Efnisyfirlit

• Cover
• Half Title Page
• Series Page
• Title Page
• Copyright Page
• Contents
• Editors
• Contributors
• 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
• 1.2.2.1 Increased (Hyper-Excitable/Exaggerated) Reflexes
• 1.2.2.2 Spasms and Clonus
• 1.2.2.3 Altered Tone or the Response of a Relaxed Muscle to an Externally Imposed Stretch
• 1.2.2.4 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
• References
• 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
• 2.5.3.1 Presynaptic Inhibition
• 2.5.3.2 Post-Activation Depression
• 2.5.4 Transmission in Group II Pathways
• 2.5.5 Pathophysiological Role of Changes in Postsynaptic Inhibition of Motoneurons
• 2.5.5.1 Disynaptic Reciprocal Ia Inhibition
• 2.5.5.2 Recurrent Inhibition
• 2.5.5.3 Autogenetic Ib Inhibition
• 2.5.5.4 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
• References
• 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
• References
• 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
• 4.4.1.1 Benzodiazepines
• 4.4.1.2 Oral Baclofen
• 4.4.1.3 Gabapentin and Pregabalin
• 4.4.2 Injection Therapies
• 4.4.2.1 Botulinum Toxin
• 4.4.2.2 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
• 4.6.3.1 Case Study
• 4.7 Conclusion
• References
• 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
• References
• 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
• References
• 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
• 7.5.1.1 Treatments for Generalised Spasticity: Oral Medications
• 7.5.1.2 Baclofen
• 7.5.1.3 Tizanidine
• 7.5.1.4 Dantrolene
• 7.5.1.5 Gabapentin
• 7.5.1.6 Cannabinoids
• 7.5.1.7 Benzodiazepines
• 7.5.1.8 Evidence-Based Guidelines for Oral Antispasticity Medications: Spanish and German Consensus Document
• 7.5.1.9 Treatments for Focal Spasticity
• 7.5.1.10 Phenol Chemodenervation
• 7.5.1.11 Botulinum Toxin
• 7.5.1.12 Intrathecal (IT) Baclofen
• 7.5.2 Non-Pharmacological Treatments
• 7.5.2.1 Physical Activity/Exercise for the Management of Spasticity in MS
• 7.5.2.2 Transcutaneous Electrical Nerve Stimulation (TENS) for the Management of Spasticity in MS
• 7.5.2.3 Transcranial Magnetic Stimulation for the Treatment of Spasticity in MS
• 7.5.3 Other Non-Pharmacological Interventions for the Management of Spasticity in MS
• 7.5.3.1 Surgery
• 7.5.4 Strategy for the Management of Spasticity in MS
• References
• 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
• 8.7.5.1 Botulinum Toxins
• 8.7.5.2 Case 2
• 8.7.5.3 Phenol and Alcohol Neurolysis
• 8.7.6 Intrathecal Therapies
• 8.7.7 Surgical Interventions
• 8.7.8 Controversial and Promising Treatments
• References
• 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
• 9.2.3.1 Cellular Changes
• 9.2.3.2 Changes in Descending and Ascending Tract Function
• 9.2.3.3 Changes in Cortical Activation with Movement
• 9.2.4 Symptoms Associated with HSP
• 9.2.4.1 Limb Stiffness
• 9.2.4.2 Paresis
• 9.2.4.3 Sensory Loss
• 9.2.4.4 Bladder
• 9.2.4.5 Bony Changes
• 9.2.4.6 Fatigue
• 9.2.4.7 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
• 9.2.9.1 Pharmacological and Surgical Treatment of Spasticity
• 9.2.9.2 Physical Interventions
• 9.2.9.3 Service Delivery
• 9.3 Spinocerebellar Degenerations
• 9.3.1 Autosomal Dominant
• 9.3.2 SCA3 or Machado-Joseph Disease
• 9.3.2.1 Symptomatic Management
• 9.3.3 Autosomal Recessive
• 9.3.4 Friedreich’s Ataxia and Late-Onset Friedreich’s Ataxia
• 9.3.4.1 Management of FDRA
• 9.3.4.1.1 Co-enzyme Q10 and Idebenone
• 9.3.4.1.2 Symptomatic Management
• 9.4 Motor Neuron Disorders and Familial Amyotrophic Lateral Sclerosis
• 9.4.1 Amyotrophic Lateral Sclerosis
• 9.4.1.1 Prevalence and Genetics
• 9.4.1.2 Pathology
• 9.4.1.3 Clinical Presentation
• 9.4.2 Interventions
• 9.4.2.1 Disease-Modifying Therapy
• 9.4.2.2 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
• References
• Index