Various stimuli including asthma, allergies, exercise, stress, and irritants such as smoke, dust, fumes, liquids, and food can trigger laryngospasm. It is common in drowning, both as a direct response to inhalation of water, and as a complication during rescue and resuscitation due to aspiration of vomit.

In some individuals laryngospasm can occur spontaneously or as a result of reflux or impaired swallowing. GERD is a common cause of spontaneous laryngospasm. Treating GERD can lessen the frequency of spasms. The onset of spasms may be caused by a viral infection.

It is also a complication associated with anesthesia. The spasm can happen often without any provocation, but tends to occur after tracheal extubation. In children, the condition can be particularly deadly, leading to cardiac arrest within 30–45 seconds, and is a possible cause of death associated with the induction of general anesthesia in the pediatric population. It can sometimes occur during sleep, waking up the sufferer. This usually occurs when the person has gastric acidity and develops re-flux during sleep, where the gastric acid causes irritation which will cause the spasm attack.

It is also a symptom of Hypoparathyroidism

Minor laryngospasm will generally resolve spontaneously in the majority of cases.

Laryngospasm in the operating room is treated by hyperextending the patient's neck and administering assisted ventilation with 100% oxygen. In more severe cases it may require the administration of an intravenous muscle relaxant, such as Succinylcholine, and reintubation.

When Gastroesophageal Reflux Disease (GERD) is the trigger, treatment of GERD can help manage laryngospasm. Proton pump inhibitors such as Dexlansoprazole (Dexilant), Esomeprazole (Nexium), and Lansoprazole (Prevacid) reduce the production of stomach acids, making reflux fluids less irritant. Prokinetic agents reduce the amount of acid available by stimulating movement in the digestive tract.

Spontaneous laryngospasm can be treated by staying calm and breathing slowly, instead of gasping for air. Drinking (tiny sips) of ice water to wash away any irritants that may be the cause of the spasm can also help greatly.

Patients who are prone to laryngospasm during illness can take measures to prevent irritation such as antacids to avoid acid reflux, and constantly drinking water or tea keep the area clear of irritants.

Additionally, laryngospasms can result from hypocalcemia, causing muscle spasms and/or tetany. Na+ channels remain open even if there is very little increase in the membrane potential. This affects the small muscles of the vocal folds.

Besides complications of surgery and anesthesia in general, there may be drainage, swelling, or redness of the incision, gagging or coughing during eating or drinking, or pneumonia due to aspiration of food or liquids. Undesirable complications are estimated to occur in 10-30% of cases. If medical therapy is unsuccessful and surgery cannot be performed due to concurrent disease (such as heart or lung problems) or cost, euthanasia may be necessary if the animal's quality of life is considered unacceptable due to the disease.

Mild cases are managed by limiting activity, keeping a healthy body weight, and avoiding exposure to high ambient temperatures. Mild sedatives can be used to decrease anxiety and panting and therefore improve respiration. Corticosteroids may also be administered in acute cases to decrease inflammation and edema of the larynx.

Severe acute symptoms, such as difficulty breathing, hyperthermia, or aspiration pneumonia, must be stabilized with sedatives and oxygen therapy and may require steroid or antibiotic medications. Sometimes a tracheotomy is required to allow delivery of oxygen. Once the patient is stabilized, surgical treatment may be beneficial especially when paralysis occurs in both aretynoid cartilages (bilateral paralysis). The surgery (aretynoid lateralization, or a "laryngeal tieback") consists of suturing one of the aretynoid cartilages in a maximally abducted (open) position. This reduces the signs associated with inadequate ventilation (such as exercise intolerance or overheating) but may exacerbate the risk of aspiration and consequent pneumonia. Tying back only one of the aretynoid cartilages instead of both helps reduce the risk of aspiration. Afterwards the dog will still sound hoarse, and will need to be managed in the same way as those with mild cases of LP.

Recent studies have found that many dogs with laryngeal paralysis have decreased motility of their esophagus. Animals with a history of regurgitation or vomiting should be fully evaluated for esophageal or other gastrointestinal disorders. Dogs with megaesophagus or other conditions causing frequent vomiting or regurgitation are at high risk for aspiration pneumonia after laryngeal tie-back. Permanent tracheostomy is an alternative surgical option for these dogs to palliate their clincical signs.

