Copyrtghl Munkhguurd 1999

ACTA PSYCHIATRICA
SCANDINAVICA

Synopsis of function and dysfunction of the

frontal lobe
Fuster JM. Synopsis of function and dysfunction of the frontal lobe. J. M. Fuster
Acta Psychiatr Scand 1999: 99 (Suppl. 395): 51-57. ( Munksgaard 1999. Department of Psychiatry and Brain Research Institute.
School of Medicine, University of California at Los
Angeles, Los Angeles, CA, USA

The cortex of the frontal lobe reaches maximum phylogenetic development

in the brain of the human. It is cortex devoted to the organization of action in
all neurobiological and cognitive domains - skeletal movement. eye
movement, speech and logical reasoning. Thus the frontal cortex may be
called ‘motor cortex’ in the widest sense. The association cortex of the frontal
lobe, commonly called prefrontal cortex, is in charge of the temporal
organization of behaviour, speech and thinking. Prefrontal lesions frequently
lead to disorders of temporal organization, especially in thinking and the
spoken language. The prefrontal cortex serves temporal organization by co-
ordinating three cognitive operations that are essential for the formation of
‘gestalts’ in the time domain: (i) preparatory set; (ii) working memory; and
(iii) inhibitory control of interference. Temporal organization is disturbed in Key words prefrontal cortex, cognition.
the schizophrenic patient, probably because of a functional disorder of the psychopathology
connectivity between the prefrontal cortex and other cortical areas, as well as Joaquin M Fuster. UCLA Neuropsychiatric Institute.
limbic and striatal structures (a ‘disconnection syndrome’). 750 Westwood Piam, Los Angeles, CA 90024 USA

Introduction
The cortex of the frontal lobe is the highest level of
a hierarchy of structures of the nerve axis devoted
to the representation and execution of actions. The
base of that hierarchy is constituted by the
motoneurones and anterior roots of the spinal
cord. Above that, in ascending order, are the motor
nuclei of the mesencephalon, the cerebellum, and
parts of the dicncephalon, including certain nuclei
of the hypothalamus, the thalamus and the basal
ganglia.
The frontal cortex itself is hierarchically orga-
nized. At the base of the cortical motor hierarchy is
the primary motor cortex, which is in charge of the
representation and execution of elementary skele-
tal movements. Above it is the premotor cortex,
which serves more complex movements defined by
goal and trajectory, including certain premotor
areas involved in speech. At the summit is the
cortex of association of the frontal lobe, which is
commonly designated the prefrontal cortex. This
cortex represents the broad schemas of action in
the skeletal and speech domains, and in addition it
is critically involved in the enactment of those
schemas or plans.
Because of these,representational and operant
functions, the prefrontal cortex is essential for the
temporal organization of behaviour and the spoken
language. Also included in the functional purview
of the prefrontal cortex is the organized action in
the internal domain of rational thinking. In
summary, the prefrontal cortex is ‘motor’ cortex
of the highest order in that it supports the cognitive
functions that co-ordinate the execution of the
most elaborate and novel actions of the organism.
For good reason it has been named the ‘executive
of the brain’ and the ‘organ of creativity’.
In this article I shall focus on the cognitive
functions of the prefrontal cortex and the con-
sequences of their failure. Before dealing with
these subjects, however, I shall deal briefly with
some basic facts about development, anatomy and
neurochemistry (for a more extensive review, see
1).
Phylogenetically as well as ontogenetically, the
prefrontal cortex is one of the last regions of the
neocortex to develop. In evolution, it reaches
maximal relative growth in the human brain,
where it constitutes nearly one-third of the totality
of the neocortex. In ontogenetic development, the
prefrontal cortex is one of the last regions to

51
Fuster
undergo the myelination of its afferent, efferent
and intrinsic fibres. It is also slow to reach full
maturity by other criteria, such as the number and
volume of cells, and the size and number of the
dendritic spines of its neurones. In the normal
human individual, full prefrontal maturation is not
reached until late adolescence. This long develop-
mental process is probably related to the slow
maturation of the cognitive functions that the
prefrontal cortex supports, including the slow
development of the highest and most character-
istically human of all cognitive activities, namely
the spoken language. These activities are organized
mainly by the cortex of the dorsolatcral convexity
of the frontal lobe, which in both phylogeny and
ontogeny grows relatively more than the orbito-
medial prefrontal cortex.
