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280524173X

DOES CEREBRAL MALARIA CONSTITUTE A RISK FACTOR FOR SPECIAL EDUCATIONAL NEEDS?

Penny Anne Holding

Thesis submitted for the Degree of Doctor of Philosophy

1997

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ProQuest Number: 10014389

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ABSTRACT

In a malarial endemic area it is pre-school children who are at most risk of developing cerebral malaria. This study was designed to increase the understanding of the expected outcome for survivors through investigating both

cognitive and behavioural aspects of development.

A broad assessment battery was developed, taking into account both potential neurological impairments, and the particular social and cultural background of the children being assessed. Tasks, adapted from the Kaufman Assessment Battery for Children, and measuring information processing skills formed the core. The battery also included measures of attention, visuo-motor speed, language, and behaviour. Modifications were made to all the tests used, following assessment of the reliability and validity of the tools within the study population.

A matched pairs design was applied, each "case" being matched on age; sex; and measures of socio-economic and nutritional status. The 87 pairs were assessed at 6 years old, (approximately 50 months post discharge). An investigation was made of the symptoms of the acute stage of the disease, to determine if there were any distinctive characteristics associated with poor outcome.

Results on the information processing battery showed no impairments in performance for the majority of children, although a significantly greater number of cases had an impaired performance. This sub-group were identified as in need

of specialist educational facilities. A combination of coma; hypoglycaemia; and fits provided the best-fit predictive model for membership of the impaired sub­ group.

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cases and controls. This combination of deficits is suggestive of an immaturity in the development of survivors, which, if it should continue, may place these children at risk of educational difficulties at higher levels of schooling, when tasks

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ACKNOWLEDGEMENTS

It would not have been possible to plan, execute, nor complete this study without

the support and advice which has been so freely offered to me, and for which I am extremely grateful. My most particular thanks g o t o :

• The assessment team: Sidi, Khamis, Thadeus, Joseph, Leonard, Bernard and Mzee Magongo.

• My other colleagues at KEMRI-Wellcome, Kilifi for their technical assistance, advice, and patience. Most especially the inspirational guidance of Kevin Marsh.

• Psychologists and child development specialists around the world who have responded to my queries with useful suggestions and guidance. Not least of which has been Alan Kaufman, for his support of my use of his assessment battery; Michael Boivin, who provided a great deal of information on his African studies; and Jane Kvalsvig, who shared insight into the contextual details of research in Africa.

• The Behavioural Sciences Unit at ICH for providing me a home.

• My family, both close and extended, for their continued support throughout the ups and downs of this research.

• Jim Stevenson, whose insightful and stimulating supervision has made it all

possible.

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CONTENTS

Page

SECTION 1 : INTRODUCTION. BACKGROUND AND THEORETICAL FRAMEWORK

A: Introduction 26

Chapter 1 : The Elements of the Study 27

Chapter 2: Malaria: the disease and the implications 29 for cognitive development

The relationship of transmission to morbidity 31

Cerebral Malaria 33

C.M.: The impact on survivors 34

C.M.: The impact on the community 34

C.M.: A continuum of deficits? 35

C.M.: Measuring the nature and extent 33

of impairment

B: Cognitive Development And Cognitive Impairment: 38 The Theoretical Framework

Chapter 3: Cognitive Development - A Vygotskian Framework 39

Stages of Development 39

Functional Systems 40

Agents of Change 41

The Socio-Historical Context Of Learning 42

The Process of Development 43

Thought and Speech 46

The Development of Concepts 47

The Specific Influence Of Literacy 49

And Schooling

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Page The socio-cultural influence on impairment 49

Capacity and Performance 51

Vygotsky and malaria 52

Summary and Implications 52

Chapter 4: Luria's Neural Base to Cognitive Functioning 54

The Roots of Development 54

Equipotentiality versus Localisation 55

Assessment and Syndrome Analysis 56

Syndrome analysis: a case study 57

Models of Functional Systems, and Models of Development 57

The Two Forms of Synthesis or Processing 58

The Three Principal Functional Units Of The Brain 59 The hierarchical structure of functional units 60

The laws governing cortical maturation 61

Normal and Abnormal Development 62

Dynamic Development 63

Summary and Implications 64

Chapter 5: The Information Integration Model 66

The Coding Component 66

Simultaneous Processing 68

Successive Processing 69

Examples of Assessment Materials 69

Determinants of the selection of processing strategy 69

age/developmental stage 70

the influence of the socio-cultural environment 71

Information processing, achievement and schooling 72 Application versus slection of processing strategies 72

The Attention Component 73

The Planning Component 73

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Page

Validity of the Model 74

Application Of The Model To The Understanding Of Impaired Performance 77

Summary and Implications 78

C: The Relationship Between Cognitive Function And Disease 80

Chapter 6: Cerebral Malaria: The Potential Mechanisms 81

Cerebral Insults 81

Coma 81

Fits/Seizures 82

Hyperpyrexia 85

Hypoglycaemia 85

The Evidence Of Other Encephalopathies 86

Reye's Syndrome 87

Meningitis 88

General Health and Development 92

Other parasitic infections 92

Nutrition 95

Malnutrition 95

Anaemia/iron deficiency 96

Other nutritional deficiencies 98

Summary 98

Chapter 7: Predicting Impairment and Recovery 100

Predicting Impairment 101

The site of the lesion and the localisation of brain function 101 The age of onset: early plasticity versus early vulnerability 103

Gender 105

Stages of Development - A theoretical model for the prediction of 105 impairment

Influences Upon Recovery 108

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Page

A threshold of damage 109

Vulnerability of functions 109

Socio-economic status 111

Other environmental influences 114

The Threshold Hypothesis 116

Summary ' 119

Chapter 8: A Summary of the Implications for 120

the Study of Cerebral Malaria

Cerebral Insults 120

Coma 121

Fits/Seizures 121

Hypoglycaemia 122

Hyperpyrexia 123

Malnutrition 123

Anaemia 124

Other Parasitic Infections 125

Socio-Economic Status 125

Summary and Development of Hypotheses 126

SECTION 2: THE METHODOLOGY AND ITS DEVELOPMENT 129

Chapter 9: Assessment in Context: culture, cognition and assessment 130

Standardised Tests: strengths and weaknesses 130

The Issue of Test Bias 132

Culture Free Assessments 135

“The Developmental Niche” 138

The physical and social setting in which the child lives 138

Dynamic Assessment 141

The physical and social setting in which the child lives (cont.) 144

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Page

Specific linguistic environment 148

Customs of child care 149

The psychology of the caretaker 151

Test Format and Test Procedure: accounting for culture 153

Chapter 10: Familiarisation , 155

The Observation and Sampling of Behaviours and Activities 155 Assessing Different Materials and Presentations 156

