The most frequent cause of the syndrome is brain damage to the frontal lobe. Brain damage leading to the dysexecutive pattern of symptoms can result from physical trauma such as a blow to the head or a stroke or other internal trauma.

It is important to note that frontal lobe damage is not the only cause of the syndrome. It has been shown that damage, such as lesions, in other areas of the brain may indirectly affect executive functions and lead to similar symptoms. There is not one specific pattern of damage that leads to DES, as multiple affected brain structures and locations have led to the symptoms. This is one reason why the term frontal lobe syndrome is not preferred.

DES often occurs with other disorders, which is known as comorbidity. Many studies have examined the presence of DES in patients with schizophrenia. Results of schizophrenic patients on the "Behavioural Assessment of the Dysexecutive Syndrome (BADS)" test (discussed below) are comparable to brain injured patients. Further, results of BADS have been shown to correlate with phases of schizophrenia. Patients in the chronic phase of the disorder have significantly lower scores than those who are acute. This is logical due to the similarities in executive disruptions that make everyday life difficult for those with schizophrenia and symptoms that form DES.

Patients with Alzheimer's disease have been shown to exhibit impairment in executive functioning as well. The effects of DES symptoms on the executive functions and working memory, such as attentiveness, planning and remembering recently learned things, are some of the earliest indicators of Alzheimer's.

Studies have also indicated that chronic alcoholism (see Korsakoff's syndrome) can lead to a mild form of DES according to results of BADS.

Perseveration of thought indicates an inability to switch ideas or responses. An example of perseveration is, during a conversation, if an issue has been fully explored and discussed to a point of resolution, it is not uncommon for something to trigger the reinvestigation of the matter. This can happen at any time during a conversation.

Physical brain injury, trauma or damage

- Perseveration is particularly common with those who have had traumatic brain injury.

- Perseveration is sometimes a feature of frontal lobe lesions, and of other conditions involving dysfunction or dysregulation within the frontal lobe. This is especially true when the lateral orbitofrontal cortex or inferior prefrontal convexity (Brodmann areas 47/12) are affected.

- Perseveration is also sometimes seen as a symptom of aphasia.

Other neurological conditions

- Perseveration may also refer to the obsessive and highly selective interests of individuals on the autism spectrum. This term is most connected to Asperger syndrome.

- In attention deficit hyperactivity disorder (ADHD), perseveration or "hyperfocus" commonly occurs as an impairment of set shifting and task switching. The resistance to transition may be a coping mechanism or the brain's method to compensate for the lack of ability to regulate the application of attention.

- In people who are both intellectually gifted and suffer a learning disability, the state of hyperfocus and flow can be confounded with perseverance.

- Apart from their direct symptoms, people with obsessive–compulsive disorder can have specific problems with set shifting and inhibition of prepotent responses.

Confounds (conditions with similar appearing symptoms)

- Perseveration may be confused with habitual behaviours in a number of other conditions and disorders, such as obsessive–compulsive disorder, including post-traumatic stress disorder (PTSD), body dysmorphic disorder, trichotillomania, and habit problems. However, in animal experiments it can be shown when repetitive behaviour is a cognitive perseveration rather than a motor disorder. For example, under low doses of amphetamine an animal will perseverate in maintaining an arbitrary object preference even when different motor responses are required to maintain that preference.

Unproven:

- Several researchers have tried to connect perseveration with a lack of memory inhibition (the person repeats the answer because they have not been able to forget a past question and move on to the current subject); however, this connection could not be found, or was small.

Perseveration according to psychology, psychiatry, and speech-language pathology, is the repetition of a particular response (such as a word, phrase, or gesture) regardless of the absence or cessation of a stimulus. It is usually caused by a brain injury or other organic disorder. Symptoms include "lacking ability to transition or switch ideas appropriately with the social context, as evidenced by the repetition of words or gestures after they have ceased to be socially relevant or appropriate", or the "act or task of doing so", and are not better described as stereotypy (a highly repetitive idiosyncratic behaviour).

In a broader sense, it is used for a wide range of functionless behaviours that arise from a failure of the brain to either inhibit prepotent responses or to allow its usual progress to a different behavior, and includes impairment in set shifting and task switching in social and other contexts.

The primary definition of perseveration in biology and clinical psychiatry involves some form of response repetition or the inability to undertake set shifting (changing of goals, tasks or activities) as required, and is usually evidenced by behaviours such as words and gestures continuing to be repeated despite absence or cessation of a stimulus.

