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.

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.

Psycholinguistics pertain to the psychological and neurobiological components that allow humans to acquire, utilize, comprehend, and produce language. The tests most commonly used for psycholinguistic testing include the Dutch version of , syntactic comprehension test, and the Token test. Psycholinguistics allow physicians to narrow down and rule out other disorders that may be similar to FCMS when diagnosing a patient.

As seen in the case of Elsie Nicks, the puncture or removal of a cyst causing akinetic mutism can relieve symptoms almost immediately. However, if the cyst fills up again, the symptoms can reappear.

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.

Although MCS patients are able to demonstrate cognitively mediated behaviors, they occur inconsistently. They are, however, reproducible or can be sustained long enough to be differentiated from reflexive behavior. Because of this inconsistency, extended assessment may be required to determine if a simple response (e.g. a finger movement or a blink) occurred because of a specific environmental event (e.g. a command to move the finger or to blink) or was merely a coincidental behavior. Distinguishing between VS and MCS is often difficult because the diagnosis is dependent on observation of behavior that show self or environmental awareness and because those behavioral responses are markedly reduced. One of the more common diagnostic errors involving disorders of consciousness is mistaking MCS for VS which may lead to serious repercussions related to clinical management.

Giacino et al. have suggested demonstration of the following behaviors in order to make the diagnosis of MCS.

- Following simple commands.

- Gestural or verbal yes/no responses (regardless of accuracy).

- Intelligible verbalization.

- Purposeful behavior such as those that are contingent due to appropriate environmental stimuli and are not reflexive. Some examples of purposeful behavior include:

- appropriate smiling or crying in response to the linguistic or visual content of emotional but not to neutral topics or stimuli.

- vocalizations or gestures that occur in direct response to the linguistic content of questions.

- reaching for objects that demonstrates a clear relationship between object location and direction of reach.

- touching or holding objects in a manner that accommodates the size and shape of the object.

- pursuit eye movement or sustained fixation that occurs in direct response to moving or salient stimuli.

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.

Minimally conscious state (MCS) is defined as a condition of severely altered consciousness in which minimal but definite behavioral evidence of self or environmental awareness is demonstrated.

A lack of motivation has been reported in 25–50% of patients with Alzheimer's disease. While depression is also common in patients with this disease, aboulia is not a mere symptom of depressions because more than half of the patients with Alzheimer's disease with aboulia do not suffer from depression. Several studies have shown that aboulia is most prevalent in cases of severe dementia which may result from reduced metabolic activity in the prefrontal regions of the brain. Patients with Alzheimer's disease and aboulia are significantly older than patients with Alzheimer's who do not lack motivation. Going along with that, the prevalence of aboulia increased from 14% in patients with a mild case Alzheimer's disease to 61% in patients with a severe case of Alzheimer's disease, which most likely developed over time as the patient got older.

Fink and Taylor developed a catatonia rating scale to identify the syndrome. A diagnosis is verified by a benzodiazepine or barbiturate test. The diagnosis is validated by the quick response to either benzodiazepines or electroconvulsive therapy (ECT). While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.

Some practitioners believe there would be evidence indicating anxiolytics to be helpful in treating children and adults with selective mutism, to decrease anxiety levels and thereby speed the process of therapy. Use of medication may end after nine to twelve months, once the person has learned skills to cope with anxiety and has become more comfortable in social situations. Medication is more often used for older children, teenagers, and adults whose anxiety has led to depression and other problems.

Medication, when used, should never be considered the entire treatment for a person with selective mutism. While on medication, the person should be in therapy to help them learn how to handle anxiety and prepare them for life without medication.

Antidepressants have been used in addition to self-modeling and mystery motivation to aid in the learning process.

Contrary to popular belief, people with selective mutism do not necessarily improve with age. Effective treatment is necessary for a child to develop properly. Without treatment, selective mutism can contribute to chronic depression, further anxiety, and other social and emotional problems.

Consequently, treatment at an early age is important. If not addressed, selective mutism tends to be self-reinforcing. Others may eventually expect an afflicted child to not speak and therefore stop attempting to initiate verbal contact. Alternatively, they may pressure the child to talk, increasing their anxiety levels in situations where speech is expected. Due to these problems, a change of environment may be a viable consideration. However, changing school is worth considering only if the alternative environment is highly supportive, otherwise a whole new environment could also be a social shock for the individual and/or deprive them of any friends or support they have currently. Regardless of the cause, increasing awareness and ensuring an accommodating, supportive environment are the first steps towards effective treatment. Most often afflicted children do not have to change schools or classes and have no difficulty keeping up except on the communication and social front. Treatment in teenage or adult years can be more difficult because the afflicted individual has become accustomed to being mute.

The exact treatment depends on the person's age, any comorbid mental illnesses, and a number of other factors. For instance, stimulus fading is typically used with younger children because older children and teenagers recognize the situation as an attempt to make them speak, and older people with this condition and people with depression are more likely to need medication.

