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.

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.

Developmental Verbal Dyspraxia can be diagnosed by a speech language pathologist (SLP) through specific exams that measure oral mechanisms of speech. The oral mechanisms exam involves tasks such as pursing lips, blowing, licking lips, elevating the tongue, and also involves an examination of the mouth. A complete exam also involves observation of the patient eating and talking. Tests such as the Kaufman Speech Praxis test, a more formal examination, are also used in diagnosis.

A differential diagnosis of DVD/CAS is often not possible for children under the age of 2 years old. Even when children are between 2–3 years, a clear diagnosis cannot always occur, because at this age, they may still be unable to focus on, or cooperate with, diagnostic testing.

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 is no one definitive test for ideomotor apraxia; there are several that are used clinically to make an ideomotor apraxia diagnosis. The criteria for a diagnosis are not entirely conserved among clinicians, for apraxia in general or distinguishing subtypes. Almost all the tests laid out here that enable a diagnosis of ideomotor apraxia share a common feature: assessment of the ability to imitate gestures. A test developed by Georg Goldenberg uses imitation assessment of 10 gestures. The tester demonstrates the gesture to the patient and rates him on how whether the gesture was correctly imitated. If the first attempt to imitate the gesture was unsuccessful, the gesture is presented a second time; a higher score is given for correct imitation on the first trial, then for the second, and the lowest score is for not correctly imitating the gesture. The gestures used here are all meaningless, such as placing the hand flat on the top of the head or flat outward with the fingers towards the ear. This test is specifically designed for ideomotor apraxia. The main variation from this is in the type and number of gestures used. One test uses twenty-four movements with three trials for each and a trial-based scoring system similar to the Goldenberg protocol. The gestures here are also copied by the patient from the tester and are divided into finger movements, e.g. making a scissor movement with the forefinger and middle finger, and hand and arm movements, e.g. doing a salute. This protocol combines meaningful and meaningless gestures. Another test uses five meaningful gestures, such as waving goodbye or scratching your head and five meaningless gestures. Additional differences in this test are a verbal command to initiate the movement and it distinguishes between accurate performance and inaccurate but recognizable performance. One test utilizes tools, including a hammer and a key, with both a verbal command to use the tools and the patient copying the tester's demonstrated use of the tools. These tests have been shown to be individually unreliable, with considerable variability between the diagnoses delivered by each. If a battery of tests is used, however, the reliability and validity may be improved. It is also highly advisable to include assessments of how the patient performs activities in daily life. One of the newer tests that has been developed may provide greater reliability without relying on a multitude of tests. It combines three types of tool use with imitation of gestures. The tool use section includes having the patient pantomime use with no tool present, with visual contact with the tool, and finally with tactile contact with the tool. This test screens for ideational and ideomotor apraxia, with the second portion aimed specifically at ideomotor apraxia. One study showed great potential for this test, but further studies are needed to reproduce these results before this can be said with confidence. This disorder often occurs with other degenerative neurological disorders such as Parkinson's disease and Alzheimer's Disease. These comorbidities can make it difficult to pick out the specific features of ideomotor apraxia. The important point in distinguishing ideomotor apraxia is that basic motor control is intact; it is a high level dysfunction involving tool use and gesturing. Additionally, clinicians must be careful to exclude aphasia as a possible diagnosis, as, in the tests involving verbal command, an aphasic patient could fail to perform a task properly because they do not understand what the directions are.

Although qualitative and quantitative studies exist, there is little consensus on the proper method to assess for apraxia. The criticisms of past methods include failure to meet standard psychometric properties as well as research-specific designs that translate poorly to non-research use.

The Test to Measure Upper Limb Apraxia (TULIA) is one method of determining upper limb apraxia through the qualitative and quantitative assessment of gesture production. In contrast to previous publications on apraxic assessment, the reliability and validity of TULIA was thoroughly investigated. The TULIA consists of subtests for the imitation and pantomime of non-symbolic (“put your index finger on top of your nose”), intransitive (“wave goodbye”) and transitive (“show me how to use a hammer”) gestures. Discrimination (differentiating between well- and poorly performed tasks) and recognition (indicating which object corresponds to a pantomimed gesture) tasks are also often tested for a full apraxia evaluation.

However, there may not be a strong correlation between formal test results and actual performance in everyday functioning or activities of daily living (ADLs). A comprehensive assessment of apraxia should include formal testing, standardized measurements of ADLs, observation of daily routines, self-report questionnaires and targeted interviews with the patients and their relatives.

