The diagnosis of frontal lobe disorder can be divided into the following three categories:

- Clinical history

Frontal lobe disorders may be recognized through a sudden and dramatic change in a person's personality, for example with loss of social awareness, disinhibition, emotional instability, irritability or impulsiveness. Alternatively the disorder may become apparent because of mood changes such as depression, anxiety or apathy.

- Examination

On mental state examination a person with frontal lobe damage may show speech problems, with reduced verbal fluency. Typically the person is lacking in insight and judgment, but does not have marked cognitive abnormalities or memory impairment (as measured for example by the mini-mental state examination). With more severe impairment there may be echolalia or mutism. Neurological examination may show primitive reflexes (also known as frontal release signs) such as the grasp reflex. Akinesia (lack of spontaneous movement) will be present in more severe and advanced cases.

- Further investigation

A range of neuropsychological tests are available for clarifying the nature and extent of frontal lobe dysfunction. For example, concept formation and ability to shift mental sets can be measured with the Wisconsin Card Sorting Test, planning can be assessed with the Mazes subtest of the WISC. Individuals with Pick's disease will show frontal cortical atrophy on MRIs. Frontal impairment due to head injuries, tumours or cerebrovascular disease will also be apparent on brain imaging.

Sensory processing disorder since 1994 is accepted in the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC:0-3R) and is not recognized as a mental disorder in medical manuals such as the ICD-10 or the DSM-5.

Diagnosis is primarily arrived at by the use of standardized tests, standardized questionnaires, expert observational scales, and free play observation at an occupational therapy gym. Observation of functional activities might be carried at school and home as well. Some scales that are not exclusively used in SPD evaluations are used to measure visual perception, function, neurology and motor skills.

Depending on the country, diagnosis is made by different professionals, such as occupational therapists, psychologists, learning specialists, physiotherapists and/or speech and language therapists. In some countries it is recommended to have a full psychological and neurological evaluation if symptoms are too severe.

Assessment of patients with DES can be difficult because traditional tests generally focus on one specific problem for a short period of time. People with DES can do fairly well on these tests because their problems are related to integrating individual skills into everyday tasks. The lack of everyday application of traditional tests is known as low ecological validity.

It is estimated that up to 16.5% of elementary school aged children present elevated SOR behaviors in the tactile or auditory modalities. However, this figure might represent an underestimation of Sensory Over Responsivity prevalence, since this study did not include children with developmental disorders or those delivered preterm, who are more likely to present it.

This figure is, nonetheless, larger than what previous studies with smaller samples had shown: an estimate of 5–13% of elementary school aged children.

Incidence for the remaining subtypes is currently unknown.

The Behavioural Assessment of the Dysexecutive Syndrome (BADS) was designed to address the problems of traditional tests and evaluate the everyday problems arising from DES. BADS is designed around six subtests and ends with the Dysexecutive Questionnaire (DEX). These tests assess executive functioning in more complex, real-life situations, which improves their ability to predict day-to-day difficulties of DES.

The Dysexecutive Questionnaire (DEX) is a 20-item questionnaire designed to sample emotional, motivational, behavioural and cognitive changes in a subject with DES. One version is designed for the subject to complete and another version is designed for someone who is close to the individual, such as a relative or caregiver. Instructions are given to the participant to read 20 statements describing common problems of everyday life and to rate them according to their personal experience. Each item is scored on a 5-point scale according to its frequency from "never" (0 point) to "very often" (4 points).

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

There are several measures that can be employed to assess the executive functioning capabilities of an individual. Although a trained non-professional working outside of an institutionalized setting can legally and competently perform many of these measures, a trained professional administering the test in a standardized setting will yield the most accurate results.

In terms of treatment for frontal lobe disorder, general supportive care is given, also some level of supervision could be needed. The prognosis will depend on the cause of the disorder, of course. A possible complication is that individuals with severe injuries may be disabled, such that, a caregiver may be unrecognizable to the person.

Another aspect of treatment of frontal lobe disorder is speech therapy. This type of therapy might help individuals with symptoms that are associated with aphasia and dysarthria.