More broadly in clinical psychology, it describes mental or physical behaviours which are not excessive in terms of quantity but are apparently both functionless and involve a narrow range of behaviours, and are not better described as stereotypy (a highly repetitive idiosyncratic behaviour).

In general English, perseveration (vb: "to perseverate") refers to insistent or redundant repetition, not necessarily in a clinical context.

Thought disorder (TD) or formal thought disorder (FTD) refers to disorganized thinking as evidenced by disorganized speech. Specific thought disorders include derailment, poverty of speech, tangentiality, illogicality, perseveration, and thought blocking.

Psychiatrists consider formal thought disorder as being one of two types of disordered thinking, with the other type being delusions. The latter involves "content" while the former involves "form". Although the term "thought disorder" can refer to either type, in common parlance it refers most often to a disorder of thought "form" also known as formal thought disorder.

Eugen Bleuler, who named schizophrenia, held that thought disorder was its defining characteristic. However, formal thought disorder is not unique to schizophrenia or psychosis. It is often a symptom of mania, and less often it can be present in other mental disorders such as depression. Clanging or echolalia may be present in Tourette syndrome. Patients with a clouded consciousness, like that found in delirium, also have a formal thought disorder.

However, there is a clinical difference between these two groups. Those with schizophrenia or psychosis are less likely to demonstrate awareness or concern about the disordered thinking. Clayton and Winokur have suggested that this results from a fundamental inability to use the same type of Aristotelian logic as others. On the other hand, patients with a clouded consciousness, referred to as "organic" patients, usually do demonstrate awareness and concern, and complain about being "confused" or "unable to think straight"; Clayton and Winokur suggest that this is because their thought disorder results, instead, from various cognitive deficits.

The concept of thought disorder has been criticized as being based on circular or incoherent definitions. For example, thought disorder is inferred from disordered speech, based on the assumption that disordered speech arises because of disordered thought. Incoherence, or word salad, refers to speech that is unconnected and conveys no meaning to the listener.

Furthermore, although thought disorder is typically associated with psychosis, similar phenomena can appear in different disorders, potentially leading to misdiagnosis—for example, in the case of incomplete yet potentially fruitful thought processes.

It has been suggested that individuals with autism spectrum disorders (ASD) display language disturbances like those found in schizophrenia; a 2008 study found that children and adolescents with ASD showed significantly more illogical thinking and loose associations than control subjects. The illogical thinking was related to cognitive functioning and executive control; the loose associations were related to communication symptoms and to parent reports of stress and anxiety.

In psychology and neuroscience, executive dysfunction, or executive function deficit, is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control.

Executive dysfunction is not the same as dysexecutive syndrome, a term coined by Alan Baddeley to describe a common pattern of dysfunction in executive functions, such as deficiencies in planning, abstract thinking, flexibility and behavioural control. This group of symptoms, usually resulting from brain damage, tend to occur together. However, the existence of dysexecutive syndrome is controversial.

Cerebellar cognitive affective syndrome (CCAS), also called "Schmahmann's syndrome" is a condition that follows from lesions (damage) to the cerebellum of the brain. This syndrome, described by Dr. Jeremy Schmahmann and his colleagues refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

Ideational apraxia (IA) is a neurological disorder which explains the loss of ability to conceptualize, plan, and execute the complex sequences of motor actions involved in the use of tools or otherwise interacting with objects in everyday life. Ideational apraxia is a condition in which an individual is unable to plan movements related to interaction with objects, because he has lost the perception of the object's purpose. Characteristics of this disorder include a disturbance in the concept of the sequential organization of voluntary actions. The patient appears to have lost the knowledge or thought of what an object represents. This disorder was first seen 100 years ago by Doctor Arnold Pick, who described a patient who appeared to have lost their ability to use objects. The patient would make errors such as combing their hair with the wrong side of the comb or placing a pistol in his mouth. From that point on, several other

researchers and doctors have stumbled upon this unique disorder. IA has been described under several names such as, agnosia of utilization, conceptual apraxia or loss of knowledge about the use of tools, or semantic amnesia of tool usage. The term apraxia was first created by Steinthal in 1871 and was then applied by Gogol, Kusmaul, Star, and Pick to patients who failed to pantomime the use of tools. It was not until the 1900s, when Liepmann refined the definition, that it specifically described disorders that involved motor planning, rather than disturbances in the patient’s visual perception, language, or symbolism.