As stated above, apraxia should not be confused with aphasia; however, they frequently occur together. It has been stated that apraxia is so often accompanied by aphasia that many believe that if a person displays AOS; it should be assumed that the patient also has some level of aphasia.

One of the most significant problems associated with CBD is the inability to perform a definitive diagnosis while an individual exhibiting the symptoms associated with CBD is still alive. A clinical diagnosis of CBD is performed based upon the specified diagnostic criteria, which focus mainly on the symptoms correlated with the disease. However, this often results in complications as these symptoms often overlap with numerous other neurodegenerative diseases. Frequently, a differential diagnosis for CBD is performed, in which other diseases are eliminated based on specific symptoms that do not overlap. However, some of the symptoms of CBD used in this process are rare to the disease, and thus the differential diagnosis cannot always be used.

Postmortem diagnosis provides the only true indication of the presence of CBD. Most of these diagnoses utilize the Gallyas-Braak staining method, which is effective in identifying the presence of astroglial inclusions and coincidental tauopathy.

MRI is often done to diagnose PSP. MRI may show atrophy in the midbrain with preservation of the pons giving a "hummingbird" sign appearance.

Diagnosis may be clinical if associated with dementia and other etiologies. In cases caused by stroke, MRI will show a corresponding stroke in the inferior parietal lobule. In the acute stage, this will be bright (restricted diffusion) on the DWI sequence and dark at the corresponding area on the ADC sequence.

Magnetic resonance imaging (MRI) is used to detect morphological brain abnormalities associated with ADCP in patients that are either at risk for ADCP or have shown symptoms thereof. The abnormalities chiefly associated with ADCP are lesions that appear in the basal ganglia. The severity of the disease is proportional to the severity and extent of these abnormalities, and is typically greater when additional lesions appear elsewhere in the deep grey matter or white matter. MRI also has the ability to detect brain malformation, periventricular leukomalacia (PVL), and areas affected by hypoxia-ischemia, all of which may play a role in the development of ADCP. The MRI detection rate for ADCP is approximately 54.5%, however this statistic varies depending on the patient’s age and the cause of the disease and has been reported to be significantly higher.

PSP is frequently misdiagnosed as Parkinson's disease because of the slowed movements and gait difficulty, or as Alzheimer's disease because of the behavioral changes. It is one of a number of diseases collectively referred to as Parkinson plus syndromes. A poor response to levodopa along with symmetrical onset can help differentiate this disease from PD. Also, patients with the Richardson variant tend to have an upright or arched-back posture as opposed to the stooped-forward posture of other Parkinsonian disorders, although PSP-Parkinsonism (see below) may show the stooped posture. Early falls are characteristic, especially with Richardson-syndrome.

At this time the cause of PCA is unknown; similarly, there are no fully accepted diagnostic criteria for the disease. This is partially due to the gradual onset of PCA symptoms, the variety of symptoms, the rare nature of the disease and younger age of patients (initial symptoms appear in patients of 50–60 years old). In 2012, the first international conference on PCA was held in Vancouver, Canada. Continued research and testing will hopefully result in accepted and standardized criteria for diagnosis.

PCA patients are often initially misdiagnosed with an anxiety disorder or depression. Some believe that patients may experience depression or anxiety due to their awareness of their symptoms, such as decrease in their vision capabilities, yet they are unable to control this decline in their vision or the progressive nature of the disease. The early visual impairments of a PCA patient have often led to an incorrect referral to an ophthalmologist, which can result in unnecessary cataract surgery.

Due to the lack of biological marks of PCA, neuropsychological examinations should be used for diagnosis. Neuroimaging can also assist in diagnosis of PCA. The common tools used for Neuroimaging of both PCA and AD patients are magnetic resonance imaging (MRI's), a popular form of medical imaging that uses magnetic fields and radio waves, as well as single-photon emission computed tomography, an imaging form that uses gamma rays, and positron emission tomography, another imaging tool that creates 3D images with a pair of gamma rays and a tracer. Images of PCA patient’s brains are often compared to AD patient images to assist diagnosis. Due to the early onset of PCA in comparison to AD, images taken at the early stages of the disease will vary from brain images of AD patients. At this early stage PCA patients will show brain atrophy more centrally located in the right posterior lobe and occipital gyrus, while AD brain images show the majority of atrophy in the medial temporal cortex. This variation within the images will assist in early diagnosis of PCA; however, as the years go on the images will become increasingly similar, due to the majority of PCA patients also having AD later in life because of continued brain atrophy. A key aspect found through brain imaging of PCA patients is a loss of grey matter (collections of neuronal cell bodies) in the posterior and occipital temporal cortices within the right hemisphere.

