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.

In most cases, the cause of laryngeal paralysis is unknown or idiopathic. However, the disorder may arise secondary to general neuropathies, generalized neuromuscular diseases, muscular diseases, neoplasia either in the cervical (neck) region or the cranial mediastinum, or trauma. This acquired form occurs predominantly in middle-aged to old large breed or giant breed dogs such as the Labrador Retriever, golden retriever, Siberian Husky, Newfoundland, and St. Bernard. Usually these dogs are born with a normal larynx, but over time the nerves and muscles that control the laryngeal cartilages lose function.

Laryngeal paralysis may also be congenital in some breeds (e.g. Bouvier des Flandres, Dalmatians, Siberian huskies, and bulldogs), appearing in dogs between two and six months of age. Affected puppies may have difficulty swallowing and breathing, they may gag frequently, and their bark often sounds abnormal. In Dalmatians it is part of another condition called 'laryngeal paralysis-polyneuropathy complex.' Affected puppies should not be used for breeding.

Choke collars are not thought to be a significant risk factor for this disorder. However, after LP is diagnosed it is usually recommended to stop using a collar or anything else around the dog's neck and to switch to a harness instead.

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

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.

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.

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

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

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.

A hoarse voice, also known as hoarseness or dysphonia, is when the voice involuntarily sounds breathy, raspy, or strained, or is softer in volume or lower in pitch. It can be associated with a feeling of unease or scratchiness in the throat. Hoarseness is often a symptom of problems in the vocal folds of the larynx. It may be caused by laryngitis, which in turn may be caused by an upper respiratory infection, a cold, or allergies. Cheering at sporting events, speaking loudly in noisy situations, talking for too long without resting your voice, singing loudly, or speaking with a voice that's too high or too low can also cause temporary hoarseness. A number of other causes for losing one's voice exist, and treatment is generally by resting the voice and treating the underlying cause. If the cause is misuse or overuse of the voice drinking plenty of water may alleviate the problems.

It appears to occur more commonly in females and the elderly. Furthermore, certain occupational groups, such as teachers and singers, are at increased risk.

Long-term hoarseness, or hoarseness that persists over three weeks, especially when not associated with a cold or flu should be assessed by a medical doctor. It is also recommended to see a doctor if hoarseness is associated with coughing up blood, difficulties swallowing, a lump in the neck, pain when speaking or swallowing, difficulty breathing, or complete loss of voice for more than a few days. For voice to be classified as "dysphonic", abnormalities must be present in one or more vocal parameters: pitch, loudness, quality, or variability. Perceptually, dysphonia can be characterised by hoarse, breathy, harsh, or rough vocal qualities, but some kind of phonation remains.

Dysphonia can be categorized into two broad main types: organic and functional. The type of dysphonia is dependent on the cause of the pathology. While the causes of dysphonia can be divided into five basic categories, all of them result in an interruption of the ability of the vocal folds to vibrate normally during exhalation, which affects the voice. The assessment and diagnosis of dysphonia is done by a multidisciplinary team, and involves the use of a variety of subjective and objective measures, which look at both the quality of the voice as well as the physical state of the larynx. Multiple treatments have been developed to address organic and functional causes of dysphonia. Dysphonia can be targeted through direct therapy, indirect therapy, medical treatments, and surgery. Functional dysphonias may be treated through direct and indirect voice therapies, whereas surgeries are recommended for chronic, organic dysphonias.

There is no known treatment for FTS, as the cause is not yet known. There are conflicting reports on whether the paralysis is reversible; some sources claim that moving an elephant away from the area in which it contracted the condition will allow it to recover, while others claim that damage to the trunk is irreversible.

In some extreme cases, wildlife managers have killed affected elephants for humane reasons.

Although the exact cause of spasmodic dysphonia (i.e., laryngeal dystonia) is still unknown, epidemiological, genetic and neurological pathogenic factors have been proposed in recent research.

Risk factors include:

- Being female

- Being middle aged

- Having a family history of neurological diseases (e.g., tremor, dystonia, meningitis and other neurological diseases)

- Stressful events

- Upper respiratory tract infections

- Sinus and throat illnesses

- Heavy voice use

- Cervical dystonia

- Childhood measles or mumps

- Pregnancy and parturition

It has not been established whether these factors directly impact the development of spasmodic dysphonia (SD), however these factors could be used to identify possible and/or at-risk patients.