The following increase an individual's chances for acquiring VCD:

- Upper airway inflammation (allergic or non-allergic rhinitis, chronic sinusitis, recurrent upper respiratory infections)

- Gastroesophageal reflux disease

- Past traumatic event that involved breathing (e.g. near-drowning, suffocation)

- Severe emotional trauma or distress

- Female gender

- Playing a wind instrument

- Playing a competitive or elite sport

Causes of diffuse esophageal spasm are not well understood. It is thought, however, that many cases are caused by uncontrolled brain signals running to nerve endings. Therefore, suppression medication is often the first line therapy such as anti depressants and anti-epileptic medication are prescribed. It has also been reported that very cold or hot beverages can trigger an esophageal spasm. Avoidance therapy benefits some people, but it has not been medically proven.

The exact cause of VCD is not known, and it is unlikely that a single underlying cause exists. Several contributing factors have been identified, which vary widely among VCD patients with different medical histories. Physical exercise (including, but not limited to, competitive athletics) is one of the major triggers for VCD episodes, leading to its frequent misdiagnosis as exercise-induced asthma. Other triggers include airborne pollutants and irritants such as smoke, dust, gases, soldering fumes, cleaning chemicals such as ammonia, perfumes, and other odours. Gastroesophageal reflux disease (GERD) and rhinosinusitis (inflammation of the paranasal sinuses and nasal cavity) may also play a role in inflaming the airway and leading to symptoms of VCD as discussed below.

Laryngeal hyperresponsiveness is considered the most likely physiologic cause of VCD, brought on by a range of different triggers that cause inflammation and/or irritation of the larynx (voice box). The glottic closure reflex (or laryngeal adductor reflex) serves to protect the airway, and it is possible that this reflex becomes hyperactive in some individuals, resulting in the paradoxical vocal fold closure seen in VCD. Two major causes of laryngeal inflammation and hyperresponsiveness are gastroesophageal reflux disease (GERD) and postnasal drip (associated with rhinosinusitis, allergic or nonallergic rhinitis, or a viral upper respiratory tract infection (URI)). Rhinosinusitis is very common among patients with VCD and for many patients, VCD symptoms are ameliorated when the rhinosinusitis is treated. GERD is also common among VCD patients, but only some experience an improvement in VCD symptoms when GERD is treated. Other causes of laryngeal hyperresponsiveness include inhalation of toxins and irritants, cold and dry air, episodic croup and laryngopharyngeal reflux (LPR).

VCD has long been strongly associated with a variety of psychological or psychogenic factors, including conversion disorder, major depression, obsessive-compulsive disorder, anxiety (especially in adolescents), stress (particularly stress relating to competitive sports), physical and sexual abuse, post-traumatic stress disorder, panic attacks, factitious disorder and adjustment disorder. It is important to note that anxiety and depression may occur in certain patients as a "result" of having VCD, rather than being the cause of it. Psychological factors are important precipitating factors for many patients with VCD; although exercise is also a major trigger for episodes of VCD, some patients experience VCD co-occurring with anxiety regardless of whether or not they are physically active at the time of the VCD/anxiety episode. Experiencing or witnessing a traumatic event related to breathing (such as a near-drowning or life-threatening asthma attack, for example), has also been identified as a risk factor for VCD.

VCD has also been associated with certain neurologic diseases including Arnold-Chiari malformation, cerebral aqueduct stenosis, cortical or upper motor neuron injury (such as that resulting from stroke), amyotrophic lateral sclerosis (ALS), parkinsonism syndromes and other movement disorders. However, this association occurs only rarely.

No cure for the condition as such exists. A number of treatments may provide partial relief:

- Botox injections may temporarily disable the muscle and provide relief for 3-4 months per injection

- Muscle relaxants

- Lorazepam (Ativan), diazepam (Valium) and other benzodiazepines relax the smooth muscle in the throat, slowing or halting contractions. In some people, benzodiazepines may have addictive properties.

- Stress reduction

- High stress levels make these spasms more noticeable

- It is advisable to take note of when your symptoms are at their worst

- Warm fluids

- Hot fluids may be helpful for some people with cricopharyngeal spasm (or other esophageal disorders)

The risk may be reduced by administering a non-particulate antacid (e.g. Sodium Citrate) or an H-antagonist like Ranitidine.

Up to now, prevalence studies investigating rates of dysphonia on a large-scale level have been limited. According to a large sample of 55 million patients seeking health-care treatment in the United States, dysphonia can be found in approximately 1% of the population. Higher rates are reported in females and elderly adults, however, dysphonia can be found in both sexes and across age groups. It is proposed that higher rates in females are due to anatomical differences of the vocal mechanism.

Certain occupational groups may be more prone to developing voice disorders, namely dysphonia. Occupations that require extensive use of voice may be at a greater risk such as teachers and singers. However, the evidence is highly variable and must be interpreted carefully.

Ressurance to the patient when no cause can be found.

In case of a cause treat the cause.

