The cause of<unk>  is heterogeneous, as many neurocognitive processes are involved in the<unk>  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<unk>  through dynamic interaction with neurological characteristics. Studies in cognitive neuroscience suggest that<unk>  functions are widely distributed throughout the brain, though a few areas have been isolated as primary contributors.<unk>  is studied extensively in clinical neuropsychology as well, allowing correlations to be drawn between such dysexecutive symptoms and their neurological correlates.<unk>  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.<unk>  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<unk> , a disorder such as attention-deficit/hyperactivity disorder is a classification given to a set of subjectively-determined symptoms implicating<unk>  – current models indicate that such clinical symptoms are caused by<unk> . Neurophysiology As previously mentioned,<unk>  functioning is not a unitary concept. Many studies have been conducted in an attempt to pinpoint the exact regions of the brain that lead to<unk> , producing a vast amount of often conflicting information indicating wide and inconsistent distribution of such functions. A common assumption is that disrupted<unk>  control processes are associated with pathology in prefrontal brain regions. 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<unk>  functions such as the basal ganglia and cerebellum. In most cases of<unk> , deficits are attributed to either frontal lobe damage or<unk> , or to disruption in fronto-subcortical connectivity. Neuroimaging with PET and fMRI has confirmed the relationship between<unk>  function and functional frontal pathology. Neuroimaging studies have also suggested that some constituent functions are not discretely localized in prefrontal regions. Functional imaging studies using different tests of<unk>  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<unk>  function are associated with abnormal function in the globus pallidus and appear to be the genuine result of basal ganglia damage. With substantial cognitive load, fMRI signals indicate a common network of frontal, parietal and occipital cortices, thalamus, and the cerebellum. This observation suggests that<unk>  function is mediated by dynamic and flexible networks that are characterized using functional integration and effective connectivity analyses. The complete circuit underlying<unk>  function includes both a direct and an indirect circuit. The neural circuit responsible for<unk>  functioning is, in fact, located primarily in the frontal lobe. This main circuit originates in the dorsolateral prefrontal cortex/orbitofrontal cortex and then projects through the striatum and thalamus to return to the prefrontal cortex. Not surprisingly, plaques and tangles in the frontal cortex can cause disruption in functions as well as damage to the connections between prefrontal cortex and the hippocampus. Another important point is in the finding that structural MRI images link the severity of white matter lesions to deficits in cognition. The emerging view suggests that cognitive processes materialize from networks that span multiple cortical sites with closely collaborative and over-lapping functions. 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. Genetics Certain genes have been identified with a clear correlation to<unk>  and related psychopathologies. According to Friedman et al. (2008), the heritability of<unk>  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<unk> , 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<unk>  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<unk>  in schizophrenia and schizotypal behaviour.
Executive dysfunction
Dyssynergia
Musical anhedonia
Social-emotional agnosia
Language disorder
Social degeneration
Memory disorder
Apraxia of speech