Assessing an Appropriate Level of Difficulty 156

Chapter 11 : The Main Pilot Study 157

The Assessment Team 157

Content of the Assessment Battery 157

Procedure 158

Subjects 159

Results 159

Description of the subject group 159

Family Background Interview 160

Chapter 12: Information Processing- The K-ABC and the Kilifi Battery 162

Description of the Battery of Sub-Tests 163

Simultaneous Scale 163

Magic Window 163

Face Recognition 164

Gestalt Closure 164

Matrix Analogies 164

Triangles/Construction 164

Sequential Processing Scale 165

Hand Movements 165

Number Recall 165

Word Order 165

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Page

Arithmetic 166

Pilot Study of Kilifi Simultaneous-Sequential Sub-tests 166

Procedure 166

Results 167

Practice Effects 171

Goals of the K-ABC ' 171

The Theoretical And Research Basis And The Definition Of Intelligence 172

Studies of construct validity 174

Evidence from the interpretive manual 174

The verbal component 175

The attention component 179

Developmental differences in factor structure 180

Cross-cultural validation 181

The Laotian Study 182

The Zairian Study 183

Educational Implications 184

Predictive Validity 184

Appropriate Redemption: Aptitude-Treatment-lnteraction 185

Dealing with Novelty 187

Sensitivity to Different Groups of Children 188

Issues of Design 188

Summary and Conclusions 189

A more complete test battery 191

Chapter 13: Achievement 192

Arithmetic 192

Rhyming and Alliteration 193

Chapter 14: Attention 196

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Page

Intervention and Remediation 202

The Evidence of Specific Disorders of Attention 203

Attention deficit disorders 203

Acquired brain disorders 205

Epilepsy and seizure activity 206

Meningitis ' 207

Traumatic brain injury 207

The Selection of An Attention Task 208

Task Description and Development 209

Chapter 15: Planning/Adaptive Intelligence 211

Problem Solving 212

Chapter 16: Relative Hand Skill and Developmental Disorders 214 The Development of Handedness , the Normal and the Pathological 214

The Right Shift Theory of Handedness 215

Is Left-Handedness Pathological 216

Relative Hand Skill and Cognitive Impairment 217

Speed and Cognitive Impairment 218

Task Description and Development 218

Pilot study pegboard 218

Main study pegboard 219

Chapter 17: Speech and Language Development 220

Development of the Language Assessment 225

Stage 1 : Pre-pilot study 225

Stage 2: Pilot study 225

Stage 3: Final procedure 226

Language Comprehension 226

Expressive Language 228

The expressive language checklist 230

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Page

Discourse Analysis and Pragmatic Errors 231

The measurement of pragmatic errors in the current context 234

Assessing the semantic level 236

Assessing the syntactic level 237

Assessing the phonological level 238

Summary " 239

Chapter 18: Behaviour 241

Introduction 241

Why is the Investigation of Behaviour Important ? 243

Persistence of Behaviour Problems 246

Risk Factors Associated with Onset and Persistence 246

Approaches to the Analysis of Behaviour 248

How Context Specific are Behaviour Measures? 249

What Constitutes a Behavioural Problem? Issues of culture and age 251

Prevalence of Behavioural Disorders 252

Sex Differences 253

Sampling Techniques: Which method to use? 254

Development of the Kilifi Behavioural Assessment 257

The Behaviour Questionnaire for Parents 257

Initial pilot work 257

Procedure 257

Main pilot study results 259

Behavioural observations 260

Main pilot study results 261

Chapter 19 Health Screening 263

Current Nutritional Status 263

Development of the procedure 263

Hearing 264

Otoscopic screening 264

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Page

Pure tone audiometry 264

Vision 264

Inspection 265

Screening for visual acuity 265

Screening for visual field 265

SECTION 3: DEVELOPMENTAL SEQUELAE OF MALARIA: THE MAIN

STUDY 266

Chapter 20: Main Study: Outline And Procedures 267

The Assessment Team 267

Subjects and Matching 267

Inclusion Criteria 268

Exclusion Criteria 268

Sample Size 269

Matching 269

Content 270

Procedure 271

Health screening 271

Assessment sessions 272

Analysis of Results 273

Chapter 21 : Background Details: Comparing CASES and CONTROLS 274

Sample Size for Analysis 274

Part 1 : Matching 274

Combined level of matching 274

Verification of matching 276

Summary 281

Part 2: Background Details at the Time of Follow Up 281

Socio-economic measures 281

Family composition and schooling 282

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Page

Employment and income source 284

Developmental history 287

Health status, past and present 288

Summary 292

Chapter 22: Health Screening Assessment 293

Nutritional status 293

Hearing 293

Sight 294

Chapter 23: Investigations of Procedure and Methodology 296 Factor Structure of the Kilifi Assessment Battery 296

Nutritional Status and Performance 299

Test Performance and Environmental Indicators 301

School experience 301

Gender differences 302

Mother can speak English 304

Family school index 305

Others : a summary table 306

Assessor Effect Upon Test Performance 306

Behavioural Measures 308

Chapter 24: Description of the Performance on 311

the Assessment Battery

Information Processing 311

Achievement 312

Attention/Planning 312

Visuo-Motor Speed 313

Language 313

Behaviour 314

Test taking behaviour 314

Parental report of behaviour in the home 314

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Page

Summary 315

Chapter 25: Differences in Performance 316

Information Processing 316

Achievement 318

Attention/Planning - 318

Visuo-Motor Speed 318

Language 318

Behaviour 320

Observation of test taking behaviour 320

Parental report of behaviour in the home 320

Summary 321

Chapter 26: Comparison Of The Pattern Of Performance 322 Between Cases and Controls

Impaired Performance, and the Comparison of “Outliers”. 322

Information processing 328

Handedness 329

Attention/Planning 329

Language 330

Behaviour 332

Gender 334

Summary 334

Chapter 27: The Composition of the Impaired Case Group 336

The Performance Profile 336

Looking at possible gender effects 338

Predicting Group Membership from Clinical Variables 339 Predicting Group Membership from Neurological Impairment on Discharge 341 Protection and Risk : Socio-Environmentai and General Health Factors 342

