The Neuroanatomy of Attention

Christopher M. Filley, M.D.1

ABSTRACT

Attention is a complex neurobehavioral domain that is essential

for all higher functions. Large areas of the brain are devoted to attention,
reflecting its importance in the entire range of mental operations. Cur-

Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.

rently, two major distributed neural networks are recognized as mediating
complementary aspects of attentional function. One is a diffuse system that
distributes attention globally. This attentional system is subserved by a
widespread network of thalamic and bihemispheric structures in which the
frontal lobes are particularly important. The second network, a focal system
that distributes attention to salient aspects of spatial experience, is lateral-
ized to frontal and parietal regions of the right hemisphere. Both atten-
tional networks are comprised of cortical and subcortical gray matter struc-
tures, as well as connecting white matter tracts that integrate these regions
into functional ensembles. Neurological disorders frequently produce dra-
matic syndromes reflecting dysfunction of these networks. Among these
syndromes are the acute confusional state, which results from disturbance
of the diffuse system, and left neglect, which follows disruption of the right
hemisphere system. The neuroanatomy of attention is crucial for under-
standing important neurobehavioral syndromes and their treatment.

KEYWORDS: Attention, neuroanatomy, acute confusional state,

neglect, neural networks

Learning Outcomes: As a result of this activity, the reader will be able to describe (1) the neuroanatomical
representation of attention in the human brain and (2) the clinical syndromes of inattention that result from var-
ious neurological disorders.

In 1890, the American psychologist and sion by the mind, in clear and vivid form, of one
philosopher William James wrote in his monu- out of what seem several simultaneous possible
mental The Principles of Psychology, “Everyone objects or trains of thought. Focalization, con-
knows what attention is. It is the taking posses- centration, of consciousness are its essence. It

