It is clear that prefrontal cortex
is a vital component of the circuitry sub serving executive function, posterior
cortical regions and subcortical structures collaborate with prefrontal cortex
to mediate successful executive processes.3,4 There is also evidence
that patients with subcortical ischaemic vascular disease show selective
deficits on tests of executive function (Cummings, 1994). In all disorder the
executive deficits are attributed to either frontal lobe damage or dysfunction
or to disruption in fronto subcortical connectivity.In most cases of executive
dysfunction, deficits are attributed to either frontal lobe damage or
dysfunction or to disruption in fronto-subcortical connectivity3.
Neuroimaging with PET and fMRI has confirmed the relationship between executive
function and functionalontal pathology3. Neuroimaging studies have also
suggested that some constituent functions are not discretely localized in
Functional imaging studies using
different tests of executive function have implicated the dorsolateral
prefrontal cortex to be the primary site of cortical activation during these
tasks.6In addition, PET studies of patients with Parkinson’s disease have
suggested that tests of executive function are associated with abnormal
function in the globus pallidus and appear to be the genuine result of basal
ganglia damage.3 With substantial cognitive load, fMRI signals indicate a
common network of frontal, parietal and occipital cortices, thalamus, and the
cerebellum.7 This observation suggests that executive function is
mediated by dynamic and flexible networks that are characterized using
functional integration and effective connectivity analyses.8The
complete circuit underlying executive function includes both a direct and an
The neural circuit responsible for
executive functioning is, in fact, located primarily in the frontal lobe 6.
The emerging view suggests that cognitive processes materialize from
networks that span multiple cortical sites with closely collaborative and
overlapping functions.5 A challenge for future research will be to
map the multiple brain regions that might combine with each other in a vast
number of ways, depending on the task requirements.9
Etiology: - The etiology of
executive dysfunction is heterogeneous10, as many neurocognitive
processes are involved in the executive system and each may be compromised by a
range of genetic and environmental factors. Learning and development of long-term
memory play a role in the severity of executive dysfunction through dynamic
interaction with neurological characteristics.
Executive processes are closely
integrated with memory retrieval capabilities for overall cognitive control; in
particular, goal/task-information is stored in both short-term and long term
memory, and effective performance requires effective storage and retrieval of
this information (Verbruggen & Logan 2008). Certain genes have been
identified with a clear correlation to executive dysfunction and related
psychopathologies. According to Friedman et al (2008), the heritability of
executive functions is among the highest of any psychological trait. The
dopamine receptor D4 gene (DRD4) with 7'-repeating polymorphism (7R) has been repeatedly
shown to correlate strongly with impulsive response style on psychological
tests of executive dysfunction, particularly in clinical ADHD2
Testing and Measurement:-There are
several measures that can be employed to assess the executive functioning capabilities
of an individual.
Clock Drawing Test
The Clock Drawing Test (CDT) is a
brief cognitive task that can be used by physicians who suspect neurological
dysfunction based on history and physical examination, it is relatively easy.
The cognitive mechanism involved in
the Stroop task is referred to as directed attention. The Stroop task requires
the participant to engage in and allows assessment of processes such as
attention management, speed and accuracy of reading words and colours and of
inhibition of competing stimuli4. The stimulus is a colour word that is printed
in a different colour than what the written word reads.
Wisconsin Card Sorting Test
The Wisconsin Card Sorting Test
(WCST), is used to determine an individual's competence in abstract reasoning,
and the ability to change problem-solving strategies when needed.4
These abilities are primarily determined by the frontal lobes and basal
ganglia, which are crucial components of executive functioning making the WCST
is a good measure for this purpose11.
Executive Dysfunction in Clinical
Populations The Clinical presentation of severe executive dysfunction that is
unrelated a specific disease or disorder is classified as a dysexecutive
Syndrome, and often appears following damage to the frontal lobes of the
cerebral cortex12. As a result, executive dysfunction is implicated
etiologically and/or co-morbidly in many psychiatric illnesses, which often
show the same symptoms as the dysexecutive Syndrome. It has been assessed and
researched extensively in relation to cognitive developmental disorders,
psychotic disorders, affective disorders, and conduct disorders, as well as
neurodegenerative diseases and acquired brain injury (ABI).
