aspects of Spasticity in SCI
		6.1.2 Spinal Shock, Recovery of Spinal Excitability, and Development of Spastic Movement Disorder
		6.1.3 Pattern of Spastic Movement Disorder Depends on Patho-Anatomy
	6.2 Pathophysiology-Based Treatment of Spasticity
		6.2.1 Clinical Signs of Spasticity
		6.2.2 Spastic Movement Disorder
		6.2.3 Therapeutic Consequences
	6.3 Patient Selection and Therapeutic Approach
		6.3.1 Indication for Treatment of Spasticity in SCI
		6.3.2 Clinical Assessment of Spasticity in SCI
		6.3.3 Clinical Presentation and Anatomical Distribution of Spasticity
		6.3.4 Physiological Effects of Training
		6.3.5 The Mainstay of Spasticity Treatment in SCI Is Physical Therapy
		6.3.6 Oral Systemic Anti-Spastic Pharmacotherapy
		6.3.7 Intrathecal Anti-Spastic Pharmacotherapy
		6.3.8 Focal Anti-Spastic Pharmacotherapy: Chemodenervation
		6.3.9 Surgical Correction of Contractures
		6.3.10 Focal Anti-Spastic Surgical Treatment: Selective Dorsal Rhizotomy
	6.4 The Complex Spastic SCI Patient: Selection of Therapeutic Approach
		6.4.1 Case 1: Combination Therapies: Oral Systemic and Focal
		6.4.2 Case 2: Combination Therapies: Intrathecal Systemic and Focal
Chapter 7: Clinical Management of Spasticity and Contractures in Multiple Sclerosis
	7.1 Multiple Sclerosis; Incidence, Epidemiology, and Disease Course
	7.2 Pathophysiology of MS and Spasticity
	7.3 Disease-Modifying Therapy in MS
	7.4 Spasticity in MS
	7.5 Management of Spasticity in MS
		7.5.1 Pharmacological Treatments Treatments for Generalised Spasticity: Oral Medications Baclofen Tizanidine Dantrolene Gabapentin Cannabinoids Benzodiazepines Evidence-Based Guidelines for Oral Antispasticity Medications: Spanish and German Consensus Document Treatments for Focal Spasticity Phenol Chemodenervation Botulinum Toxin Intrathecal (IT) Baclofen
		7.5.2 Non-Pharmacological Treatments Physical Activity/Exercise for the Management of Spasticity in MS Transcutaneous Electrical Nerve Stimulation (TENS) for the Management of Spasticity in MS Transcranial Magnetic Stimulation for the Treatment of Spasticity in MS
		7.5.3 Other Non-Pharmacological Interventions for the Management of Spasticity in MS Surgery
		7.5.4 Strategy for the Management of Spasticity in MS
Chapter 8: Clinical Assessment and Management of Spasticity and Contractures in Traumatic Brain Injury
	8.1 Introduction
	8.2 Impact of Contractures and Spasticity on Recovery
	8.3 Clinical Presentations
	8.4 Brain Injury Complications That May Worsen Spasticity
	8.5 Treatment Goals
		8.5.1 Case 1
	8.6 Assessment
		8.6.1 Clinical Assessment
		8.6.2 Biomechanical Assessment
	8.7 Management
		8.7.1 Physical Modalities
		8.7.2 Stretching and Casting for Contracture vs. Spasticity Management
		8.7.3 Electrical Stimulation
		8.7.4 Oral Medications
		8.7.5 Focal Therapies Botulinum Toxins Case 2 Phenol and Alcohol Neurolysis
		8.7.6 Intrathecal Therapies
		8.7.7 Surgical Interventions
		8.7.8 Controversial and Promising Treatments
Chapter 9: Hereditary Spastic Paraparesis and Other Hereditary Myelopathies
	9.1 Introduction
	9.2 Distal Axonopathies: Hereditary Spastic Paraparesis
		9.2.1 Prevalence and Genetics
		9.2.2 Clinical Presentation
		9.2.3 Pathology Cellular Changes Changes in Descending and Ascending Tract Function Changes in Cortical Activation with Movement
		9.2.4 Symptoms Associated with HSP Limb Stiffness Paresis Sensory Loss Bladder Bony Changes Fatigue Mood and Quality of Life
		9.2.5 Impact of Spasticity and Associated Symptoms on Functional Ability
		9.2.6 Balance
		9.2.7 Walking
		9.2.8 Outcome measurement
		9.2.9 Interventions Pharmacological and Surgical Treatment of Spasticity Physical Interventions Service Delivery
	9.3 Spinocerebellar Degenerations
		9.3.1 Autosomal Dominant
		9.3.2 SCA3 or Machado-Joseph Disease Symptomatic Management
		9.3.3 Autosomal Recessive
		9.3.4 Friedreich’s Ataxia and Late-Onset Friedreich’s Ataxia Management of FDRA Co-enzyme Q10 and Idebenone Symptomatic Management
	9.4 Motor Neuron Disorders and Familial Amyotrophic Lateral Sclerosis
		9.4.1 Amyotrophic Lateral Sclerosis Prevalence and Genetics Pathology Clinical Presentation
		9.4.2 Interventions Disease-Modifying Therapy Symptomatic management
	9.5 Leukodystrophies
		9.5.1 Demyelinating and Dysmyelinating Disorders
		9.5.2 Hypomyelinating Disorders
		9.5.3 Spongiform Disorders
		9.5.4 Cystic Disorders
	9.6 Adrenoleukodystrophy
		9.6.1 Prevalence and Genetics
		9.6.2 Clinical Presentation
		9.6.3 Interventions
	9.7 Summary
Document Text Contents
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Spasticity and Contractures in
Clinical Practice and Research