Matching variables 342

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Page

Summary of Results 344

Chapter 28: Discussion 347

Introduction 347

A: Describing the Pattern of Impairments Found 347

Summary of results 347

Behaviour 350

Parental rating 350

Gender 351

Test session behaviour 352

Language 354

Attention/Planning 356

Concluding the Evidence on Group Differences 358

B: Predicting Outcome from the Severity of the Damage 361

Neurological Impairment on Discharge 362

Other Clinical Variables as Predictors 363

Coma 363

Hypoglycaemia 364

Seizures 365

Hyperpyrexia 366

Parasitisation/summary on other clinical variables 367 The Association Between Clinical Variables and Cognitive 367 Impairment : The best fit predictive model

Factors Affecting Vulnerability and Protection 369

Pre-insult history 369

Nutritional status 370

Conclusion to pre-insult investigations 371

Age of onset 372

Gender 373

Post insult factors influencing outcome 374

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Page

Family size 374

School attendance 374

Income and social environmental measures 376

General health 377

Sensory impairment 378

Conclusion to post-insult investigations 378

General Summary of Case Group Analysis 379

0: Methodological Issues 380

Construct validity 380

Simultaneous/Sequential 380

Planning/Attention 381

Achievement 382

The third factor 382

Test of speed 382

Language 383

Behaviour 383

Predictive validity 384

Gender 385

An evaluative summary 386

Summary and Conclusion on the Kilifi Assessment Battery 387

Chapter 29: Summary, Conclusions And Implications For Future 389 Research

Future Research 391

References 393

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APPENDICES

Appendix 1

Appendix 2

Appendix 3

Appendix 4

Appendix 5

Appendix 6

Appendix 7

Appendix 8

Appendix 9

Description of Pragmatic Errors

Expressive Language Checklist

Parent Questionnaire

Key to Behavioural Observation

Box Plots of Raw Scores

Bar Charts of Raw Scores, showing outliers

Distribution of Performance Llevels, standard deviation groups

Blantyre Coma Scales

Examples of Assessment Materials Record Booklet

Gestalt Closure drawings

Verbal Comprehension drawings Construction- drawings

Visual Search sheets (word order stimuli) Instruction Sheets

Page

430

432

435

438

441

443

445

448

449

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TABLES AND FIGURES

Page

Figure 1.1 The parasite in the human host 29

Figure 1.2 Malaria, the progression to death 31

Table 5.1 Results of confirmatory factor analysis on PASS model 75

Figure 7.1 Categories of impairment 100

Figure 7.2 Brain reserve capacities and the threshold hypothesis 117 Figure 8.1 Hypothetical distribution of performance 126

Table 12.1 Pilot study results: Magic Window 167

Table 12.2 Pilot study results: Face Recognition a 167 Table 12.3 Pilot study results: Face Recognition b 168

Table 12.4 Pilot study results: Gestalt Closure 168

Table 12.5 Pilot study results: Matrix Analogies a 168 Table 12.6 Pilot study results: Matrix Analogies b 169

Table 12.7 Pilot study results: Construction a 169

Table 12.8 Pilot study results: Construction b 169

Table 12.9 Pilot study results: Hand Movements a 170 Table 12.10 Pilot study results: Hand Movements b 170

Table 12.11 Pilot study results: Number Recall 170

Table 12.12 Pilot study results: Word Order simple 171 Table 12.13 Pilot study results: Word Order interference 171

Table 12.14 Construct validity : K-ABC 174

Table 12.15 Construct validity :Kilifi Battery 175

Table 12.16 Construct validity :The verbal component 177 Table 12.17 Inter-correlations- K-ABC vs. WISC-R 178 Table 12.18 Construct validity :The attention component 180

Table 12.19 Construct validity : Laotian Study 183

Table 12.20 Construct validity : Zairian Study 184

Table 13.1 Pilot study results: Arithmetic 193

Table 13.2 Pilot study results: Rhyming 194

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Table 13.3b Pilot study results: Alliteration b

Table 14.1 Pilot study results: Attention Table 16.1 Pilot study results: Pegboard one Table 16.2 Pilot study results: Pegboard two

Table 17.1 Pilot study results: Verbal Comprehension Table 17.2 Pilot study results: Syntax

Table 17.3 Pilot study results: Articulation

Figure 18.1 Quay’s categories of behaviour disorders Table 18.1 Test Session Observation Schedule results Figure 21.1 Level of matching

Figure 21.3 Age at admission: Cases Figure 21.4 Age at admission: Controls Figure 21.5 Time since admission: Cases Figure 21.4 Time since admission: Controls Table 21.1 Age at time of assessment Table 21.2 Matching variables: malnutrition Table 21.3 Matching Variables: malnutrition Table 21.4 Matching variables: mother’s English Table 21.5 Matching variables: mother’s English

Table 21.6 Matching variables: mean corpuscular volume Table 21.7 Matching variables: mean corpuscular volume Table 21.8 Matching variables: mother’s occupation Table 21.9 Matching variables: mother’s occupation Table 21.10 Matching variables: mother’s schooling

Table 21.11 Matching variables: mother’s schooling Table 21.12 Matching variables: hookworm density Table 21.13 Matching variables: hookworm density

Table 21.14 Matching variables: mid-upper arm circumference

Table 21.15 Matching variables: mid-upper arm circumference Table 21.16 Family composition and schooling

Figure 21.6 Level of School Attendance

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Page

Table 21.17 Main caretaker 283

Table 21.18 Main caretaker cross-tabulation 283

Table 21.19 Contact with father 283

Table 21.20 Contact with father: cross-tabulation 283 Table 21.21 Households with only one language used 284

Table 21.22 Languages spoken to the child 284

Table 22.23 Languages spoken by the child 284

Table 21.24 Mother’s current occupation 285

Table 21.25 Mother’s current occupation: cross-tabulation 285

Table 21.26 Father’s occupation 286

Table 21.27 Father’s occupation-reduced categories 286

Table 21.28 Main source of family income 286

Table 21.29 Main source of family income-reduced categories 286

Figure 21.7 Developmental milestones 287

Table 21.30 Crying at birth 288

Figure 21.8 Age at weaning 288

Figure 21.9 Hospital admissions: controls 289

Table 21.31 Length of stay in hospital 290

Table 21.32 Fits/Seizures 290

Table 21.33 Kwashiorkor 291

Figure 21.10 Current health status 291

Table 22.1 Mid-upper arm circumference at assessment 293

Figure 22.1 Outcome of hearing screening 294

Figure 22.2 Outcome of acuity screening 295

Table 23.1 Kilifi Battery - Six factor solution 297 Table 23.2 Kilifi Battery - Three factor solution 298 Table 23.3 MANOVA - simultaneous processing vs. nutritional status 300

Table 23.4 MANOVA - sequential processing vs. nutritional status 300 Table 23.5 MANOVA - co-operation factor vs. nutritional status 300

