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Signs of laryngeal paralysis include voice change (the dog's bark becomes hoarse-sounding), gagging or coughing (often during or after eating or drinking), exercise intolerance, inspiratory stridor (noisy breathing on inspiration), difficulty breathing, and in severe cases cyanosis or syncope (fainting). Secondary problems may also occur, including aspiration or edema in the lungs, though often the problem remains an upper respiratory problem. Affected dogs are vulnerable to heat stroke and heat exhaustion due to their limited ability to cool themselves down by panting, but the disorder itself can be mistaken for heat stroke.
Signs may occur at any time, but initially owners may only notice that their dog's bark sounds different, that their dog can't run as much as before, or that the dog has trouble in hot weather in unilateral cases because the unaffected side can compensate for the paralysed side. However most unilateral cases will eventually progress to include both sides of the larynx, a more serious problem with symptoms appearing more often.
Signs are usually worse in hot and humid weather, during exercise, during times of stress or excitement, and in obese pets. Acute or late-stage symptoms are usually unmistakable and require immediate emergency treatment.
Laryngeal paralysis in animals is a condition in which the nerves and muscles that control the movements of one or both arytenoid cartilages of the larynx cease to function, and instead of opening during inspiration and closing during swallowing, the arytenoids remain stationary in a somewhat neutral position. Specifically, the muscle that causes abduction of the arytenoid cartilage, the cricoarytenoideus dorsalis muscle, ceases to function. This leads to inadequate ventilation during exercise and during thermoregulatory panting as well as incomplete protection of the airway during swallowing.
One of the commonest forms of laryngeal paralysis develops in geriatric medium to large breed dogs, in particular the Labrador retriever, but also some other breeds. This had been traditionally known as idiopathic largyngeal paralysis ("ILP": idiopathic means "of unknown cause"), and was believed to be a result of a condition affecting the nerves of the larynx (bilateral mononeuropathy of the recurrent laryngeal nerves). However investigations into ILP by two groups in Michigan and Tennessee between 2005 - 2013 showed that the condition was not limited to, or specifically a result of, dysfunction of the laryngeal nerves. Instead it was the most visible symptom of a slowly progressing polyneuropathy of old age, which also affected other nerves in the body. This finding, now generally believed correct following further research, has led to the proposed renaming of this type of laryngeal paralysis from "Idiopathic laryngeal paralysis" ("ILP") to "Geriatric onset laryngeal paralysis polyneuropathy" ("GOLPP").
Animals affected by laryngeal paralysis have reduced tolerance for exercise and heat and an increased risk of aspiration pneumonia. The condition is not generally regarded as causing pain, other than physical distress and anxiety caused by any difficulty in breathing or emotional distress from any difficulty with physical movement. Where laryngeal paralysis is related to a general progressive polyneuropathy, as in GOLPP, the nervous system will gradually degenerate causing increasing difficulty in management of the limbs (especially rear limbs), swallowing and breathing, and eventually in most cases euthanasia. Laryngeal paralysis is fairly common in large breed and geriatric dogs, particularly in the Labrador retriever, is rarely found in cats, and can also occur in horses where it is referred to as roaring, roarer's syndrome, or medically as laryngeal hemiplegia or recurrent laryngeal neuropathy (RLN). Laryngeal paralysis can be unilateral or bilateral depending upon dysfunction of one or both arytenoid cartilages.
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.
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.
Dysphonia is a broad clinical term which refers to abnormal functioning of the voice. More specifically, a voice can be classified as “dysphonic” when there are abnormalities or impairments in one or more of the following parameters of voice: pitch, loudness, quality, and variability. For example, abnormal pitch can be characterized by a voice that is too high or low whereas abnormal loudness can be characterized by a voice that is too weak or loud. Similarly, a voice that has frequent, inappropriate breaks characterizes abnormal quality while a voice that is monotone (i.e., very flat) or inappropriately fluctuates characterizes abnormal variability. While hoarseness is used interchangeably with the term dysphonia, it is important to note that the two are not synonymous. Hoarseness is merely a subjective term to explain the perceptual quality (or sound) of a dysphonic voice. While hoarseness is a common symptom (or complaint) of dysphonia, there are several other signs and symptoms that can be present such as: breathiness, roughness, and dryness. Furthermore, a voice can be classified as dysphonic when it poses problems in the functional or occupational needs of the individual or is inappropriate for their age or sex.
