Selective mutism (SM) is an umbrella term for the condition of otherwise well-developed children who cannot speak or communicate under certain settings. The exact causes that affect each child may be different and yet unknown. There have been attempts to categorize, but there are no definitive answers yet due to the under-diagnosis and small/biased sample sizes. Many people are not diagnosed until late in childhood only because they do not speak at school and therefore fail to accomplish assignments requiring public speaking. Their involuntary silence makes the condition harder to understand or test. Parents often are unaware of the condition since the children may be functioning well at home. Teachers and pediatricians also sometimes mistake it for severe shyness or common stage fright.

Selective mutism occurs in all ethnic groups. The majority of reported cases are of white and multiethnic children. However this could be due to under-diagnosis and under-reporting in other ethnic groups.

Most children with selective mutism are hypothesized to have an inherited predisposition to anxiety. They often have inhibited temperaments, which is hypothesized to be the result of over-excitability of the area of the brain called the amygdala. This area receives indications of possible threats and sets off the fight-or-flight response. Given the very high overlap between social anxiety disorder and selective mutism (as high as 100% in some studies), it is possible that social anxiety disorder causes selective mutism.

Some children with selective mutism may have trouble processing sensory information. This would cause anxiety and a sense of being overwhelmed in unfamiliar situations, which may cause the child to "shut down" and not be able to speak (something that some autistic people also experience). Many children with selective mutism have some auditory processing difficulties.

About 20–30% of children with SM have speech or language disorders that add stress to situations in which the child is expected to speak.

Despite the change of name from "elective" to "selective", a common misconception remains that a selectively mute child is defiant or stubborn. In fact, children with SM have a lower rate of oppositional behavior than their peers in a school setting. Some previous studies on the subject of selective mutism have been dismissed as containing serious flaws in their design. According to a more recent systematic study it is believed that children who have selective mutism are not more likely than other children to have a history of early trauma or stressful life events. Another recent study by Dummit et al., in 1997 did not find any evidence of trauma in their sample of children. Recent evidence has shown that trauma does not explain why most children with selective mutism develop the condition. Many children who have selective mutism almost always speak confidently in some situations. Children who have experienced trauma however are known to suddenly stop speaking.

Children and adults with selective mutism are fully capable of speech and understanding language but fail to speak in certain situations, though speech is expected of them. The behaviour may be perceived as shyness or rudeness by others. A child with selective mutism may be completely silent at school for years but speak quite freely or even excessively at home. There is a hierarchical variation among people with this disorder: some people participate fully in activities and appear social but do not speak, others will speak only to peers but not to adults, others will speak to adults when asked questions requiring short answers but never to peers, and still others speak to no one and participate in few, if any, activities presented to them. In a severe form known as "progressive mutism", the disorder progresses until the person with this condition no longer speaks to anyone in any situation, even close family members.

Selective mutism is by definition characterized by the following:

- Consistent failure to speak in specific social situations (in which there is an expectation for speaking, e.g., at school) despite speaking in other situations.

- The disturbance interferes with educational or occupational achievement or with social communication.

- The duration of the disturbance is at least 1 month (not limited to the first month of school).

- The failure to speak is not due to a lack of knowledge of, or comfort with, the spoken language required in the social situation.

- The disturbance is not better accounted for by a communication disorder (e.g., childhood-onset fluency disorder) and does not occur exclusively during the course of autism spectrum disorder, schizophrenia, or another psychotic disorder.

Selective mutism is strongly associated with other anxiety disorders, particularly social anxiety disorder. In fact, the majority of children diagnosed with selective mutism also have social anxiety disorder (100% of participants in two studies and 97% in another). Some researchers therefore speculate that selective mutism may be an avoidance strategy used by a subgroup of children with social anxiety disorder to reduce their distress in social situations.

Particularly in young children, SM can sometimes be confused with an autism spectrum disorder, especially if the child acts particularly withdrawn around his or her diagnostician, which can lead to incorrect treatment. Although autistic people may also be selectively mute, they often display other behaviors—hand flapping, repetitive behaviors, social isolation even among family members (not always answering to name, for example)—that set them apart from a child with selective mutism. Some autistic people may be selectively mute due to anxiety in social situations that they do not fully understand. If mutism is entirely due to autism spectrum disorder, it cannot be diagnosed as selective mutism as stated in the last item on the list above.

The former name "elective mutism" indicates a widespread misconception among psychologists that selective mute people choose to be silent in certain situations, while the truth is that they often wish to speak but have difficulty doing so. To reflect the involuntary nature of this disorder, the name was changed to "selective mutism" in 1994.