Like other disabilities, adequate accommodations are needed for the afflicted to succeed at school, work, and in the home. Under the U.S. federal law and the Individuals with Disabilities Education Act (IDEA), those with the disorder qualify for services based upon the fact that they have an impairment that hinders their ability to speak, thus disrupting their lives. This assistance is typically documented in the form of an Individual Educational Plan (IEP). Post-secondary accommodations are also available for people with disabilities.

Under another law, Section 504 of the Rehabilitation Act of 1973, public school districts are required to provide a free, appropriate public education to every "qualified handicapped person" residing within their jurisdiction. If the child is found to have impairments that substantially limit a major life activity (in this case, learning), the education agency has to decide what related aids or services are required to provide equal access to the learning environment.

The U.S. Food and Drug Administration (FDA) has not approved any drug for the direct treatment of stuttering. However, the effectiveness of pharmacological agents, such as benzodiazepines, anticonvulsants, antidepressants, antipsychotic and antihypertensive medications, and dopamine antagonists in the treatment of stuttering has been evaluated in studies involving both adults and children.

A comprehensive review of pharmacological treatments of stuttering in 2006 concluded that few of the drug trials were methodologically sound. Of those that were, only one, not unflawed study, showed a reduction in the frequency of stuttering to less than 5% of words spoken. In addition, potentially serious side effects of pharmacological treatments were noted, such as weight gain, sexual dysfunctions and the potential for blood pressure increases. There is one new drug studied especially for stuttering named pagoclone, which was found to be well-tolerated "with only minor side-effects of headache and fatigue reported in a minority of those treated".

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.

Those who are physically mute may have problems with the parts of the human body required for human speech (the esophagus, vocal cords, lungs, mouth, or tongue, etc.).

Trauma or injury to Broca's area, located in the left inferior frontal cortex of the brain, can cause muteness.

In a typical 2-year-old child, about 50% of speech may be intelligible. A 4-year-old child's speech should be intelligible overall, and a 7-year-old should be able to clearly produce most words consistent with community norms for their age. Misarticulation of certain difficult sounds ("l", "r",

"s", "z", "th", "ch", "dzh", and "zh") may be normal up to 8 years. Children with speech sound disorder have pronunciation difficulties inappropriate for their age, and the difficulties are not caused by hearing problems, congenital deformities, motor disorders or selective mutism.

The DSM-5 diagnostic criteria are as follows:

- A. Persistent difficulty with speech sound production that interferes with speech intelligibility or prevents verbal communication of messages.

- B. The disturbance causes limitations in effective communication that interfere with social participation, academic achievement, or occupational performance, individually or in any combination.

- C. Onset of symptoms is in the early developmental period.

- D. The difficulties are not attributable to congenital or acquired conditions, such as cerebral palsy, cleft palate, deafness or hearing loss, traumatic brain injury, or other medical or neurological conditions.

For most children, the disorder is not lifelong and speech difficulties improve with time and speech-language treatment. Prognosis is poorer for children who also have a language disorder, as that may be indicative of a learning disorder.

Before beginning treatment, an assessment is needed, as diagnosing stuttering requires the skills of a certified speech-language pathologist (SLP).

While there is no complete cure for stuttering, several treatment options exist that help individuals to better control their speech. Many of the available treatments focus on learning strategies to minimize stuttering through speed reduction, breathing regulation, and gradual progression from single-syllable responses to longer words, and eventually more complex sentences. Furthermore, some stuttering therapies help to address the anxiety that is often elicited as a result of stuttering, and consequently exacerbates stuttering symptoms. This method of treatment is referred to as a comprehensive approach, in which the main emphasis of treatment is directed toward improving the speaker's attitudes toward communication and minimizing the negative impact stuttering can have on the speaker's life. Treatment from a qualified S-LP can benefit people who stutter of any age.

Speech language pathologists teach people who stutter to control and monitor the rate at which they speak. In addition, people may learn to start saying words in a slightly slower and less physically tense manner. They may also learn to control or monitor their breathing. When learning to control speech rate, people often begin by practising smooth, fluent speech at rates that are much slower than typical speech, using short phrases and sentences. Over time, people learn to produce smooth speech at faster rates, in longer sentences, and in more challenging situations until speech sounds both fluent and natural. When treating stuttering in children, some researchers recommend that an evaluation be conducted every three months in order to determine whether or not the selected treatment option is working effectively. "Follow-up" or "maintenance" sessions are often necessary after completion of formal intervention to prevent relapse.

Muteness or mutism () is an inability to speak, often caused by a speech disorder, hearing loss, or surgery. Someone who is mute may be so due to the unwillingness to speak in certain social situations.

Errors produced by children with speech sound disorders are typically classified into four categories:

- Omissions: Certain sounds are not produced — entire syllables or classes of sounds may be deleted; e.g., fi' for fish or 'at for cat.

- Additions (or Epentheses/Commissions): an extra sound or sounds are added to the intended word; e.g. puh-lane for plane.