Bronchospasm are caused by a number of reasons. Lower respiratory tract conditions such as asthma, chronic obstructive pulmonary disease (COPD), and emphysema can result in contraction of the airways. Other causes are side effects of topical decongestants such as oxymetazoline and phenylephrine. Both of these medications activate alpha-1 adrenergic receptors that result in smooth muscle constriction. Non-selective beta blockers are known to facilitate bronchospasm as well. Beta blockers bind into the β2 receptors and block the action of epinephrine and norepinephrine from binding to its receptors, causing shortness of breath.

There are two sphincters in the oesophagus. They are normally contracted and they relax when one swallows so that food can pass through them going to the stomach. They then squeeze closed again to prevent regurgitation of the stomach contents. If this normal contraction becomes a spasm, these symptoms begin.

Diffuse esophageal spasm (DES) is a condition characterized by uncoordinated contractions of the esophagus, which may cause difficulty swallowing (dysphagia) or regurgitation. In some cases, it may cause symptoms such as chest pain, similar to heart disease. The cause of DES remains unknown.

Certain abnormalities on x-ray imaging are commonly observed in DES, such as a "corkscrew" or "rosary bead esophagus", although these findings are not unique to this condition. Specialized testing called manometry can be performed to evaluate the motor function of the esophagus, which can help identify abnormal patterns of muscle contraction within the esophagus that are suggestive of DES. The treatment of DES consists primarily of medications, such as acid suppressing agents (like proton pump inhibitors), calcium channel blockers, hyoscine butylbromide, or nitrates. In only extremely rare cases, surgery may be considered. People with DES have higher incidences of gastroesophageal reflux disease (GERD) and anxiety.

PND is suggested to be a cause of extra-oral halitosis, especially when a sinus infection is also present. Acid reflux or heartburn is believed to aggravate and in some cases cause post-nasal drip. Post-nasal drip can be a cause of laryngeal inflammation and hyperresponsiveness, leading to symptoms of vocal cord dysfunction (VCD).

Historically it is said that a patient is at risk if they have:

- Residual gastric volume of greater than 25ml, with

- pH of less than 2.5

However these are indirect measurements and are not factors that directly influence aspiration risk.

Patients with a high risk should have a rapid sequence induction. High risk is defined as these factors:

1. Non-elective surgical procedure

2. Light anaesthesia/unexpected response to stimulation

3. Acute or chronic, upper or lower GI pathology

4. Obesity

5. Opioid medication

6. Neurological disease, impaired conscious level, or sedation

7. Lithotomy position

8. Difficult intubation/airway

9. Gastrointestinal reflux

10. Hiatal hernia

Medication challenge tests, such as the methacholine challenge test, have a lower sensitivity for detection of exercise-induced bronchoconstriction in athletes and are also not a recommended first-line approach in the evaluation of exercise-induced asthma.

Mannitol inhalation has been recently approved for use in the United States.

It should be noted, however, that a relatively recent review of the literature has concluded that there is currently insufficient available evidence to conclude that either mannitol inhalation or eucapnic voluntary hyperventilation are suitable alternatives to exercise challenge testing to detect exercise-induced bronchoconstriction and that additional research is required.

It is not clear exactly what causes esophageal spasms. Sometimes esophageal spasms start when someone eats hot or cold foods or drinks. However, they can also occur with eating or drinking. The increased release of acetylcholine may also be a factor, but the triggering event is not known.

Bronchospasm or a bronchial spasm is a sudden constriction of the muscles in the walls of the bronchioles. It is caused by the release (degranulation) of substances from mast cells or basophils under the influence of anaphylatoxins. It causes difficulty in breathing which can be very mild to severe.

Bronchospasms appear as the feature of asthma, chronic bronchitis and anaphylaxis. Bronchospasms are a possible side effect of some drugs: pilocarpine (which is used to treat illness resulting from the ingestion of deadly nightshade, as well as other things), beta blockers (used to treat hypertension), a paradoxical result of using LABA drugs (to treat COPD) and other drugs. Bronchospasms can present as a sign of giardiasis.

Bronchospasms are one of several conditions associated with cold housing.

Some of the things that can cause bronchospasms are: consuming foods, taking medicines, allergic responses to insects, and fluctuating hormone levels, particularly in women.

A few of the more common allergens are foods such as eggs, milk, peanuts, walnuts, tree and other nuts, fish, especially shellfish, soy and wheat; insect bites and stings, especially bee stings; and other medicines, especially penicillin and its derivatives.