Table 23.6 MANOVA-current nutritional status 300

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Page

Table 23.8 MANOVA - sequential processing vs. school attendance 302 Table 23.9 MANOVA - co-operation factor vs. school attendance 302 Table 23.10 MANOVA - simultaneous processing vs. gender 303

Table 23.11 MANOVA - sequential processing vs. gender 303 Table 23.12 MANOVA - co-operation factor vs. gender 303 Table 23.13 Comparison of group means for gender groups 304 Table 23.14 MANOVA - simultaneous processing vs. English spoken 304 Table 23.15 MANOVA - sequential processing vs. English spoken 305 Table 23.16 MANOVA - co-operation factor vs. English spoken 305 Table 23.17 MANOVA - simultaneous processing vs. family school index 305 Table 23.18 MANOVA - sequential processing vs. family school index 306 Table 23.19 MANOVA - co-operation factor vs. family school index 306

Table 23.20 MANOVA- a summary table 306

Table 23.21 Assessor by Group 307

Table 23.22 MANOVA - simultaneous processing vs. assessor 307 Table 23.23 MANOVA - sequential processing vs. assessor 307 Table 23.24 MANOVA - co-operation factor vs. assessor 307 Table 23.25 Comparison of Test Scores by assessor 308 Table 23.26 Factor reduction on observational measures 308 Table 23.27 Correlations between behaviour measures 310

Table 24.1a Simultaneous Processing Scale 311

Table 24.1b Sequential Processing Scale 311

Table 24.2 Achievement 312

Table 24.3a Attention - raw scores 312

Table 24.3b Attention - composite scores 313

Table 24.4 Visuo-Motor Speed 313

Table 24.5 Language Measures 314

Table 24.6a Behavioural observation 318

Table 24.6b Behaviour questionnaire 315

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Table 25.3 MANOVA - information processing scales

Page 317

Table 25.4 MANOVA - language measures 318

Figure 25.1a Syntax 319

Figure 25.1b Semantics 319

Figure 25.1c Articulation 320

Table 25.5 Expressive language ratings 320

Table 25.6 Behaviour observation 320

Figure 26.1 Outliers by sub-test 323

Table 26.1 Significance tests of proportion of outliers 323

Figure 26.2 Outlier scores 324

Table 26.2 Levels of cognitive impairment 324

Figure 26.3 Gentile ranks: Visuo-Motor Speed 325

Figure 26.4 Gentile ranks: Arithmetic 325

Figure 26.5 Gentile ranks: Gonstruction 325

Figure 26.6 Gentile ranks: Face Recognition 326

Figure 26.7 Gentile ranks: Gestalt Glosure 326

Figure 26.8 Gentile ranks: Matrix Analogies 326

Figure 26.9 Gentile ranks: Magic Window 326

Figure 26.10 Gentile ranks: Hand Movements 327

Figure 26.11 Gentile ranks: Number Recall 327

Figure 26.12 Gentile ranks: Word Order 327

Figure 26.13 Gentile ranks: Verbal Gomprehension 328

Figure 26.14 Box plot: difference score 328

Table 26.3 Balance between information processing scales 329

Table 26.4 Balance between scale scores 329

Table 26.5 Attention: difference in error types 330

Figure 26.15 Gentile ranks: attention/planning 330

Figure 26.16 Pragmatic errors by type: cases 331

Figure 26.17 Pragmatic errors by type: controls 331

Figure 26.18 Behaviour questionnaire composite score 332

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Table 26.7 Correlation between performance and behaviour

Page 334

Table 26.8 MANOVA: case/control by gender 334

Figure 27.1 Outliers by sub-test: performance measures 336

Figure 27.2 Outliers by sub-test : ratings 337

Figure 27.3 Gender distribution outliers by performance measures 338 Figure 27.4 Gender distribution outliers by ratings 338

Table 27.1 Clinical variables 339

Table 27.2 Univariate analyses of clinical variables 340

Table 27.3 Best prediction logistic regression model 341 Table 27.4 Neurological impairment and cognitive impairment 342 Table 27.5 Matching variables - significance levels 343 Table 27.6 Background measures - significance levels 345

Figure 27.5 Outcome - death 345

Figure 27.6 Outcome - cognitive impairment 345

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SECTION 1: INTRODUCTION. BACKGROUND AND THEORETICAL FRAMEWORK

A: INTRODUCTION

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CHAPTER 1: THE ELEMENTS OF STUDY

This study investigates the link between brain insult, cognitive development and the measurement of cognitive ability, particularly as it relates to the impact of

cerebral malaria.

Cerebral Malaria is a severe form of malarial disease which has been associated with the development of gross neurological impairments in up to 20% of survivors. It is the most common acute encephalopathy in children in Africa, and possibly in the world. Yet, prior to the inception of this study there was no published literature on the effect on the longer term cognitive development of affected children. Thus little information exists regarding either the nature or degree of any cognitive impairments associated with cerebral malaria (C.M.). An understanding of the extent of the impact of C.M. on cognitive development, and the nature and persistence of associated cognitive deficits, would aid a) the allocation of appropriate educational resources, and may aid b) the clinical management of affected children.

Following an introduction to malarial disease. Section One provides details of a theoretical framework to the investigation, which attempts to pull together the disparate strands involved. This is supplied by a synthesis of two strongly connected theoretical approaches, those of Vygotsky and Luria. There are a number of features of their work which make it appropriate to the current context. Firstly, they provide a theory of intelligence and cognitive development which link

the biological and the cultural. Secondly, whilst their primary focus is on normally occurring developmental processes, they also examine the effects of possible disruptions and interventions on the process of development. Their theoretical approaches also provide direct guidelines for assessment, but these will be

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measurement process , but also to provide a framework for the interpretation of results.

The methodology required to answer the question "Does cerebral malaria constitute a risk factor for special educational needs?" has to take into account two extremely important issues. One concerns the nature of the disease itself, such that the measurements applied are sensitive to the possible impact of cerebral malaria. To provide such guidelines it was thus necessary to turn to the literature spanning a wide range of related topics, including that on malarial disease; other brain diseases and insults; and issues related to the risk factors for cognitive sequelae of brain insult in childhood. Each of these topics will be looked at in turn in chapters six to eight, in a section entitled ‘The relationship between cognitive function and disease”.

Having identified the cognitive functions which may be affected, the second issue, as it is impossible to isolate the investigation from the socio-cultural context of the disease, concerns the selection of assessment material appropriate within the particular cultural setting. This required the development of a test battery for use with the current study population. The work involved constitutes the first half of this study. Section 2: ‘The methodology and its development” reports the background to, and the results of, the test battery development.

