Psychogenic aphonia is often seen in patients with underlying psychological problems. Laryngeal examination will usually show bowed vocal folds that fail to adduct to the midline during phonation. However, the vocal folds will adduct when the patient is asked to cough. Treatment should involve consultation and counseling with a speech pathologist and, if necessary, a psychologist.

In this case, the patient's history and the observed unilateral immobility rules out function aphonia.

Aphonia is defined as the inability to produce voiced sound. A primary cause of aphonia is bilateral disruption of the recurrent laryngeal nerve, which supplies nearly all the muscles in the larynx. Damage to the nerve may be the result of surgery (e.g., thyroidectomy) or a tumor.

Aphonia means "no sound". In other words, a person with this disorder has lost his/her voice.

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.

Selective mutism previously known as "elective mutism" is an anxiety disorder very common among young children, characterized by the inability to speak in certain situations. It should not to be confused with someone who is mute and cannot communicate due to physical disabilities. Selectively mute children are able to communicate in situations in which they feel comfortable. About 90% of children with this disorder have also been diagnosed with social anxiety. It is very common for symptoms to occur before the age of five and do not have a set time period. Not all children express the same symptoms. Some may stand motionless and freeze in specific social settings and have no communication.

Alalia is a disorder that refers to a delay in the development of speaking abilities in children. In severe cases, some children never learn how to speak. It is caused by illness of the child or the parents, the general disorders of the muscles, the shyness of the child or that the parents are close relatives.

Anarthria is a severe form of dysarthria. The coordination of movements of the mouth and tongue or the conscious coordination of the lungs are damaged.

Aphasia can rob all aspects of the speech and language. It is a damage of the cerebral centres of the language.

Aphonia is the inability to produce any voice. In severe cases the patient loses phonation. It is caused by the injury, paralysis, and illness of the larynx.

Conversion disorder can cause loss of speaking ability.

Feral children grow up outside of human society, and so usually struggle in learning any language.

Some people with autism never learn to speak.

Most intellectually disabled children learn to speak, but in the severe cases they can't learn speech (IQ 20-25). Children with Williams syndrome have good language skills with mean IQ 50. Children with Down syndrome often have impaired language and speech.

Speech and language impairment are basic categories that might be drawn in issues of communication involve hearing, speech, language, and fluency.

A speech impairment is characterized by difficulty in articulation of words. Examples include stuttering or problems producing particular sounds. Articulation refers to the sounds, syllables, and phonology produced by the individual. Voice, however, may refer to the characteristics of the sounds produced—specifically, the pitch, quality, and intensity of the sound. Often, fluency will also be considered a category under speech, encompassing the characteristics of rhythm, rate, and emphasis of the sound produced

A language impairment is a specific impairment in understanding and sharing thoughts and ideas, i.e. a disorder that involves the processing of linguistic information. Problems that may be experienced can involve the form of language, including grammar, morphology, syntax; and the functional aspects of language, including semantics and pragmatics

An individual can have one or both types of impairment. These impairments/disorders are identified by a speech and language pathologist.

The following are brief definitions of several of the more prominent speech disorders:

Many of the symptoms are not limited to the disorder, as they may resemble a number of conditions that affect the upper and lower airway. Such conditions include asthma, angioedema, vocal cord tumors, and vocal cord paralysis.

People with vocal cord dysfunction often complain of "difficulty in breathing in” or “fighting for breath”, which can lead to subjective respiratory distress, and in severe cases, loss of consciousness. They may report tightness in the throat or chest, choking, stridor on inhalation and wheezing, which can resemble the symptoms of asthma. These episodes of dyspnea can be recurrent and symptoms can range from mild to severe and prolonged in some cases. Agitation and a sense of panic are not uncommon and can result in hospitalization.

Different subtypes of vocal cord dysfunction are characterized by additional symptoms. For instance, momentary aphonia can be caused by laryngospasm, an involuntary spasm of the vocal cords and a strained or hoarse voice may be perceived when the vocal cord dysfunction occurs during speech, resulting in spasmodic dysphonia.