Individuals with schizophrenia
It may demonstrate amnesia for
portions of their episodic memory. Observed damage to explicit, consciously
accessed, memory is generally attributed to the fragmented thoughts that
characterize the disorder.
These fragmented thoughts are
suggested to produce a similarly fragmented organization in memory during
encoding and storage, making retrieval more difficult. However, implicit memory
is generally preserved in patients with schizophrenia (Ward. 2006).
Persons with schizophrenia also tend
to demonstrate deficits in response inhibition and cognitive flexibility (Thoma
Patients often demonstrate
noticeable deficits in the central executive component of working memory as
conceptualized by Baddeley and Hitch. However, performance on tasks associated
with the phonological loop and visuospatial sketchpad are typically less
affected Ward, 2006.
More specifically, patients with
schizophrenia show impairment to the central executive component of working
memory, specific to tasks in which the visuospatial system is required for
central executive control (Oram et al. 2005).
Individuals with ADHD often
experience problems with organization, discipline, and setting priorities, and
these difficulties often persist from childhood through adulthood10. In both
children and adults with ADHD, an underlying executive dysfunction involving
the prefrontal regions and other interconnected subcortical structures has been
found.10As a result people with ADHD commonly perform more poorly than matched
controls on interference control, mental flexibility and semantic verbal
Autism Spectrum Disorder
Autism is diagnosed based on the
presence of markedly abnormal or impaired development in social interaction and
communication and a markedly restricted repertoire of activities and interests.
Individuals with autism commonly show impairment in three main areas of
executive functioning: a) fluency; b) planning; and c) cognitive flexibility 8.
Fluency refers to the ability to
generate novel ideas and responses, findings have suggested that children with
autism generate fewer novel words and ideas and produce less complex responses
than matched controls.
Persons with autism demonstrate
impairment on tasks requiring planning abilities relative to typically
functioning controls, with this impairment maintained over time. As might be
suspected, in the case of autism comorbid with learning disability, an additive
deficit is observed in many cases.
Poor mental flexibility, as
demonstrated in individuals with autism, is characterized by perseverative,
stereotyped behaviour, and deficits in both the regulation and modulation. In
general individuals show relatively spared performance on tasks that do not
require mentalizing. These include: use of desire and emotion words, sequencing
behavioural, pictures and the recognition of basic facial emotional
expressions. In contrast, individuals with autism typically demonstrated
impaired performance on tasks.
These include: false beliefs, use of
belief and idea words, sequencing mentalistic pictures, and recognizing complex
emotions such as admiring or scheming (Ward, 2006).
Executive dysfunction in bipolar
disorder associated particularly with the manic state, and is largely accounted
for in terms of the formal thought disorder that is a feature of mania (Dixon
et al., 2004). Individuals affected by bipolar disorder exhibit deficits in
strategic thinking, inhibitory control, working memory, attention and
initiation that are independent of affective state15. However
patients with bipolar disorder with a history of psychosis demonstrated greater
impairment on measures of executive functioning and spatial working memory
compared with bipolar patients without a history of psychosis suggesting that
psychotic symptoms are correlated with executive dysfunction15.