Attention: Its Neuroanatomical Bases, Forms, Disorders, Assessment, and Treatment in Adults with Specific Neurological
Disorders; Editors in Chief, Nancy Helm-Estabrooks, Sc.D., and Nan Bernstein Ratner, Ed.D.; Guest Editor, Laura L.
Murray, Ph.D. Seminars in Speech and Language, volume 23, number 2, 2002. Address for correspondence and reprint
requests: Christopher M. Filley, M.D., UCHSC B-183, 4200 East Ninth Avenue, Denver, Colorado 80262. 1Behavioral
Neurology Section, Denver Veterans Affairs Medical Center, and the Department of Neurology and Psychiatry, University
of Colorado School of Medicine, Denver, Colorado. Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh
Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. 0734-0478,p;2002,23;02,089,098,ftx,en;ssl00110x. 89
90 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 23, NUMBER 2 2002
implies withdrawal from some things in order
to deal effectively with others. . . .”1 Despite
the appeal of this simple and eloquent descrip-
tion, attention has proved to be a singularly elu-
sive phenomenon in psychology and neuro-
science, and despite the more than a century of
research since James’ time, many questions re-
main unanswered. The organization of atten-
tion in the human brain is not clearly under-
stood, and even a uniformly accepted definition
of the word has yet to emerge.
Paradoxically, the neurology of attention
can be gainfully studied even if its definition
and phenomenological details remain unre-
solved. A major line of inquiry, permitting a
more sophisticated understanding of attention,
is the considerable clinical experience with in-
dividuals who have attentional disorders. Ad-
ditional information has been derived from
experimental studies of humans and higher
primates. Another more recent contributor to
this area of study has been a growing literature
on the functional neuroimaging of attention
that has enabled more precise localization of
neural networks devoted to attention.
In this article, the neuroanatomy of at-
tention in the human brain is reviewed and
summarized from a clinical perspective. A dis-
cussion of the often-confusing terminology
pertaining to attention will serve as a point of
departure, with particular consideration of the
distinction between attention and arousal.
Then, the two prominent attentional systems
of the brain will be considered, as well as clini-
cal syndromes resulting from disturbances in
these systems. The article ends with a discus-
sion of attention as a neurobehavioral domain
to which the idea of distributed neural net-
works is readily applicable.
TERMINOLOGY
Attention has been defined in many ways, and
various subcategories of the concept have been
proposed in attempts to refine the meaning of
attention in particular contexts. Whereas these
distinctions are useful for detailed studies of
human cognition, it is probably best for clinical
purposes to begin with a basic working defini-
tion of attention. Generally speaking, attention
can be defined as the ability to maintain a co-
herent line of thought or action.2
Attention is closely related to arousal, but
there is an important distinction between these
two phenomena. Arousal can be regarded sim-
ply as the degree of wakefulness exhibited by
the individual. In their classic monograph on
stupor and coma, Plum and Posner3 discuss
arousal in terms of the “level” of consciousness
and distinguish it from the “content” of con-
sciousness, which refers to the higher cognitive
and emotional functions. To illustrate this dis-
tinction, language, one component of the con-
tent of consciousness, is only possible if a suffi-
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
cient level of consciousness exists. Clinically,
some patients display normal arousal, whereas
others deviate from this state in a variety of
ways. Sleep is a normal departure from arousal,
whereas disorders of arousal range from stupor
and coma to agitation and hyperalertness.4
The neuroanatomy of arousal has been rela-
tively well-understood since the 1940s, when the
brainstem and thalamus emerged as crucial brain
structures responsible for this phenomenon (Fig.
1). Classic ablation experiments in nonhuman
animals established that the brainstem ascending
reticular activating system (ARAS) profoundly
influences arousal as manifested by electroen-
cephalographic (EEG) activity5 and that a dif-
fuse thalamocortical projection system activates
the entire cerebrum.6 It is now recognized that
the ARAS and its relays in the thalamus, the in-
tralaminar and midline nuclei, are critical for
normal arousal, and more recent functional neu-
roimaging studies have confirmed these observa-
tions.7 Arousal can thus be conceptualized as de-
pending on the concerted action of the ARAS
and thalamus that serves to activate the entire
brain. With this framework, it is easier to under-
stand the clinical dictum of Plum and Posner3
that coma requires either a structural lesion of
the brainstem ARAS or bilateral damage to the
cerebral hemispheres.
Although disorders of arousal are always ac-
companied by attentional deficits, the converse is
not true. One example of this dissociation is the
case of a patient with a subtle acute confusional
state who may be inattentive, distractible, and
perseverative but has normal arousal as judged
by the degree of wakefulness. Arousal can also be
preserved in severely impaired patients with
 NEUROANATOMY OF ATTENTION/FILLEY 91

Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.

Figure 1 Drawing of the brain in the midsagittal plane illustrating the major structures responsible for arousal
and attention. Arousal is mediated by the brainstem ARAS and its rostral terminus, the thalamus (T). From the
thalamus, numerous white matter fibers project to the cerebral cortex, forming the neuroanatomical basis of
diffuse attention.