The incidence of selective mutism is not certain. Due to the poor understanding of this condition by the general public, many cases are likely undiagnosed. Based on the number of reported cases, the figure is commonly estimated to be 1 in 1000, 0.1%. However, a 2002 study in "The Journal of the American Academy of Child and Adolescent Psychiatry" estimated the incidence to be 0.71%.

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.

There are a number of factors that could potentially contribute to the development of feeding and eating disorders of infancy or early childhood. These factors include:

- Physiological – a chemical imbalance effecting the child's appetite could cause a feeding or eating disorder.

- Developmental – developmental abnormalities in oral-sensory, oral-motor, and swallowing can impact the child's eating ability and elicit a feeding or eating disorder.

- Environmental – simple issues such as inconsistent meal times can cause a feeding or eating disorder. Giving the child food that they are not developmentally acquired for can also cause these disorders. Family dysfunction and sociocultural issues could also play a role in feeding or eating disorders.

- Relational – when the child is not securely attached to the mother, it can cause feeding interactions to become disturbed or unnatural. Other factors, such as parental emotional unavailability and parental eating disorders, can cause feeding and eating disorders in their children.

- Psychological and behavioral – these factors include one involving the child's temperament. Characteristics such as being anxious, impulsive, distracted, or strong-willed personality types are ones that could affect the child's eating and cause a disorder. The individual could have learned to reject food due to a traumatic experience such as choking or being force fed.

Elective mutism was defined as a refusal to speak in almost all social situations (despite normal ability to do so), while selective mutism is considered to be a "failure" to speak in specific situations and is strongly associated with social anxiety disorder. In contrast to selective mutism, someone who is electively mute may not speak in any situation, as is usually shown in books and movies. Elective mutism is often attributed to defiance or the effect of trauma.

With ADHD being one of the most common disorders diagnosed in childhood, the causes are often studied, yet still inconclusive. Many researchers say ADHD is caused by genetic factors, yet other studies are being done to expand on the Cause. One research study showed that children who carry a certain gene associated with ADHD had a thinner layer of tissue in the areas of the brain associated with attention. As the children grew older, the brain tissue thickened and their ADHD symptoms improved. Environmental factors, such as the mother smoking or drinking during pregnancy is connected to children with ADHD. Children exposed to lead at a young age will also have an increased chance of developing ADHD. Brain injuries could cause ADHD, yet only a small number of children diagnosed fit into this category. Researchers have looked into sugar intake as the cause of ADHD, but have found little to support that theory.

Language delays are the most frequent developmental delays, and can occur for many reasons. A delay can be due to being a “late bloomer,” or a more serious problem. The most common causes of speech delay include

- Hearing loss

- Slow development

- Intellectual Disability

Such delays can occur in conjunction with a lack of mirroring of facial responses, unresponsiveness or unawareness of certain noises, a lack of interest in playing with other children or toys, or no pain response to stimuli.

Other causes include:

- Psychosocial deprivation - The child doesn't spend enough time talking with adults. Research on early brain development shows that babies and toddlers have a critical need for direct interactions with parents and other significant care givers for healthy brain growth and the development of appropriate social, emotional, and cognitive skills.

- Television viewing is associated with delayed language development. Children who watched television alone were 8.47 times more likely to have language delay when compared to children who interacted with their caregivers during television viewing. As recommended by the American Academy of Pediatrics (AAP), children under the age of 2 should watch no television at all, and after age 2 watch no more than one to two hours of quality programming a day. Therefore, exposing such young children to television programs should be discouraged. Parents should engage children in more conversational activities to avoid television-related delays to their children language development, which could impair their intellectual performance.

- Stress during pregnancy is associated with language delay.

- Being a twin

- Attention deficit hyperactivity disorder

- Autism (a developmental disorder) - There is strong evidence that autism is commonly associated with language delay. Asperger syndrome, which is on the autistic spectrum, however, is not associated with language delay.

- Selective mutism (the child just doesn't want to talk)

- Cerebral palsy (a movement disorder caused by brain damage)

- Genetic abnormalities - In 2005, researchers found a connection between expressive language delay and a genetic abnormality: a duplicate set of the same genes that are missing in sufferers of Williams-Beuren syndrome. Also so called XYY syndrome can often cause speech delay.

- Correlation with male sex, previous family history, and maternal education has been demonstrated.

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)

Akinetic mutism is a symptom during the final stages of Creutzfeldt–Jakob disease (a rare degenerative brain disease) and can help diagnose patients with this disease. It can also occur in a stroke that affects both anterior cerebral artery territories. Another cause is neurotoxicity due to exposure to certain drugs such as tacrolimus and cyclosporine.

