The idea for the present volume grew from discussions that the four of us had among ourselves and with our colleagues at recent scientific meetings. All of us were impressed by the wealth of empirical data that was being generated by investigators interested in brain damage and recovery from both behavioral and biological orientations. Nevertheless, we were concerned about the relative paucity of attempts to evaluate the data provided by new technologies in more than a narrow context or to present new theories or reexamine time-honored ideas in the light of new findings. We recognized that science is guided by new technologies, by hard data, and by theories and ideas. Yet we were forced to conclude that, although investi� gators were often anxious to publicize new methods and empirical fmdings, the same could not be said about broad hypotheses, underlying concepts, or in� ferences and speculations that extended beyond the empirical data. Not only were many scientists not formally discussing the broad implications of their data, but, when stimulating ideas were presented, they were more likely to be heard in the halls or over a meal than in organized sessions at scientific meetings.

Contenuti

1 Toward a Definition of Recovery of Function.- 1. The Problem Defined.- 2. Definitions of Recovery of Function.- 3. Recovery or Behavioral Sparing?.- 4. Recovery or Compensation?.- 5. Recovery as Absolute and Inferential.- 6. Mechanisms of Recovery.- 7. Summary and Conclusions.- References.- 2 Neural System Imbalances and the Consequence of Large Brain Injuries.- 1. Introduction.- 2. Subtotal Lesions.- 2.1. Normalization and Recovery of Function.- 2.2. Some Limitations.- 3. Complete Lesions.- 3.1. Recovery without Normalization.- 3.2. The Nature of the Behavioral Deficit.- 3.3. Some Supporting Data.- 3.4. The Chronic Consequence of Large Injuries.- 4. Conclusions.- References.- 3 Bases of Inductions of Recoveries and Protections from Amnesias.- 1. Introduction.- 2. Training Effects.- 3. Drug Effects.- 4. Memory and Remembering.- 5. Controversial Issues.- References.- 4 Neural Spare Capacity and the Concept of Diaschisis: Functional and Evolutionary Models.- 1. Introduction.- 1.1. Intimations of Spare Capacity.- 1.2. Do Large Ablations More Readily Reveal Spare Capacity?.- 1.3. Evolutionary and Functional Puzzle of Spare Capacity.- 2. The Elements of Brain Information Processing Are Diffuse Domains.- 2.1. Unrealistic Aspects of Machine Metaphors and the Bugaboo Mosaic.- 2.2. Diffuse Domains Are Adequate for Maintaining Distinctions: A Metaphor of the Brain as an Immense Set of Counters.- 2.3. Von Monakow’s Concept of Diaschisis.- 2.4. Experimental Studies of Diaschisis.- 2.5. Diaschisis in the Model.- 2.6. Implications of the Model for Understanding Early Brain Damage.- 3. Error and Reliability when Large Numbers of Subsystems Interact.- 3.1. Introduction to Neuroeconomics: Costs and Benefits in the Natural Selection of Spare Neural Capacity.- 3.2. Two Types of Safety Factor: Reiteration (Redundancy) and Aiming High.- 3.3. Numerical Demonstration of the Importance of the Reiterative Safety Factor.- 3.4. Implications of the Numerical Demonstration for Ablation Research.- 3.5. Reiterations Are Unlikely to Comprise Large, Complex Units.- 3.6. Relevance of Research on Brain Size for the Safety Factor Hypothesis.- 3.7. Implications when There Is Additional Loss of Tissue.- 4. Five Possible Nonneural Preadaptations for Safety Factor.- 4.1. Developmental Heterochrony.- 4.2. The Head as a Releaser of Imprinting at Birth.- 4.3. The Visual Proportions of Infants as Affectional Releasers.- 4.4. A Large Head on a Large Body Is Fearsome rather than Cute.- 4.5. Surface/Volume Ratio in Thermoregulation.- 5. An Important Implication of Nonneural Natural Selection Factors for Neural Information Processing, Diaschisis, and Recovery.- 6. Summary.- References.- 5 Kurt Goldstein and Recovery of Function.