Researchers have also explored the possibility of a genetic component to SD. Three genes have been identified that may be related to the development of focal or segmental dystonia: TUBB4A, THAP1 and TOR1A genes. However, a recent study that examined the mutation of these three genes in 86 SD patients found that only 2.3% of the patients had novel/rare variants in THAP1 but none in TUBB4A and TOR1A. Evidence of a genetic contribution for dystonia involving the larynx is still weak and more research is needed in order to establish a causal relationship between SD and specific genes.

SD is a neurological disorder rather than a disorder of the larynx, and as in other forms of dystonia, interventions at the end organ (i.e., larynx) have not offered a definitive cure, only symptomatic relief. The pathophysiology underlying dystonia is becoming better understood as a result of discoveries about genetically based forms of the disorder, and this approach is the most promising avenue to a long-term solution.

SD is classified as a neurological disorder. However, because the voice can sound normal or near normal at times, some practitioners believe it to be psychogenic, that is, originating in the affected person's mind rather than from a physical cause. No medical organizations or groups take this position. A comparison of SD patients compared with vocal fold paralysis (VFP) patients found that 41.7% of the SD patients met the DSM-IV criteria for psychiatric comorbidity compared with 19.5% of the VFP group. However, another study found the opposite, with SD patients having significantly less psychiatric comorbidity compared to VFP patients: "The prevalence of major psychiatric cases varied considerably among the groups, from a low of seven percent (1/14) for spasmodic dysphonia, to 29.4 percent (5/17) for functional dysphonia, to a high of 63.6 percent (7/11) for vocal cord paralysis." A review in the journal Swiss Medicine Weekly states that "Psychogenic causes, a 'psychological disequilibrium', and an increased tension of the laryngeal muscles are presumed to be one end of the spectrum of possible factors leading to the development of the disorder". Alternatively, many investigators into the condition feel that the psychiatric comorbidity associated with voice disorders is a result of the social isolation and anxiety that patients with these conditions feel as a consequence of their difficulty with speech, as opposed to the cause of their dysphonia. The opinion that SD is psychogenic is not upheld by experts in the scientific community.

SD is formally classified as a movement disorder, one of the focal dystonias, and is also known as laryngeal dystonia.

Klumpke's paralysis is a form of paralysis involving the muscles of the forearm and hand, resulting from a brachial plexus injury in which the eighth cervical (C8) and first thoracic (T1) nerves are injured either before or after they have joined to form the lower trunk. The subsequent paralysis affects, principally, the intrinsic muscles of the hand (notably the interossei, thenar and hypothenar muscles) and the flexors of the wrist and fingers (notably flexor carpi ulnaris and ulnar half of the flexor digitorum profundus). Forearm pronators and wrist flexors may be involved, as may dilators of the iris and elevators of the eyelid (both of which may be seen in the case of associated Horner's syndrome). The classic presentation of Klumpke's palsy is the “claw hand” where the forearm is supinated and the wrist and fingers are flexed. If Horner syndrome is present, there is miosis (constriction of the pupils) in the affected eye.

The injury can result from difficulties in childbirth. The most common aetiological mechanism is caused by a traumatic vaginal delivery. The risk is greater when the mother is small or when the infant is of large weight. Risk of injury to the lower brachial plexus results from traction on an abducted arm, as with an infant being pulled from the birth canal by an extended arm above the head or with someone catching himself by a branch as he falls from a tree. Lower brachial plexus injuries should be distinguished from upper brachial plexus injuries, which can also result from birth trauma but give a different syndrome of weakness known as Erb's palsy.

Other trauma, such as motorcycle accidents, that have similar spinal cord injuries to C-8 & T-1, also show the same symptom's of Klumpke's paralysis.

DSMA1 is usually fatal in early childhood. The patient, normally a child, suffers a progressive degradation of the respiratory system until respiratory failure. There is no consensus on the life expectancy in DSMA1 despite a number of studies being conducted. A small number of patients survive past two years of age but they lack signs of diaphragmatic paralysis or their breathing is dependent on a ventilation system.

Klumpke Palsy is listed as a 'rare disease' by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Klumpke palsy, or a subtype of Klumpke palsy, affects fewer than 200,000 people in the US population.