For some PCA patients, neuroimaging may not result with a clear diagnosis; therefore, careful observation of the patient in relation to PCA symptoms can also assist in the diagnosis of the patient. The variation and lack of organized clinical testing has led to continued difficulties and delays in the diagnosis of PCA in patients.

There is no curative treatment for this condition. Supportive management is helpful.

Imaging studies have shown differing results which probably represents the heterogeneity of language problems than can occur in PNFA. However, classically atrophy of left perisylvian areas is seen.

Comprehensive meta-analyses on MRI and FDG-PET studies identified alterations in the whole left frontotemporal network for phonological and syntactical processing as the most consistent finding. Based on these imaging methods, progressive nonfluent aphasia can be regionally dissociated from the other subtypes of frontotemporal lobar degeneration, frontotemporal dementia and semantic dementia.

Diagnosis of pseudobulbar palsy is based on observation of the symptoms of the condition. Tests examining jaw jerk and gag reflex can also be performed. It has been suggested that the majority of patients with pathological laughter and crying have pseudobulbar palsy due to bilateral corticobulbar lesions and often a bipyrimidal involvement of arms and legs. To further confirm the condition, MRI can be performed to define the areas of brain abnormality.

Due to the progressive, continuous nature of the disease, improvement over time seldom occurs in patients with PPA as it often does in patients with aphasias caused by trauma to the brain.

In terms of medical approaches to treating PPA, there are currently no drugs specifically used for patients with PPA, nor are there any specifically designed interventions for PPA. A large reason for this is the limited research that has been done on this disease. However, in some cases, patients with PPA are prescribed the same drugs Alzheimer's patients are normally prescribed.

The primary approach to treating PPA has been with behavioral treatment, with the hope that these methods can provide new ways for patients to communicate in order to compensate for their deteriorated abilities. Speech therapy can assist an individual with strategies to overcome difficulties. There are three very broad categories of therapy interventions for aphasia: restorative therapy approaches, compensatory therapy approaches, and social therapy approaches. Rapid and sustained improvement in speech and dementia in a patient with primary progressive aphasia utilizing off-label perispinal etanercept, an anti-TNF treatment strategy also used for Alzheimer's, has been reported. A video depicting the patient's improvement was published in conjunction with the print article. These findings have not been independently replicated and remain controversial.

Movement and posture limitations are aspects of all CP types and as a result, CP has historically been diagnosed based on parental reporting of developmental motor delays such as failure to sit upright, reach for objects, crawl, stand, or walk at the appropriate age. Diagnosis of ADCP is also based on clinical assessment used in conjunction with milestone reporting. The majority of ADCP assessments now use the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (formerly the International Classification of Impairments Disease, and Handicaps), measures of motor impairment that are effective in assessing severe CP. ADCP is typically characterized by an individual’s inability to control their muscle tone, which is readily assessed via these classification systems.

Currently, the specific causes for PPA and other degenerative brain disease similar to PPA are unknown. Autopsies have revealed a variety of brain abnormalities in people who had PPA. These autopsies, as well as imaging techniques such as CT scans, MRI, EEG, single photon emission computed tomography (SPECT), and positron emission tomography (PET), have generally revealed abnormalities to be almost exclusively in the left hemisphere.

Assessments for developmental coordination disorder typically require a developmental history, detailing ages at which significant developmental milestones, such as crawling and walking, occurred. Motor skills screening includes activities designed to indicate developmental coordination disorder, including balancing, physical sequencing, touch sensitivity, and variations on walking activities.

The American Psychiatric Association has four primary inclusive diagnostic criteria for determining if a child has developmental coordination disorder.

The criteria are as follows:

1. Motor Coordination will be greatly reduced, although the intelligence of the child is normal for the age.

2. The difficulties the child experiences with motor coordination or planning interfere with the child's daily life.

3. The difficulties with coordination are not due to any other medical condition

4. If the child does also experience comorbidities such as mental retardation; motor coordination is still disproportionally affected.