There is no cure for neurocognitive disorder or the diseases that cause it. Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to maintain a better quality of life for everyone involved. Speech therapy has been shown to help with language impairment.

Studies suggest that diets with high Omega 3 content, low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such a newly developed “computerized brain training programs” can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence, the ability to adapt and deal with new problems or challenges the first time encountered, and in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information. If it is caused by an underlying cause such as Alzheimer's disease or infections, the cause may be treated but the amnesia may not be.

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.

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 to train non-professional staff to administer a CDT. Therefore, this is a test that can easily be administered in educational and geriatric settings and can be utilized as a precursory measure to indicate the likelihood of further/future deficits. Also, generational, educational and cultural differences are not perceived as impacting the utility of the CDT.

The procedure of the CDT begins with the instruction to the participant to draw a clock reading a specific time (generally 11:10). After the task is complete, the test administrator draws a clock with the hands set at the same specific time. Then the patient is asked to copy the image. Errors in clock drawing are classified according to the following categories: omissions, perseverations, rotations, misplacements, distortions, substitutions and additions. Memory, concentration, initiation, energy, mental clarity and indecision are all measures that are scored during this activity. Those with deficits in executive functioning will often make errors on the first clock but not the second. In other words, they will be unable to generate their own example, but will show proficiency in the copying task.

Since the term of "reversible" has been used, it simply implies a high possibility of recovery from the disease. Cunha (1990) examined the recovery process of 26 patients with reversible dementia. Unfortunately, only 2 patients have found as return to normal function indicated by the MMSE scores. Poor results have also been reported in Copeland et al. (1992)'s studies, as 1 out of 21 DD patients had fully recovered. Thus, attention should be arisen that the diagnosis of reversible or pseudodementia needs to be given with extreme care, and the recovery pattern for individual patient remains uncertain.

Diagnosis of Wernicke–Korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. Wernicke's encephalopathy typically presents with ataxia and nystagmus, and Korsakoff's psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning.

Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke's encephalopathy, patients will have marked degeneration of the mamillary bodies. Thiamine (vitamin B) is an essential coenzyme in carbohydrate metabolism and is also a regulator of osmotic gradient. Its deficiency may cause swelling of the intracellular space and local disruption of the blood-brain barrier. Brain tissue is very sensitive to changes in electrolytes and pressure and edema can be cytotoxic. In Wernicke's this occurs specifically in the mammillary bodies, medial thalami, tectal plate, and periaqueductal areas. Sufferers may also exhibit a dislike for sunlight and so may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various "memory circuits" within the brain. An example of a memory circuit is the Papez circuit.

The current treatments for CCAS focus on relieving the symptoms. One treatment is a cognitive-behavioral therapy (CBT) technique that involves making the patient aware of his or hers cognitive problems. For example, many CCAS patients struggle with multitasking. With CBT, the patient would have to be aware of this problem and focus on just one task at a time. This technique is also used to relieve some motor symptoms. In a case study with a patient who had a stroke and developed CCAS, improvements in mental function and attention were achieved through reality orientation therapy and attention process training. Reality orientation therapy consists of continually exposing the patient to stimuli of past events, such as photos. Attention process training consists of visual and auditory tasks that have been shown to improve attention. The patient struggled in applying these skills to “real-life” situations. It was the help of his family at home that significantly helped him regain his ability to perform activities of daily living. The family would motivate the patient to perform basic tasks and made a regular schedule for him to follow.

Transcranial magnetic stimulation (TMS) has also been proposed to be a possible treatment of psychiatric disorders of the cerebellum. One study used TMS on the vermis of patients with schizophrenia. After stimulation, the patients showed increased happiness, alertness and energy, and decreased sadness. Neuropsychological testing post-stimulation showed improvements in working memory, attention, and visual spatial skill. Another possible method of treatment for CCAS is doing exercises that are used to relieve the motor symptoms. These physical exercises have been shown to also help with the cognitive symptoms.