The prefrontal cortex is the most highly inter-
connected of all the neocortical regions. It receives
afferent fibres from the brainstem, the hypothala-
mus, the limbic system (amygdala and hippocam-
pus), the thalamus (especially the anterior and
mediodorsal nuclei) and other areas of the
neocortex, notably the association cortex of post-
rolandic regions. Brainstem, hypothalamic and
limbic inputs probably bring to the prefrontal
cortex information about the internal milieu,
whereas the inputs from the hippocampus are
probably essential for the formation of motor
memory. Inputs from the posterior cortex are
apparently involved in sensory-motor integrations
at the highest level. The prefrontal cortex recipro-
cates the afferent inputs from all of those cerebral
structures with output efferents to them.
A number of neurotransmitter systems con-
verge on the prefrontal cortex and are active
within it. Most prominent among these are the
dopamine systems, a norepinephrine system, the
cholinergic system originating in the basal nucleus
of Meynert, and the GABAergic system. Several
types of dopamine receptors of the prefrontal
cortex have been postulated to malfunction in
schizophrenia. The cholinergic system appears to
be deficient in Alzheimer’s disease and other
dementias.
Temporal organization of behaviour
During the past few decades, largely as a result of
neuropsychological and neurophysiological studies
of the human and the monkey, a picture has
emerged of the prefrontal cortex as the highest
structure responsible for the organization of
behaviour in the time domain. This role of the
prefrontal cortex is now deemed to be essential for
the sequencing of novel and complex behaviour,
52
including speech, and extending to sequences of
logical reasoning. In order to understand this role
of the prefrontal cortex in what has come to be
termed ‘executive function’, it is important to
consider, first and foremost, that the prefrontal
cortex has both representational and operant
functions. Let us briefly deal with the former
before we approach the latter.
The prefrontal cortex is a substrate of motor
memory. In this part of the cerebral mantle,
especially its dorsolateral aspects, the highest
schemes or plans of behaviour are formed and
represented. These schemas or plans of behaviour
are established in the prefrontal cortex, presumably
under the agency of inputs from the amygdala, the
hippocampus and the posterior (postrolandic)
cortex, in addition to inputs from the brainstem
that are believed to be responsible for maintaining
the drive and motivation of the organism. The
schemas themselves probably consist of distributed
networks of prefrontal neurones formed by tem-
poral coincidence of those inputs. By temporal
coincidence synapses are modulated, with the
effect of facilitating their conduction ability and
thus knitting the network together (2). The
activation of the network above a certain level
leads to the enactment of the plan and the sequence
of behaviour directed to the attainment of its goal.
In order for the behaviour to become temporally
organized in the enactment of the action plan,
functions of temporal integration need to be
brought into play. Temporal structures or ‘gestalts’
of behaviour require, above all, the organism’s
capacity to mediate cross-temporal contingencies
- in other words, its capacity to fulfil the following
logical operations: ‘Tf now this, then later that; and
if earlier that, then now this.’ It should be noted
that this applies to skeletal behaviour as well as to
thinking and speech.
In neural terms, that function of cross-temporal
mediation is accomplished by at least three
subfunctions or operational components. These
are believed to be the three basic cognitive
functions - the information-processing functions
- of the prefrontal cortex: (i) short-term motor
memory or preparatory set for forthcoming
action; (ii) short-term perceptual memory (work-
ing memory) for retention of sensory information
on which that action is to depend; and (iii)
inhibitory control of interference, to suppress all
internal or external information that might
interfere with the action at hand - in other
words, with the behavioural gestalt in progress.
All three functions of the prefrontal cortex have
received support from neuropsychology and
primate neurophysiology (1).