Globus pharyngis (also known as globus sensation, globus or, somewhat outdatedly, globus hystericus, commonly referred to as having a "lump in one's throat"), is the persistent sensation of having phlegm, a pill or some other sort of obstruction in the throat when there is none. Swallowing can be performed normally, so it is not a true case of dysphagia, but it can become quite irritating. One may also feel mild chest pain or even severe pain with a clicking sensation when swallowing.
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.
Mendelson's syndrome is characterised by a bronchopulmonary reaction following aspiration of gastric contents during general anaesthesia due to abolition of the laryngeal reflexes. The main clinical features are signs of general hypoxia, two to five hours after anaesthesia. Such features may include cyanosis, dyspnea, fever, pulmonary wheeze, crepitant rales, rhonchi, and tachycardia with a low blood pressure. Decreased arterial oxygen tension is also likely to be evident. Pulmonary edema can cause sudden death or death may occur later from pulmonary complications.
Symptoms include intrinsic minus hand deformity, paralysis of intrinsic hand muscles, and C8/T1 Dermatome distribution numbness. Involvement of T1 may result in Horner's syndrome, with ptosis, and miosis. Weakness or lack of ability to use specific muscles of the shoulder or arm.It can be contrasted to Erb-Duchenne's palsy, which affects C5 and C6.
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).
Extraesophageal symptoms result from exposure of the upper aerodigestive tract to gastric contents. This causes a variety of symptoms, including hoarseness, postnasal drip, sore throat, difficulty swallowing, indigestion, chronic cough, wheezing, globus pharyngeus, and chronic throat-clearing. Some people with LPR have heartburn, while others have little to no heartburn as refluxed stomach contents do not remain in the esophagus long enough to irritate the surrounding tissue. Individuals with more severe forms of LPR may experience abrasion of tooth enamel due to intermittent presence of gastric contents in the oral cavity.
Additionally, LPR can cause inflammation in the vocal tract which results in the symptom of dysphonia or hoarseness. Hoarseness is considered to be one of the primary symptoms of LPR and is associated with complaints such as strain, vocal fatigue, muskuloskeletal tension, and hard glottal attacks, all of which can reduce a person's ability to communicate effectively. Moreover, LPR patients may try to compensate for their hoarseness by increasing muscular tension in their vocal tract. This hyper-functional technique adopted in response to the inflammation caused by LPR can lead to a condition called muscle tension dysphonia and may persist even after the hoarseness and inflammation has disappeared. A speech-language pathologist will often need to be involved to help resolve this maladaptive, compensatory pattern through the implementation of voice therapy.
LPR presents as a chronic and intermittent disease in children. LPR in children and infants tends to manifest with a unique set of symptoms. Symptoms seen in children with LPR include a cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia. Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, feeding difficulties, aspiration, regurgitation, and failure to thrive. Moreover, LPR in children is commonly concomitant with laryngeal disorders such as laryngomalacia, subglottic stenosis, and laryngeal papillomatosis.
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.
Mendelson's syndrome is chemical pneumonitis or aspiration pneumonitis caused by aspiration during anaesthesia, especially during pregnancy. Aspiration contents may include gastric juice, blood, bile, water or an association of them.
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.
