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.

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.

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.

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.

Speech-language pathologists (SLPs) offer many services to children with speech or language disabilities.

The symptoms of VCD are often inaccurately attributed to asthma, which in turn results in the unnecessary and futile intake of corticosteroids, bronchodilators and leukotriene modifiers, although there are instances of comorbidity of asthma and VCD.

The differential diagnosis for vocal cord dysfunction includes vocal fold swelling from allergy, asthma, or some obstruction of the vocal folds or throat. Anyone suspected of this condition should be evaluated and the vocal folds (voice box) visualized. In individuals who experience a persistent difficulty with inhaling, consideration should be given to a neurological cause such as brain stem compression, cerebral palsy, etc.

The main difference between VCD and asthma is the audible stridor or wheezing that occurs at different stages of the breath cycle: VCD usually causes stridor on the inhalation, while asthma results in wheezing during exhalation. Patients with asthma usually respond to the usual medication and see their symptoms resolve. Clinical measures that can be done to differentiate VCD from asthma include:

- rhinolaryngoscopy: A patient with asthma will have normal vocal cord movement, while one with VCD will display vocal cord abduction during inhalation

- spirometry: A change in the measure following the administration of a bronchodilator is suggestive of asthma rather than VCD

- chest radiography: The presence of hyperinflation and peribronchial thickening are indicative of asthma, as patients with VCD will show normal results.

The most effective diagnostic strategy is to perform laryngoscopy during an episode, at which time abnormal movement of the cords, if present, can be observed. If the endoscopy is not performed during an episode, it is likely that the vocal folds will be moving normally, a 'false negative' finding.

Spirometry may also be useful to establish the diagnosis of VCD when performed during a crisis or after a nasal provocation test. With spirometry, just as the expiratory loop may show flattening or concavity when expiration is affected in asthma, so may the Inspiratory loop show truncation or flattening in VCD. Of course, testing may well be negative when symptoms are absent.

Diagnosis of post-polio syndrome can be difficult, since the symptoms are hard to separate from complications due to the original poliomyelitis infection, and from the normal infirmities of aging. There is no laboratory test for post-polio syndrome, nor are there any other specific diagnostic criteria. Three important criteria are recognized, including: previous diagnosis of polio, long interval after recovery and the gradual onset of weakness.

In general, PPS is a diagnosis of exclusion whereby other possible causes of the symptoms are eliminated. Neurological examination aided by other laboratory studies can help to determine what component of a neuromuscular deficit occurred with polio and what components are new and to exclude all other possible diagnoses. Objective assessment of muscle strength in PPS patients may not be easy. Changes in muscle strength are determined in specific muscle groups using various muscle scales which quantify strength, such as the Medical Research Council (MRC) scale. Magnetic resonance imaging (MRI), neuroimaging, and electrophysiological studies, muscle biopsies, or spinal fluid analysis may also be useful in establishing a PPS diagnosis.

The psychological mechanism of conversion can be the most difficult aspect of a conversion diagnosis. Even if there is a clear antecedent trauma or other possible psychological trigger, it is still not clear exactly how this gives rise to the symptoms observed. Patients with medically unexplained neurological symptoms may not have any psychological stressor, hence the use of the term "functional neurological symptom disorder" in DSM-V as opposed to "conversion disorder", and DSM-V's removal of the need for a psychological trigger.

The treatment for post-polio syndrome is generally palliative and consists of rest, analgesia (pain relief) and utilisation of mechanisms to make life easier such as powered wheelchairs. There are no reversive therapies. Fatigue is usually the most disabling symptom; energy conservation can significantly reduce fatigue episodes. Such conservation can be achieved with lifestyle changes, reducing workload and daytime sleeping. Weight loss is also recommended if patients are obese. In some cases, the use of lower limb orthotics can reduce energy usage.

Medications for fatigue, such as amantadine and pyridostigmine, have not been found to be effective in the management of PPS. Muscle strength and endurance training are more important in managing the symptoms of PPS than the ability to perform long aerobic activity. Management should focus on treatments such as hydrotherapy and developing other routines that encourage strength but do not affect fatigue levels. The recent trend is towards use of intravenous immunoglobulin (IVIG) which has yielded promising, albeit modest results, but there is insufficient evidence to recommend it as a treatment.

PPS increases the stress on the musculoskeletal system due to increasing muscular atrophy. A recent study showed that in a review of 539 PPS patients, 80 percent reported pain in muscles and joints and 87 percent had fatigue. Joint instability can cause significant pain in individuals with PPS and should be adequately treated with painkillers. Supervised activity programs and decreasing mechanical stress with braces and adaptive equipment are recommended.

Because PPS can fatigue facial muscles, as well as cause dysphagia (difficulty swallowing), dysarthria (difficulty speaking) or aphonia (inability to produce speech), persons with PPS may become malnourished due to difficulty eating. Compensatory routines can help relieve these symptoms such as eating smaller portions at a time and sitting down whilst eating. PPS with respiratory involvement requires special management such as breathing exercises, chest percussion with a stethoscope on regular occasions for observation of the disease and management of secretions. Failure to properly assess PPS with respiratory involvement can increase the risk of missing aspiration pneumonia (an infection of the lower respiratory tract) in an individual. Severe cases may require permanent ventilation or tracheostomy. Sleep apnoea may also occur. Other management strategies that may lead to improvement include smoking cessation, treatment of other respiratory diseases and vaccination against respiratory infections such as influenza.

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.

FDG positron emission tomography (PET) may be useful to detect the condition early. Other imaging studies including MRI, CT scans, and X-rays may reveal inflammation and/or damaged cartilage facilitating diagnosis.

It is useful to do a full set of pulmonary function tests, including inspiratory and expiratory flow-volume loops. Patterns consistent with either extrathoracic or intrathoracic obstruction (or both) may occur in this disease. Pulmonary function tests (flow-volume loops) provide a useful noninvasive means of quantifying and following the degree of extrathoracic airway obstruction in relapsing polychondritis.