Other causes of akinetic mutism are as follows:

- Respiratory arrest and cerebral hypoxia

- Acute cases of encephalitis lethargica

- Meningitis

- Hydrocephalus

- Trauma

- Tumors

- Aneurysms

- Olfactory groove meningioma

- Cyst in third ventricle

- Toxical lesions and infections of central nervous system

- Delayed post-hypoxic leukoencephalopathy (DPHL)

- Creutzfeldt–Jakob disease (mesencephalic form)

Another cause of both akinesia and mutism is ablation of the cingulate gyrus. Destruction of the cingulate gyrus has been used in the treatment of psychosis. Such lesions result in akinesia, mutism, apathy, and indifference to painful stimuli. The anterior cingulate cortex is thought to supply a "global energizing factor" that stimulates decision making. When the anterior cingulate cortex is damaged, it can result in akinetic mutism.

Many different causes of aboulia have been suggested. While there is some debate about the validity of aboulia as a separate disease, experts mostly agree that aboulia is the result of frontal lesions and not with cerebellar or brainstem lesions. As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward, aboulia may be a dopamine-related dysfunction. Aboulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere.

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

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

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.

A speech sound disorder is a speech disorder in which some speech sounds (called phonemes) in a child's (or, sometimes, an adult's) language are either not produced, not produced correctly, or are not used correctly. The term protracted phonological development is sometimes preferred when describing children's speech to emphasize the continuing development while acknowledging the delay.

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.

Most speech sound disorders occur without a known cause. A child may not learn how to produce sounds correctly or may not learn the rules of speech sounds on his or her own. These children may have a problem with speech development, which does not always mean that they will simply outgrow it by themselves. Many children do develop speech sounds over time but those who do not often need the services of a Speech-Language Pathologist to learn correct speech sounds.

Some speech sound errors can result from other syndromes or disorders such as:

- developmental disorders (e.g. autism)

- genetic disorders (e.g. Down syndrome)

- hearing loss, including temporary hearing loss, such as from ear infections

- cleft palate or other physical anomalies of the mouth

- illness

- neurological disorders (e.g. cerebral palsy)

Injuries to the frontal lobe and/or the basal ganglia can interfere with an individual's ability to initiate speech, movement, and social interaction. Studies have shown that 5-67% of all patients with traumatic brain injuries and 13% of patients with lesions on their basal ganglia suffer from some form of diminished motivation.

Aboulia has also been associated with amphetamine withdrawal. It may complicate rehabilitation when a stroke patient is uninterested in performing tasks like walking despite being capable of doing so. It should be differentiated from apraxia, when a brain injured patient has impairment in comprehending the movements necessary to perform a motor task despite not having any paralysis that prevents performing the task; that condition can also result in lack of initiation of activity.

Strokes are one of the most common causes of Foix-Chavany-Marie Syndrome. The type of strokes associated with this syndrome include embolic and thrombotic strokes. Strokes affecting the middle cerebral artery and the branches that pass through or near the operculum are characteristic of FCMS.

Symptoms of infections specifically HIV and Herpes simplex encephalitis can cause FCMS. Numerous lesions can develop with HIV infections, which likely result in the development of FCMS.

One of the defining characteristics of minimally conscious state is the more continuous improvement and significantly more favorable outcomes post injury when compared with vegetative state. One study looked at 100 patients with severe brain injury. At the beginning of the study, all the patients were unable to follow commands consistently or communicate reliably. These patients were diagnosed with either MCS or vegetative state based on performance on the JFK Coma Recovery Scale and the diagnostic criteria for MCS as recommended by the Aspen Consensus Conference Work-group. Both patient groups were further separated into those that suffered from traumatic brain injury and those that suffered from non-traumatic brain injures (anoxia, tumor, hydrocephalus, infection). The patients were assessed multiple times over a period of 12 months post injury using the Disability Rating Scale (DRS) which ranges from a score of 30=dead to 0=no disabilities. The results show that the DRS scores for the MCS subgroups showed the most improvement and predicted the most favorable outcomes 12 months post injury. Amongst those diagnosed with MCS, DRS scores were significantly lower for those with non-traumatic brain injuries in comparison to the vegetative state patients with traumatic brain injury. DRS scores were also significantly lower for the MCS non-traumatic brain injury group compared to the MCS traumatic brain injury group. Pairwise comparisons showed that DRS scores were significantly higher for those that suffered from non-tramuatic brain injuries than those with traumatic brain injuries. For the patients in vegetative states there were no significant differences between patients with non-traumatic brain injury and those with traumatic brain injuries. Out of the 100 patients studied, 3 patients fully recovered (had a DRS score of 0). These 3 patients were diagnosed with MCS and had suffered from traumatic brain injuries.