Symptoms of spasmodic dysphonia can come on suddenly or gradually appear over the span of years. They can come and go for hours or even weeks at a time, or remain consistent. Gradual onset can begin with the manifestation of a hoarse voice quality, which may later transform into a voice quality described as strained and breaks in phonation. These phonation breaks have been compared to stuttering in the past, but there is a lack of research in support of spasmodic dysphonia being classified as a fluency disorder. It is commonly reported by people with spasmodic dysphonia that symptoms almost only occur on vocal/speech sounds that require phonation. Symptoms are less likely to occur at rest, while whispering, and/or on speech sounds that do not require phonation. It is hypothesized this occurs because of an increase in sporadic, sudden, and prolonged tension found in the muscles around the larynx during phonation. This tension affects the abduction and adduction (opening and closing) of the vocal folds. Consequently, the vocal folds are unable to retain subglottal air pressure (required for phonation) and breaks in phonation can be heard throughout the speech of people with spasmodic dysphonia.
Regarding types of spasmodic dysphonia, the main characteristic of spasmodic dysphonia, breaks in phonation, is found along with other varying symptoms. The voice quality of adductor spasmodic dysphonia can be described as “strained-strangled” from tension in the glottal region. Voice quality for abductor spasmodic dysphonia can be described as breathy from variable widening of the glottal region. Vocal tremor may also be seen in spasmodic dysphonia. A mix and variance of these symptoms are found in mixed spasmodic dysphonia.
Symptoms of spasmodic dysphonia typically appear in middle aged people, but have also been seen in people in their twenties, with symptoms emerging as young as teenage years.
Usually, the first respiratory symptoms are dyspnea and paradoxical respirations which then escalate within the first few months of life to diaphragmatic paralysis. The symptoms of diaphragmatic paralysis come on very rapidly and without warning, and the patient is often rushed to a hospital where they are placed on a ventilator for respiratory support. Due to the severe nature of diaphragmatic paralysis the patient eventually needs continuous ventilation support to survive. Continuous ventilation, however, may in itself cause damage to the anatomy of the lungs.
In addition to diaphragmatic paralysis other issues may arise: as the name suggests, the distal limbs are most affected with symptoms of weakness, restricting mobility due to (near-)paralysis of the distal limbs as well as the head and neck. Also, dysfunction of the peripheral nerves and the autonomic nervous system may occur. Due to these dysfunctions the patients have been shown to suffer from excessive sweating and irregular heartbeat. The deep tendon reflex is also lost in patients with DSMA1.
Uterine growth retardation and poor foetal movement have been observed in severe DSMA1 cases.
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.
As a result of cholinergic crisis, the muscles stop responding to the bombardment of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis.
This crisis may be masked by the concomitant use of atropine along with cholinesterase inhibitor in order to prevent side effects. Flaccid paralysis resulting from cholinergic crisis can be distinguished from myasthenia gravis by the use of the drug edrophonium (Tensilon), which worsens the paralysis caused by cholinergic crisis, but strengthens the muscle in the case of myasthenia gravis. (Edrophonium is an cholinesterase inhibitor hence increases the concentration of acetylcholine present).
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.
Crutch paralysis is a form of paralysis which can occur when either the radial nerve or part of the brachial plexus, containing various nerves that innervate sense and motor function to the arm and hand, is under constant pressure, such as by the use of a crutch. This can lead to paralysis of the muscles innervated by the compressed nerve. Generally, crutches that are not adjusted to the correct height can cause the radial nerve to be constantly pushed against the humerus. This can cause any muscle that is innervated by the radial nerve to become partially or fully paralyzed. An example of this is wrist drop, in which the fingers, hand, or wrist is chronically in a flexed position because the radial nerve cannot innervate the extensor muscles due to paralysis. This condition, like other injuries from compressed nerves, normally improves quickly through therapy.
Hoarseness is the most common presenting symptom, while pain, stridor or laryngeal obstruction are unusual complaints. They may cause significant respiratory obstruction leading to dyspnoea or respiratory distress and even cyanosis, and jugular and epigastric retractions. Congenital lesions may present with severe airway obstruction at birth calling for emergency intervention and intubation.
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.
Laryngocele refers to a congenital anomalous air sac communicating with the cavity of the larynx, which may bulge outward on the neck.
It may also be acquired, as seen in glassblowers, due to continual forced expiration producing increased pressures in the larynx which leads to dilatation of the laryngeal ventricle (Sinus of Morgagni). It is also seen in people with chronic obstructive airway disease.