Medications that help relieve deficits in traumatic brain injuries in adults have been proposed as candidates to treat CCAS. Bromocriptine, a direct D2 agonist, has been shown to help with deficits in executive function and spatial learning abilities. Methylphendiate has been shown to help with deficits in attention and inhibition. Neither of these drugs has yet been tested on a CCAS population. It may also be that some of the symptoms of CCAS improve over time without any formal treatment. In the original report of CCAS, four patients with CCAS were re-examined one to nine months after their initial neuropsychological evaluation. Three of the patients showed improvement in deficits without any kind of formal treatment, though executive function was still found to be one standard deviation below average. In one patient, the deficits worsened over time. This patient had cerebellar atrophy and worsened in visual spatial abilities, concept formation, and verbal memory. It should be noted that none of these treatments were tested on a large enough sample to determine if they would help with the general CCAS population. Further research needs to be done on treatments for CCAS.

Confabulations can also be detected using a free recall task, such as a self-narrative task. Participants are asked to recall stories (semantic or autobiographical) that are highly familiar to them. The stories recalled are encoded for errors that could be classified as distortions in memory. Distortions could include falsifying true story elements or including details from a completely different story. Errors such as these would be indicative of confabulations.

The progression of the degeneration caused by bvFTD may follow a predictable course. The degeneration begins in the orbitofrontal cortex and medial aspects such as ventromedial cortex. In later stages, it gradually expands its area to the dorsolateral cortex and the temporal lobe. Thus, the detection of dysfunction of the orbitofrontal cortex and ventromedial cortex is important in the detection of early stage bvFTD. As stated above, a behavioural change may occur before the appearance of any atrophy in the brain in the course of the disease. Because of that, image scanning such as MRI can be insensitive to the early degeneration and it is difficult to detect early-stage bvFTD.

In neuropsychology, there is an increasing interest in using neuropsychological tests such as the Iowa gambling task or Faux Pas Recognition test as an alternative to imaging for the diagnosis of bvFTD. Both the Iowa gambling task and the Faux Pas test are known to be sensitive to dysfunction of the orbitofrontal cortex.

Faux Pas Recognition test is intended to measure one’s ability to detect faux pas types of social blunders (accidentally make a statement or an action that offends others). It is suggested that people with orbitofrontal cortex dysfunction show a tendency to make social blunders due to a deficit in self-monitoring. Self-monitoring is the ability of individuals to evaluate their behaviour to make sure that their behaviour is appropriate in particular situations. The impairment in self-monitoring leads to a lack of social emotion signals. The social emotions such as embarrassment are important in the way that they signal the individual to adapt social behaviour in an appropriate manner to maintain relationships with others. Though patients with damage to the OFC retain intact knowledge of social norms, they fail to apply it to actual behaviour because they fail to generate social emotions that promote adaptive social behaviour.

The other test, the Iowa gambling task, is a psychological test intended to simulate real-life decision making. The underlying concept of this test is the somatic marker hypothesis. This hypothesis argues that when people have to make complex uncertain decisions, they employ both cognitive and emotional processes to assess the values of the choices available to them. Each time a person makes a decision, both physiological signals and evoked emotion (somatic marker) are associated with their outcomes and it accumulates as experience. People tend to choose the choice which might produce the outcome reinforced with positive stimuli, thus it biases decision-making towards certain behaviours while avoiding others. It is thought that somatic marker is processed in orbitofrontal cortex.

The symptoms observed in bvFTD are caused by dysfunction of the orbitofrontal cortex, thus these two neuropsychological tests might be useful in detecting the early stage bvFTD. However, as self-monitoring and somatic marker processes are so complex, it likely involves other brain regions. Therefore, neuropsychological tests are sensitive to the dysfunction of orbitofrontal cortex, yet not specific to it. The weakness of these tests is that they do not necessarily show dysfunction of the orbitofrontal cortex.

In order to solve this problem, some researchers combined neuropsychological tests which detect the dysfunction of orbitofrontal cortex into one so that it increases its specificity to the degeneration of the frontal lobe in order to detect the early-stage bvFTD. They invented the Executive and Social Cognition Battery which comprises five neuropsychological tests.

- Iowa gambling task

- Faux Pas test

- Hotel task

- Mind in the Eyes

- Multiple Errands Task

The result has shown that this combined test is more sensitive in detecting the deficits in early bvFTD.