The overactivity of the bronchioles' muscle is a result of exposure to a stimulus which under normal circumstances would cause little or no response. The resulting constriction and inflammation causes a narrowing of the airways and an increase in mucus production; this reduces the amount of oxygen that is available to the individual causing breathlessness, coughing and hypoxia.

Bronchospasms are a serious potential complication of placing a breathing tube during general anesthesia. When the airways spasm or constrict in response to the irritating stimulus of the breathing tube, it is difficult to maintain the airway and the patient can become apneic.

First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.

The International Olympic Committee recommends the eucapnic voluntary hyperventilation (EVH) challenge as the test to document exercise-induced asthma in Olympic athletes. In the EVH challenge, the patient voluntarily, without exercising, rapidly breathes dry air enriched with 5% for six minutes. The presence of the enriched compensates for the losses in the expired air, not matched by metabolic production, that occurs during hyperventilation, and so maintains levels at normal.

Esophageal spasm is rare. Often, symptoms that may suggest esophageal spasm are the result of another condition such as gastroesophageal reflux disease (GERD) or achalasia. The symptoms can also include dysphagia, regurgitation, noncardiac chest pain, heartburn, globus pharyngis (which is a feeling that something is stuck in the throat) or a dry cough.

The "lump in the throat" sensation that characterizes globus pharyngis is often caused by inflammation of one or more parts of the throat, such as the larynx or hypopharynx, due to cricopharyngeal spasm, gastroesophageal reflux (GERD), laryngopharyngeal reflux or esophageal versatility.

In some cases the cause is unknown and symptoms may be attributed to a cause "i.e." a somatoform or anxiety disorder. It has been recognised as a symptom of depression, which responds to anti-depressive treatment.

Differential diagnosis must be made from Eagle syndrome which uses the patient's description of "something caught in my throat" as a diagnostic tool. Eagle syndrome is an elongation of the styloid process causing irritation to nerves and muscles in the region resulting in a number of unusual symptoms.

The results of recent studies have strongly suggested that GERD is a major cause of globus, though this remains under considerable debate.

A less common cause, distinguished by a "lump in the throat" accompanied with clicking sensation and considerable pain when swallowing, may be due to thyroid-cartilage rubbing against anomalous asymmetrical laryngeal anatomy "e.g." the superior cornu abrading against the thyroid lamina, surgically trimming the offending thyroid-cartilage provides immediate relief in all cases. However this cause is frequently misdiagnosed, despite requiring a simple clinical examination involving careful palpation of the neck side to side which elicits the same click sensation (laryngeal crepitus) and pain as when swallowing, most cases are due to prior trauma to the neck. High resolution computed tomographic (CT) or MRI scan of the larynx is usually required to fully understand the anomalous laryngeal anatomy. Anterior displacement of the thyroid ala on the affected side while swallowing can help resolve symptoms.

LPR is often regarded as a subtype of GERD that occurs when stomach contents flow upward through the esophagus and reach the level of the larynx and pharynx. However, LPR is associated with a distinct presentation of symptoms. LPR and GERD frequently differ in the relative prevalence of heartburn and throat clearing. While heartburn is present in over 80% of GERD cases, it occurs in only 20% of LPR cases. Throat clearing shows the opposite prevalence pattern, occurring in approximately 87% of LPR cases and in fewer than 5% of GERD cases. Unlike GERD, LPR also poses a risk for bronchitis or pneumonitis as reflux of stomach acid to the level of the larynx can result in aspiration. LPR is also commonly associated with erythema, or redness, as well as edema in the tissues of the larynx that are exposed to gastric contents. In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophageal tissue exposed to the refluxed material.

Differences in the molecular structure of the epithelial tissue lining the laryngopharyngeal region may be partly responsible for the different symptomatic manifestations of LPR in comparison to GERD. In contrast to the resistant stratified squamous epithelium lining the esophagus, the larynx is lined by ciliated respiratory epithelium, which is more fragile and susceptible to damage. While the epithelium lining the esophagus is capable of withstanding as many as 50 instances of exposure to gastric contents each day, which is the uppermost estimate considered to be within the range of normal physiologic functioning, injury to laryngeal epithelium can occur following exposure to only small amounts of acidic gastric contents.

LPR was not discussed as a separate condition from GERD until the 1970s and 1980s. However, at around the same time that GERD was first recognized as a clinical entity in the mid-1930s, a link between gut symptoms and airway disease was suggested. Later, acid-related laryngeal s and granulomas were reported in 1968. Subsequent studies suggested that acid reflux might be a contributory factor in other laryngeal and respiratory conditions. In 1979, the link between these airway symptoms and reflux of gastric contents was first documented. At the same time, treatment of reflux disease results was shown to eliminate these airway symptoms.