The Fregoli delusion, or the delusion of doubles, is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know.

The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras delusion, psychiatrists believe it is related to a breakdown in normal face perception.

The cause of IA is still somewhat of a mystery to most researchers. That is because there is no localized focal point in the brain that shows where this deficit will occur. Since 1905 Liepmann proposed a hypothesis of an action processing system that is found in the left hemisphere of the brain, which is dedicated to skilled, motor planning that guides the movement of the body. Yet, he still was never able to produce two patients with the same brain damage that showed ideational apraxia. The major ideas of where IA is found are in the left posterior temporal-parietal junction. Possibly damage to the lateral sulcus also known as Sylvian fissure may contribute to an individual’s deterioration of object recognition. Another possible area of damage leading to IA is the submarginal gyrus, which is located in the parietal lobe of the brain. Overall, IA is an autonomous syndrome, linked to damage in the left hemisphere involving semantic memory disorders rather than a defect in motor control.

Several severe injuries or diseases can cause IA in a wide range of patients. Alzheimer's patients are the largest cohort groups that express IA. Other groups that are often seen with this dysfunction are stroke victims, traumatic brain injuries, and dementia. Interestingly, the damage is almost always found in the dominant hemisphere (i.e. usually the left hemisphere) of the patient.

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.

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 attention-deficit/hyperactivity disorder is a classification given to a set of subjectively-determined symptoms implicating executive dysfunction – current models indicate that such clinical symptoms are caused by executive dysfunction.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

In 2006, the U.S. Department of Education indicated that more than 1.4 million students were served in the public schools' special education programs under the speech or language impairment category of IDEA 2004. This estimate does not include children who have speech/language problems secondary to other conditions such as deafness; this means that if all cases of speech or language impairments were included in the estimates, this category of impairment would be the largest. Another source has estimated that communication disorders—a larger category, which also includes hearing disorders—affect one of every 10 people in the United States.

ASHA has cited that 24.1% of children in school in the fall of 2003 received services for speech or language disorders—this amounts to a total of 1,460,583 children between 3 –21 years of age. Again, this estimate does not include children who have speech/language problems secondary to other conditions. Additional ASHA prevalence figures have suggested the following:

- Stuttering affects approximately 4% to 5% of children between the ages of 2 and 4.

- ASHA has indicated that in 2006:

- Almost 69% of SLPs served individuals with fluency problems.

- Almost 29% of SLPs served individuals with voice or resonance disorders.

- Approximately 61% of speech-language pathologists in schools indicated that they served individuals with SLI

- Almost 91% of SLPs in schools indicated that they servedindividuals with phonological/articulation disorder

- Estimates for language difficulty in preschool children range from 2% to 19%.

- Specific Language Impairment (SLI) is extremely common in children, and affects about 7% of the childhood population.

Once it has been positively identified, pharmacotherapy follows. Antipsychotic drugs are the frontrunners in treatment for Fregoli and other DMSs. In addition to antipsychotics, anticonvulsants and antidepressants are also prescribed in some treatment courses. If a Fregoli patient has other psychological disorders, treatment often results in the use of trifluoperazine.

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

List of symptoms that has been observed in those with autistic catatonia:

- Stupor

- Mutism

- Hyperactivity

- Agitation

- Excitement

- Posing

- Negativism

- Rigidity

- Waxy flexibility

- Automatic obedience

- Combativeness (during excitement)

- Aggressivity

- Stereotypies

- Tics

- Grimacing

- Echolalia

- Echopraxia

- Perseveration

- Verbigeration

- Staring

- Withdrawal

- Immobility

- Challenging behaviour

- Tremor

- Slowness

- Amotivation

- Grasp reflex

- Mannerism

- Gaze fixation

- Choreoathetoid movements of the trunk and extremities

- Autonomic instability (during excitement)

- Cannot start actions

- Cannot stop actions (if during excitement episodes needs acute psychiatric care)

- Freezing

- Impulsivity

- Bizarre/psychotic

- Sleep problems

- Urinary or Fecal incontinence

- Odd gait

- Passivity

- Reversal of day and night

- Eyerolling

- Stiff muscles

- Catalepsy

- Physiological pillow

- Difficulty crossing lines

- Gegenhalten

- Mitgehen

- Mitmachen

- Ambitendency

- Rituals

Nonverbal learning disorder (also known as nonverbal learning disability, NLD, or NVLD) is a learning disorder characterized by verbal strengths as well as visual-spatial, motor, and social skills difficulties. It is sometimes confused with Asperger Syndrome or high IQ. Nonverbal learning disorder has never been included in the American Psychiatric Association's "Diagnostic and Statistical Manual of Mental Disorders" or the World Health Organization's "International Classification of Diseases".