Screening tests which can be used to assess developmental coordination disorder include:-

- Movement Assessment Battery for Children (Movement-ABC – Movement-ABC 2)

- Peabody Developmental Motor Scales- Second Edition (PDMS-2)

- Bruininks-Oseretsky Test of Motor Proficiency (BOTMP-BOT-2)

- Motoriktest für vier- bis sechsjährige Kinder (MOT 4-6)

- Körperkoordinationtest für Kinder (KTK)

- Test of Gross Motor Development, Second Edition (TGMD-2)

- Maastrichtse Motoriek Test (MMT)

- Wechsler Adult Intelligence Scale (WAIS-IV)

- Wechsler Individual Achievement Test (WAIT-II)

- Test of Word Reading Efficiency (TOWRE-2)

- Developmental Coordination Disorder Questionnaire (DCD-Q)

- Children's Self-Perceptions of Adequacy in, and Predilection for Physical Activity (CSAPPA)

Currently there is no single gold standard assessment test.

A baseline motor assessment establishes the starting point for developmental intervention programs. Comparing children to normal rates of development may help to establish areas of significant difficulty.

However, research in the "British Journal of Special Education" has shown that knowledge is severely limited in many who should be trained to recognise and respond to various difficulties, including developmental coordination disorder, dyslexia and deficits in attention, motor control and perception (DAMP). The earlier that difficulties are noted and timely assessments occur, the quicker intervention can begin. A teacher or GP could miss a diagnosis if they are only applying a cursory knowledge.

"Teachers will not be able to recognise or accommodate the child with learning difficulties in class if their knowledge is limited. Similarly GPs will find it difficult to detect and appropriately refer children with learning difficulties."

There is no cure for Gerstmann syndrome. Treatment is symptomatic and supportive. Occupational and speech therapies may help diminish the dysgraphia and apraxia. In addition, calculators and word processors may help school children cope with the symptoms of the disorder.

Given the complexity of the medical problems facing ideomotor apraxia patients, as they are usually suffering from a multitude of other problems, it is difficult to ascertain the impact that it has on their ability to function independently. Deficits due to Parkinson's or Alzheimer's disease could very well be sufficient to mask or make irrelevant difficulties arising from the apraxia. Some studies have shown ideomotor apraxia to independently diminish the patient's ability to function on their own. The general consensus seems to be that ideomotor apraxia does have a negative impact on independence in that it can reduce an individual's ability to manipulate objects, as well as diminishing the capacity for mechanical problem solving, owing to the inability to access information about how familiar parts of the unfamiliar system function. A small subset of patients has been known to spontaneously recover from apraxia; this is rare, however. One possible hope is the phenomenon of hemispheric shift, where functions normally performed by one hemisphere can shift to the other in the event that the first is damaged. This seems to necessitate, however, that some portion of the function is associated with the other hemisphere to begin with. There is dispute over whether the right hemisphere of the cortex is involved at all in the praxis system, as some evidence from patients with severed corpus callosums indicates it may not be.

Although there is little that can be done to substantially reverse the effects of ideomotor apraxia, Occupational Therapy can be effective in helping patients regain some functional control. Sharing the same approach in treating ideational apraxia, this is achieved by breaking a daily task (e.g. combing hair) into separate components and teaching each distinct component individually. With ample repetition, proficiency in these movements can be acquired and should eventually be combined to create a single pattern of movement.

Articulation problems resulting from dysarthria are treated by speech language pathologists, using a variety of techniques. Techniques used depend on the effect the dysarthria has on control of the articulators. Traditional treatments target the correction of deficits in rate (of articulation), prosody (appropriate emphasis and inflection, affected e.g. by apraxia of speech, right hemisphere brain damage, etc.), intensity (loudness of the voice, affected e.g. in hypokinetic dysarthrias such as in Parkinson's), resonance (ability to alter the vocal tract and resonating spaces for correct speech sounds) and phonation (control of the vocal folds for appropriate voice quality and valving of the airway). These treatments have usually involved exercises to increase strength and control over articulator muscles (which may be flaccid and weak, or overly tight and difficult to move), and using alternate speaking techniques to increase speaker intelligibility (how well someone's speech is understood by peers). With the speech language pathologist, there are several skills that are important to learn; safe chewing and swallowing techniques, avoiding conversations when feeling tired, repeat words and syllables over and over in order to learn the proper mouth movements, and techniques to deal with the frustration while speaking. Depending on the severity of the dysarthria, another possibility includes learning how to use a computer or flip cards in order to communicate more effectively.