Page 156

145Clinical Management of Spasticity and Contractures in Spinal Cord Injury

In contrast, short latency reflexes neither in healthy subjects nor in
patients with spasticity contribute significantly to muscle activity during
natural movements [19]. These observations indicate that the muscle activ-
ity required during movement performance (e.g., to support the body dur-
ing the stance phase of stepping) develops on a lower level of organisation
after a CNS damage [19,61,66]. Consequently, the muscle tone required is not
achieved by a modulated muscle activation as it is the case in healthy sub-
jects. Instead, muscle hypertonus develops with the stretching of the toni-
cally activated muscle. This represents a more simple mode of muscle tone
generation, which is also based on structural alterations of a muscle second-
ary to a CNS lesion, i.e., a loss of sarcomeres [66], muscle fibre changes and
increase of structurally deteriorated extracellular matrix [14–16]. Increased
passive tension in the muscle is unrelated to stretch reflex activation. At the
single-fibre level, elevated passive tension was found in muscle cells express-
ing fast myosin heavy chain isoforms, especially MyHC-IIx, but not in those
expressing slow MyHC. Type IIx fibres were present in higher-than-normal
proportions in spastic muscles, whereas type I fibres were proportionately
reduced [16]. This is equivalent to an alteration of the contractile properties
toward tonic muscle characteristics. According to these authors, ultrastruc-
tural changes of the extracellular matrix such as expanded connective tis-
sue, but also decreased mitochondrial volume fraction and appearance of
intracellular amorphous material, suggest that the global passive muscle
stiffening in SCI spasticity is caused by structural and functional adapta-
tions outside and inside the muscle cells, which alter their passive mechani-
cal properties. This change compensates in part for the loss of neurogenic
muscle activation and allows, for example, for support of the body during
the stance phase of stepping. However, the performance of quick/fast move-
ments becomes impossible by this mode of regulation of muscle stiffness.
Muscle spasms do not play a role in this. Patients with spasticity do not only
suffer from an impaired motor output but a defective control and processing
of afferent signals contribute to the movement performance [65].

Thus, in patients with spasticity, in comparison with healthy subjects,
muscle activity is enhanced in the passive state, i.e., during the clinical exam-
ination, but is reduced during active natural movements. The spastic signs
observed during the clinical examination can therefore hardly be translated
to the movement disorder. Clinically, spastic signs are more pronounced in
damage of the spinal cord compared to a cerebral lesion. However, from a
pathophysiological point of view there exist only quantitative but no qualita-
tive differences.

6.2.3 Therapeutic Consequences

Exaggerated reflexes do little to contribute to the movement disorder that
impairs the patient. Nevertheless, most anti-spastic drugs are directed to
reduce the activity of short-latency reflexes mediated by group Ia fibres in

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146 Neurological Rehabilitation

order to reduce muscle stiffness. However, mobile patients require spastic
muscle stiffness to support their body during stepping to compensate for
paresis [61]. Therefore, anti-spastic drugs can accentuate paresis and conse-
quently can lead to a worsening of function. Similarly, some authors argue
that botulinum toxin type A is assumed to result in a largely cosmetic effect
on spastic signs without functional improvement [67,68], although this toxin
might reduce the activity of the intrafusal fibres [69,70]. Intrathecal baclofen
might also reduce hyperactive reflexes without producing significant weak-
ness [71–73]. In conclusion, therapeutic interventions in patients with spastic
paresis due to an incomplete SCI should be focused on the training, relearn-
ing, and activation of residual motor function [74,75], and the prevention
of secondary complications, such as muscle contractures [76]. Anti-spastic
drug therapy might predominantly benefit immobilised patients by reduc-
ing muscle stiffness and relieving muscle spasms [77], which might in turn
improve nursing care for these patients. In cases where function is ham-
pered by a focal imbalance of specific muscle groups resulting in movement
impairment or contracture, focal botulinum toxin is known to be effective
in improving pain, helping to avoid or to reduce contractures, and facilitat-
ing function. Its action is by a weakening and relaxation of muscle activity
resulting in a biomechanical change in the muscle’s function. It makes the
muscle amenable to stretching and lengthening in order to restore to some
extent the interaction of antagonists. Thus, in addition, the weakening of the
agonist allows to some extent a strengthening of the antagonist muscles and
thereby it is possible to restore some of the disturbed antagonistic balance
[78]. This is independent of mobility of the patient but will require at least
some mobility of the affected limb when targeting functional improvement.