In psychiatry, stilted speech or pedantic speech is communication characterized by situationally inappropriate formality. This formality can be expressed both through abnormal prosody as well as speech content that is "inappropriately pompous, legalistic, philosophical, or quaint". Often, such speech can act as evidence for autism spectrum disorder (ASD) or a thought disorder, a common symptom in schizophrenia or schizotypal personality disorder.

To diagnose stilted speech, researchers have previously looked for the following characteristics:

- speech conveying more information than necessary

- vocabulary and grammar expected from formal writing rather than conversational speech

- unneeded repetition or corrections

While literal and long-winded word content is often the most identifiable feature of stilted speech, such speech often displays irregular prosody, especially in resonance. Often, the loudness, pitch, rate, and nasality of pedantic speech vary from normal speech, resulting in the perception of pedantic or stilted speaking. For example, overly loud or high-pitched speech can come across to listeners as overly forceful while slow or nasal speech creates an impression of condescension.

These attributions, which are commonly found in patients with ASD, partially account for why stilted speech has been considered a diagnostic criteria for the disorder. Stilted speech, along with atypical intonation, semantic drift, terseness, and perseveration, are all qualities known to be commonly impaired during conversation with adolescents on the autistic spectrum. Often, stilted speech found in children with ASD will also be especially stereotypic or rehearsed.

Patients with schizophrenia are also known to experience stilted speech. This symptom is attributed to both an inability to access more commonly used words and a difficulty understanding pragmatics, or the relationship between language and context. However, stilted speech appears as less common symptom compared to a certain number of other symptoms of the psychosis (Adler "et al" 1999). This element of cognitive disorder is also exhibited as a symptom in the narcissistic personality disorder (Akhtar & Thomson 1982).

In its more common usage, "stilted speech" is a term used to describe overly-formal, unnatural-sounding speech.

TGA attacks are associated with some form of precipitating event in at least one-third of cases. The most commonly cited precipitating events include vigorous exercise (including sexual intercourse), swimming in cold water or enduring other temperature changes, and emotionally traumatic or stressful events. There are reports of TGA-like conditions following certain medical procedures and disease states. One study reports two cases of familial incidence (in which two members of the same family experienced TGA), out of 114 cases considered. This indicates the possibility that there could be a slight familial incidence.

If the definition of a precipitating event is widened to include events days or weeks earlier, and to take in emotionally stressful burdens such as money worries, attending a funeral or exhaustion due to overwork or unusual childcare responsibilities, a large majority, over 80%, of TGA attacks are said to correlate with precipitating events.

The role of psychological co-factors has been addressed by some research. It is the case that people in a state of TGA exhibit measurably elevated levels of anxiety and/or depression. Emotional instability may leave some people vulnerable to stressful triggers and thus be associated with TGA. Individuals who have experienced TGA, compared with similar people with TIA, are more likely to have some kind of emotional problem (such as depression or phobias) in their personal or family history or to have experienced some kind of phobic or emotionally challenging precipitating event.

The prognosis of "pure" TGA is very good. It does not affect mortality or morbidity and unlike earlier understanding of the condition, TGA is not a risk factor for stroke or ischemic disease. Rates of recurrence are variously reported, with one systematic calculation suggesting the rate is under 6% per year. TGA "is universally felt to be a benign condition which requires no further treatment other than reassurance to the patient and his or her family."

"The most important part of management after diagnosis is looking after the psychological needs of the patient and his or her relatives. Seeing a once competent and healthy partner, sibling or parent become incapable of remembering what was said only a minute ago is very distressing, and hence it is often the relatives who will require reassurance."

TGA may have multiple etiologies and prognoses. Atypical presentations may masquerade as epilepsy and be more properly considered TEA. In addition to such probable TEA cases, some people experiencing amnestic events diverging from the diagnostic criteria articulated above may have a less benign prognosis than those with "pure" TGA.