More recent techniques based on the principles of motor learning (PML), such as LSVT (Lee Silverman voice treatment) speech therapy and specifically LSVT may improve voice and speech function in PD. For Parkinson's, aim to retrain speech skills through building new generalised motor programs, and attach great importance to regular practice, through peer/partner support and self-management. Regularity of practice, and when to practice, are the main issues in PML treatments, as they may determine the likelihood of generalization of new motor skills, and therefore how effective a treatment is.

Augmentative and alternative communication (AAC) devices that make coping with a dysarthria easier include speech synthesis and text-based telephones. These allow people who are unintelligible, or may be in the later stages of a progressive illness, to continue to be able to communicate without the need for fully intelligible speech.

The prognosis for individuals with apraxia varies. With therapy, some patients improve significantly, while others may show very little improvement. Some individuals with apraxia may benefit from the use of a communication aid.

However, many people with apraxia are no longer able to be independent. Those with limb-kinetic and/or gait apraxia should avoid activities in which they might injure themselves or others.

Occupational therapy, physical therapy, and play therapy may be considered as other references to support patients with apraxia. These team members could work along with the SLP to provide the best therapy for people with apraxia. However, because people with limb apraxia may have trouble directing their motor movements, occupational therapy for stroke or other brain injury can be difficult.

No medication has been shown useful for treating apraxia.

There are some brief tests (5–15 minutes) that have reasonable reliability to screen for dementia.

While many tests have been studied, presently the mini mental state examination (MMSE) is the best studied and most commonly used. The MMSE is a useful tool for helping to diagnose dementia if the results are interpreted along with an assessment of a person's personality, their ability to perform activities of daily living, and their behaviour. Other cognitive tests include the abbreviated mental test score (AMTS), the, "Modified Mini-Mental State Examination" (3MS), the "Cognitive Abilities Screening Instrument" (CASI), the Trail-making test, and the clock drawing test. The MOCA (Montreal Cognitive Assessment) is a very reliable screening test and is available online for free in 35 different languages. The MOCA has also been shown somewhat better at detecting mild cognitive impairment than the MMSE.

Another approach to screening for dementia is to ask an informant (relative or other supporter) to fill out a questionnaire about the person's everyday cognitive functioning. Informant questionnaires provide complementary information to brief cognitive tests. Probably the best known questionnaire of this sort is the "Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)". There is not sufficient evidence to determine how accurate the IQCODE is for diagnosing or predicting dementia. The Alzheimer's Disease Caregiver Questionnaire is another tool. It is about 90% accurate for Alzheimer's and can be completed online or in the office by a caregiver. On the other hand, the "General Practitioner Assessment Of Cognition" combines both, a patient assessment and an informant interview. It was specifically designed for the use in the primary care setting.

Clinical neuropsychologists provide diagnostic consultation following administration of a full battery of cognitive testing, often lasting several hours, to determine functional patterns of decline associated with varying types of dementia. Tests of memory, executive function, processing speed, attention, and language skills are relevant, as well as tests of emotional and psychological adjustment. These tests assist with ruling out other etiologies and determining relative cognitive decline over time or from estimates of prior cognitive abilities.

There is no cure for DVD/CAS, but with appropriate, intensive intervention, people with the disorder can improve significantly.

DVD/CAS requires various forms of therapy which varies with the individual needs of the patient. Typically, treatment involves one-on-one therapy with a speech language pathologist (SLP). In children with DVD/CAS, consistency is a key element in treatment. Consistency in the form of communication, as well as the development and use of oral communication are extremely important in aiding a child's speech learning process.

Many therapy approaches are not supported by thorough evidence; however, the aspects of treatment that do seem to be agreed upon are the following:

- Treatment needs to be intense and highly individualized, with about 3-5 therapy sessions each week

- A maximum of 30 minutes per session is best for young children

- Principles of motor learning theory and intense speech-motor practice seem to be the most effective

- Non-speech oral motor therapy is not necessary or sufficient

- A multi-sensory approach to therapy may be beneficial: using sign language, pictures, tactile cues, visual prompts, and Augmentative and Alternative Communication (AAC) can be helpful.

Although these aspects of treatment are supported by much clinical documentation, they lack evidence from systematic research studies. In ASHA's position statement on DVD/CAS, ASHA states there is a critical need for collaborative, interdisciplinary, and programmatic research on the neural substrates, behavioral correlates, and treatment options for DVD/CAS.