The cause of executive dysfunction is
heterogeneous, 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. Studies in
cognitive neuroscience suggest that executive functions are widely distributed throughout the brain, though a few areas have been isolated as primary contributors. Executive dysfunction is studied extensively in clinical
neuropsychology as well, allowing correlations to be drawn between such dysexecutive symptoms and their neurological correlates. A 2015 study confirmed that executive dysfunction has a positive correlation with neurodevelopmental disorders such as
autism spectrum disorder (ASD) or
attention deficit hyperactivity disorder (ADHD). 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. Executive dysfunction characterizes many of the symptoms observed in numerous
clinical populations. In the case of
acquired brain injury and neurodegenerative diseases there is a clear neurological etiology producing dysexecutive symptoms. Conversely,
syndromes and
disorders are defined and diagnosed based on their symptomatology rather than etiology. Thus, while Parkinson's disease, a
neurodegenerative condition, causes executive dysfunction, a disorder such as ADHD is a classification given to a set of subjectively-determined symptoms implicating executive dysfunction – models from the 1990s and 2000s indicate that such clinical symptoms are caused by executive dysfunction. This is supported to some extent by the primary literature, which shows both pre-frontal activation and communication between the pre-frontal cortex and other areas associated with executive functions such as the
basal ganglia and
cerebellum. In most cases of executive dysfunction, deficits are attributed to either frontal lobe damage or dysfunction, or to disruption in fronto-subcortical connectivity. 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. In 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 This observation suggests that executive function is mediated by dynamic and flexible networks that are characterized using functional integration and effective connectivity analyses. The emerging view suggests that cognitive processes materialize from networks that span multiple cortical sites with closely collaborative and over-lapping functions. 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
ADHD. The catechol-o-methyl
transferase gene (
COMT) codes for an enzyme that degrades
catecholamine neurotransmitters (DA and NE), and its Val158Met polymorphism is linked with the modulation of task-oriented cognition and behavior (including set shifting) and the experience of reward, which are major aspects of executive functioning. COMT is also linked to methylphenidate (stimulant medication) response in children with ADHD. Both the DRD4/7R and COMT/Val158Met polymorphisms are also correlated with executive dysfunction in schizophrenia and schizotypal behaviour.
Evolutionary perspective The prefrontal lobe controls two related executive functioning domains. The first is mediation of abilities involved in planning,
problem solving, and understanding information, as well as engaging in working memory processes and controlled attention. In this sense, the prefrontal lobe is involved with dealing with basic, everyday situations, especially those involving metacognitive functions. The second domain involves the ability to fulfill biological needs through the coordination of cognition and emotions which are both associated with the frontal and prefrontal areas. The prefrontal lobe in humans has been associated both with metacognitive executive functions and emotional executive functions. Theory and evidence suggest that the frontal lobes in other primates also mediate and regulate emotion, but do not demonstrate the metacognitive abilities that are demonstrated in humans. This uniqueness of the executive system to humans implies that there was also something unique about the environment of ancestral humans, which gave rise to the need for executive functions as adaptations to that environment. Some examples of possible adaptive problems that would have been solved by the evolution of an executive system are: social exchange, imitation and observational learning, enhanced pedagogical understanding, tool construction and use, and effective communication. In a similar vein, some have argued that the unique metacognitive capabilities demonstrated by humans have arisen out of the development of a sophisticated language (symbolization) systems and culture. Moreover, in a developmental context, it has been proposed that each executive function capability originated as a form of public behaviour directed at the external environment, but then became self-directed, and then finally, became private to the individual, over the course of the development of self-regulation. These shifts in function illustrate the evolutionarily salient strategy of maximizing longer-term social consequences over near-term ones, through the development of an internal control of behaviour. == Testing and measurement ==