preparatory set
Set is motor attention. It is attention directed to the
action in preparation. Thus this form of attention is
focused on the representation of the plan and, at the
Same time, on components of established, long-
term motor memory, which are activated ad hoc for
the execution of every integral piece of the
sequence of behaviour in progress, from its
initiation to its goal.
The mechanisms whereby a scheme of behaviour
in an activated motor network of frontal cortex
becomes the agent of preparation for action are as
yet unclear. However, it seems likely that one
electrical correlate of set is the so-called contingent
negative variation (CNV), a slow surface potential
that develops over the frontal lobe during the time
interval between a sensory stimulus and a motor
response contingent upon it. Another electrical
correlate is the Bereitschaftspotential or ‘readiness
potential,’ which is another slow surface potential
(this one briefer) that develops over the motor
cortex just before the motor response.
By the use of microelectrodes in behaving
monkeys, we have found cells in the dorsolateral
prefrontal cortex which might well perform that
function of preparatory set. While a monkey delays
action and prepares for it, in the context of a delay
task (e.g. delayed matching to sample, spatial
delayed response), we have observed neurones
that by their frequency of discharge appear to be
attuned to the impending motor response. That
discharge is greater or smaller depending on the
characteristics of the action that the monkey is
expecting to execute. Furthermore, the cells’
discharge accelerates as that action becomes
imminent, and the degree of acceleration varies
in proportion to the certainty with which the animal
can predict those characteristics. (Uncertainty is
introduced into the test by associating different
colours with different probabilities of a required
response of the forelimb, either to the right or to
the left.)
In summary, the presence of cells that appear to
predict future actions - albeit only in the short
term - indicates that there are mechanisms in the
dorsolateral prefrontal cortex not only for evoking
that future - the ‘memory of the future’ (3) -but
for preparing the motor apparatus for it. Those
mechanisms perhaps involve the priming of struc-
tures in lower stages of the motor hierarchy for the
impending action (e.g. premotor cortex, basal
ganglia, pyramidal system). The probable relation-
ship between the behaviour of those ‘set cells’ of
the monkey and the recognized role of the
prefrontal cortex of the human in the formulation
and execution of plans is obvious (see below).
Prefrontal function
Working memory
Intermixed with the ‘set cells’ in the dorsolateral
prefrontal cortex of the monkey, one can find so-
called ‘memory cells.’ These appear to have the
temporally opposite function. Instead of looking
forward in time, to the impending motor action,
they look back in time to the sensory information, a
few seconds or minutes earlier, on which that action
is to be partly based. These cells react specifically to
the sensory cues and, during the waiting (delay)
period before the motor response, their discharge
decelerates. Memory cells are probably the neuro-
nal components of activated networks that con-
stitute the physiological substrate for the well-
known role of the prefrontal cortex in working
memory.
Again, working memory is a function first
surmised by neuropsychological analysis of pre-
frontal syndromes in the human and the monkey.
This analysis provided precursory evidence that
short-term or recent memory deficits are common
components of those syndromes. The animal
evidence was particularly revealing. A long line
of experiments initiated by Jacobsen (4) demon-
strated that monkeys with dorsolateral prefrontal
ablations have severe difficulties in learning and
performing all kinds of so-called ‘delay tasks’, i.e.
tasks in which the subject must retain in memory,
through a delay, an item of sensory information for
subsequent performance of a motor act. The deficit
can also be produced by reversible (cryogenic)
inactivation of the prefrontal cortex (5, 6). Micro-
electrode studies of the monkey and the discovery
of memory cells (7,8) established conclusively that
there is a physiological substrate of neurones, in the
dorsolateral prefrontal cortex of the primate, for
that memory function which so often previously
had been found to fail in humans and animals with
lesions of that cortex.
Later, cognitive psychology (9) coined the term
‘working memory’ to describe the temporary, ‘on-
line’, memory function that humans use in certain
tasks and to solve certain problems. Along with
that term came the theoretical construct of the
cognitive operations involved in that kind of active
memory, which primate researchers had been
variously referring to as provisional memory,
operant memory, or simply short-term memory.