In summary, those with minimally conscious state and non-traumatic brain injuries will not progress as well as those with traumatic brain injuries while those in vegetative states have an all around lower to minimal chance of recovery.

Because of the major differences in prognosis described in this study, this makes it crucial that MCS be diagnosed correctly. Incorrectly diagnosing MCS as vegetative state may lead to serious repercussions related to clinical management.

In 1877, a German physician named the disorder "aphasia voluntaria" to describe children who were able to speak normally but often "refused" to.

In 1980, a study by Torey Hayden identified four "subtypes" of Elective Mutism:

- Symbiotic mutism: the most common form, caused by a vocal and dominating mother and absent father (very rarely the other way around) and characterized by the use of mutism as controlling behavior around other adults.

- Speech phobic mutism: the least common, in which the child showed distinct fear at hearing a recording of his or her voice. This also involved ritualistic behaviors, which may reflect OCD, and was thought to be caused by the child having been told to keep a family secret.

- Reactive mutism: a reaction to trauma and/or abuse, with all children showing symptoms of depression and being notably withdrawn, usually showing no facial expressions. Notably, Hayden admits that some children put in this category had no apparent incident to react to, but they were included because of their symptoms.

- Passive-aggressive mutism: silence is used as a display of hostility, connected to antisocial behavior. Some of the children in her study had reportedly not been mute until age 9-12.

The "Diagnostic and Statistical Manual of Mental Disorders" (DSM), first published in 1952, first included Elective Mutism in its third edition, published in 1980. Elective mutism was described as "a continuous refusal to speak in almost all social situations" despite normal ability to speak. While "excessive shyness" and other anxiety-related traits were listed as associated features, predisposing factors included "maternal overprotection", mental retardation, and trauma. Elective mutism in the third edition revised (DSM III-R) is described similarly as in the third edition except for specifying that the disorder is "not" related to social anxiety disorder.

In 1994, the fourth edition of the DSM reflected the name change to selective mutism and redefined the disorder.

Frontal lobe disorder is an impairment of the frontal lobe that occurs due to disease or head trauma. The frontal lobe of the brain plays a key role in higher mental functions such as motivation, planning, social behaviour, and speech production. A frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, degenerative diseases, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical clinical signs, use of simple screening tests, and specialist neurological testing.

The signs and symptoms of frontal lobe disorder can be indicated by Dysexecutive syndrome which consists of a number of symptoms which tend to occur together. Broadly speaking, these symptoms fall into three main categories; cognitive (movement and speech), emotional or behavioural. Although many of these symptoms regularly co-occur, it is common to encounter patients who have several, but not all of these symptoms. This is one reason why some researchers are beginning to argue that dysexecutive syndrome is not the best term to describe these various symptoms. The fact that many of the dysexecutive syndrome symptoms can occur alone has led some researchers to suggest that the symptoms should not be labelled as a "syndrome" as such. Some of the latest imaging research on frontal cortex areas suggests that executive functions may be more discrete than was previously thought.

Signs/symptoms can be divided as follows:

In cases where the causes are environmental, the treatment is to eliminate or reduce these causes first of all, and then to fit patients with a hearing aid, especially if they are elderly. When the loss is due to heredity, total deafness is often the end result. On the one hand, persons who experience gradual deterioration of their hearing are fortunate in that they have learned to speak. Ultimately the affected person may bridge communication problems by becoming skilled in sign language, speech-reading, using a hearing aid, or accepting elective surgery to use a prosthetic devices such as a cochlear implant.

In some cases, the loss is extremely sudden and can be traced to specific diseases, such as meningitis, or to ototoxic medications, such as Gentamicin. In both cases, the final degree of loss varies. Some experience only partial loss, while others become profoundly deaf. Hearing aids and cochlear implants may be used to regain a sense of hearing, with different people experiencing differing degrees of success. It is possible that the affected person may need to rely on speech-reading and/or sign language for communication.

In most cases the loss is a long term degradation in hearing loss. Discrediting earlier notions of presbycusis, Rosen demonstrated that long term hearing loss is usually the product of chronic exposure to environmental noise in industrialized countries (Rosen, 1965). The U.S. Environmental Protection Agency has asserted the same sentiment and testified before the U.S. Congress that approximately 34 million Americans are exposed to noise pollution levels (mostly from roadway and aircraft noise) that expose humans to noise health effects including the risk of hearing loss (EPA, 1972).

Certain genetic conditions can also lead to post-lingual deafness. In contrast to genetic causes of pre-lingual deafness, which are frequently autosomal recessive, genetic causes of post-lingual deafness tend to be autosomal dominant.