- 1. Introduction.- 2. Methodological Assumptions and Empirical Origins.- 3. Theoretical Approach.- 4. Localization.- 5. Psychological Deficits following Brain Damage.- 6. Psychological Testing of Brain-Damaged Patients.- 7. Recovery and Rehabilitation.- 8. Significance for Neuropsychology.- References.- 6 Assumptions about the Brain and Its Recovery from Damage.- 1. Mechanisms of Brain Function.- 2. MacLean and the Triune Brain.- 3. Multiple Functions of Neural Systems.- 4. The Effects of Damage.- 4.1. Are Any Changes “Absolute”?.- 4.2. Motivational Changes following Brain Damage.- 5. Secondary Effects of Brain Damage.- 6. Residual Visual Abilities.- 7. The Extent of Stroke-Induced Damage.- References.- 7 Mass Action and Equipotentiality Reconsidered.- 1. Introduction and Historical Roots.- 2. Do We Need Mass Action and Equipotentiality?.- 2.1. Principles of Cortical Function.- 2.2. Principles of Behavior.- 3. Evidence of Recovery and Nonrecovery.- 3.1. Distinguishing between Getting Better and Recovery.- 3.2. Examining the Evidence for “Recovery of Function”.- 3.3. Recovery, Mass Action, and Equipotentiality.- 4. Conclusions.- References.- 8 Margaret Kennard and Her “Principle” in Historical Perspective.- 1. Introduction.- 2. Education and Background.- 3. Lesion Development and Motor Function.- 4. Historical Antecedents.- 5. Deficits following Early Lesions.- 6. Theoretical Formulations.- 7. Serial Lesions.- 8. Other Pursuits and Later Contributions.- 9. Conclusions.- References.- 9 Infant Brain Injury: The Benefit of Relocation and the Cost of Crowding.- 1. Introduction.- 2. The Relocation of Speech.- 2.1. The Phenomenon.- 2.2. Two Necessary Conditions for Speech Relocation.- 2.3. The Cost of Relocation: Crowding of Functions.- 2.4. Conclusions.- 3. Relocation of Functions and Crowding in Animals.- 3.1. Hemispheric Specialization and Asymmetry.- 3.2. Bilateral Brain Injury and Relocation.- 3.3. Infant Lesions and Compound Cue Discriminations.- 4. Some Final Comments.- References.- 10 Arguments against Redundant Brain Structures.- 1. Introduction.- 2. Too Much Brain.- 3. Neuronal Redundancy during Infancy.- 4. Restatement of Problem.- 5. The Motor System.- 6. The Visual System.- 7. The Auditory System.- 8. The Somatosensory System.- 9. Autonomic Functions.- 10. Comment.- References.- 11 Another Look at Vicariation.- 1. Vicariation: Relationship to Localization of Function.- 2. What Is Recovery?.- 3. Vicariation and Other Theories of Recovery.- 4. Attempts to Locate Recovered Function.- 5. Changing Concepts of Brain Function and Another Look at Vicariation.- 6. Conclusions.- References.- 12 Hughlings Jackson’s Theory of Localization and Compensation.- 1. Introduction.- 2. Some Aspect of Jackson’s Role in the Development of Modern Neurology.- 3. Jackson’s Theory of Localization and Its Derivative: Compensation.- 4. Critique: Historical and Contemporary.- 4.1. Time Frames.- 4.2. The Motor Model.- References.- 13 The Parcellation Theory and Alterations in Brain Circuitry after Injury.- 1. Introduction.- 2. Invasion.- 3. Overlap of Connections Is a Feature of Primitive and Developing Brains.- 4. Ontogenetic Parcellation.- 5. Cytodiversification.- 6. Experimentally Induced Sprouting and Accidental Brain Injury.- 7. Conclusion.- References.- 14 Trophic Hypothesis of Neuronal Cell Death and Survival.- 1. Introduction.- 2. Key Terms and Concepts.- 3. The Neuronotrophic Factor Hypothesis.- 4. Nerve Growth Factor: Its Presence and Competence in the CNS.- 5. Nerve Growth Factor’s Functional Roles in the CNS.- 6. Summary and Conclusions.- References.- 15 Sensory Cortical Reorganization following Peripheral Nerve Injury.- 1. Somatotopic Order in the Primary Somatosensory Cortex.- 2. Control of Somatotopic Order.- 3. Acetylcholine as a Permissive Agent for Neuronal Plasticity.- 4. Neuronal Responses following Deafferentation.- 5. The Effects of Acetylcholine on Neurons in Normal Somatosensory Cortex.