Section 3 deals with the application of this battery to the assessment of the impact of cerebral malaria upon subsequent development. Conclusions are then drawn regarding the management of affected children both subsequent to the disease episode, and during the illness itself.

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CHAPTER 2 MALARIA: THE DISEASE AND THE IMPLICATIONS FOR COGNITIVE DEVELOPMENT.

"Such is the gravity of the maiaria problem in some countries, that not only is the health of the population threatened, but also the social and economic development of the communities. " (Phillips 1983 p 1 )

Malaria is a pathogenic parasite transmitted to humans via mosquito bites.

'■"V

LIVER

When, and if, the parasite multiplies it enters

RED BLOOD CELLS

Haemolysis releases the stage of parasite capable of infecting new

li

RED BLOOD CELLS

SEQUESTRATION

Infected RBC’s adhere to cell linings of the internal organs, causing

li

REDUCED FLOW OF BLOOD and thus of oxygen and glucose

Figure 1.1 The Parasite In The Human Host

There are four malaria parasites which can infect humans; Plasmodium

falciparum, vivax, ovale, and malarias. The following discussion will concentrate upon the malaria parasite Plasmodium falciparum because the majority of severe, life threatening, complications occur as a consequence of P.falciparum

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estimates that there are 1-2 million malaria related deaths a year, the vast majority being in children aged 1-5 years (Warrell et al 1990), with about 90% of

P.falciparum related deaths concentrated in sub-Saharan Africa (World Bank 1993). Annual malaria related mortality rates in children are cited as being

between 24 per thousand in Zaire to 12 per thousand in Nigeria (Molyneux et al. 1989). Studies in the Kilifi District of Kenya have shown a minimum mortality rate of 1.1 per thousand in the under fives, based upon hospital records. However, as only 20% of all deaths were found to occur in hospital, the malaria mortality rate in the community is likely to be much higher (Snow et al 1993).

As with mortality, morbidity rates are difficult to measure accurately as the majority of endemic areas are rural, although the scale of the problem can also be estimated through hospital records (Greenwood et al 1991). For example in The Gambia 45% of all paediatric admissions were found to be related to

P.falciparum malaria (Brewster et al 1990). In coastal Kenya a study of 7538 paediatric admissions over a period of 2.5 years detected P.falciparum in the peripheral blood films of 40% of these children, with 25% of admissions recieving a primary diagnosis of malaria (Marsh et al 1995). Hospital surveilance in Kilifi, Kenya also looked at the incidence rate for under fives, of severe malaria by geographical origin of admissions, with rates as high as 46 per thousand recorded (Snow et al 1993).

In endemic areas it is not unusual to find 100% of the population infected with the malaria parasite, although this is not matched by the same levels of morbidity or mortality (Marsh 1992). High levels of malaria parasitaemia in the individual are associated with disease, but the relationship is not linear. It is not certain what causes the infection to turn to disease, or even what makes the disease take on

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be rapid, taking between 1-3 days (Greenwood et al 1987). Severe disease is characterised by one, or a combination of the following: prolonged convulsions; coma; severe anaemia (Hb <5g/dl); hypoglycaemia (glucose concentration <40 mg/d I) and respiratory distress associated with severe metabolic acidosis (Warrell et al 1990, Marsh et al 1995). Once developed several of these patho­ physiological processes associated with severe malaria appear to run a course separate to the level of parasitization of the individual, and their effect upon the individual may also be separate from the actual malaria infection.

Figure 1.2

Malaria, the progression to death.

1000

Uninfected 400

bitten by 100

infected Infected Infected

mosquito (asympt (sympto

omatic) matic)

2 Severe

illness

1 Death

(reproduced from Marsh (1992) p.856)

The Relationship Of Transmission To Morbidity

Not all infective mosquito bites lead to malarial disease, and the proportion producing an infection varies widely between regions. In some areas it has found

to be as low as 1 in 20 (Mbogo 1994). Figure 1.2 is based on the average of many studies, and shows the passage of progression from mosquito bite to death, illustrating the decreasing numbers of people involved as the severity of

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the outcome increases. The entomological inoculation rate (number of infectious bites per person per annum) is used as a marker for transmission pressure (Mbogo 1994, Mbogo et al 1995). Paradoxically, in areas of lower transmission pressure significant levels of malaria mortality and morbidity exist. These levels may actually decline under situations of very intense transmission (Snow et al

1994). The most marked differences observed between areas of high and low transmission are in the age profile of malaria admissions. For example, in Ifakara, Tanzania, an area of high transmission, the highest rates of malaria admissions were among children less than 1 year old. Whilst in Kilifi, Kenya, with much lower transmission, the highest rates of malaria admission were in children aged 1 - 4 years (Snow et al 1994). The explanation for this most probably centers on the speed at which protective immunity against malaria develops, a factor also held as important in determining the specific nature of malarial disease at different ages (see below for more details).

As has already been stated, in endemic areas the susceptibility to serious illness changes with age (Marsh 1992). During the first few months, probably largely due to the passive transfer of maternal antibodies in utero, there appears to be protection against disease, though not to parasitization. This immunity reduces at around 6 months of age, with the majority of extreme cases, and death, concentrated in those between one and three - four years old, the exact range varying with transmission rates (Brewster et al 1990, Marsh 1992, Snow et al

1997). Active immunity develops over early childhood, depending on the degree of exposure to infective bites. For example in the Kilifi District of Kenya the frequency of severe disease begins to diminish at around 5 years, becoming very low in adolescence and adulthood. On average each child could be expected to have experienced 4-5 discrete periods of illness by the time they are 6 years old.

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1990, Marsh et al 1995). In the same studies the mean ages of occurance for cerebral malaria were recorded at 45 months and 40 months respectively. Transmission rates impact upon the spread of disease, such that in areas of lower transmission cerebral malaria is a more common feature of clinical

admissions. In the comparison of data taken from Kilifi and Ifakara, referred to above, cerebral malaria was found to be nearly four times as common in the lower transmission site (Snow et al 1994).

Cerebral Malaria

Cerebral malaria (C.M.) is the most common fatal syndrome of P. falciparum. Altered consciousness/coma, associated with widespread abnormalities of brain functioning, is the single most characteristic feature (see earlier list of other associated symptoms). There is some controversy over the defintion of impaired consciousness as it relates to cerebral malaria (Marsh et al 1995). W.H.O. criteria for C.M. centre upon deep coma, with an inability to make a localising response. A modification of this has been adopted in Kilifi to allow comparison with other research previously carried out on African children (Molyneux et al 1989, Brewster 1990). This alters the defintion to include a wider continuum of severity of illness, the diagnosis requiring impaired consciousness, with a Blantyre score of 4 or less (see Appendix 1 for specific details, Marsh et al (1995)).

