cambridge university press principles and practice of lifespan developmental neuropsychology mar 2010 kho tài liệu bách khoa

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Principles and Practice of Lifespan
Developmental Neuropsychology



Principles
and Practice of Lifespan
Developmental
Neuropsychology
Jacobus Donders
Scott J. Hunter


CAMBRIDGE UNIVERSITY PRESS

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Cambridge University Press
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Published in the United States of America by Cambridge University Press, New York
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Information on this title: www.cambridge.org/9780521896221
© Cambridge University Press 2010
This publication is in copyright. Subject to statutory exception and to the
provision of relevant collective licensing agreements, no reproduction of any part
may take place without the written permission of Cambridge University Press.
First published in print format 2010

ISBN-13

978-0-511-67360-3

eBook (EBL)

ISBN-13

978-0-521-89622-1

Hardback

Cambridge University Press has no responsibility for the persistence or accuracy
of urls for external or third-party internet websites referred to in this publication,
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.


Contents
Contact information for authors page vii
Biography for Jacobus Donders and Scott J. Hunter

Introduction
Jacobus Donders and Scott J. Hunter

Section I: Theory and models
1

6c Synthesis of chapters on learning disabilities:
overview and additional perspectives

H. Lee Swanson 163

1

3

7a Infants and children with spina bifida
Heather B. Taylor, Susan H. Landry, Lianne
English and Marcia Barnes 169

A lifespan review of developmental
neuroanatomy
John Williamson 3

2a Developmental models in pediatric
neuropsychology
Jane Holmes Bernstein 17
2b Models of developmental neuropsychology:
adult and geriatric
Tyler J. Story and Deborah K. Attix 41
3

Multicultural considerations in lifespan
neuropsychological assessment
Thomas Farmer and Clemente Vega 55

4

Structural and functional neuroimaging
throughout the lifespan

Brenna C. McDonald and Andrew J. Saykin

Section II: Disorders

xi

69

83

7b Adolescence and emerging adulthood in
individuals with spina bifida: a developmental
neuropsychological perspective
Kathy Zebracki, Michael Zaccariello, Frank
Zelko and Grayson N. Holmbeck 183
7c Spina bifida/myelomeningocele and
hydrocephalus across the lifespan:
a developmental synthesis
Ilana Gonik, Scott J. Hunter and Jamila
Cunningham 195
8 Cerebral palsy across the lifespan
Seth Warchausky, Desiree White and Marie
Van Tubbergen 205
9a Intellectual disability across the lifespan
Bonnie Klein-Tasman and Kelly Janke 221

5a Attention deficit hyperactivity disorder
in children and adolescents
David Marks, Joey Trampush and Anil Chacko 83

9b Lifespan aspects of PDD/autism spectrum
disorders (ASD)
Julie M. Wolf and Sarah J. Paterson 239

5b Attention deficit hyperactivity disorder
in adults
Margaret Semrud-Clikeman and Jodene
Goldenring Fine 97

9c Autism spectrum disorders and intellectual
disability: common themes and points
of divergence
Marianne Barton, Colby Chlebowski and
Deborah Fein 251

5c Attention deficit hyperactivity disorder:
a lifespan synthesis
Jeffrey M. Halperin, Anne-Claude V. Bedard and
Olga G. Berwid 113
6a Learning disorders in children and adolescents
Gregory M. Stasi and Lori G. Tall 127
6b Learning disorders in adults
Elizabeth P. Sparrow 143

10a Hearing loss across the lifespan:
neuropsychological perspectives
Betsy Kammerer, Amy Szarkowski and Peter
Isquith 257
10b Visual impairment across the lifespan:
neuropsychological perspectives

Lisa M. Noll and Lana L. Harder 277


Contents

11a

Traumatic brain injury in childhood
Michael W. Kirkwood, Keith Owen Yeates and
Jane Holmes Bernstein 299

11b

Adult outcomes of pediatric traumatic
brain injury
Miriam Beauchamp, Julian Dooley and Vicki
Anderson 315

11c

11d

Traumatic brain injury in older
adults
Felicia C. Goldstein and Harvey
S. Levin 345

11e

Traumatic brain injury across the

lifespan: a long-term developmental
perspective
Jacobus Donders 357

12a

Pediatric aspects of epilepsy
Lindsey Felix and Scott J. Hunter

12b

13a

vi

Neurobehavioral aspects of traumatic brain
injury sustained in adulthood
Tresa Roebuck-Spencer, James Baños, Mark
Sherer and Thomas Novack 329

13b

Lifespan aspects of brain tumors
Celiane Rey-Casserly 393

14

Lifespan aspects of endocrine disorders
Geoffrey Tremont, Jennifer Duncan Davis and
Christine Trask 409

15

Metabolic and neurodegenerative disorders
across the lifespan
Richard Ziegler and Elsa Shapiro 427

16a

Psychopathological conditions in children
and adolescents
Abigail B. Sivan 449

16b

Psychopathological conditions in adults
Anthony C. Ruocco, Elizabeth Kunchandy
and Maureen Lacy 455

16c

Neuropsychological aspects of
psychopathology across the lifespan:
a synthesis
Alexandra Zagoloff and Scott J. Hunter 469

359

A lifespan perspective of cognition in
epilepsy

Michael Seidenberg and Bruce Hermann

Index
371

Leukemia and lymphoma across the lifespan
Kevin R. Krull and Neelam Jain 379

477

The color plates are to be found between pp. 276
and 277


Contact information for authors
Vicki Anderson, Ph.D.
Department of Psychology
Royal Children’s Hospital
Parkville, Victoria, Australia

Anil Chako, Ph.D.
Department of Psychiatry
Mount Sinai Medical Center
New York, NY

Deborah K. Attix, Ph.D.
Department of Psychiatry and Behavioral Sciences
Duke University Medical Center
Durham, NC

Colby Chlebowski, M.A.
Department of Psychology
University of Connecticut
Storrs, CT

James Baños, Ph.D., ABPP-Cn
Department of Physical Medicine & Rehabilitation
University of Alabama, Birmingham
Birmingham, AL

Jamila Cunningham, M.A.
Department of Psychology
Loyola University
Chicago, IL

Marcia Barnes, Ph.D.
Children’s Learning Institute
University of Texas Health Science Center at Houston
Houston, TX

Jennifer Duncan Davis, Ph.D.
Department of Psychiatry and Human Behavior
Warren Alpert School of Medicine of Brown University
Providence, RI

Marianne Barton, Ph.D.
Department of Psychology
University of Connecticut
Storrs, CT

Jacobus Donders, Ph.D.
Department of Psychology
Mary Free Bed Rehabilitation Hospital
Grand Rapids, MI

Miriam Beauchamp, Ph.D.
Department of Psychology
Royal Children’s Hospital
Parkville, Victoria, Australia

Julian Dooley, Ph.D.
Murdoch Childrens Research Institute
Melbourne, Australia

Anne-Claude V. Bedard, Ph.D.
Department of Psychiatry
Mount Sinai Medical Center
New York, NY
Jane Holmes Bernstein, Ph.D.
Neuropsychology Program
Children’s Hospital Boston
Department of Psychiatry
Harvard Medical School
Boston, MA
Olga G. Berwid, Ph.D.
Department of Psychiatry
Mount Sinai Medical Center
New York, NY