major brain destruction; individuals in a veg-
etative state8 have paradoxically normal arousal
and sleep-wake cycles, despite the absence of
all other neurobehavioral functions.4 Thus, al-
though attentional deficits are typically com-
mingled with disorders of arousal, attention can
be impaired even when arousal is normal. Selec-
tive deficits of attention imply relatively circum-
scribed involvement of brain regions subserving
attentional functions.
A myriad of terms have been used to de-
scribe varieties of attention, many of which are
more useful in specific experimental contexts
than they are in daily clinical practice. Three
subtypes of attention, however, are useful and
help to simplify a consideration of the neu-
roanatomy of attention.4 Selective attention is
the general capacity to focus awareness on rele-
vant stimuli for very brief periods of time (i.e.,
a few seconds). Sustained attention, sometimes
called concentration or vigilance, is the selec-
tive attention to stimuli for a more extended
time period. Directed attention refers to atten-
tion to the contralateral side of space, also
known as the contralateral hemispace.
THE DIFFUSE ATTENTIONAL
SYSTEM
Among the many capacities organized by the
human brain, one of the most crucial is that
which permits the focusing of mentation on
important events that come to consciousness.
Humans are continually subjected to a flood of
sensory input, both from external sources and
from within, that would overwhelm the neu-
robehavioral capacities of the brain without
92 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 23, NUMBER 2 2002
some kind of filtering mechanism. The ability
to attend to relevant aspects of experience in-
fluences all aspects of behavior and is critical
for the effective operation of any higher cogni-
tive or emotional system. Every teacher, for ex-
ample, is familiar with the necessity for stu-
dents to “pay attention” in school lest even the
best efforts of pedagogy go for nothing.
At its most fundamental level, attention is
represented in the human brain as a widespread
collection of interconnected structures that has
been called the attentional matrix.9 This diffuse
system is responsible for maintaining a tonic level
of attention (which, to confuse matters, may be
referred to as arousal in some attention research,
for example, O’Donnell10 and Murray11) that
permits the monitoring of both external and in-
ternal sensory events. In so doing, this process
ensures that the individual is continually updated
about exteroceptive and interoceptive sensory
data that can exert a major impact on functional
adaptation. Although the neuroanatomy of this
diffuse system is still poorly understood, some
progress has been made in identifying its struc-
tural components.
As a rule, the most important structures
mediating diffuse attention are the thalamus
and the cerebral hemispheres (Fig. 1). The
centrally located thalamus in fact participates
in both arousal and attention, in the former by
virtue of its input from the ARAS in the upper
brainstem and in the latter because of its con-
nections to the cerebral hemispheres. The ex-
tensive linkage of the thalamus and the hemi-
spheres provides the essential substrate for the
phenomena of diffuse attention. In particular,
the thalamus makes connections with the cere-
bral cortex, which is vital for the engagement
of the cortices in the many cognitive domains
to which they are dedicated. In this context,
the white matter tracts connecting the thala-
mus with the cerebral cortex deserve mention.
Disorders of cerebral white matter are increas-
ingly recognized as producing a broad array of
neurobehavioral disturbances, including disor-
ders of attention.4,12
An important distinction needs to be
made between the specialized attentional phe-
nomena exhibited by individual cortical regions
and the more global attentional competence
displayed by the brain as a whole. Specific cor-
tical regions can be shown to display atten-
tional capacities in the domains for which they
are specialized (e.g., a task requiring visual at-
tention will result in selectively increased activ-
ity of the visual cortices9). This kind of anatom-
ically segregated attention, however, cannot be
readily tested clinically, so global attention is
more often the focus of the clinical assessment.
Of all cortical regions, damage to the frontal
lobes is most commonly associated with global
attentional dysfunction. Thus the frontal lobes
constitute a particularly important component
of the diffuse attentional system.
The frontal lobes are the largest lobes of
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
the human brain and the most recently ac-
quired in evolution. These areas are implicated
in all higher functions, most particularly those
referred to as “executive functions,” but they
also have a special relationship with selective
and sustained attention. Patients with bilateral
dorsolateral frontal lesions may display pro-
nounced inattention in concert with their defi-
cits in executive function and working memory,
and those with medial frontal lesions may be
profoundly inattentive as a result of apathy or
abulia.4,13 In addition, children with attention
deficit disorder with hyperactivity (ADHD)
have been found to manifest decreased frontal
lobe blood flow that increases after treatment
with methylphenidate.14 Considerable evidence
also supports the hypothesis that the right
frontal lobe may be specialized for the mainte-
nance of attention, particularly for sustained at-
tention. Adults with right frontal lesions have
deficits in sustained attention,15 and functional
neuroimaging studies in normal subjects have
identified this region as important in visual
vigilance.16 Moreover, some functional neu-
roimaging evidence suggests that hypometabo-
lism of the right frontal lobe occurs in adults
with ADHD.17
ACUTE CONFUSIONAL STATE
The most common disorder of attention in
clinical practice is the acute confusional state
(ACS). Like attention, confusion is a difficult
concept to define, but for purposes of this dis-
cussion, confusion can be considered the in-
ability to maintain a coherent line of thought