C.M. has a mortality rate of betweeen 10 - 40% (Greenwood et al 1987, Molyneux et al 1989, Marsh et al 1995). The cerebral insult which results from this form of severe malaria is the patho-physiological basis for the development of long term neurological sequelae. There are a number of mechanisms which

have been suggested as implicated in the onset of cerebral insult in severe malarial disease. For example, the sequestration of infected cells in the cerebral

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unknown. Secondly, cases of C.M. where no obstruction of the microvasculature has been found are not uncommon (Marsh et al 1996). Other mechanisms implicated in the onset of neurological disturbance are: Raised intra-cranial

pressure, associated with acute brain swelling (Newton et al 1991, Newton et al 1994); Seizures (Waruiru et al 1996, Crawley et al 1996); Severe metabolic disruptions, particularly of blood glucose, and lactic acid levels (Marsh et al

1996); and the prescence of high concentrations of tumour necrosis factor and other cytokines (Clark & Rocket 1996). Cytokines are produced as part of the bodies immune response. When their concentrations become very highly concentrated, it is proposed that the immune response itself becomes pathogenic (Clark & Rocket 1996). Finally, preliminary evidence from Kilifi suggests that excitotoxic mechanisms may also be present in cerebral malaria (Dobbie et al in prep.). Excitoxicity refers to the ability of naturally occuring substances, such as glutamate and amino acids, to destroy neurons when, for example, their quantity is significantly increased (Choi 1992). Such mechanisms are hypothesised to contribute to the pathogenesis of central neuronal cell loss (Choi 1992), and may therefore also have an important role to play in pathogenesis of cerebral malaria.

C.M: The impact on survivors.

Although the majority of survivors appear to make a full recovery, in studies in the Gambia, Malawi, Kenya, Tanzania and Nigeria between 5-20% of children have been found to remain with gross neurological sequelae over six months after recovery from C.M. (Molyneux et al 1989, Brewster et al 1990, Bondi 1992, Peshu et al in preparation). The following have been identified as being amongst the most common: monoparesis (weakening of a single limb); cortical blindness (loss of the capacity to distinguish forms or patterns); aphasia (inability to

express or understand words), ataxia (inability to co-ordinate voluntary movements), and hemiplegia (paralysis of one side of the body).

C.M.: The impact on the community.

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unit in the Kilifi District of Kenya has concentrated on a defined study area which is under continuous demographic surveillance. It is estimated that in this area each child has a 1:15 chance of having developed severe, life threatening malaria warranting in-patient care before his/her fifth birthday. At this age

children start to attend nursery classes (there are approximately 30 in the area). Of the 1,800 children reaching this age every year there will be about 120 who have had severe malaria, 30+ of whom are survivors of cerebral malaria, (potentially one per class). A number of these, about 3-6, will have gross

neurological sequelae, and may need long term support from health and educational facilities. To date no published data is available to indicate the prevalence of more subtle impairments, and the question of how many, if any, of the remaining survivors have more subtle conditions requiring special educational support remains to be answered.

C.M.: A continuum of deficit?

It is hypothesized that there are essentially two possibilities. Firstly that there are no "hidden" impairments. This would be the case if cognitive functions are unaffected unless the cerebral insult is sufficient to also manifest itself in gross neurological deficits. Research on brain damage in children is supportive of this "critical level" for damage, before which the young brain appears to recover lost functioning, but beyond which it is unable to do so (The Kennard Principle and the "crowding effect" cited in Fingers et al 1988, and described in Chapter 7). A threshold of severity of damage for intellectual impairment is also discussed by Chadwick and colleagues in studies of children with head injuries (Chadwick et al 1981).

The second possibility is that in addition to those children with gross neurological

sequelae there is a larger group whose impairments are of a more subtle cognitive or behavioural nature, and which might only become apparent at school entry. This would be the case if the gross impairments identified are part of a

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that whilst the presenting features associated with eventual neurological sequelae are, in the main, the same as those associated with mortality (that is coma and hypoglycaemia) (Brewster et al 1990; Molyneux et al 1989; Marsh et al 1995), there are additional features which are associated with neurological sequelae alone. These include severe fitting, which may also contribute to the development of more subtle sequelae. Futher research on the longer term

development of all survivors of C.M., is required in order to establish whether deficits follow an all or nothing principle, or whether a continuum of impairments emerge.

C.M.: Measuring the nature and extent of impairment.

In reviewing research on parasitic infections and cognitive functions Kvalsvig (1988) points out that for an assessment battery to be sensitive to the effect of an infection there needs to be prior knowledge of the cognitive functions which are likely to be affected by the disease in question, relevant tests can then be included to assess these functions. Despite the importance of cerebral malaria in the non-industrialised world only one study was located in literature on the effects of cerebral malaria on cognitive functioning. This compared the performance, on a battery of psychological tests, of nine adults defined as having cerebral malaria, with a non-cerebral malaria group (KastI et al 1968). The tests were administered both during illness, and at discharge. Whilst the cerebral group was found to perform at a significantly lower level on tasks of short term memory, visuo-spatial organization, sequential processing and speed of

processing when ill, the two groups no longer differed on discharge. The pattem of results found was interpreted to mean that although during illness there is evidence of cerebral dysfunction, the adult brain appears to recover fully when health is restored. It needs to be stressed, however, this is a non-comparable

group to that of the current study. Firstly the assessemnts were made upon adults, and secondly the defintion of cerebral malaria given did not necessarily include impaired consciousness. Therefore these results are of little current relevance.

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The results of another, much more closely comparable study, was published after the data collection on the current study had been completed (Muntendam et al 1996). It therefore could have no influence upon the design of the current study. The study was carried out in the Gambia on 36 matched pairs of children, one of

each pair being a survivor of C.M.. Their performance was compared on a battery of eleven neuropsychological tests. No evidence was found of a serious long-term impairment on the C.M. children. This study will be reviewed in more detail in the discussion section of the current study.

In the abscence of any further direct precedents, a wider literature, relating to the

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B: COGNITIVE DEVELOPMENT AND COGNITIVE IMPAIRMENT - THE THEORETICAL FRAMEWORK

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CHAPTER 3 COGNITIVE DEVELOPMENT - A VYGOTSKIAN FRAMEWORK

"At the beginning of development there stands the act, independent of the word, then at the end of it there stands the word which becomes the act, the word makes man’s action free. (Vygotsky & Luria 1994 p.170)

This chapter is an interpretation of Vygotsky's theoretical explanations of the path of cognitive development. It aims to describe the main influences upon cognitive development, and the main causes of differential development. In so doing it also aims to draw implications for the design and implementation of the current study.