Lianne English

Department of Psychology
University of Guelph
Guelph, Ontario, Canada
Thomas Farmer, Psy.D.
The Chicago School of Professional Psychology
Chicago, IL
Deborah Fein, Ph.D.
Department of Psychology
University of Connecticut
Storrs, CT
Lindsey Felix, Ph.D.
Alexian Brothers
Neuroscience Institute
Chicago, IL


Contact information for authors

Jodene Goldenring Fine, Ph.D.
Department of Psychiatry
Michigan State University
East Lansing, MI

Betsy Kammerer, Ph.D.
Deaf and Hard of Hearing Program
Children’s Hospital Boston
Waltham, MA

Felicia C. Goldstein, Ph.D.
Department of Neurology

Emory University School of Medicine and Wesley
Woods Center on Aging
Atlanta, GA

Michael W. Kirkwood, Ph.D.
Department of Physical Medicine & Rehabilitation
The Children’s Hospital
Aurora, CO

Ilana Gonik, Ph.D
Department of Psychiatry
Loyola University Medical Center
Maywood, IL
Jeffrey M. Halperin, Ph.D
Department of Psychology
Queens College, CUNY
Flushing, NY

Kevin R. Krull, Ph.D.
Department of Epidemiology and Cancer
Control
St. Jude Children’s Research Hospital
Memphis, TN

Lana L. Harder, Ph.D.
Department of Psychiatry
University of Texas Southwestern Medical School
Children’s Medical Centre

Elizabeth Kunchandy, Ph.D.

Rehabilitation Care Service
VA – Pudget Sound
Seattle, WA

Bruce Hermann, Ph.D.
Department of Neurology
University of Wisconsin Madison School of Medicine
Madison, WI

Maureen Lacy, Ph.D.
Department of Psychiatry
University of Chicago
Chicago, IL

Grayson N. Holmbeck, Ph.D.
Department of Psychology
Loyola University of Chicago
Chicago, IL

Susan H. Landry, Ph.D.
The University of Texas Health Science Center
Department of Pediatrics
Children’s Learning Institute
Houston, TX

Scott J. Hunter, Ph.D.
Departments of Psychiatry & Pediatrics
University of Chicago
Chicago, IL
Peter Isquith, Ph.D.

Department of Psychiatry
Dartmouth Medical School
Hanover, NH
Neelam Jain, Ph.D.
Department of Epidemiology and Cancer Control
St. Jude Children’s Research Hospital
Memphis, TN

viii

Bonnie Klein-Tasman, Ph.D.
Department of Psychology
University of Wisconsin, Milwaukee
Milwaukee, WI

Kelly Janke, M.A.
Department of Psychology
University of Wisconsin, Milwaukee
Milwaukee, WI

Harvey S. Levin, Ph.D.
Cognitive Neuroscience Laboratory
Departments of Physical Medicine and Rehabilitation,
Neurosurgery and Psychiatry
Baylor College of Medicine
Houston, TX
David Marks, Ph.D.
Department of Psychiatry
Mount Sinai Medical Center
New York, NY

Brenna C. McDonald, PsyD
Departments of Radiology and Neurology
Indiana University School of Medicine
Indianapolis, IN


Contact information for authors

Lisa M. Noll, Ph.D.
Learning Support Center for Child Psychology
Texas Children’s Hospital
Houston, TX
Thomas Novack, Ph.D.
Department of Physical Medicine & Rehabilitation
University of Alabama, Birmingham
Birmingham, AL
Sarah J. Paterson, Ph.D.
Department of Pediatrics
Children’s Hospital of Philadelphia
Philadelphia, PA
Celiane Rey-Casserly, Ph.D.
Department of Psychiatry
Children’s Hospital and Harvard Medical School,
Boston
Boston, MA
Tresa Roebuck-Spencer, Ph.D., ABPP-Cn
Department of Psychology
National Rehabilitation Hospital
Washington DC
Anthony C. Ruocco, Ph.D.

Department of Psychiatry
University of Illinois at Chicago
Chicago, IL
Andrew J. Saykin, PsyD
Departments of Radiology, Neurology, and Psychiatry
Indiana University School of Medicine
Indianapolis, IN
Michael Seidenberg, Ph.D.
Department of Psychology
Rosalind Franklin University of Medicine and Science
North Chicago, IL
Margaret Semrud-Clikeman, Ph.D.
Departments of Psychology & Psychiatry
Michigan State University
East Lansing, MI
Elsa Shapiro, Ph.D.
Pediatric Clinical Neuroscience
University of Minnesota Medical Center
Minneapolis, MN
Mark Sherer, Ph.D., ABPP-Cn
TIRR Memorial Hermann
Baylor College of Medicine
Houston, TX

Abigail B. Sivan, Ph.D.
Department of Psychiatry & Behavioral Science
Feinberg School of Medicine
Northwestern University
Chicago, IL
Elizabeth P. Sparrow, Ph.D.

Sparrow Neuropsychology, P.A.
Durham, NC
Gregory M. Stasi, Ph.D.
Rush Neurobehavioral Center
Skokie, IL
Tyler J. Story, Ph.D.
Division of Neurology
Duke University Medical Center
Durham, NC
H. Lee Swanson, Ph.D.
Graduate School of Education
University of California-Riverside
Riverside, CA
Amy Szarkowski, Ph.D.
Deaf and Hard of Hearing Program
Children’s Hospital Boston
Waltham, MA
Lori G. Tall, PsyD
Rush Neurobehavioral Center
Skokie, IL
Heather B. Taylor, Ph.D.
The University of Texas Health Science Center
Department of Pediatrics
Children’s Learning Institute
Houston, TX
Joey Trampush, M.A.
Department of Psychology
CUNY Graduate Center
New York, NY
Christine Trask, Ph.D.

Department of Psychiatry and Human Behavior
Warren Alpert School of Medicine of Brown
University
Providence, RI
Geoffrey Tremont, Ph.D.
Neuropsychology Program, Rhode Island Hospital
Providence, RI

ix


Contact information for authors

Marie Van Tubbergen, Ph.D.
Department of Physical Medicine and
Rehabilitation
University of Michigan
Ann Arbor, MI
Clemente Vega
Yale University School of Medicine
Department of Neurosurgery
New Haven, CT
Seth Warschausky, Ph.D.
Department of Physical Medicine and
Rehabilitation
University of Michigan
Ann Arbor, MI
Desiree White, Ph.D.
Department of Psychology
Washington University

St. Louis, MO
John Williamson, Ph.D.
Department of Neurology and
Rehabilitation
University of Illinois at Chicago
Chicago, IL
Julie M. Wolf, Ph.D.
Yale Child Study Center
New Haven, CT

x

Keith Owen Yeates, Ph.D.
The Research Institute at Nationwide Children’s
Hospital
Columbus, OH
Michael Zaccariello, Ph.D.
Department of Psychiatry and Psychology
Mayo Clinic
Alexandra Zagoloff, M.S.
Department of Psychology
Illinois Institute of Technology
Chicago, IL
Kathy Zebracki, Ph.D.
Department of Behavioral Sciences,
Rush University Medical Center,
Pediatric Psychologist,
Shriners Hospital for Children,
Chicago, IL
Frank Zelko, Ph.D.