Many of the symptoms are not specific to vocal cord dysfunction and can resemble a number of conditions that affect the upper and lower airway.

"Episodes" can be triggered suddenly or develop gradually and triggers are numerous. Primary causes are believed to be gastroesophageal reflux disease (GERD), extra-esophageal reflux (EERD), exposure to inhaled allergens, post-nasal drip, exercise, or neurological conditions that can cause difficulty inhaling only during waking. Published studies emphasize anxiety or stress as a primary cause while more recent literature indicates a likely physical etiology. This disorder has been observed from infancy through old age, with the observation of its occurrence in infants leading some to believe that a physiological cause such as reflux or allergy is likely. Certain medications, such as antihistamines for allergies, cause drying of the mucous membranes, which can cause further irritation or hypersensitivity of the vocal cords.VCD can mimic asthma, anaphylaxis, collapsed lungs, pulmonary embolism, or fat embolism, which can lead to an inaccurate diagnosis and inappropriate, potentially harmful, treatment. Some incidences of VCD are misdiagnosed as asthma, but are unresponsive to asthma therapy, including bronchodilators and steroids. Among adult patients, women tend to be diagnosed more often. Among children and teenage patients, VCD has been linked with high participation in competitive sports and family orientation towards high achievement.

Vocal cord dysfunction co-occurs with asthma approximately 40% of the time. This frequently results in a misdiagnosis of asthma alone. Even young children can tell the difference between an asthma attack (primarily difficulty exhaling) and a VCD attack (primarily difficulty inhaling). Knowing the difference between the two will help those who have both know when to use the rescue inhaler prescribed or when to use the breathing recovery exercises trained by a speech-language pathologist.

Conversion disorder begins with some stressor, trauma, or psychological distress. Usually the physical symptoms of the syndrome affect the senses or movement. Common symptoms include blindness, partial or total paralysis, inability to speak, deafness, numbness, difficulty swallowing, incontinence, balance problems, seizures, tremors, and difficulty walking. These symptoms are attributed to conversion disorder when a medical explanation for the afflictions cannot be found. Symptoms of conversion disorder usually occur suddenly. Conversion disorder is typically seen in individuals aged 10 to 35, and affects between 0.011% and 0.5% of the general population.

Conversion disorder can present with motor or sensory symptoms including any of the following:

Motor symptoms or deficits:

- Impaired coordination or balance

- Weakness/paralysis of a limb or the entire body (hysterical paralysis or motor conversion disorders)

- Impairment or loss of speech (hysterical aphonia)

- Difficulty swallowing (dysphagia) or a sensation of a lump in the throat

- Urinary retention

- Psychogenic non-epileptic seizures or convulsions

- Persistent dystonia

- Tremor, myoclonus or other movement disorders

- Gait problems (astasia-abasia)

- Loss of consciousness (fainting)

Sensory symptoms or deficits:

- Impaired vision (hysterical blindness), double vision

- Impaired hearing (deafness)

- Loss or disturbance of touch or pain sensation

Conversion symptoms typically do not conform to known anatomical pathways and physiological mechanisms. It has sometimes been stated that the presenting symptoms tend to reflect the patient's own understanding of anatomy and that the less medical knowledge a person has, the more implausible are the presenting symptoms. However, no systematic studies have yet been performed to substantiate this statement.

Conversion disorder presents with symptoms that typically resemble a neurological disorder such as stroke, multiple sclerosis, epilepsy or hypokalemic periodic paralysis. The neurologist must carefully exclude neurological disease, through examination and appropriate investigations. However, it is not uncommon for patients with neurological disease to also have conversion disorder.

In excluding neurological disease, the neurologist has traditionally relied partly on the presence of positive signs of conversion disorder, i.e. certain aspects of the presentation that were thought to be rare in neurological disease but common in conversion. The validity of many of these signs has been questioned, however, by a study showing that they also occur in neurological disease. One such symptom, for example, is "la belle indifférence", described in DSM-IV as "a relative lack of concern about the nature or implications of the symptoms". In a later study, no evidence was found that patients with functional symptoms are any more likely to exhibit this than patients with a confirmed organic disease. In DSM-V, "la belle indifférence" was removed as a diagnostic criteria.