Functional neuroimaging studies have implicated abnormalities in the
dorsolateral prefrontal cortex and the anterior cingulate cortex as being
volumetrically different in individuals with bipolar disorder 13
Persons with PD show deficits in the
areas of: a) spatial working memory; b) central executive aspects of working
memory; c) loss of episodic memories; d) locating events in time. Parkinson’s
disease (PD) primarily involves damage to subcortical brain structures and is
often associated with movement difficulties, in addition to problems with
memory and thought processes (Ward, 2006). In the PD often demonstrate difficulties
in working memory, a component of executive functioning. Cognitive deficits
found in early PD process appear to involve primarily the fontro-executive
functions 14. Moreover, studies of the role of dopamine in the
cognition of PD patients have suggested that PD patients with reduced dopamine
supplementation are more impaired in their performance on measures of executive
functioning (Grossman et al. 2002). This suggests that dopamine may contribute
to executive control processes. Increased distractibility, problems in set
formation and maintaining and shifting attention sets, deficits in executive
functions such as self-directed planning, problems solving, and working memory
have been reported in PD patients14.
Spatial working memory PD patients
often demonstrate difficulty in updating changes in spatial information and
often become disoriented. They do not keep track of spatial contextual
information in the same way that a typical person would do almost
automatically. Similarly, they often have trouble remembering the locations of
objects that they have recently seen, and thus also have trouble with encoding
this information into long-term memory.
Central executive aspects PD is
often characterized by a difficulty in regulating and controlling one’s stream
of thought, and how memories are utilized in guiding future behaviour. However,
some recent research suggests that PD patients may actually be less persistent
in pursuing goals than typical persons and may abandon tasks sooner when they
encounter problems of a higher level of difficulty 14.
The loss of episodic memories in PD
patients typically demonstrates a temporal gradient wherein older memories are
generally more preserved than newer memories. Also, while forgetting event
content is less compromised in Parkinson’s than in Alzheimer’s, the opposite is
true for event data memories.
Locating events in time, PD patients
often demonstrate deficits in their ability to sequence information, or date
events. Part of the problems is hypothesized to be due to a more fundamental
difficulty in coordinating or planning retrieval strategies, rather than
failure at the level of encoding or storing information in memory. This deficit
is also likely to be due to an underlying difficulty in properly retrieving
script information. PD patients often exhibit signs of irrelevant intrusions,
incorrect ordering of events, and omission of minor components in their script
retrieval, leading to disorganized and inappropriate application of script
Conclusions and future directions
Executive function is, by
definition, complex, and this review has only scratched the surface of the
current debates concerning the neuronal basis of executive function and
dysfunction. It is clear that although the prefrontal cortex is a vital
component of the circuitry subserving executive function, posterior cortical
regions and subcortical structures collaborate with prefrontal cortex to
mediate successful executive processing. The advent of functional neuroimaging
techniques has provided the means to study the neuronal basis of human executive
function directly. Early imaging experiments attempted to dissociate component processes
of executive function and attribute them to discrete prefrontal foci. Although
there is some evidence for both functional and material specificity in
prefrontal cortices, it appears that this is more a matter of degree than
reflecting fixed and fundamental dissociations. It is also clear that the same
prefrontal regions mediate very different executive functions. An increasingly
influential view is, therefore, that we should not be looking for one-to-one mappings
between structure and function. Rather, we should be using more sophisticated analysis
approaches to study flexible and dynamic changes in effective and functional connectivity
between brain regions. This has dramatic implications for our understanding of normal
and abnormal executive functions. From a clinical perspective, a dynamic
network approaches is synchronous with the rising trend for disconnection models
of neurological and psychiatric disorders. Important challenges for the future
will be to gain a more through understanding of these models, and to construct
theoretical frameworks for understanding the mechanisms of both disconnection
and functional re-organisation.
Neuronal mechanisms of executive control by the prefrontals cortex. Neurosci
Res 2001; 39: 147–65.
Stuss DT, Benson
DF. Neuropsychological studies of the frontal lobes. Psychol Bull 1984;
(2003). Executive functions and their disorders. British Medical Bulletin.
Saint-Cyr JA, Lang AE. Frontal lobe dysfunction in Parkinson’s disease. Brain
1986; 109: 845–83.
Just, M., Reichle, E. (2000). Working memory and executive function: evidence
from neuroimaging. Current Opinion in Neurobiology. 10; 195-199.