Recently, moreover, both imaging and neurocognitive testing studies question whether TGA is as benign as has been thought. MRI scans of the brain in one study showed that among people who had experienced TGA, all had cavities in the hippocampus, and these cavities were far more numerous, larger, and more suggestive of pathological damage than in either healthy controls or a large control group of people with tumor or stroke. Verbal and cognitive impairments have been observed days after TGA attacks, of such severity that the researchers estimated the effects would be unlikely to resolve within a short time frame. A large neurocognitive study of patients more than a year after their attack has shown persistent effects consistent with amnestic mild cognitive impairment (MCI-a) in a third of the people who had experienced TGA. In another study, "selective cognitive dysfunctions after the clinical recovery" were observed, suggesting a prefrontal impairment. These dysfunctions may not be in memory "per se" but in retrieval, in which speed of access is part of the problem among people who have had TGA and experience ongoing memory problems.

Considered to be neurologically based, nonverbal learning disorder is characterized by verbal strengths as well as visual-spatial, motor, and social skills difficulties. People with this disorder may not at times comprehend nonverbal cues such as facial expression or tone of voice. Challenges with mathematics and handwriting are common.

While various nonverbal impairments were recognized since early studies in child neurology, there is ongoing debate as to whether/or the extent to which existing conceptions of NLD provide a valid diagnostic framework. As originally presented "nonverbal disabilities" (p. 44) or "disorders of nonverbal learning" (p. 272) was a category encompassing non-linguistic learning problems (Johnson and Myklebust, 1967). "Nonverbal learning disabilities" were further discussed by Myklebust in 1975 as representing a subtype of learning disability with a range of presentations involving "mainly visual cognitive processing," social imperception, a gap between higher verbal ability and lower performance IQ, as well as difficulty with handwriting. Later neuropsychologist Byron Rourke sought to develop consistent criteria with a theory and model of brain functioning that would establish NLD as a distinct syndrome (1989).

Questions remain about how best to frame the perceptual, cognitive and motor issues associated with NLD.

The DSM-5 (Diagnostic and Statistical Manual) and ICD-10 (International Classification of Diseases) do not include NLD as a diagnosis.

Assorted diagnoses have been discussed as sharing symptoms with NLD—these conditions include Right hemisphere brain damage and Developmental Right Hemisphere Syndrome, Developmental Coordination Disorder, Social-Emotional Processing Disorder, Asperger syndrome, Gerstmann syndrome and others.

Labels for specific associated issues include visual-spatial deficit, dyscalculia, dysgraphia, as well as dyspraxia.

In their 1967 book "Learning Disabilities; Educational Principles and Practices", Doris J. Johnson and Helmer R. Myklebust characterize how someone with these kinds of disabilities appears in a classroom: "An example is the child who fails to learn the meaning of the actions of others...We categorize this child as having a deficiency in social perception, meaning that he has an inability which precludes acquiring the significance of basic nonverbal aspects of daily living, though his verbal level of intelligence falls within or above the average." (p. 272). In their chapter "Nonverbal Disorders Of Learning" (p. 272-306) are sections titled "Learning Though Pictures," (274) "Gesture," (281) "Nonverbal Motor Learning," (282) "Body Image," (285) "Spatial Orientation," (290) "Right-Left Orientation," (292) "Social Imperception," (295) "Distractibility, Perseveration, and Disinhibition." (298)

Palinacousis is an auditory form of perseveration — continuing to hear a sound after the physical noise has disappeared. The condition is often associated with lesions of the temporal lobe.

Acquired disorders result from brain injury, stroke or atrophy, many of these issues are included under the Aphasia umbrella.

Brain damage, for example, may result in various forms of aphasia if critical areas of the brain such as Broca's or Wernicke's area are damaged by lesions or atrophy as part of a dementia.

Of the published cases of palinopsia from posterior cortical lesions or seizures, 93% described hallucinatory palinopsia. Hallucinatory palinopsia may be caused by many types of posterior cortical lesions such as neoplasms, infarctions, hemorrhages, arteriovenous malformations, aneurysm, abscesses, and tuberculomas. Hallucinatory palinopsia from seizures may be secondary to a focal cortical lesion or may be secondary to a non-structural disturbance. Causes of seizures that are reported to cause palinopsia include metabolic disturbances (hyperglycemia, carnitine deficiency), ion channel disturbances, Creutzfeldt–Jakob disease, and seizures of unknown cause.