or action.2 Patients with a confusional state
thus have a singular deficit in attention that in-
terferes with the performance of all other men-
tal operations. Confusion typically results from
acute toxic, metabolic, or structural disorders
of the brain, and ACS is the usual setting in
which this behavior appears. In addition, a
chronic confusional state (CCS), in which an
acute insult or series of insults persists over a
more lengthy period, is also recognized, and
this syndrome with time resembles or evolves
into subcortical dementia.4
In contrast to CCS, ACS presents as a
rapidly evolving disorder of attention with
variable disturbance in the level of conscious-
ness. Two major forms of ACS can be distin-
guished: (1) a “hyperactive-hyperalert” state
with agitation; hallucinations (typically visual);
and often tremulousness, fever, and tachycardia
and (2) a “hypoactive-hypoalert” state charac-
terized by apathy, lethargy, and somnolence.18
In either case, confusion in patients with ACS
results from a reduced capacity to focus, shift,
and sustain attention. The word “delirium” is
invoked by many to describe all such cases, but
this descriptor is most appropriately applied to
the hyperactive-hyperalert form of ACS, best
exemplified by the striking clinical syndrome
of delirium tremens that is caused by abrupt al-
cohol withdrawal in patients with severe alco-
holism. The term ACS is preferable for the full
spectrum of patients with acute confusion be-
cause it most succinctly captures the core neu-
robehavioral deficit.
The pathogenesis of ACS reflects damage
to cerebral areas that normally subserve diffuse
attentional competence. Thus, because diffuse
attention is a widely represented capacity in-
volving the thalamus, the cerebral cortex, and
their white matter connections, disorders that
affect the brain as a whole are the most com-
mon causes of ACS.4 Toxic and metabolic dis-
turbances resulting from systemic intoxication
(e.g., alcohol) or disease (e.g., hypoxia from
respiratory arrest) are capable of producing a
confusional state, alternatively known as toxic-
metabolic encephalopathy.4 Because no struc-
tural damage occurs in most cases of toxic-
metabolic encephalopathy, the outcome is
usually favorable when the offending toxin or
disease is effectively addressed. Diffuse dys-
NEUROANATOMY OF ATTENTION/FILLEY 93
function of the cortical and subcortical gray
matter has long been assumed to underlie
toxic-metabolic encephalopathy, but more re-
cent evidence indicates that the same clinical
picture may occur when the cerebral white
matter is selectively affected by toxins19 or
metabolic disorders.12 In addition, focal struc-
tural lesions of the brain can produce ACS.
Centrally located tumors, for example, may
disrupt attention by interfering with thalamic
function.3,4 Traumatic brain injury leads to
both acute and chronic inattention by damag-
ing the cortical gray matter by contusions, the
deep white matter by diffuse axonal injury, or
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
both.4 Stroke in the cerebral hemispheres may
also produce this syndrome. As can be pre-
dicted from the prominent role of the frontal
lobes in attention, ACS has been observed
after infarction of the frontal lobes related to
rupture of anterior communicating artery
aneurysms.20 Infarction of the right parietal
lobe because of occlusion of the right middle
cerebral artery may also produce ACS,21 an im-
portant observation that pertains to the role of
the right hemisphere in spatial attention.
THE RIGHT HEMISPHERE
ATTENTIONAL SYSTEM
In contrast to the diffuse attentional system,
there is also a system in the human brain that
enables the narrowing of the attentional focus on
motivationally relevant spatial stimuli. Whereas
the diffuse system permits the awareness of se-
lected elements from a wide array of exogenous
and endogenous events, this second system spe-
cifically allows for the distribution of attention to
focal spatial stimuli. This distributed neural net-
work has been called the spatial attentional sys-
tem, and it functions to distribute attentional re-
sources to the contralateral hemispace.9 The
spatial attentional system is strongly lateralized
to the right hemisphere, specifically the posterior
parietal cortex, the dorsolateral prefrontal cortex
in the vicinity of the frontal eye field, and the
cingulate gyrus.9 In addition, subcortical areas,
including the thalamus, striatum, superior col-
liculus, and connecting white matter tracts, also
participate in this network.9 For purposes of this
article, the term “right hemisphere attentional