Neuropsychology Service, Children’s Memorial Hospital
Department of Psychiatry and Behavioral Science
Feinberg School of Medicine, Northwestern University
Chicago, IL
Richard Ziegler, Ph.D.
Pediatric Clinical Neuroscience
University of Minnesota Medical Center
Minneapolis, MN


Biography for Jacobus Donders
Jacobus Donders obtained his PhD from the University
of Windsor in 1988. He completed his internship at
Henry Ford Hospital in Detroit, MI, and his residency
at the University of Michigan in Ann Arbor, MI.
He is currently the Chief Psychologist at Mary Free
Bed Rehabilitation Hospital in Grand Rapids, MI.
Dr. Donders is board-certified by the American
Board of Professional Psychology in both Clinical
Neuropsychology and Rehabilitation Psychology. He
has served on multiple editorial and professional executive boards, has authored or co-authored more than
100 publications in peer-reviewed journals, and has
co-edited two books about neuropsychological intervention. He is a Fellow of the National Academy
of Neuropsychology and of Divisions 40 (Clinical
Neuropsychology) and 22 (Rehabilitation Psychology)
of the American Psychological Association. His main
research interests include construct and criterion validity of neuropsychological test instruments and prediction of outcome in congenital disorders and acquired
brain injury.

Biography for Scott J. Hunter

Scott J. Hunter is an Associate Professor of
Psychiatry, Behavioral Neuroscience, and Pediatrics
in the Pritzker School of Medicine at the University
of Chicago, where he serves as the Director of
Pediatric Neuropsychology and Coordinator for

Child Psychology training. Dr. Hunter obtained his
PhD in Clinical and Developmental Psychology from
the University of Illinois at Chicago in 1996. He
completed his internship at Northwestern University
School of Medicine’s Stone Institute of Psychiatry,
and residencies in Pediatric Neuropsychology and
Developmental Disabilities in the Departments
of Pediatrics and Neurology at the University of
Rochester. He serves as an ad-hoc editor for a number
of peer-reviewed publications, and has authored or
co-authored multiple peer-reviewed articles, presentations, and book chapters. He co-edited Pediatric
Neuropsychological Intervention (CUP, 2007) with
Jacobus Donders. Both clinically and in his research,
Dr. Hunter specializes in identifying and characterizing neurocognitive and behavioral dysfunction in
children with complex medical and neurodevelopmental disorders.
To Harry van der Vlugt, my original mentor, for
sharing his lifespan wisdom and support.
Jacobus Donders
This book is dedicated to the memory of Arthur
Benton and Rathe Karrer, who each mentored my
professional development, and to Richard Renfro, for
his ongoing support and understanding during the
development and completion of this project.
Scott J. Hunter

Introduction
Jacobus Donders and Scott J. Hunter

Neuropsychology is the science and practice of evaluating and understanding brain–behavior relationships and
providing recommendations for intervention that can be
implemented in the daily lives of persons when brain
dysfunction compromises functioning at home or
school, on the job, or in the community at large. The
associated target behaviors and skills can range from
specific cognitive abilities to emotional and psychosocial
functioning. This specialty has advanced significantly
over the past several years, but recent well-respected
published works about common neuropsychological
disorders have tended to focus primarily or exclusively
on either children or adults, or have provided separate
discussions of conditions that are traditionally seen more
commonly at either end of the age spectrum (e.g.
Morgan and Ricker [1], Snyder et al. [2]). Similarly,
there is a dearth of comprehensive discussions in the
available literature to date of various neuropsychological
syndromes in their different manifestations across the
lifespan, and the longitudinal development and longerterm outcomes of such conditions. This has contributed
to a sometimes unwarranted bifurcation within the field,
where developmental course has been left out of the
diagnostic and treatment equation. In response, the primary goal of this volume is to provide an integrated
review of neuropsychological function and dysfunction
from early childhood through adulthood and, where

possible, old age, to support the understanding and
consideration of the role development plays in the presentation and outcome of neuropsychological disorders
across the lifespan.
Each chapter in this volume is intended as an empirical review of the current state of knowledge concerning
the manifestation and evaluation of common neuropsychological disorders as well as their intervention, with
additional consideration of what still needs to be done to
improve efficacy of practice and research. The first section provides a review of the general principles behind
lifespan developmental neuropsychology. The second
section examines a number of commonly encountered neurodevelopmental, behavioral, and cognitive

disorders. For many of the disorders, there is one chapter
focusing on pediatric aspects of the condition, one
emphasizing adult and/or geriatric concerns, and a summary commentary chapter that consolidates and synthesizes the knowledge shared across the age-specific review
chapters, with a focus on identifying and guiding areas of
further research and practice in the domain. For some
conditions (e.g. cerebral palsy) there are currently simply
not enough data about outcomes into adulthood to
warrant a separate chapter, whereas for other diagnostic
groups (especially some of the neurodegenerative ones,
which are often associated with death prior to adulthood), the emphasis is placed on the time frame in
which they most commonly occur. However, for several
other disorders (e.g. traumatic brain injury), there is a
wealth of information about the correlates of new-onset
cases of the condition at different ages, as well as longitudinal outcomes.
Each of the chapters in this volume was written by
one or more authors who specialize in clinical practice
as well as research with the disorder being discussed.
As a result, these experts give the reader an up-to-date
account of the state of the art of the field at this time,
and make suggestions for improvement in approaches

toward assessment, intervention, and empirical investigation of the disorders as they present across the
lifespan. We hope that this book will provide a vantage
point from which to explore lifespan developmental
aspects of a wide range of commonly encountered
neuropsychological disorders. We anticipate that it
will be of interest not only to pediatric neuropsychologists but also to professionals in rehabilitation, neurology, and various allied health fields.

References
1. Morgan JE, Ricker JH. Textbook of Clinical
Neuropsychology. New York: Taylor & Francis; 2008.
2. Snyder PJ, Nussbaum PD, Robins, DL. Clinical
Neuropsychology: A Pocket Handbook for Assessment, 2nd
edn. Washington DC: American Psychological
Association; 2006.