Another feature thought to be important was that symptoms tended to be more severe on the non-dominant (usually left) side of the body. There have been a number of theories about this, such as the relative involvement of cerebral hemispheres in emotional processing, or more simply, that it was "easier" to live with a functional deficit on the non-dominant side. However, a literature review of 121 studies established that this was not true, with publication bias the most likely explanation for this commonly held view. Although agitation is often assumed to be a positive sign of conversion disorder, release of epinephrine is a well-demonstrated cause of paralysis from hypokalemic periodic paralysis.

Misdiagnosis does sometimes occur. In a highly influential study from the 1960s, Eliot Slater demonstrated that misdiagnoses had occurred in one third of his 112 patients with conversion disorder. Later authors have argued that the paper was flawed, however, and a meta-analysis has shown that misdiagnosis rates since that paper was published are around 4%, the same as for other neurological diseases.

After a period of prolonged stability individuals who had been infected and recovered from polio begin to experience new signs and symptoms, characterised by muscular atrophy (decreased muscle mass), weakness, pain and fatigue in limbs that were originally affected or in limbs that didn't seem to have been affected at the time of the initial polio illness. PPS is a very slowly progressing condition marked by periods of stability followed by new declines in the ability to carry out usual daily activities. Most patients become aware of their decreased capacity to carry out daily routines due to significant changes in mobility, decreasing upper limb function and lung capability. Fatigue is often the most disabling symptom; even slight exertion often produces disabling fatigue and can also intensify other symptoms. Problems breathing or swallowing, sleep-related breathing disorders, such as sleep apnea and decreased tolerance for cold temperatures are other notable symptoms.

Increased activity during intervening healthy years between the original infection and onset of PPS can amplify the symptoms. Thus, contracting poliomyelitis at a young age can result in particularly disabling PPS symptoms.

Post-polio syndrome (PPS, or post-poliomyelitis syndrome or post-polio sequelae) is a condition that affects approximately 25 to 40 percent of people who have previously survived an acute attack of poliomyelitis —a viral infection of the nervous system—after the initial infection. Typically the symptoms appear 15 to 30 years after recovery from the original paralytic attack, at an age of 35 to 60. Symptoms include acute or increased muscular weakness, pain in the muscles, and fatigue. The same symptoms may also occur years after a nonparalytic polio (NPP) infection.

The precise mechanism that causes PPS is unknown. It shares many features with chronic fatigue syndrome, but unlike that disorder, it tends to be progressive, and can cause loss of muscle strength. Treatment is primarily limited to adequate rest, conservation of available energy, and supportive measures, such as leg braces and energy-saving devices such as powered wheelchairs, analgesia (pain relief) and sleep aids.

Inflammation occurs in the laryngeal, tracheal and bronchial cartilages. Both of these sites are involved in 10% of persons with RP at presentation and 50% over the course of this autoimmune disease, and is more common among females.

The involvement of the laryngotracheobronchial cartilages may be severe and life-threatening; it causes one-third of all deaths among persons with RP.

Laryngeal chondritis is manifested as pain above the thyroid gland and, more importantly, as dysphonia with a hoarse voice or transient aphonia. Because this disease is relapsing, recurrent laryngeal inflammation may result in laryngomalacia or permanent laryngeal stenosis with inspiratory dyspnea that may require emergency tracheotomy as a temporary or permanent measure.

Tracheobronchial involvement may or may not be accompanied with laryngeal chondritis and is potentially the most severe manifestation of RP.

The symptoms consist of dyspnea, wheezing, a nonproductive cough, and recurrent, sometimes severe, lower respiratory tract infections.

Obstructive respiratory failure may develop as the result of either permanent tracheal or bronchial narrowing or chondromalacia with expiratory collapse of the tracheobronchial tree. Endoscopy, intubation, or tracheotomy has been shown to hasten death.

Relapsing polychondritis may affect many different organ systems of the body. At first, some people with the disease may have only nonspecific symptoms such as fever, weight loss, and malaise.