Confabulations can also be researched by using continuous recognition tasks. These tasks are often used in conjunction with confidence ratings. Generally, in a recognition task, participants are rapidly presented with pictures. Some of these pictures are shown once; others are shown multiple times. Participants press a key if they have seen the picture previously. Following a period of time, participants repeat the task. More errors on the second task, versus the first, are indicative of confusion, representing false memories.

As described, Korsakoff 's syndrome usually follows or accompanies Wernicke's encephalopathy. If treated quickly, it may be possible to prevent the development of Korsakoff's syndrome with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke-Korsakoff's syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke's encephalopathy will not necessarily progress to WKS.

In order to reduce the risk of developing WKS it is important to limit the intake of alcohol or drink in order to ensure that proper nutrition needs are met. A healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing WKS. This prevention method may specifically help heavy drinkers who refuse to or are unable to quit.

As certain of pseudodementia remains potentially treatable, it is essential that they are distinguished from primarily dementia of the Alzheimer's type (DAT), and multi-infarct dementia (MID). For instance, pseudodementia associated with depression (DD) has been found as the most frequently appearing, while as many as 10% to 20% patients are misdiagnosed as primary degenerative dementia (PDD) or vice versa. A significant overlapping in cognitive and neuropsychological dysfunction in DD and PDD patients seemed to increase the difficulty in diagnosis. However, differences in the severity of impairment and quality of patients' responses could be observed, and DD patients exhibited a greater depressive symptomatology. Additionally, a test of antisaccadic movements may be used to differentiate DD from PDD patients. as PDD patients significantly display poorer performance on this test. A general comparison between aspects of DD and PDD is shown below.

In general, pseudodementia patients present a considerable cognitive deficits, including disorders in learning, memory and psychomotor performance. Substantial evidences from brain imaging such as CT scanning and positron emission tomography (PET) have also revealed abnormalities in brain structure and function.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Symptoms of frontotemporal dementia progress at a rapid, steady rate. Patients suffering from the disease can survive between 2–15 years. Eventually patients will need 24-hour care for daily function.

CSF leaks are a known cause of reversible frontotemporal dementia.

Serotonin and norepinephrine reuptake inhibitor, venlafaxine, were given to case study KS four months after initial stroke that started symptoms of witzelsucht. Changes back to his original behavior were noticeable after daily dose of 37.5 mg of venlafaxine for two weeks. In subsequent two months, inappropriate jokes and hypersexual behavior were rarely noticed. Due to the rareness of this disorder, not much research into potential treatments has been conducted.

Agnosia is the inability to recognize certain objects, persons or sounds. Agnosia is typically caused by damage to the brain (most commonly in the occipital or parietal lobes) or from a neurological disorder. Treatments vary depending on the location and cause of the damage. Recovery is possible depending on the severity of the disorder and the severity of the damage to the brain. Many more specific types of agnosia diagnoses exist, including: associative visual agnosia, astereognosis, auditory agnosia, auditory verbal agnosia, prosopagnosia, simultanagnosia, topographical disorientation, visual agnosia etc.

The types of imaging techniques that are most prominently utilized when studying and/or diagnosing CBD are:

- magnetic resonance imaging (MRI)

- single-photon emission computed tomography (SPECT)

- fluorodopa positron emission tomography (FDOPA PET)

Developments or improvements in imaging techniques provide the future possibility for definitive clinical diagnosis prior to death. However, despite their benefits, information learned from MRI and SPECT during the beginning of CBD progression tend to show no irregularities that would indicate the presence of such a neurodegenerative disease. FDOPA PET is used to study the efficacy of the dopamine pathway.

Despite the undoubted presence of cortical atrophy (as determined through MRI and SPECT) in individuals experiencing the symptoms of CBD, this is not an exclusive indicator for the disease. Thus, the utilization of this factor in the diagnosis of CBD should be used only in combination with other clinically present dysfunctions.

There are no standard diagnostic criteria. Misophonia is distinguished from hyperacusis, which is not specific to a given sound and does not involve a similar strong reaction, and from phonophobia, which is a fear of a specific sound, but it may occur with either.

It is not clear whether people with misophonia usually have comorbid conditions, nor whether there is a genetic component.