- 6. Cellular Mechanisms.- 7. The Hypothesis.- 8. Summary.- References.- 16 Is Dendritic Proliferation of Surviving Neurons a Compensatory Response to Loss of Neighbors in the Aging Brain?.- 1. Introduction.- 2. The Aging Brain.- 3. Regressive Influences.- 4. Balance of Influences.- References.- 17 Practical and Theoretical lssues in the Use of Fetal Brain Tissue Transplants to Promote Recovery from Brain Injury.- 1. Introduction.- 2. Specificity of Neural Connections between Host and Transplant Tissue.- 2.1. Some New Experimental Tests of Transplant Specificity.- 2.2. Are Transplants Morphologically “Normal”?.- 2.3. Is Homologous Embryonic Tissue Required to Obtain Recovery?.- 3. Is There a Critical Postoperative Period for Transplant Effectiveness?.- 4. Do Trophic Factors Play a Role in Transplant-Induced Recovery?.- 4.1. Recovery Seems to Persist when Transplants Are Removed.- 4.2. Do Transplants Release or Stimulate the Production of Trophic Substances?.- 4.3. Glial Cells May Play an Important Role in Transplant-Mediated Functional Recovery.- 5. Systemic Injections of Trophic Factors Can also Promote Functional Recovery.- 6. Problems and Risks in Using Embryonic Brain Tissue Grafts for the Treatment of Brain Injury.- 7. Conclusions.- References.- 18 Functional Electrical Stimulation and Its Application for the Rehabilitation of Neurologically Injured Individuals.- 1. Early History of Electrical Stimulation in Medicine.- 2. Recent History of Functional Electrical Stimulation for Patient Therapy in Spinal Cord Injury.- 3. Functional Electrical Stimulation.- 4. An Isokinetic Muscle Exerciser for Strength Training.- 5. An Aerobic Exercise Bicycle for Endurance Training.- 6. Physiological Changes and Physical Conditioning Responses to FES-Induced Active Physical Therapy.- 6.1. Background Information.- 6.2. Functional Electrical Stimulation as a Therapeutic Modality.- 6.3. Cardiovascular Responses.- 6.4. Thermoregulatory Responses.- 6.5. Muscular Response.- 7. Functional Electrical Stimulation and Walking.- 8. Summary.- References.- 19 Recovery of Language Disorders: Homologous Contralateral or Connected Ipsilateral Compensation?.- 1. Introduction.- 2. Right Hemisphere Compensation.- 3. Ipsilateral Structural Compensation.- 4. Factors in Recovery from Aphasia.- 4.1. Initial Severity.- 4.2. Time from Onset.- 4.3. Etiology.- 4.4. Lesion Size.- 5. Variations in Language Laterality and Anatomic Asymmetry.- 6. Conclusions.- References.- 20 Sensory Substitution and Recovery from “Brain Damage”.- 1. Introduction.- 2. Sensory Substitution.- 2.1. Vision Substitution.- 2.2. Tactile Auditory Substitution.- 2.3. Cutaneous Sensory Substitution in Leprosy Patients.- 2.4. Braille and Sign Language.- 2.5. Electromyographic Sensory Feedback.- 3. Physiological Considerations.- 3.1. Peripheral Factors.- 3.2. Central Nervous System Factors.- 4. Perceptual Considerations.- 5. Practical Considerations.- 6. Conclusions.- References.- 21 Emotion and Motivation in Recovery and Adaptation after Brain Damage.- 1. Introduction.- 2. Arousal, Emotion, and Motivation after Brain Damage.- 3. Some Clinical Examples of the Importance of Emotion and Motivation in Recovery after Brain Damage.- 4. The Problem of Motivation in Neurological Rehabilitation and the Limits of the Damaged Neurological System.- 5. The Relative Importance of Frontal Lobe Injury versus Temporal Lobe Injury for Recovery of Emotional and Motivational Deficits.- 6. A Note about Awareness and Its Importance in Psychiatric and Neurologically Oriented Therapies.- 7. Summary and Conclusions.- References.- 22 Recovery of Function: Sources of Controversy.- 1. Introduction.- 2. Assessing the Functional Organization of the Brain.- 3. Variability and the Concept of “Normative” Performance.- 4. Multiple Brain Changes and Causality.- 5. Recovery and the Null Hypothesis.- 6. Conclusions.- References.

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