Section I
Chapter

Theory and models

1

A lifespan review of developmental
neuroanatomy
John Williamson

On the development of functional
neural systems

The structure of the brain is in constant flux from the
moment of its conception to the firing of its final nerve
impulse in death. As the brain develops, functional
networks are created that underlie our cognitive and
emotional capacities. Our technologies for evaluating
these functional systems have changed over time as
well, evolving from lesion-based case studies, neuropathological analyses, in vivo neurophysiological techniques (e.g. electroencephalography), and in vivo
structural evaluation (CT scan, magnetic resonance
imaging (MRI), diffusion tensor imaging (DTI)), to
in vivo functional methodologies (functional magnetic
resonance imaging (fMRI), positron emission tomography (PET)). And with these rapidly developing technologies, we are able to more thoroughly test some of
the earlier hypotheses that were developed about the
nature and function of the brain.
Although attempts to localize mental processes to
the brain may be traced to antiquity, the phrenologists
Gall and Spurtzheim may have initiated the first modern attempt, by hypothesizing that language is confined
to the frontal lobes [1]. While these early hypotheses
were largely ignored as phrenology fell in ill-repute,
they were resurrected in the early 1860s by Paul
Broca, who, inspired by a discussion of the phrenologists’ work, sparked a renewed interest in localization of
brain function with his seminal case studies on aphasia
[2]. Broca’s explorations were among the earliest examples of lateralized language dominance.
Recently, high-resolution structural MRI was applied
to preserved specimens taken from two of Broca’s
patients, to examine the localization of damage on the
surface and interior of the brains. This modern technology revealed extensive damage in the medial regions of
the brain and highlighted inconsistencies with previous
hypotheses in the area of the brain identified by Broca,
which is now identified as Broca’s area [3]. This is
interesting, both from a historical perspective and also

with respect to our current understandings of the brain
systems involved in the behavioral presentations Broca
described (beyond the articulatory functions of the inferior frontal gyrus); specifically the extent of behavioral
changes identified by Broca is now more accurately
reflected by the apparent neuropathology.
A contemporary of Broca’s, John Hughlings
Jackson, offered a different perspective regarding localization. While Jackson had no problem with the notion
of probabilistic behavior profiles with specific brain
lesions (e.g. a left inferior frontal lesion most likely will
affect expressive speech), he did not agree with the
prevailing idea at the time that these lesion/behavior
observations represented a confined center of function
[4]. Jackson proposed a vertical organization of brain
functions, with each level (e.g. brain stem, motor and
sensory cortex, and prefrontal cortex) containing a representation, or component of the function of interest.
Though this idea was at the periphery of opinion at the
time, when strict localizationist theory was gaining
momentum, it has come to form the basis of modern
thought regarding the mechanisms of brain and behavior
relationships.
Holes and gaps in the models of strict localization of
behaviors to specific, contained brain regions became
more salient to the mainstream neuroscience community
over time (cf. the disrepute of phrenology and conflicting
findings from lesion/behavior studies). In response, Karl
Lashley’s search for the memory engram typified another
era in the exploration of brain–behavior relationships.
Using an experimental approach rather than the classic
case study method, Lashley, famously unable to localize

memory function in rats (through progressive brain ablation), introduced the constructs of equipotentiality and
mass action [5]. Equipotentiality is the concept that all
brain tissue is equally capable of taking over the function
of any other brain tissue (demonstrated in the visual
cortex) and, relatedly, mass action references the idea
that the behavioral impact of a lesion is dependent on
its size, not its location. Also, although less popularized,


Section I: Theory and models

4

he suggested that, at any given time, the pattern of neural
activity is more important than location when understanding higher cognitive functions [6]. Although plasticity in the human brain does not conform to notions of
equipotentiality, recent research on stem-cell treatments
in neurodegenerative diseases has reinvigorated the construct in an albeit new form. Guillame and Zhang [7]
review the use of embryonic stem cells as a neural cell
replacement technique and strides in functional integration, axonal growth, and neurotransmitter release (e.g. the
development of dopamine-producing cells in mouse
brains after stem cell implantation).
Historically, political and social influences on the
philosophy of science trended Western societies away
from the study of brain structures in the understanding of behavior after World War I [8]. In contrast,
researchers in the former Soviet Union continued that
approach. For example, while in opposition to the idea
of equipotentiality, Filimonov (cited in Luria, 1966 [9,
10]), a Soviet neurologist, presented the concepts of
functional pluripotentialism and graded localization
of functions. Specifically, he postulated that no cerebral formation is responsible for one unique task, and

that the same tissue is involved in multiple tasks, given
the right conditions. These concepts signaled a move
from strict localization approaches to understanding
brain–behavior relationships to a dynamic functional
systems approach (i.e. back to a Jacksonian view), most
notably attributed to Alexandr Romanovich Luria. His
approach to neuropsychological investigation stood
in contrast to Western psychometric methods, by
instead focusing on the effect of specific brain lesions
on localized/adjacent functional systems (syndrome
analysis) [10].
Luria stated that simple to more complex behavioral
operations are not localized to a particular brain region,
but instead managed by an “elaborate apparatus consisting of various brain structures” [11]. Though other
definitions of functional systems, or even neural networks, have since been posited, this early view eloquently described the construct. Luria proposed that
all functional systems must involve three core blocks
including (1) the arousal block, (2) the sensory input
block, and (3) the output/planning unit. Structurally,
the arousal unit referenced reticular formation and
related structures that impact cortical arousal; the sensory input unit referenced post central-fissure structures and the integration of cross-modal sensory data;
and the output/planning unit referenced primarily the
frontal lobes and involved planning and execution of
behavior [12].

Luria presented a theory of functional systems
development based on these three functional units. He
suggested that the three functional units develop hierarchically in the form of increasingly complex cortical
zones. These zones correspond to primary, secondary,
and tertiary motor and sensory areas, which develop in
order of complexity, with the tertiary planning unit

(anatomically demarcated by prefrontal areas) appearing last [12]. Luria’s developmental theory mirrors
Jackson’s proposal that neuro-anatomical development
proceeds upward from the spinal cord to neocortex and
from the posterior to anterior [4].
Functional systems, of course, are organized
within a far more complicated web than Luria’s original three-tiered theory. Still, modern brain researchers have “run” with the idea of the functional system.
Recent research has explored questions of the nature
of top-down control (vertical integration), with some
investigators arguing for specific areas within the
stream as primary originators (e.g. lateral prefrontal
cortex [13]), while others argue for different cortical
systems as top-down controllers (e.g. fronto-parietal
and cingulo-opercular control networks [14]).
Functional neuroanatomy is the basis of our
understanding of the human condition, as is an understanding of how that anatomy interacts with the body
and its environment; a complex dance. What we do
know is that almost any behavior, even a slight deviation in heartbeat interval, may be influenced by
myriad factors within the nervous system. A deviation
of heartbeat interval can be influenced by fluctuations
in physical activity, thinking, and emotional status [15,
16]. Our exploration of brain–behavior relationships
is further complicated by language, and more specifically the definition of constructs that are chosen to
define these relationships. Take, for example, our
understanding of a change in heartbeat interval and
its relationship to emotion. Constructs such as fear,
anger, sadness, and happiness describe rather large
subsets of behavior. In order to capture these emotions
at a brain level, Arne Ohman has suggested that emotion is a “flexibly organized ensemble of responses,
which uses whatever environmental support is available to fulfill its biological function” [17].
This is a noticeably loose definition. It has to be with

constructs such as emotional memory [18], expressive
aprosodia and receptive aprosodia [19], emotional intelligence [20], approach and withdrawal [21], and terms
such as melancholy, wistfulness, euphoria, mirth, and
doldrums floating around in the collective consciousness
of researchers and the lay public. To understand that


A lifespan review of developmental neuroanatomy

minute shift in heartbeat interval, we need to understand
the emotional state of our subject. To evaluate the functional systems involved in that heartbeat shift, we need to
understand the interconnecting pathways involved in
vagal (cranial nerve X) control of the heart (direct parasympathetic nervous system influence is necessary in a
beat-to-beat change in heart rate). What structures connect to the vagus? What structures connect to those
structures? Are there afferent feedback loops? How do
these control systems develop? The so-called “decade of
the brain” has extended and we have an ever-developing
complexity in our understanding of the brain’s role in
defining what it means to be human. It is an exciting time
to be a neuropsychologist.
The development of functional neuroanatomy
across the lifespan is a complicated topic. This chapter,
necessarily, is not a comprehensive review of the subject,
but is instead a detailed introduction. As such, the
purpose of the following sections is to discuss current
research and our current knowledge regarding the neuroanatomical structures that are of particular interest
with regard to understanding cognitive and emotional
development. The chapter is therefore organized as
follows: (1) Brain structure. In this section, we cover
cellular structures and brain areas in their prototypical

forms, discussing general associated functions. (2) Brain
development across the lifespan. This section covers the
mechanism of brain development and notable changes
over time in anatomy and function.