94 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 23, NUMBER 2 2002
system” will serve as a convenient label for this
neural network.
An important neuroanatomical distinction
in considering the right hemisphere attentional
system is between its posterior and anterior
components. A useful contrast has been drawn
between the “posterior system,” centered in the
parietal lobe and concerned with sensory sur-
veillance and stimulus selection, and the “ante-
rior system,” organized in the frontal lobes and
dedicated to the executive functions of control
and action.22 Mesulam9 has refined this di-
chotomous depiction with a more detailed por-
trayal in which the parietal lobe is responsible
for detecting and representing relevant spatial
information and the frontal lobe has two com-
plementary roles. The dorsolateral prefrontal
cortex is charged with the direction of atten-
tional resources toward an appropriate response
to the assembled information, and the cingulate
gyrus is responsible for maintaining motivation
and effort during the execution of the atten-
tional task.9
Abundant clinical and experimental evi-
dence has led to the notion that the right
hemisphere in most people can be considered
dominant for attention.4,9,23 Just as the left
hemisphere is dominant for language and re-
lated cognitive domains in most individuals,
the right appears to have superiority for medi-
ating directed attention.23 Experience in clini-
cal neurology has long indicated that right
hemisphere lesions are associated with more
frequent, severe, and lasting attentional disor-
ders than are comparably sized and placed le-
sions of the left hemisphere.4,9,23,24 Moreover,
experimental data from normal humans have
confirmed these observations. Intracarotid in-
jections of amobarbital cause contralateral vi-
sual neglect (see later) after right-side but not
left-side injection.25 Studies with EEG have
shown that desynchronization of the right
hemisphere appears after stimulation of either
side, whereas desynchronization of the left
hemisphere develops only after right-side stim-
ulation, implying that the right hemisphere has
a more extensive capacity to respond to exter-
nal stimulation.26
In light of these observations, the organi-
zation of the right hemisphere attentional sys-
tem can be conceptualized by reference to a
differential lateralization of attentional compe-
tence (Fig. 2). This system, the primary loci of
which are in the right frontal and parietal lobes,
is capable of surveying both sides of extraper-
sonal and personal space, whereas the compara-
ble system in the left hemisphere can only at-
tend to the contralateral (right) hemispace.
Thus, a patient with a destructive lesion of the
right hemisphere will have reduced access to the
left hemispace; in contrast, one with a left
hemisphere lesion is more likely to have pre-
served bilateral surveillance because the right
hemisphere is intact. This scheme provides a
satisfying explanation for the frequent clinical
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
observation that left hemisphere lesions, much
as they often produce major linguistic and re-
lated deficits, result at most in minor and tran-
sient contralateral neglect. Neglect from a right
hemisphere lesion, on the other hand, is often a
persistent, devastating syndrome.
NEGLECT
Neglect is a syndrome of failure to report, re-
spond to, or orient to stimuli in the contralateral
extrapersonal or intrapersonal environment, and
this definition requires that the deficit is not due
to elemental sensory or motor impairment.27
Neglect, one of the most intriguing syndromes
in behavioral neurology, in its complete form
manifests as a remarkable unawareness of the
contralateral hemispace or body. Despite an
otherwise normal neurological examination, an
individual with severe neglect is effectively cut
off from one side of his or her external and per-
sonal world. This disorder can be so pervasive
that, even in the absence of other neurological
deficits, it precludes functional competence. In
fact, individuals with lasting neglect are less
likely to live independently than are those with
aphasia and right hemiparesis.27
From the previous discussion, it is apparent
that left neglect is much more common and clin-
ically meaningful than right neglect is. Thus, the
syndrome is frequent, even expected, in patients
with large, acute, destructive lesions of the right
hemisphere. In addition to acute focal diseases,
such as infarction, hemorrhage, and trauma, ne-
glect may result from more subacute or chronic
neuropathology such as neoplasms and degener-
 NEUROANATOMY OF ATTENTION/FILLEY 95

Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.

Figure 2 Drawing of the superior surface of the brain that schematically represents the dominance of the
right hemisphere for directed attention. The right side of the cerebrum has the capacity to survey both sides of
extrapersonal and intrapersonal space, whereas the left side can only survey the contralateral space.

ative disorders, including Alzheimer’s disease.
Clinical observations in affected patients can be
striking. The syndrome may reveal itself in be-
haviors such as failing to eat food on the left side
of a plate, to dress the left side of the body, or
even to shave the left side of the face. Severe ne-
glect also has dire implications for driving a
motor vehicle. Even with primary visual func-
tion intact, which is typically the case, left ne-
glect can effectively prevent a driver from pay-
ing attention to any sensory stimuli in the left
side of space. In contrast, loss of vision in one
side of space (hemianopsia) can be recognized
and adapted to by the individual and is therefore
far less hazardous than neglect is.
In keeping with the dichotomy of the pos-
terior versus anterior attentional systems dis-
cussed earlier, Heilman and colleagues27 used
observations from clinical subjects and experi-
mental animals to draw a distinction between
sensory and motor neglect. Sensory neglect may
be hemispatial or personal and may be found
in one or more of the three major modalities of
vision, audition, and somesthesis. This deficit
is detected clinically by testing for extinction
using the method of double simultaneous stim-
ulation. Sensory stimuli are applied bilaterally
to a patient through a given sensory modality,
and if the patient does not report the stimulus
on one side, then that side is said to exhibit
extinction. Sensory neglect is most strongly as-
sociated with right parietal lesions.27 Motor ne-
glect, also known as intentional neglect, gener-
ally involves reduced action in an affected limb
96 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 23, NUMBER 2 2002
and may take many forms.27 Motor impersis-
tence is the failure to sustain already initiated
movements; hypokinesia is delay in movement
initiation; and akinesia, the most severe form,
implies an inability to initiate movement. The
dorsolateral prefrontal region plays a critical
role in the intentional system of the brain.27
Treatment of neglect is generally disap-
pointing. Lasting neglect syndromes are usu-
ally due to large structural lesions that may
permit only limited recovery with the passage
of time. Once the underlying disorder has been
addressed, little can be done medically; phar-
macological interventions have not proven
helpful.27 Management of the environment
with such techniques as training, cueing, and
the like may be of some value (see Cherney28
for a more detailed review of neglect assess-
ment and treatment).
ATTENTION AND NEURAL
NETWORKS
Attention is a complex neurobehavioral capacity
without which the expression of all other higher
functions of the human brain is impossible. The
representation of attention in the brain is thus
widespread, consistent with its essential role in
human mental life. Two complementary systems
exist to mediate different aspects of attention.
The diffuse attentional system of the thalamus
and the cerebral cortices and their white matter
connections functions to maintain global aware-
ness of both exogenous and endogenous features
of experience. The right hemisphere attentional
system, involving highly interconnected areas of
the right frontal and parietal lobes, operates to
select salient spatial elements from the external
or intrapersonal environment and then to orga-
nize an appropriate motor response to these
stimuli.
Damage to either of these systems can
produce major neurobehavioral sequelae. The
common denominator of the two major clini-
cal syndromes—ACS and left neglect—is in-
attention, and, indeed, the neuropsychological
performance of patients with these syndromes
can be indistinguishable.29 The clinical phe-
nomenology of these syndromes, however, is
usually sufficiently distinct to allow their dif-
ferentiation by neurobehavioral evaluation. Pa-
tients with ACS have a global deficit in selec-
tive attention that limits the ability to focus on
any stimuli, whereas those with left neglect
have an inability to direct attention to one side
of their sensory experience. Whereas it may
seem that left neglect should be less disabling
because it is limited to one hemispace, clinical
experience shows that neglect of the left hemi-
space imposes unique burdens on functional
adaptation and may be as devastating as ACS
and often more persistent. Unfortunately, some
individuals may experience both syndromes
simultaneously.
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
Each of the attentional systems discussed
earlier can be envisioned as a neural network
that is widely distributed throughout relevant
areas of the brain. This network model has
come to dominate current thinking on the
organization of mental phenomena4,9 and is
strongly supported by advanced neuroimaging
techniques.30 Neural networks are comprised
of cortical and subcortical gray matter struc-
tures that are connected by white matter tracts.
These white matter tracts make up nearly one
half the volume of the human brain,12 and the
connectivity conferred by their complex inter-
hemispheric and intrahemispheric trajectories
is enormous (Fig. 3). Similarly, the spectrum
of neurobehavioral disorders that follow cere-
bral white matter damage is extremely broad,
ranging from subtle attentional disorders to
dementia, stupor, and coma.4,12,19,31 Both gray
and white matter components are therefore in-
timately involved with the mediation of atten-
tion and all other higher functions. One of the
emerging challenges in clinical neuroscience is
the detailed understanding of neural networks
that include both gray and white matter com-
ponents.9,12
CONCLUSION
The knowledge of attention and its repre-
sentation in the brain has been derived from
patients with attentional dysfunction, experi-
mental studies of humans and higher primates,
and, most recently, functional neuroimaging in-
vestigations. The understanding of this funda-
mental but elusive cognitive domain, originally