Stages of development

In Vygotskian theory change can be characterised as occurring in stages. The early stages being dominated by natural processes and elementary mental functions. The later stages are dominated by social processes and higher mental functions (Wertsch 1985). The passage from one stage to another is accounted for not by quantitative differences, but by qualitative shifts (Vygotsky 1966/1991 ) \ Take for example the development of memory, this does not develop simply by being able to remember ever increasing amounts, but by becoming "logical memory", guided by meaning and deliberately applied by the child. In a series of experiments described by Leont’ev (1932/1994) the memory functions of young children were found to depend upon direct memory, that is memory functioning which is not organised with the use of memory aids (mnemonic devices). Changes with age were not caused by merely a quantitative increase in capacity. Rather the integration of mnemonic devices into memory function, that is the integration of thought with memory, appeared to create a qualitatively different form of memory, mediated memory. The use of mnemonic devices was found to dominate in the performance of adults on memory tasks

(Leont'ev 1932/1994).

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In the case of attention, change is said to be from behaviour which functions by being attracted by an external source, to becoming dependent upon the child's own thinking, that is 'selective attention' (Leont'ev 1932/1994). The theory suggests, as the example of memory given above also illustrates, that the end point is the development of conscious activity and deliberate mastery, where

consciousness is defined as the state of awareness and understanding (Vygotsky 1934/1986).

Functional Systems

Describing development purely in terms of individual functions, such as memory,

perception and attention, is inappropriate within the Vygotskian framework, as mental functions are seen to be combined in a highly complex inter-relationship. Individual functions do not develop separately because they do not operate in isolation from other mental functions. Rather, successful completion of any psychological activity depends upon their operating together. In Vygotsky's words,

"the fate of each functional ingredient of consciousness thus depends upon the deveiopment of the entire system." (Vygotsky 1934/1986 p 167).

This was illustrated in a lecture given by Vygotsky on the development of perception (Vygotsky 1960/1987). A series of experiments was described which investigated the processes involved in the perception of magnitude. Of particular interest was how compensation for changes in distance was achieved, when

judging relative size. For example how are two pencils of identical length, one close and one far, perceived as being equal in size, even though on a sensory level the retinal image of the further pencil is smaller? These experiments involved judgements of relative size being made for different combinations of: objects, projected images, and the dependence upon memory of an object

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constancy of perceptions are closely inter-linked with memory functions (Vygotsky 1960/1987).

Each level of maturity is characterised by a different relationship between mental

functions. In the course of development behaviour becomes governed by increasingly more complex, and inter-related systems of functions (Vygotsky & Luria 1994). However regression to earlier less complex and more independent functioning can happen when damage or decay affects the physiological

structure of the brain (Vygotsky 1966/1991).

Agents of Change

A common thread underlying change and development across all functions and domains, though not necessarily occurring simultaneously in each domain, is the mastery and use of tools and signs. Tools (also referred to as technical tools) are objects used to complete a task, such as a stick for digging. Vygotsky differentiated between human tools and animal tools. The differences between the ape and the young child lie primarily in the different combinations of psychological functions that guide the use of the tool (Vygotsky & Luria 1994). The behaviour of the ape takes place within a narrow time frame. A problem is encountered, e.g. termites are found down a narrow hole, a stick is seen and used to solve the problem by digging the termites out. Visual perception therefore dominates the process (Kohler cited in Vygotsky 1960/1987). Human activity is not so dependent upon visual perception, but is guided by a combination which includes memory functions. For example, a stick may be specifically sought from another location, or, later in development, it may be carried in anticipation of its use. Human activity is therefore more purposeful and directive.

Signs and symbols (psychological tools) are also important in distinguishing between animal and human intellect. They are central to the development of

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speech; counting systems; mnemonic techniques/devices; art; writing; maps etc. (Wertsch 1985). Since, as stated earlier, development is a process of qualitative change, the process of learning these mediational means will facilitate both the specific psychological activity to which they are being applied, and change the

very nature of thought, of psychological activity in general (Vygotsky 1934/1986).

The essential difference between technical and psychological tools is that the former are external and act externally to the person to change the object of the

activity being undertaken, whilst signs and symbols are psychological, in that they alter mental functioning internally. Psychological tools act more as a catalyst to activity, not altering the external object directly, but influencing the ability of

internal mental processes to complete the activity (Vygotsky and Luria 1994).

The Socio-Historical Context Of Learning

The tools available to the individual have been referred to as "socio-cultural technologies" (Rogoff 1989/1991), the selection being largely determined by those used in the immediate cultural environment. In Vygotskian theory learning and development occur within the social context, which is also referred to as the historical domain (Wertsch 1985). The young child experiences acts outside of itself, which are often being carried out in relation to itself. It is the process of assigning meaning to this activity, and of bringing it into voluntary control, which is central to the development of higher mental functions (Vygotsky & Luria 1994). The action is given meaning by the 'adult' involved, (not necessarily an adult per se, but at least a person operating at a higher level of mental functioning). The child does not need to understand the purpose of the activity, or share a common goal with the adult, to take an active part. S/he eventually acquires that meaning

as his/her own, but not necessarily in the same form as it was presented. The process of the internalisation of meaning is not one of passive acquisition, of a straightforward transferral of knowledge. Rather it is a process of transformation,

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Yssevich; Leont'ev; cited in Vygotsky & Luria 1994). Zankov's tests required the subjects to memorise word lists, with abstract figures provided as potential memory aids. Young children ignored the aids. Older children did use them, but only after transforming the figures into meaningful symbols. Thus if a symbol

presented could, through rotation or inversion, be made to resemble the object to which it was attached, only then would it be used. (E.g. a triangle might be used to remember ice-cream cone, but a square would not).

This description of the child as an active learner is similar to that supplied by Piaget in relation to the concepts of assimilation and accommodation (Vygotsky 1934/1986). The difference between the two theoretical approaches arises in the importance attached to the context in which psychological activity occurs. From the Vygotskian perspective child development is a social activity, s/he is not the Piagetian solitary thinker. Thinking develops through social guidance, and is thus moulded and developed, and may even be constrained, by it. That is not to say that the child is only a product of his/her environment. Vygotsky described two equally important roots of development, the natural/biological, and the social/historical. They begin independently, with biological development pre­ dating the social. As internalisation of the social experiences increases they do not supplant the biological processes. Rather the two become interdependent, creating a qualitatively different potential from that to be expected if they should act independently. The biological influence upon development is not expanded upon in the same detail as the social-historical by Vygotsky himself. It is to the closely related work of his colleague, Luria, that one must turn for a working model of brain functions and the brain - behaviour link.