Brain structure
The nervous system is composed of central (CNS),
peripheral (PNS), and enteric branches. The brain
and spinal cord form the CNS. Nerves that connect
the spinal cord and brain to peripheral structures such
as the heart compose the PNS. The enteric nervous
system controls the gastrointestinal system primarily
via communication with the parasympathetic and
sympathetic nervous systems.

Brain cells
The brain has two classes of cells, neurons and glia. There
are many different types of cells within each class,
although they all share characteristics that distinguish
these nervous system cells from other cells in the body.
Generally stated, neurons are specialized electro-chemical
signal transmitters and receivers. Glia serve a supporting
role in the brain (e.g. nutritional and scavenger functions,
growth factors, blood–brain barrier components, and

myelin–white matter creation) and have a role in neurogenesis during development (e.g. radial glia as neuron
progenitors [22]).

Neurons
Within the adult neocortex, there are billions of neurons and 10 to 50 times more glia. The total number of

synapses is estimated to be approximately 0.15 quadrillion. Myelinated white matter is estimated to span
between 150 000 and 180 000 kilometers in the young
adult [23, 24].
Neurons are composed of a cell body, axon, and
dendritic fields. The cell body contains less than
a tenth of the cell’s entire volume, with the remainder contained within the axon and dendrites [25].
Synapses are interaction points between neurons.
An individual neuron communicates via action
potential. Action potentials are all-or-none electrical
events which are excited (promoted) or inhibited
(prevented) based on the nature of synaptic stimulation (e.g. the nature of chemical and electrical
stimulation via neurotransmitters and graded potentials). A single neuron may be in direct contact (via
synapse) with thousands of other neurons. The firing
rate of a neuron is influenced by the summation of
inhibitory and excitatory events along the axon and
dendritic–synaptic interactions among the numerous connections. Speed of transmission is a function
of white matter width and myelination.
White matter may be myelinated or unmyelinated.
Myelination increases transmission speed. Myelin
sheathes (covering axons) are generated by specialized
glial cells in the brain called oligodendroglia, and in the
periphery by cells called Schwann cells.
Neurons may be classified as unipolar, pseudounipolar, or bipolar depending on the cell body form and
number and arrangement of processes. Functional characteristics are also used in classification (e.g. afferent
neurons that conduct signals from the periphery to the
CNS are also called sensory neurons, and efferent neurons that conduct signals from the CNS to the periphery
are also called motor neurons). Further, neurotransmitter receptor types are also used to describe neurons.
For example, neurons containing serotonin or glutamate are referenced as serotonergic or glutaminergic
neurons [26].

Neurotransmitters
Neurotransmitters are chemical agents that bind to
specialized receptors on neurons. Neurotransmitters

5


Section I: Theory and models

specifically relevant to neuropsychology include,
but are not limited to, serotonin (e.g. depression/
anxiety), acetylcholine (e.g. memory), dopamine
(e.g. motor), norepinephrine (e.g. depression), glutamate (e.g. memory), and gamma-aminobutyric acid
(e.g. anxiety). The effect of a particular neurotransmitter on a functional system is largely determined
by receptor types. Each neurotransmitter can bind to
multiple receptor types. The distribution of receptor
types is not even throughout the brain and may
influence emotional state/traits, disease outcomes
in mental health, and response to psychopharmacologically active medications. For example, protein
expression of serotonin receptors in the prefrontal
cortex differentiates successful suicidal patients and
controls [27]. Asymmetry in serotonin receptors is
found in depressed patients with greater right prefrontal receptor density than left compared with controls
[28]. Moreover, higher baseline binding potential in
chronic depression pharmacological treatment is
associated with worse outcomes [29]. For a more
comprehensive review of neuronal structure and
function, see Levitan and Kaczmarek [30].

Cranial nerves

6

There are 12 cranial nerves. A solid understanding
of the effects of cranial nerve lesions, or the effects
of upstream lesions on cranial nerve activity, is an
important tool for neuropsychologists in evaluating
patient presentation. Cranial nerves have both sensory and motor functions. For example, cranial nerve
level control of the muscles of the eye is distributed
across three nerves (the oculomotor, trochlear, and
abducens nerves), whereas sensory information from
the eye is transmitted via the optic nerve. The optic
nerve projects from the retina, to the thalamus,
through the temporal and parietal cortices, and to
the calcerine cortex in the occipital lobe. Processing
is not performed at the level of the cranial nerves,
which only serve to connect/transmit information
from processing centers. Testing cranial nerve function can, however, give clues as to the nature of a
lesion. For example, the optic radiations of the optic
nerve travel close to the surface of the cortex of the
temporal lobe. A unilateral lesion of the temporal
lobe can cause a contralateral visual field cut.
Examining associated behavioral changes can suggest
a location for a functional lesion. For a more detailed
review of cranial nerve functions and assessment see
Monkhouse [31].

Rhombencephalon
The rhombencephalon, or hindbrain, is composed of
the medulla oblongata, the pons, and the cerebellum.

Functionally, the hindbrain contains several structures
involved in neural networks regulating autonomic
nervous system (ANS) function and arousal. Cranial
nerves regulating the ANS (vagus), and movements of
the mouth, throat, neck, and shoulders (glossopharyngeal, hypoglossal, trigeminal, spinal accessory) are
found in the hindbrain. Additional structures include
the reticular formation (basic autonomic functions,
respiration), nucleus of the solitary tract (in actuality,
this refers to several structures) and the nucleus ambiguus. The nucleus ambiguus and the nucleus of the
solitary tract are the primary interface junctions for
the vagus nerve, which enervates the viscera. In thinking about the development of brain structures and
functional systems relevant to emotional and cognitive
behaviors, it may be helpful to consider phylogeny and
lessons from comparative neuroscience.
Transitioning from reptiles to mammals, we see
the emergence of myelinated vagus. Returning to our
earlier example of emotion and changes in heartbeat
intervals, Porges [32, 33] discusses the impact of this
system and its development on social engagement
behaviors in humans with his polyvagal perspective,
contrasting and elucidating the interactions of brainstem structures, peripheral afferents, cortical and
subcortical top-down control, and myelinated and
unmyelinated vagal efferents. Regulation of the autonomic nervous system is a complex component of
social behaviors and emotional response. Cortical, subcortical, and other brain structures such as the amygdala, hypothalamus, orbitofrontal cortex, and temporal
cortex all interact via direct and indirect pathways
with these hindbrain structures to influence parasympathetic and sympathetic nervous system response.
Further, the nucleus of the solitary tract receives afferent input from the periphery (e.g. baroreceptors, which
monitor and relay changes in blood pressure), which
is in turn distributed to subcortical and cortical structures for processing.
These hindbrain structures should be considered as

output and input nuclei for a range of supportive behavioral features in the human (e.g. facilitating appropriate
arousal levels for performing cognitive, exertional, and
social functions). Also contained within the rhombencephalon are the pons and cerebellum. Functionally,
these structures contribute to fine motor control via
postural and kinesthetic feedback to volitional areas