In contrast, mobile patients can benefit from a functional arm and leg
(locomotor-) training, which is associated with a recovery of function [19,61].
In animal experiments it could be shown that afferent signals induced by the
functional training to spinal cord neurons below the lesion lead to a directed
neuroplasticity [79] that is associated with a physiological mode of limb mus-
cle activation. In contrast, according to this study, a lack of training of natural
movements leads to a chaotic sprouting associated with a neuronal dysfunc-
tion, which might hamper a successful regeneration in the future in chronic
SCI subjects [80]. The clinical consequence of a functional training in mobile
patients is that with the improvement of function during the course of train-
ing less spastic muscle stiffness is required for movement performance, i.e.,
a new equilibrium between improved mobility and less pronounced signs of
spasticity becomes established [61].

As a consequence it follows that, in mobile patients, anti-spastic medi-
cation can impede recovery of natural movements, as the performance of
natural movements requires some spastic muscle stiffness for compensation
of the paresis, i.e., lack of sufficient muscle activation [81]. Robotic devices
can support this repetitive training. They allow longer training times and
can provide useful feedback information to the patient about the course of

Page 311

300 Index

invasive, permanent methods,

invasive, reversible methods,

management strategy for stroke
patients with spasticity, 128

noninvasive treatment, 123–124
stroke patients, spasticity assessment in

about, 118–119
activity and participation, 121
body function and structure,

119–121, 119t, 120t
Stroke patients, spasticity assessment in

about, 118–119
activity and participation, 121
body function/structure, 119–121,

119t, 120t
Stroke Upper Limb Capacity Scale, 121
Strumpell-Lorrain syndrome, 237
Supraspinal control of spinal networks, 69
Surface electromyography (sEMG), 121
Surface neuromuscular electrical

stimulation, 123
Surgical treatment

intrathecal baclofen, 89–91
in MS, 195
neurotomy, 89
selective dorsal rhizotomy, 91–96, 95t
for TBI, 226–227

Symptomatic management, SCA, 262


Tardieu scale, 27, 243
Tardieu Score, 17, 212t
TBI, see Traumatic brain injury (TBI)
Tendon-lengthening procedures, 195
Tendon transfers, 128
Tenotomy, 195
Tetrahydrocannabinol (THC), 155
Tetraplegia, 160
Tibial nerve, 124, 126
Timed Up and Go Test, 121
Tizanidine, 40, 124, 152, 163, 182–183

about, 3, 4
altered, 9–12

Tone Assessment Scale, 102, 214
Tongue movements, 270

Tonic supraspinal inhibition, 31
Tonus, 3, 4

for learning, 70–71
physiological effects of, 150

Transcranial magnetic stimulation
(TMS), 193–194, 240

Transcutaneous electrical nerve
stimulation (TENS), 191–193

Transmission in group II pathways,

Traumatic brain injury (TBI)
biomechanical assessment, 214–216
brain injury complications on

spasticity, 209
clinical assessment, 212–214, 213t
clinical presentations, 207–209, 208t
contractures/spasticity on recovery,

management options

electrical stimulation, 218–219
focal therapies, 220–223
intrathecal therapies, 223–226, 226t
oral medications, 219
physical modalities, 216–217
stretching/casting for contracture

vs. spasticity management,

surgical interventions, 226–227
treatment modalities, 227

overview, 204–206
treatment goals, 209–212, 210t–212t

Treadmill training, 69
Trunk control, 108


Upper limb symptoms, 270
Upper motoneuron syndrome

spasticity in, 13–14
Upper motor neuron (UMN), 204, 236,

Utrecht Arm/Hand Test (UAT), 116, 116f


Velocity-dependent response, 10f–11f
Very late-onset Friedreich’s ataxia

(VLOFA), 267

Page 312


Visual Analogue Scaling, 121
Visual problems, 259


Walking difficulties, 249–252
Walking index in SCI (WISCI), 149
Walking Test, 121

Wallerian degeneration, 88, 142
Water therapy, 151
Whole-body vibration (WBV), 194
Wolff’s law, 85n


Zone of partial preservation, 141

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