One of those operations, it was assumed, is the
‘articulatory loop’, a concept that is difficult to
apply to the monkey but which has clear implica-
tions for the construction of language, which is a
form of sequential behaviour of the human that has
a very high requirement for working memory.
In summary, it appears that the recent-memory
function of the human which is often disturbed in
53
Fuster
Dorsolateral
Orbital
Fig. I . Schematic diagram of the human brain. Prefrontal
cytoarchilectonic areas are indicated according t o the
numbering of Brodmann’s map.
prefrontal syndromes, and the short-term memory
function of the monkey which fails after prefrontal
lesion and which has a clear electrophysiological
correlate in the behaviour of memory cells, are one
and the same function - what has now come to be
commonly called working memory. In neurophy-
siological terms, it consists of the temporary
activation of a widely distributed network of
neocortical neurones, which is maintained in an
active state by prefrontal cortex inasmuch as the
information contained in the network is to be used
for prospective action. The role of the prefrontal
cortex in working memory is critical, but in view of
recent research involving microelectrode research
and neuroimaging (lo), it has to be emphasized that
the role in question is essentially based on cortico-
cortical interactions -that is, interactions between
the prefrontal cortex and areas of postrolandic
cortex. The localization of working memory in the
prefrontal cortex is an unfortunate misconception.
Inhibitory control
It has been known for a long time that patients with
prefrontal injuries are abnormally distractible, tend
to perseverate, and have difficulty in controlling
impulsivity and instinctual behaviour. Now the
convergence of human and animal neuropsychol-
ogy has led to the conclusion that such symptoms
are more frequently observed after lesions of the
orbitofrontal cortex than after lesions of any other
sector of the prefrontal cortex. Because these
symptoms commonly occur together, and because
the anatomy and connectivity of the orbital
prefrontal cortex points to commonality of patho-
physiology, it seems increasingly evident that all of
54
these manifestations of orbitofrontal damage stem
from the disorder of a common function. This
function can best be characterized as the ability of
the organism to protect goal-directed behaviour
from interference.
The interference can be of many kinds. It can
take the form of sensory stimuli that appear in the
context of the behavioural gestalt or sequence and
which, unless suppressed, are likely to lead the
behaviour astray and away from its goal. The
interference can also take the form of internal
tendencies - some inborn, others established into
learned routine. Thus, for example, it may be
interference from instinctual drives which under
certain circumstances take precedence over current
behaviour and disrupt it. Alternatively, the inter-
ference may come from well-established memories
and patterns of behaviour that may be appropriate
in another context but which currently constitute
an obstacle to present behaviour.
Unlike the set and memory functions of the
prefrontal cortex, the role of this cortex in the
inhibitory control of interference does not have
accepted electrophysiological correlates. However,
it seems very likely that inhibitory control functions
are exerted selectively through the cortical intrinsic
GABA-crgic system and the inhibitory cortico-
hypothalamic pathways which have their origin in
the orbitofrontal cortex.
Prefrontal syndromes
It now appears that those three prefrontal func-
tions, two mainly based in the dorsolateral cortex
(set and working memory) and the other in the
orbital cortex (inhibitory control), work in co-
operation to ensure the integrity and success of
every new and elaborate sequence of goal-directed
behaviour. This physiological co-operation involves
other cerebral structures to which the prefrontal
cortex is connected, and it extends to the spoken
language and internal sequences of logical reason-
ing.
In the light of these functional conclusions, it is
appropriate here to re-examine the symptomatol-
ogy of prefrontal damage in the human. The
following is not intended to provide a detailed
clinical description of prefrontal syndromes, but
merely an outline of reference for understanding
the consequences in the human of failure of the
physiological functions of the prefrontal cortex
described above.
First and foremost it needs to be recognized that
there is no such thing as ‘the frontal-lobe syn-
drome.’ The functional heterogeneity of the frontal
cortex precludes the reality of such a nosological

entity. Instead, what we can observe is the
existence of three major clusters of symptoms or
syndromes depending on the topography of the
lesion resulting from trauma or disease of the
prefrontal cortex. Each syndrome corresponds to
one of the major aspects of the associative frontal
cortex - dorsolateral, mediaUcingulate, and orbi-
tal. Figure 1 illustrates these regions and the
cytoarchitectonic areas that they include according
to Brodmann’s map.