A lifespan review of developmental neuroanatomy

(e.g. premotor and motor cortex). This includes facilitating motor movements in speech.
In addition to fine motor control, lesions of the
cerebellum have a wide range of behavioral and cognitive
consequences. The cerebellum has reciprocal connections to brainstem nuclei, hypothalamus, and prefrontal
and parietal cortices (among other areas). Behavioral
effects of cerebellar lesions observed in the literature
include autonomic disregulation [34], flattening of affect,
distractibility, impulsiveness, stereotyped behaviors,
depression [35], memory and learning dysfunction, language problems, and visuospatial effects [36]. Though
these problems in cognition and behavior are clearly less
severe than lesions in associated areas of neocortex and
some reported issues have not been replicated, the variety
of impacts suggests an important role for the cerebellum
in some of these functional systems. There are some
interesting clues as to what that role may be.
Recent research has shown additional roles of the
cerebellum in speech with lesion effects beyond dystaxic
motor impairments in speech formation. Ackerman
et al. [37] review recent clinical and functional imaging
data as they pertain to speech syndromes and potential
connections to other cognitive functions following cerebellar lesions. They argue that connections to language

areas in the cortex function as conduits to subvocalization (self speech) which is involved in verbal working
memory (a right cerebellar/left frontal interaction).
This subvocalization argument is also present in other
modalities (e.g. imagined movements). These connections, along with the hypotheses of planning and rehearsal components attributed to cerebellar activity, may
explain the increasing evidence of wide-reaching cognitive and behavioral effects with cerebellar lesions.

Mesencephalon
The midbrain includes the substantia nigra (linked
to dopamine production and Parkinson disease), the
superior and inferior colliculi (visual and auditory system actions), and a large portion of the reticular activating system (RAS). The reticular activating system,
formed in part by nuclei in the midbrain tegmentum,
plays a role in consciousness. The discovery of the RAS
was critical for understanding coma. It serves as a
modulator of sleep and wakefulness via connections
to the diencephalic structures, the thalamus (thalamic
reticular nucleus) and hypothalamus. These connections ascending from the reticular formation are part
of the ascending reticular activating system. Also nested
within the midbrain are projections from the dorsal

raphe nucleus (from the hindbrain structure, the pons).
The raphe is a source of serotonin and is also involved
in the regulation of sleep cycles.
The substantia nigra is functionally linked to the
basal ganglia, specifically the caudate nucleus and the
putamen (referred to collectively as the striatum). It is
divided into two sections, the pars compacta and the
pars reticulata. The pars compacta projects to the
striatum and the pars reticulata projects to the superior colliculus and thalamus. The substantia nigra
provides dopamine to the basal ganglia and it is part
of the extrapyramidal motor system. Lack of dopamine in the striatum leads to parkinsonian symptoms

(rigidity, tremor, slowing); the system still functions
without the substantia nigra as long as the level of
dopamine is regulated properly.
The superior and inferior colliculi are interconnected small structures in the midbrain that are
involved in visual and auditory orientation and attention. The superior colliculus receives projections from
the frontal eyefields (premotor cortex) and controls
saccadic movements. The interconnection and functional relationship to the prefrontal cortex has led to
the use of saccadic eye movement models in evaluating
the neural circuitry of schizophrenia and other psychiatric illnesses thought to involve prefrontal cortical
systems [38].

Telencephalon
The telencephalon includes the entirety of the cerebral
hemispheres including the diencephalon, limbic system, basal ganglia, and other structures. We will continue working our way through the brain from the
ventral to the dorsal and the caudal to the rostral. We
begin the discussion of the telencephalon with the
thalamus and hypothalamus.

Thalamus and hypothalamus
The thalamus and hypothalamus, among other structures, compose the diencephalon. The thalamus is a
complex bilateral structure with extensive reciprocal
connections to major structures throughout the brain,
including efferent fibers to cortical regions (thalamocortical axons) and afferent fibers from cortical regions
(corticothalamic axons). There are 11 thalamic nuclei
that are classified as either relay or association nuclei
based on their target projections. These are specific
nuclei. There are also nonspecific nuclei, stimulation
of which yields activations along a large area of cortex.
The thalamus has nuclei with projections to all major

7


Section I: Theory and models

8

sensory areas except for olfaction. Further, it is a projection site for the RAS (important role for arousal and
sleep; logical, given the sensory connections). For a
comprehensive review of thalamic nuclei and function,
please see Jones [39].
Because of the heterogeneity of nuclei, associated
functional systems, and projections of the thalamus,
it can be difficult to understand which systems are
involved in the neuropsychological sequelae of thalamic lesions. One approach is to use functional imaging
technologies, such as PET scan, to evaluate diaschesis
effects of a localized thalamic lesion [40].
The thalamus is the most likely location for a
strategic infarct (e.g. from a stroke) to cause a dementia. This is probably a consequence of the role of the
thalamus in regulating higher-brain activity. As a subcortical structure with dense connections throughout
both hemispheres, the thalamus reflects the lateralization of function of involved cortical areas. For example, contralateral attentional neglect occurs with rightsided thalamic lesions. A similar presentation is also
evident with right parieto-temporal lesions [41].
Developmentally, abnormalities in thalamic nuclei
(e.g. massa intermedia), have been associated with
future manifestations of psychiatric conditions such as
schizophrenia. The massa intermedia is detectable early
in development, within 13 to 14 weeks of gestation [42].
There is some evidence that the medial dorsonuclei
reduces in volume as schizophrenia progresses, an
area rich in connections to prefrontal cortex (an area

implicated in the expression of schizophrenia) [43].
Shimizu et al. [44] find evidence of a developmental
interaction between the massa intermedia and mediodorsonuclei in schizophrenic patients.
The hypothalamus is primarily involved in visceromotor, viscerosensory, and endocrine (oxytocin and
vasopressin) functions. It directly modulates autonomic
nervous system activity. It functions as one connection
point for limbic structures (involved in emotional regulation) to control of the autonomic nervous system.
The stria terminalis, an afferent white matter tract,
connects the amygdaloid bodies to the hypothalamus.
The hypothalamus then has direct efferent connections
to brainstem nuclei, including the output nuclei for
vagal control (nucleus ambiguus) and sympathetic neurons in the spinal cord. These connections make the
hypothalamus a critical component in functional systems involved in rage and fear responses.
The interaction of three structures, the hypothalamus, pituitary gland, and adrenal gland, is important in the regulation of mood, sexuality, stress, and

energy usage. The so-called hypothalamic-pituitaryadrenal (HPA) axis has been implicated in social
bonding and mate-pairing in comparative neuroscience and human research. Developmentally, it
has been found in prairie voles that exposure to oxytocin (a hormone produced in the HPA) early on is
associated with capacity for social bonding in adult
animals [45, 46].
Further connections also involve the hypothalamus
in memory functions (e.g. the hippocampus and mammillary bodies are connected via the fornix). Lesions to
the mammillary bodies, a hypothalamic structure, can
cause severe anterograde memory deficits. Deterioration
of this system is associated with the development of
Alzheimer’s disease.