Ottowitz, W., Savage, C. (2002). Neural network basis for abnormalities of
attention and executive function in major depressive disorder: implications for
application of the medical disease model to psychiatric disorders. Harvard
Review of Psychology. 10(2); 86-99.
Chang, L., Ernst, T., et al. (2006). Different activation patterns for working
memory load andvisual attention load. Brain Research. 158-165.
Kenworthy, L., Sirian, L., Black, D., & Wagner, A. (2002). Adaptive skills
and executive function in autism spectrum disorders. Child Neuropsychology,
Kravariti, E., Frith, C., Murray, R.M., & McGuire, P.K. (2004). Effect of
symptoms on executive function in bipolar illness. Psychological Medicine, 34,
Hurks, P., Krabbendam, L., & Jolles, J. (2008). Interference control, working
memory, concept shifting, and verbal fluency in adults with
attention-deficit/hyperactivity disorder (ADHD). Neruopsychology, 22(1), 74-84.
dopamine system genes and cognitive functions in patients with schizophrenia
and their relatives and in healthy subjects from the general
population.Neuroscience Behaviour Physiology, Andermahr, I., Gaser, C., Hager,
F., et al. (1996).37(7), 643-50.
Chan, RC. (2001).
Dysexecutive symptoms among a non-clinical sample: a study with the use of the
Dysexecutive Questionnaire. British Journal of Psychology, Aug., 92 (pt
Thompson, J.M., Gallagher, P., Goswami, U., Young, A.H., Ferrier, I.N., &
Moore, P.B. (2006). A meta-analysis of cognitive deficits in euthymic patients
with bipolar disorder. Journal of Affective Disorders, 93, 105-115
(2007). Behavioral persistence deficit in parkinson’s disease patients. Journal
of Neurology, 14, 300-304
Bearden, C.E., Barguil, M., Barrett, J., Reichenberg, A., Bowden, C.L., Soars,
J.C., & Velligan,D.I. (2007). The neurocognitive signature of psychotic
bipolar disorder. Journal of Biology Psychiatry, 62,910-916.
DeLong MR, Strick PL. Parallel organization of functionally segregated circuits
linking basal ganglia and cortex. Annu Rev Neurosci 1986; 9: 357–81.
Mitchell P, Goodwin GM. Cognitive deficits in depression: possible implications
for functional neuropathology. Br J Psychiatry 2001; 178: 200–6.
Faraone, S., Monutaeux, M., et al. (2000). Neuropsychologocal functioning in nonreferred
siblings of children with attention deficit/hyperactivity disorder. Journal of Abnormal
Psychology. 109(2); 252-265.
Vascular subcortical dementias: clinical aspects. Dementia 1994; 5: 177–8
Sahakian BJ. The neuropsychology of schizophrenia: relations with clinical and neurobiological
dimensions. Psychol Med 1995; 25: 581–94.
Galasko, D., Hanson, L., et al. (2008). Spatial deficits predict rate of
cognitive decline in autopsy-verified Funahashi. Neuronal mechanisms of
executive control by the prefrontals cortex. Neurosci Res 2001; 39: 147–65.
lewy bodies. Neuropsychology. 22(6); 729-737.
Marshall, L., Bree, M. van den, Thomas, H., Owen, M., O'Donovan, M., Thapar, A.
(2004). Association of the dopamine D4 receptor gene 7-repeat allele with
neuropsychological test performance of children with ADHD. American Journal of
Luria AR. Frontal
lobe syndromes. In: Pinken PJ, Bruyn GW. (eds) Handbook of Clinical Neurology,
vol 2. Amsterdam: North Holland, 2002; 725–57.
Nigg, J. T.
(2006). What causes ADHD?: Understanding what goes wrong and why. New York, NY:
Robbins TW, James
M, Owen AM et al. Cognitive deficits in progressive supranuclear palsy, Parkinson’s
disease and multiple systems atrophy in tests sensitive to frontal lobe
dysfunction. J Neurol Neurosurg Psychiatry 1994; 57: 79–88.