Dorsolateral syndrome
There is considerable variation in the types of
symptoms that can be exhibited by patients with
damaged dorsolateral prefrontal cortex. The result-
ing syndrome differs according to the location and
extent of the damage within that cortex. None the
less, it is possible to enumerate the manifestations
of dorsolateral pathology that are most commonly
observed. These may appear either together or in
isolation.
At the top of the list are the disorders of drive,
attention and motivation. Patients with even minor
dorsolateral prefrontal damage are generally dis-
interested in the world around them and devoid of
spontaneity in both language and behaviour. They
are less alert than normal to events in their
environment and to other people, and they
appear to lack the motivation to do things for
themselves and for others. Their life is constricted
by routine and a tendency to temporal concreteness
- their behaviour is anchored in the here and now
without perspective, either backwards or forwards,
in time. Their memory for recent events is poor,
and their capacity to plan ahead is also deficient.
On close analysis, this temporal concreteness
appears to derive directly from impairment of the
two temporally integrative functions that we have
ascribed to the dorsolateral cortex, namely working
memory and preparatory set. The working memory
disorder can be substantiated by observation of the
patient in his or her daily life, as well as by formal
testing. To some degree the deficit in short-term
memory is a consequence of the above-mentioned
impairments of drive and attention. The patient
does not remember what he or she is not interested
in or motivated to remember. However, the deficit
is largely primary, being a consequence of the
failure of the basic prefrontal mechanisms of
working memory to which I alluded earlier.
If the working memory deficit is a common
feature of the dorsolateral syndrome, the planning
deficit is virtually pathognomonic of this syndrome.
It is the most constant and specific symptom of
dorsolateral prefrontal damage. The affected indi-
Prefrontal function
vidual cannot formulate plans of future action that
deviate from the ordinary, and his or her capacity
to create new behaviour or spcech is often severely
restricted. It goes without saying that this deficit is
closely related to the above-mentioned deficit in
‘memory of thc future,’ and thus a deficit in the
ability to represent schemas of action. In addition,
however, there is the inability to execute them.
Here we are again dealing with the lack of drive,
the inability to make decisions, and the faulty
preparation for impending action -in other words,
the defect in motor set. These problems, in
aggregate, define what has been termed the
‘dysexecutive syndrome.’
Medial/cingulate syndrome
Lesions of the medial aspects of the prefrontal
cortex induce a disorder of drive and motivation
with even more constancy and saliency than lesions
of the dorsolateral cortcx. Here, whatever dis-
orders of temporal integration are discerned can be
wholly ascribed to inattention and disinterest. In
fact, apathy is the dominant affective component of
the medial/cingulate syndrome. From it derives a
lack of spontaneity in all domains of action
including, of course, the speech domain. The
patient generally moves less than before the illness,
and is hypokinetic in all rcspects. In extreme cases
- that is, in cases with large lesions of the medial
prefrontal cortex - the hypokinesia turns into
akinesia. Akinetic mutism is one of the most
characteristic disorders of medial prefrontal
damage.
Orbital syndrome
The orbital syndrome, which results from pathol-
ogy of the ventral prefrontal cortex, differs
markedly in some respects from the other two
syndromes. Here an attention disorder is again in
the foreground, but this one is different to the
attention disorder of the medial and dorsolateral
syndromes. The orbital patient suffers not so much
from disorder of the intensive aspects of attention
(i.e. failure to focus and concentrate) as from
disorder in its exclusionary aspect. The patient is
abnormally distractible, and is unable to inhibit
interference from external stimuli that are extra-
neous to context and not part of the current action.
Along with this, and probably in part related to it,
the patient tends to be hyperactive, unable to
inhibit spontaneous activity and unable to react to
those extraneous stimuli (hyper-reactivity).