Basal ganglia
The basal ganglia are a set of subcortical grey matter
structures most often associated with aspects of motor

control, though recent research demonstrates additional roles in functional systems, including cognitive
domains such as attention. Unlike primary motor cortex lesions, paralysis does not occur with basal ganglia
damage. Instead, abnormal voluntary movements at
rest, and initiation and inertia deficits are typical.
The structures included in the basal ganglia vary by
nomenclature, but commonly reference the caudate
and putamen (i.e. dorsal striatum or neo-striatum),
globus pallidus (internal and external segments), substantia nigra, and subthalamic nucleus. Other nomenclatures include the amygdala (discussed here with
limbic system structures), and the nucleus accumbens
and olfactory tubercle (ventral striatum).
There are two pathways of activity in the basal ganglia with opposing behavioral outcomes, the indirect and
the direct pathways. These pathways facilitate and inhibit
the flow of information through the thalamus and operate simultaneously (the overall effect is a function of the
current balance of activation pattern between the pathways). Activation of the direct pathway increases thalamic activity and activity of the cortex. Activation of the
indirect pathway decreases thalamic activity and activity
of the cortex. Damage to the basal ganglia can either
decrease or increase movement depending on which
structures/neurotransmitters are impacted within the
direct and indirect pathways.
Several neurodegenerative disorders are associated
with basal ganglia structures including Parkinson disease, Huntington disease, Wilson disease, and various
multisystem atrophies (MSAs). Psychiatric disorders


A lifespan review of developmental neuroanatomy

that appear in childhood including attention deficit
hyperactivity disorder (ADHD) and Tourette syndrome
are also associated with abnormalities in the basal ganglia. Recent studies have shown reduced overall caudate
volumes and lateralized differences in caudate and

globus pallidus volumes (left greater than right) in children diagnosed with ADHD [47]. Further, fractional
anisotropy, a measure of apparent white matter integrity
using a structural imaging technique called diffusion
tensor imaging (DTI), is reduced in ventral prefrontal
to caudate pathways in children with ADHD [48].
Behaviorally, this prefrontal/caudal circuit is thought to
relate to inhibitory control (e.g. a go–no go task). As for
etiological factors, there is recent evidence that early diet
can influence future caudate volumes and intellectual
aptitude [49], suggesting a potential avenue for environmental factors such as nutrition on neural structure and
cognitive/behavioral outcome.
The role of basal ganglia structures in cognitive processes is multi-factorial. Aron et al. [50] present converging evidence on the role of a fronto-basal ganglia network
in inhibiting both action and cognition. They review
both comparative and human data using go–no go
tasks and conclude that the fronto-basal ganglia systems
are critical in determining individual differences in a
variety of human behaviors, stating, “Variation to key
nodes in this circuitry (or to their connections) could
produce important individual differences, for example,
in aspects of personality, in the response to therapy
for eating disorders, and in liability toward and
recovery from addiction. Developmental, traumatic,
or experimentally induced alterations to key nodes in
the control circuit lead to psychiatric symptoms such
as inattention, perseveration, obsessional thinking
and mania, and could also have relevance for movement and stuttering.”

Limbic system
The limbic system is a network of structures involving
subcortical, cortical, and brainstem regions that play a

role in emotional behaviors including emotionally
related memory/learning and social interactions.
Important subcortical gray matter structures of the
limbic system include the amygdala, nucleus accumbens, and hypothalamic nuclei (as illustrated above in
the HPA), among others. Cortical structures include
aspects of the prefrontal cortex (orbitofrontal), cingulate gyrus, and the hippocampus.
The amygdala, probably the most central structure
(conceptually) of the limbic system, is almond-shaped

and located deep in the anterior temporal lobe. There
are multiple nuclei which can be divided into two
groups, a basolateral group and a corticomedial
group. The amygdala is rich with connections to cortical areas including the orbitofrontal cortex and temporoparietial cortex, subcortical structures including
the basal ganglia, thalamus, hypothalamus, brainstem
structures including autonomic output nuclei, and the
hippocampus (a phylogenetically older area of cortex
involved in memory consolidation).
The amygdala is involved in functional systems of
emotion, reward, learning, memory, attention, and motivation. Though researchers have strongly focused on fear
conditioning and negative emotions in the amygdala (the
role of the amygdala in fear startle reflex), it also has a
role in positive emotion. For a review of the role of the
amygdala in positive affect see Murray [51]. Direct stimulation of the amygdala via electrodes has been shown to
most probably elicit fear or anger responses. In rats,
electrical stimulation of the amygdala elicits aggressive
vocalizations [52]. In humans, in a study of 74 patients
undergoing presurgical screening for epilepsy, fear
responses were most frequent with amygdala stimulation
(higher rate for women than men) [53].
Functionally, in addition to a central role in emotional processing, the amygdala has a role in olfaction

(the corticomedial cell group is directly connected to
the olfactory bulbs), though there are also interconnections to other sensory areas. The amygdala appears
to respond to threatening sensory stimuli via mobilization of fight or flight responses [54], but it also
responds to positive sensory stimuli. The key is not
the modality of the sensory input or the valence, the
amygdala will respond to all, but whether the sensory
data contain affective content. The amygdala also
enhances cognitive performance in the context of
emotional stimuli (e.g. emotional memory formation
via linkages to the hippocampus) [55].
Developmental disorders such as autism have been
linked to abnormal changes over time in the amygdala.
In addition to increased white matter volumes and
overall head size early in autism, in a study of young
children with autism (36–56 months of age), the
amygdala was enlarged by 13–16%. Amygdala volume differences, both larger and smaller, are found in
many psychiatric conditions, including schizophrenia,
depression, bipolar disorder, generalized anxiety disorder, and borderline personality disorder. Sometimes,
conflicts appear with one study showing increased
amygdala volume in depression and another showing
decreased amygdala volume. Tebartz et al. [56] suggest