- Distortions: Sounds are changed slightly so that the intended sound may be recognized but sounds "wrong," or may not sound like any sound in the language.

- Substitutions: One or more sounds are substituted for another; e.g., wabbit for rabbit or tow for cow.

Sometimes, even for experts, telling exactly which type has been made is not obvious — some distorted forms of /r/ may be mistaken for /w/ by a casual observer, yet may not actually be either sound but somewhere in between. Further, children with severe speech sound disorders may be difficult to understand, making it hard to tell what word was actually intended and thus what is actually wrong with it. Some terms can be used to describe more than one of the above categories, such as lisp, which is often the replacement of /s/ with /th/ (a substitution), but can be a distortion, producing /s/ just behind the teeth resulting in a sound somewhere between /s/ and /th/.

There are three different levels of classification when determining the magnitude and type of an error that is produced:

1. Sounds the patient can produce

1. A: Phonemic- can be produced easily; used meaningfully and contrastively

2. B: Phonetic- produced only upon request; not used consistently, meaningfully, or contrastively; not used in connected speech

2. Stimulable sounds

1. A: Easily stimulable

2. B: Stimulable after demonstration and probing (i.e. with a tongue depressor)

3. Cannot produce the sound

1. A: Cannot be produced voluntarily

2. B: No production ever observed

Note that omissions do not mean the sound cannot be produced, and some sounds may be produced more easily or frequently when appearing with certain other sounds: someone might be able to say "s" and "t" separately, but not "st," or may be able to produce a sound at the beginning of a word but not at the end. The magnitude of the problem will often vary between different sounds from the same speaker.

Because OMS is so rare and occurs at an average age of 19 months (6 to 36 months), a diagnosis can be slow. Some cases have been diagnosed as having been caused by a virus. After a diagnosis of OMS is made, an associated neuroblastoma is discovered in half of cases, with median delay of 3 months.

The interictal EEG pattern is usually normal.

What follows are a list of frequently used measures of speech and language skills, and the age-ranges for which they are appropriate.

- Clinical Evaluation of Language Fundamentals – Preschool (3–6 years)

- Clinical Evaluation of Language Fundamentals (6–21 years)

- MacArthur Communicative Development Inventories (0–12 months)

- The Rossetti Infant-Toddler Language Scale (0–36 months)

- Preschool Language Scale (0–6 years)

- Expressive One-word Picture Vocabulary Test (2–15 years)

- Bankson-Bernthal Phonological Process Survey Test (2–16 years)

- Goldman-Fristoe Test of Articulation 2 (2–21 years)

- Peabody Picture Vocabulary Test (2.5–40 years)

According to the DSM-5, "Catatonia Associated with Another Mental Disorder (Catatonia Specifier)" (code 293.89 [F06.1]) is diagnosed if the clinical picture is dominated by at least three of the following:

- stupor (i.e., no psychomotor activity; not actively relating to environment)

- catalepsy (i.e., passive induction of a posture held against gravity)

- waxy flexibility (i.e., allow positioning by examiner and maintain position)

- mutism (i.e., no, or very little, verbal response [exclude if known aphasia])

- negativism (i.e., opposition or no response to instructions or external stimuli)

- posturing (i.e., spontaneous and active maintenance of a posture against gravity)

- mannerisms (i.e., odd, circumstantial caricature of normal actions)

- stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements)

- agitation, not influenced by external stimuli

- grimacing (i.e. making a grimace like children)

- echolalia (i.e., mimicking another's speech)

- echopraxia (i.e., mimicking another's movements)

Other disorders (used additional code 293.89 [F06.1] to indicate the presence of the comorbid catatonia):

- Catatonia associated with autism spectrum disorder.

- Catatonia associated with schizophrenia spectrum and other psychotic disorders.

- Catatonia associated with brief psychotic disorder

- Catatonia associated with schizophreniform disorder

- Catatonia associated with schizoaffective disorder

- Catatonia associated with substance-induced psychotic disorder

- Catatonia associated with bipolar and related disorders.

- Catatonia associated with major depressive disorder

- Catatonic disorder due to another medical condition.

If catatonic symptoms are present but they are don't form the catatonic syndrome, a medication-induced or substance-induced aetiology should first be considered.

Mobility issues associated with falls and freezing of gait have a devastating impact in the lives of PD patients. Fear of falling in itself can have an incapacitating effect in PD patients and can result in social seclusion leaving patients largely isolated leading to depression. Immobility can also lead to osteoporosis which in-turn facilitates future fracture development. This then becomes a vicious circle with falls leading to immobility and immobility facilitating future falls. Hip fractures from falls are the most common form of fracture among PD patients. Fractures increase treatment costs associated with health care expenditures in PD. Also, when gait is affected it often heralds the onset of Lewy body dementia.

Studies have failed to find clear evidence that language delay can be prevented by training or educating health care professionals in the subject. Overall, some of the reviews show positive results regarding interventions in language delay, but are not curative. (Commentary - Early Identification of Language Delays, 2005)