In the orbital patient, affect is labile and
unpredictable. More often than in other prefrontal
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Fuster
syndromes, euphoria is the dominant affect.
Together with a tendency towards euphoria, the
patient displays inappropriate and childish humour
(moria). H e or she is also commonly unable to
inhibit instinctive drives and often makes blatant
displays of quarrelsomeness, hypersexuality and
hyperphagia. The disinhibition of instincts, without
moral judgement to restrain them, often drives the
patient to unruly behaviour and to breaking the
law. Sociopathy is almost a hallmark of the
orbitofrontal syndrome.
In summary, as a result of damage to the orbital
prefrontal cortex the patient exhibits a number of
abnormalities of cognition and affect, as well as
emotional and social behaviour. Most of these
abnormalities, if not all of them, appear to be the
result of a deficit in the inhibitory control function
or functions of the orbital cortex.
Psychiatric implications
As can be seen from the above description,
psychological and social disorders of one kind or
another are common in patients with frontal lobe
pathology. Some of these disorders are easily
attributable to failure of the basic functions of
the prefrontal cortex that were explained earlier
and that define its role in the temporal organization
of behaviour. Others are not. In any case, the
observation of these psychological and social
disorders has sometimes weighed heavily on the
reasoning of those who endeavour to understand
the pathogenesis of certain psychiatric disorders
which, because of our ignorance, we term ‘endo-
genous’ or ‘idiopathic.’ To conclude, let us briefly
consider a couple of examples of such disorders.
One example is the attention deficit disorder
(ADD) of childhood. There is no firm evidence that
ADD is due to an underlying disorder of the frontal
lobe, yet the similarities between ADD and the
orbital prefrontal syndrome are striking. Both are
characterized by attention disorder (especially
distractibility), hyperkinesia, and unruly behaviour.
It is thus reasonable to conclude that ADD is in
some way linked to orbitofrontal pathology (1).
Moreover, since ADD is often seen to be outgrown
in late adolescence (although too late in many cases
not to have affected learning adversely), it is also
reasonable to suppose that ADD is the clinical
manifestation of a lag in the maturation of the
orbital prefrontal cortex.
Schizophrenia offers another example of extra-
polated reasoning for the involvement of a diseased
frontal lobe in mental illness. However, this case is
better grounded than the one pertaining to ADD.
The argument for prefrontal pathology in schizo-
56
phrenia is based on the following evidence: (i)
phenomenological evidence of disordered tem-
poral organization of thinking, speech and beha-
viour in the psychotic patient; (ii) evidence of
disordered dopamine systems and receptors in
schizophrenia; (iii) evidence of schizophrenics’
failure in performance of tests of frontal-lobe
function (e.g. Tower of London for planning,
Wisconsin Card Sorting Test for working memory
and interference control); and (iv) evidence, in
schizophrenia, of frontal metabolic deficit (‘hypo-
frontality’) and the absence of dorsolateral pre-
frontal activation, as determined by neuroimaging
in the performance of frontal tasks (e.g. Wisconsin
Card Sorting Test).
All of this evidence certainly argues for the
involvement of the prefrontal cortex in the
pathogenesis of schizophrenia. Nevertheless, it is
unreasonable to assume that schizophrenia is a
disease that exclusively, or even mainly, affects the
prefrontal cortex. Such a position has to contend
with the fact that no in,jury to this cortex has been
known to result in a schizophrenic syndrome. A
more reasonable position is that schizophrenia
affects a number of neurotransmitter systems,
notably the dopaminergic systems, which are
heavily represented in the prefrontal cortex.
Because this affects the connectivity of the
prefrontal cortex with limbic structures, the basal
ganglia and the rest of the neocortex, the disorder
manifests itself as the impairment of several
emotional and cognitive functions that depend on
that connectivity. Schizophrenia is a prefrontal
disorder to the extent that the prefrontal cortex is
critical for those functions. In any event, it is more
appropriate to view this disease, with all of its
various manifestations, as some kind of a ‘dis-
connection syndrome’ in which the prefrontal
cortex is affected, as are many other cerebral
structures connected to it.
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