9


Section I: Theory and models

a resolution to such conflicting results may be a function of the “dominant mode of emotional informational
processing.” They hypothesize that an enlarged amygdala may relate to depressed mood, anhedonia, phobic
anxiety, and rumination and that a smaller amygdala

may relate to emotional instability, aggression, and
psychotic anxiety.
Another limbic structure, the hippocampus, is
located ventrally and medially in the temporal lobe, and
can be divided into four regions, designated CA1, CA2,
CA3, and CA4. CA stands for cornu ammonis. A major
input pathway to the hippocampus stems from the entorhinal cortex and the main output pathway from the
fornix. The hippocampus is a critical structure to learning new information. Damage to the hippocampus can
cause severe anterograde learning deficits such as in
Korsakoff’s syndrome, a condition caused by vitamin
deficiencies in chronic alcohol abuse that damages hippocampal structures. Classically, the role of the hippocampus in memory was brought to the attention of the
scientific community via a case study in 1957 [57] of a
patient who underwent bilateral temporal lobe resections, referred to as HM. HM had intact remote and
autobiographical memory until the surgical procedure,
but was unable to learn new information subsequently.
Corkin [58] reviews 45 years of research on HM.
Laterality and extent of peripheral involvement
determine the type and severity of memory impairment
with hippocampal lesions. Involvement of projection
areas such as the entorhinal cortex increases the severity
of anterograde deficit. This is the system that deteriorates in cortical dementias such as Alzheimer’s disease.
Bilateral lesions produce dense anterograde memory
deficits. A unilateral left or right hemisphere lesion will
produce verbal or spatial memory deficits, respectively.
Normal development of the hippocampus can be
interrupted by environmental factors. Hippocampal
volumes are reduced in victims of childhood abuse
[59]. Pediatric temporal lobe epilepsy can also have a
significant impact on hippocampal development.
Hippocampal atrophy in children with epilepsy has

been shown to relate to reduced neuropsychological
performance [60].

management. The cortex is thought to be necessary
for conscious behaviors (thalamo-cortical relationships), though recent research suggests that some
level of consciousness can exist without the cortex
[61]. There are two hemispheres divided by a large
fissure called the longitudinal fissure. They are generally
superficially symmetrical and structures are mirrored
across the two. Though there are individual differences
in brain structure, on average it is known that the right
frontal lobe tends to be wider than the left and the left
planum temporale of the superior temporal cortex is
larger than the right (thought to be related to language
development). Recent neuroimaging research has also
demonstrated substantial differences in white matter
connectivity; for example, in systems underlying language functions between the left and right hemisphere
using diffusion tensor imaging [62].
Several helpful mapping systems have been created
to identify various brain regions. Brodmann’s map is
one of the best-known systems and it is based on
cellular architecture (see Fig. 1.1).

10

The cortex is divided into four lobes, the frontal,
temporal, parietal, and occipital. As was discussed earlier in the chapter on top-down control and the organization of functional systems, the cortex is the most
highly organized and complex aspect of brain

31

2

5
7

9
19
46
40
45 44

43

18

39

10
41
42

22
17

11

21
38

19

37

18

20
6

4

3 1

8

2

5
7

9
31

24
32
10

11

19

23
33

12

Cerebral cortex

4

6
8

26
29
30
25 27
35
34

18

17

28
38
38

19
37

20

Fig. 1.1. Brodmann’s map.

18


A lifespan review of developmental neuroanatomy

The motor and sensory areas of cortex are divided
by a large fissure called the central sulcus (also known
as the Rolandic fissure and cruciate fissure). This
divides frontal and parietal areas and represents
a steep functional boundary. The regions on either
side of the fissure are the primary motor cortex
(Brodmann’s area 4, anterior of the fissure) and primary somatosensory cortex (Brodmann’s areas 3, 1,
and 2, posterior of the fissure). Organizationally, it is
helpful to think in terms of primary, secondary, and
tertiary association cortex. Functions progress from
simple to complex, from unimodal to multi-modal.
Each sensory system is composed of a primary
projection area and secondary and tertiary association
areas. Functionally, the primary projection areas are
the first area of cortex to receive information from a
specific sensory system. Sensory data reaching the
primary projection area are necessary for conscious
perception. Lesion of primary sensory cortex can
result in a loss of awareness of the affected modality;
however, the individual may still respond reflexively to
the modality (e.g. blindsight). Further sensory processing occurs in secondary association cortex, but it

is still limited to one modality. Finally, tertiary association cortex (e.g. Brodmann’s area 7 in the parietal
lobe) integrates data from multiple sensory modalities.
The primary sensory projection areas are as follows: (1) vision = occipital cortex (calcerine cortex,
Brodmann’s area 17), (2) audition = superior temporal
gyrus, temporal lobe (Brodmann’s areas 41 and 42),
(3) somatosensation = postcentral gyrus, parietal cortex
(Brodmann’s areas 3, 1, and 2), (4) gustation = parietal
operculum (Brodmann’s area 43), (5) olfaction = anterior tip of the temporal lobe (Brodmann’s area 38).
The secondary and tertiary association cortices surround and extend from the primary projection areas
(e.g. visual association areas roughly correspond to
Brodmann’s areas 18 and 19).
In a normally organized brain, the left hemisphere
is dominant for language functions. Around 90%
of the population is estimated to be right-handed.
Sinistrality is a clue that a brain is not normally organized. Recent neuroimaging studies have demonstrated
different activation patterns in left-handers when processing language, with greater bilateral activations and
shifts towards right-hemisphere language processing
[63]. Assumptions about localization and lateralization of function should be treated with greater caution
in these cases. The occurrence of sinistrality appears
to be a combination of genetic and environmental
factors. Sinistrality is over-represented in several

neurological/psychiatric conditions such as epilepsy,
autism, and schizophrenia. A recent study demonstrates a potential genetic link between sinistrality
and schizophrenia [64].
The hemispheres are functionally specialized to
deal both with different kinds of information and the
same information in different ways. Although an indepth review of laterality is well beyond the scope of
this chapter, a few common areas of study include
language, neglect (attentional space), memory (nonverbal versus verbal), and emotion.

In a normally organized brain, different aspects of
language functions are divided across the hemispheres
with semantic content, production, and rhythm localized to the left hemisphere, and expressive and receptive prosody/melody localized to the right hemisphere.
Further, there is evidence that the right superior temporal lobe is instrumental in the identification of individual voices [65]. Lesions, depending on laterality and
position relative to the central sulcus (anterior or
posterior), will have expressive or receptive consequences, or both (e.g. a right frontal lesion may produce an expressive aprosodia, or inability to modulate
the tone of speech output in a meaningful way,
whereas a left frontal lesion may produce an expressive
aphasia, inability to produce speech fluently).
In emotion, laterality is not a simple matter. For
example, a model of aspects of emotional experience
that has been applied across the lifespan is proposed
by Fox and Davidson [66]. They present a view of
emotional expression with emphasis on right and
left frontal modulation. Much of Fox’s work has
consisted of developmental EEG research. Specifically, Fox infers right and left frontal activation
from localized alpha bandwidth (~8–12 Hz) suppression. Two constructs are proffered as indicative
of left versus right frontal activation respectively,
approach and withdrawal.
Approach and withdrawal behaviors as recently
conceptualized refer to social interactions. Approach
behaviors are associated with positive affect and withdrawal behaviors are associated with negative affect.
These behaviors are evident, at least in some form,
as early as infancy. In one study, with a group selection
criterion of motor reactivity and a disposition component (assessed through parent report and observation)
infants with high motor reactivity and a disposition
towards negative affect were found to be more likely
to evidence greater right frontal EEG asymmetry,
supporting the notion of right frontal mediation of
negative emotion [67].

11