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.

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.

Neuropsychology is the study of neurobiology and psychology. Neuropsychological tests are utilized for the purpose of observing an individuals’ abilities in cognitive functioning, reasoning, and memories. The tests most commonly used for neuropsychological testing include WAIS-III, Stroop test, Bourdon Wiersma test, and the Rey-Osterrieth complex figure test. These tests allow physicians to evaluate the degree to which the bilateral lesions in the operculum have been affected, and allow for the determination of proper treatment.

Scanning techniques include EEG, SPECT, MRI, and CT brain scanning. These additional techniques are useful in determining what type of lesion the patient has, and allows physicians to determine more effective ways in treating the patient.

CT scan or MRI can confirm dementia via observation of ventricular dilation and cortical substance degeneration.

Pick's disease can be confirmed via CT scan or MRI with atrophy of frontal and temporal lobe roots.

Alzheimer's is a disease confirmed by atrophy of the parietal and temporal lobe ganglia along with changes in the cortical ganglia found in a CT scan or MRI.

Along with occupational and environmental evaluation, a neurological exam, ECHO, EEG, CT-San, and X-ray of the brain may be conducted to determine disorder. Neuroimaging that detects cerebral atrophy or cardiovascular subcortical alterations can help point to psychoorganic syndrome. Strong CNS lesions are detected in POS patients. However, this is found to be difficult as many psychiatric disorders, like dementia, have common diagnosis.

Diagnosing POS is an ongoing and developing in the medical and psychiatric industry. Exact diagnosis is difficult due to many symptoms mirroring other psychological disorders in the older aged patients.

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.

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 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).

Akinetic mutism can be misdiagnosed as depression, delirium, or locked-in syndrome, all of which are common following a stroke. Patients with depression can experience apathy, slurring of speech, and body movements similar to akinetic mutism. Similarly to akinetic mutism, patients with locked-in syndrome experience paralysis and can only communicate with their eyes. Correct diagnosis is important to ensure proper treatment. A variety of treatments for akinetic mutism have been documented, but treatments vary between patients and cases.

TMoA is diagnosed by the referring physician and speech-language pathologist (SLP). The overall sign of TMoA is nonfluent, reduced, fragmentary echoic, and perseverative speech with frequent hesitations and pauses. Patients with TMoA also have difficulty initiating and maintaining speech. However, speech articulation and auditory comprehension remain typical. The hallmark sign of TMoA is intact repetition in the presence of these signs and symptoms.

TMoA, or any other type of aphasia, is identified and diagnosed through the screening and assessment process. Screening can be conducted by a SLP or other professional when there is a suspected aphasia. The screening does not diagnose aphasia, rather it points to the need for a further comprehensive assessment. A screening typically includes evaluation of oral motor functions, speech production skills, comprehension, use of written and verbal language, cognitive communication, swallowing, and hearing. Both the screening and assessment must be sensitive to the patient’s linguistic and cultural differences. An individual will be recommended to receive a comprehensive assessment if their screening shows signs of aphasia. Under the American Speech-Language-Hearing Association (ASHA) and World Health Organization (WHO) guidelines and the "International Classification of Functioning, Disability and Health" (ICF) framework, the comprehensive assessment encompasses not only speech and language, but also impairments in body structure and function, co-morbid deficits, limitations in activity and participation, and contextual (environmental and personal) factors. The assessment can be static (current functioning) or dynamic (ongoing) and the assessment tools can be standardized or nonstandardized. Typically, the assessment for aphasia includes a gathering of a case history, a self-report from the patient, an oral-motor examination, assessment of expressive and receptive language in spoken and written forms, and identification of facilitators and barriers to patient success. From this assessment, the SLP will determine type of aphasia and the patient's communicative strengths and weaknesses and how their diagnosis may impact their overall quality of life.

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.

Diagnosis for aboulia can be quite difficult because it falls between two other disorders of diminished motivation, and one could easily see an extreme case of aboulia as akinetic mutism or a lesser case of aboulia as apathy and therefore, not treat the patient appropriately. If it were to be confused with apathy, it might lead to attempts to involve the patient with physical rehabilitation or other interventions where a source of strong motivation would be necessary to succeed but would still be absent. The best way to diagnose aboulia is through clinical observation of the patient as well as questioning of close relatives and loved ones to give the doctor a frame of reference with which they can compare the patient's new behavior to see if there is in fact a case of diminished motivation. In recent years, imaging studies using a CT or MRI scan have been shown to be quite helpful in localizing brain lesions which have been shown to be one of the main causes of aboulia.

The verbal fluency test is a widely and commonly used test to assess for frontal lobe dysfunction in patients.

- Procedure:

Participants are asked to generate words beginning with letters that had previously been introduced to them (e.g.: generate a word beginning with 'A' or 'R'). They are given three 1-min trials (one trial per letter). The goal is to say as many different words possible that begin with the given letter.

- Results:

The Verbal fluency test can assess for damage in the prefrontal lobes, which has been associated with patients suffering from source amnesia. Patients with frontal lobe disorder have trouble putting verbal items into a proper sequential order, monitor personal behaviors as well as a deficient judgment in recency. All of these behaviors are required for the proper recall of the source of a memory.

The Wisconsin Card Sorting Test is widely used in clinical settings to test for cognitive impairments, such as frontal lobe disorder which has been associated with source amnesia.

- Procedure:

The visuo-spatial component of this test is devised of two sets of 12 identical cards. The figures on the cards differ with respect to color, quantity, and shape. The participants are then given a pile of additional cards and are asked to match each one to one of the previous cards.

- Results:

Patients suffering from frontal lobe dysfunction and ultimately source amnesia, will have much greater difficulty finishing this task successfully through method of strategy.

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.

There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.

Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.

SD has no known preventative measures.

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.

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.

Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on psychological evaluation of the patient, who is most likely brought to a psychologist's attention by a family member or friend believed to be an imposter by the person under the delusion.

KLS can be diagnosed when there is confusion, apathy, or derealization in addition to frequent bouts of extreme tiredness and prolonged sleep. The earliest it can be diagnosed is the second episode, this is not common. The condition is generally treated as a diagnosis of exclusion. Because KLS is rare, other conditions with similar symptoms are usually considered first.

MRIs can determine if the symptoms are caused by certain brain disorders, stroke, and multiple sclerosis. Lumbar puncture can determine if encephalitis is the cause. KLS must be differentiated from substance abuse by toxicology tests. The use of Electroencephalography (EEG) can exclude temporal status epilepticus from consideration. EEGs are normal in about 70% of KLS patients, but background slowing may sometimes be detected. In addition, low-frequency high-amplitude waves can be observed during waking hours.

Initially, KLS appears similar to bipolar depression. Patients with frontal-lobe syndromes and Klüver-Bucy syndrome also display similar symptoms, but these conditions can be differentiated by the presence of brain lesions. KLS should also be distinguished from very rare cases of menstruation-caused hypersomnia.

Hypergraphia is a behavioral condition characterized by the intense desire to write or draw. Forms of hypergraphia can vary in writing style and content. It is a symptom associated with temporal lobe changes in epilepsy, which is the cause of the Geschwind syndrome, a mental disorder. Structures that may have an effect on hypergraphia when damaged due to temporal lobe epilepsy are the hippocampus and Wernicke's area. Aside from temporal lobe epilepsy, chemical causes may be responsible for inducing hypergraphia.

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.

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.

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.