Figure 3 Drawing of the left hemisphere demonstrating the wide distribution and extensive connectivity of
the cerebral white matter (CC, corpus callosum; UF, U fibers or arcuate fibers; SOFF, superior occipitofrontal fas-
ciculus; IOFF, inferior occipitofrontal fasciculus; AF, arcuate fasciculus; UnF, uncinate fasciculus; C, cingulum).
gleaned from the clinical observations of be-
havioral neurology and neuropsychology, is
thus being enhanced by sophisticated research
techniques. A particularly important advance is
the recognition that attention depends on the
operations of at least two complementary
neural networks, each of which contributes im-
portantly to normal mentation. Complex arrays
of both gray and white matter structures partic-
ipate in these widely distributed networks. As
further knowledge of the neuroanatomy of at-
tention accumulates, the prospects for more ef-
fective treatment of individuals affected with
attentional dysfunction will likely improve.
REFERENCES
1. James W. The Principles of Psychology, Vol. 1.
New York: Henry Holt; 1900
2. Geschwind N. Disorders of attention: a frontier
in neuropsychology. Philos Trans R Soc Lond B
1982;298:173–185
3. Plum F, Posner JB. The Diagnosis of Stupor and
Coma, 3rd ed. Philadelphia: F.A. Davis, 1982
4. Filley CM. Neurobehavioral Anatomy, 2nd ed.
Boulder, CO: University Press of Colorado, 2001
NEUROANATOMY OF ATTENTION/FILLEY 97
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
5. Moruzzi G, Magoun H. Brain stem reticular for-
mation and activation of the EEG. Electroen-
cephalogr Clin Neurophysiol 1949;1:455–473
6. Morison RS, Dempsey EW. A study of thalamo-
cortical relations. Am J Physiol 1942;35:281–292
7. Paus T. Functional anatomy of arousal and atten-
tion systems in the human brain. Prog Brain Res
2000;126:65–77
8. Multi-Society Task Force on PVS. Medical aspects
of the persistent vegetative state. N Engl J Med
1994:330:1499–1508, 1572–1579
9. Mesulam M-M. Attentional networks, confusional
states, and neglect syndromes. In: Mesulam M-M.
Principles of Behavioral and Cognitive Neurology,
2nd ed. Oxford: Oxford University Press, 2000:
174–256
10. O’Donnell BF. Forms of attention and attentional
disorders. Semin Speech Lang 2001;23:99–106
11. Murray LL. Attention deficits in aphasia: presence,
nature, assessment, and treatment. Semin Speech
Lang 2001;23:107–116
12. Filley CM. The behavioral neurology of cerebral
white matter. Neurology 1998;50:1535–1540
13. Filley CM. Clinical neurology and executive dys-
function. Semin Speech Lang 2000;21:95–108