The Process Of Development

To complete this summary of the Vygotskian description of the social-historical stages of development, it is appropriate to look next at the concept of the Zone of

Proximal Development, which, in the words of Minick is;

"the primary locus of change in human psychological development”.

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The Zone of Proximal Development, or ZPD, has been defined by Vygotsky as the distance between a child's

"actual developmental level as determined by independent problem solving" and the higher level of " potential development as determined through problem solving under guidance or in collaboration with more capable peers."(Vygotsky cited in Wertsch 1985 p.67).

As an example, take two children whose test performance places them both at the 6 year level. With careful prompting one child succeeds at tasks at the 7 year level, and the other, with the same prompts, at a 9 year level. Their understanding is not therefore at the same level, as was suggested by the first measure.

Tharp and Gallimore presented a four stage model which clearly illustrates transition through the ZPD (Tharp and Gallimore 1988). During Stage 1 performance is assisted by more capable others. Instruction at this stage is characterised by the manipulation of a number of features of the activity by the adult even before the interaction with the child begins. The adult anticipates the level of functioning of the child by adjusting: the choice of the tasks to be given; the selection of tools and materials; and the form of instructions. To solve the problem of finding a missing shoe, for example, the adult may ask the older child "Where did you last remember having it ?". Task analysis would be applied for a younger child, with a series of more directed questions such as " Did you have it in the kitchen?..in the bedroom? etc.". A younger child still would be accompanied on the hunt, with appropriate verbal labels being attached to define the activity being carried out. "Let's look in the kitchen, is it here? etc.".

Modifications and reductions occur in the quantity and quality of help the child requires in order to complete a task, up until the point where, in that domain. Stage 2 in reached. At this point performance has begun to be assisted by the

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of the importance of this stage are several sources, many cited in Tharp and Gallimore, indicating that teaching overt self-instruction improves performance particularly in 'impulsive' children (Gaddes & Edgell 1994).

During Stage 3 performance is "developed, automatised and fossilized"

(Tharp and Gallimore 1988). It no longer requires external assistance, and in fact at this stage assistance might even be considered to be disruptive. For example early counting at Stage 2 may be aided by the use of external aids such as fingers or beads. At Stage 3 counting skills will have been internalised to the point where such external aids are longer used. Indeed the imposition of an external system at this level can actually slow down the completion of the activity.

The achievement of independent internally controlled performance is not the final stage however. Learning and development continue in other domains, and during Stage 4 the learner will revert to earlier stages, actively seeking assistance where necessary to master new skills. Although placed later than Stage 3, performance at Stage 4 is characterised by performance at earlier levels. Returning to the example of counting activities, and mental arithmetic, at Stage 4 the child who can now count internally will probably need to return to earlier stages when the problems involve either larger numbers, or other processes, such as subtraction, as well.

What is highlighted by the Tharp and Gallimore model is the dynamic nature of cognitive ability, a concept central to the Vygotskian approach. This has important implications for the assessment of cognitive abilities, and the measurement of levels of development. The concept of the ZPD provides a framework for developing informative assessment tools. In support of its

importance and value Vygotsky found through investigation,

"... that the child with the larger zone of proximal development will do much better in school."(Vygotsky 1934/1986 p.187).

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Indeed he stated the measurement of the ZPD had more pedagogical value than one session, test only, measures of ability. The measurement of the ZPD will be discussed in more detail in Chapter 10.

Another important theme to be touched on above is the role of instruction in cognitive development. Whilst it is of major importance in guiding development, the reference to the child being actively involved in the internalisation of the use of signs must not be forgotten. It would be erroneous therefore to see the role of instruction as exclusively to pull development behind it, although this may be the

case at times.

Thought And Speech

Amongst the signs involved in the development of higher mental functions, language is the most important (Vygotsky 1934/1986). At the point in development where the external operations mediated by language turn inwards, the specific language environment becomes an integral part of the thought processes. A comparison was made between the conceptual categorisation of Native and Anglo Americans by Carrol and Casagrande (1958), which clearly illustrates this. Subjects were required to select the two, out of three, pictures which they judged to be illustrating the same concept. It was hypothesised that the two groups would differ in the pairings made, and that these differences would be attributable to differences in linguistic structure between Hopi and English, the two languages involved. Results supported these hypotheses. For example, where the three pictures portrayed pouring, spilling and dropping, Hopi speakers classified the first two together, and English speakers the last two. In Hopi a distinction is made between dropping objects and liquid, but not between intentional and accidental pouring. Whilst to English speakers the more salient

dimension seemed to be the intentionality of the act.

After studying the results of research on apes and humans (Kohler cited in

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thought and speech have different genetic routes, initially developing independently, upon different lines. Early thought is pre-linguistic, and early speech is at a pre-intellectual level. At a later point in development thought

becomes verbal and speech rational. When the two lines of development do meet "the nature o f the development Itself changes" (Vygotsky 1934/1986 p.94). One aspect of this relationship can be illustrated by the example of studies

of aphasies, carried out by Vygotsky and colleagues (cited in Vygotsky & Luria 1994). The loss of language abilities was found to be associated with fundamental changes in behaviour, particularly evident in an inability to organise and co-ordinate functions in the completion of a task. Language appears to have been an integral part of thought processes, guiding planning and strategies. The impairment of language left the functions required to complete the tasks unimpaired, but the implementation of activity severely disrupted.

The Development of Concepts

Another perspective on the relationship between language/speech and thought, and the changing relationship between the two throughout development, comes from the study of the development of concepts. Vygotsky's description of the development of concepts was based upon experiments carried out in collaboration with Sakharov (cited in Sakharov 1930/1994 and Vygotsky 1934/1986). These experiments consisted of categorisation tasks requiring that wooden blocks, varying in size, colour and shape, be sorted according to concepts fabricated for the study, and labelled with nonsense words. The process by which solutions were sought by adults, adolescents and children was compared. Qualitative differences emerged between children and the other two age groups, in the way objects were categorised, and the way relationships between objects were perceived. In childhood the focus was upon concrete and

perceptual similarities between objects. In adolescence, continuing into adulthood, concepts emerged which were abstract and logical. In childhood the process of selection for inclusion into a category was often done on an item by item basis, with each successive item only being compared to the one

Figure

Figure 1.1 The Parasite In The Human Host
Figure 1.2
Figure 7.2 Brain Reserve Capacities and Threshold Hypothesis
Table 17.2 Syntax
+7

References

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