Voice disorders are medical conditions involving abnormal pitch, loudness or quality of the sound produced by the larynx and thereby affecting speech production. These include:

- Puberphonia

- Chorditis

- Vocal fold nodules

- Vocal fold cysts

- Vocal cord paresis

- Reinke's edema

- Spasmodic dysphonia

- Foreign accent syndrome

- Bogart–Bacall syndrome

- Laryngeal papillomatosis

- Laryngitis

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).

Across all posited aetiologies, contact granulomas are more commonly observed in male patients than in female patients, and more commonly in adult patients than in pediatric patients. In cases where gastroesophageal reflux disease is identified as the most likely cause of the granuloma, the patient is most commonly an adult man in his 30s or 40s. When contact granulomas do occur in female and pediatric patients, they usually occur post-intubation. There are no observable age or gender trends within the category of post-intubation patients suffering from contact granulomas, nor within the causation category of vocal abuse history.

Post-nasal drip (PND, also termed upper airway cough syndrome, UACS, or post nasal drip syndrome, PNDS) occurs when excessive mucus is produced by the nasal mucosa. The excess mucus accumulates in the throat or back of the nose. It is caused by rhinitis, sinusitis, gastroesophageal reflux disease (GERD), or by a disorder of swallowing (such as an esophageal motility disorder). It is frequently caused by an allergy, which may be seasonal or persistent throughout the year.

However, other researchers argue that mucus dripping down the back of the throat from the nasal cavity is a normal physiologic process that occurs in healthy individuals. Post-nasal drip has been challenged as a syndrome due to a lack of an accepted definition, pathologic tissue changes, and available biochemical tests.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as of a result of the inactivity (perhaps even inhibition) of the AChE enzyme, which normally breaks down acetylcholine. This is a consequence of some types of nerve gas, (e.g. sarin gas). In medicine, this is seen in patients with myasthenia gravis who take too high a dose of their cholinesterase inhibitor medications, or seen following general anaesthesia, when too high a dose of a cholinesterase inhibitor drug is given to reverse surgical muscle paralysis.

For patients in need of tracheal intubation to receive oral drugs, an oversized tube, excessive movement of the tube, or infection can lead to contact granulomas, but this is rare.

The disease has only been identified as distinct from SMA recently, so research is still experimental, taking place mostly in animal models. Several therapy pathways have been devised which include gene therapy, whereby an "IGHMBP2" transgene is delivered to the cell using a viral vector; small-molecule drugs like growth factors (e.g., IGF-1 and VEGF) or olesoxime; and transplantation of healthy motor neurons grown "in vitro" from the patient's stem cells. Studies in amyotrophic lateral sclerosis are also considered helpful because the condition is relatively similar to SMARD1.

Spasmodic dysphonia, also known as laryngeal dystonia, is a disorder in which the muscles that generate a person's voice go into periods of spasm. This results in breaks or interruptions in the voice, often every few sentences, which can make a person difficult to understand. The person's voice may also sound strained or they may be nearly unable to speak. Often onset is gradual and the condition is life long.

The cause is unknown. Risk factors may include family history. Triggers may include an upper respiratory infection, injury to the larynx, overuse of the voice, and psychological stress. The underlying mechanism is believed to typically involve the central nervous system, specifically the basal ganglia. Diagnosis is typically made following examination by a team of healthcare providers.

While there is no cure, treatment may improve symptoms. Most commonly this involves injecting botulinum toxin into the affected muscles of the larynx. This generally results in improvement for a few months. Other measures include voice therapy, counselling, and amplification devices. Rarely surgery may be considered.

The disorder affects an estimated 2 per 100,000 people. Women are more commonly affected. Onset is typically between the ages of 30 and 50. Severity is variable between people. In some work and social life are affected. Life expectancy is, however, normal.

Diplophonia, also known as diphthongia, is a phenomenon in which a voice is perceived as being produced with two concurrent pitches. Diplophonia is a result of vocal fold vibrations that are quasi-periodic in nature. It has been reported from old days, but there are no uniform interpretation of established mechanisms. It has been established that diplophonia can be caused by various vocal fold pathologies, such as vocal folds polyp, vocal fold nodule, recurrent laryngeal nerve paralysis or vestibular fold hypertrophy.