14. Lou HC, Henriksen L, Bruhn P. Focal cerebral hy-
poperfusion in children with dysphasia and/or
attention deficit disorder. Arch Neurol 1984;46:
48–52
98 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 23, NUMBER 2 2002
15. Rueckert L, Grafman J. Sustained attention
deficits in patients with right frontal lesions. Neu-
ropsychologia 1996;34:953–963
16. Lewin JS, Friedman L, Wu D, et al. Cortical local-
ization of human sustained attention: detection
with functional MR using a visual vigilance para-
digm. J Comput Assist Tomogr 1996;20:695–701
17. Zametkin AJ, Nordahl TE, Gross M, et al. Cere-
bral glucose metabolism in adults with hyperactiv-
ity of childhood onset. N Engl J Med 1990;323:
136l-1366
18. Lipowski JZ. Delirium: Acute Confusional States.
New York: Oxford University Press, 1990
19. Filley CM, Kleinschmidt-DeMasters BK. Toxic
leukoencephalopathy. N Engl J Med 2001;345:
425–432
20. Alexander MP, Freedman M. Amnesia after ante-
rior communicating artery rupture. Neurology
1984;34:752–757
21. Mesulam M-M, Waxman SG, Geschwind N,
Sabin TD. Acute confusional states with right
middle cerebral artery infarctions. J Neurol Neuro-
surg Psychiatry 1976;39:84–89
22. Posner MI, Dehaene S. Attentional networks.
Trends Neurosci 1994;17:75–79
23. Mesulam M-M. A cortical network for directed at-
tention and unilateral neglect. Ann Neurol 1981;
10:309–325
24. Weintraub S, Mesulam M-M. Right cerebral dom-
inance in spatial attention. Further evidence based
on ipsilateral neglect. Arch Neurol 1987;44:621–
625
25. Spiers PA, Schomer DL, Blume HW, et al. Visual
neglect during intracarotid amobarbital testing.
Neurology 1990;40:1600–1606
26. Heilman KM, Van Den Abell T. Right hemisphere
dominance for attention: the mechanism underly-
ing hemispheric asymmetries of inattention (ne-
glect). Neurology 1980;30:327–220
27. Heilman KM, Valenstein E, Watson RT. Neglect
and related disorders. Semin Neurol 2000;20:
463–470
28. Cherney LR. Unilateral neglect: a disorder of at-
tention. Semin Speech Lang 2002:23:117–128
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
29. Lee GP, Hamsher K DeS. Neuropsychological
findings in toxicometabolic confusional states. J
Clin Exp Neuropsychol 1988;10:769–778
30. Cabeza R, Nyberg L. Imaging cognition. II. an
empirical review of 275 PET and fMRI studies. J
Cogn Neurosci 2000;12:1–47
31. Filley CM, Franklin GM, Heaton RK, Rosenberg
NL. White matter dementia: clinical disorders and
implications. Neuropsychiatry Neuropsychol Behav
Neurol 1988;1:239–254