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.

With patulous Eustachian tube, variations in upper airway pressure associated with respiration are transmitted to the middle ear through the Eustachian tube. This causes an unpleasant fullness feeling in the middle ear and alters the auditory perception. Complaints seem to include muffled hearing and autophony. In addition, patulous Eustachian tube generally feels dry with no clogged feeling or sinus pressure.

Some patients with this condition are disturbed by the perceived volume of their voice, causing them to speak very quietly. Their own voice may also sound lower to other people, because the trachea has more volume when the Eustachian tube is open. The patient may also sound as if they have congestion when speaking. Some sufferers may have difficulty in normal activities. They may also experience increased breathing rate, such as that brought on by physical activity. The increased activity not only increases the rate and force of pressure changes in the airway, which is therefore transmitted more forcefully into the middle ear, but also drives increased blood flow to peripheral muscles, compounding the problem by further depleting the Eustachian tube of extracellular fluid and increasing patency. The combination can lead to severe exacerbation of the symptoms. The urge to clear the ear is often mentioned.

List of common symptoms:

- "sac-like" appearance of the vocal folds

- Hoarseness and deepening of the voice

- Trouble speaking (Dysphonia)

- Reduced vocal range with diminished upper limits

- Stretching of the mucosa (Distension)

- Shortness of breath

Reinke's edema is characterized by a "sac-like" appearance of the vocal folds. The edema is a white translucent fluid that causes a bulging (distension) of the vocal cord. The most common clinical symptom associated with Reinke's edema is an abnormally low pitched voice with hoarseness. The low pitch voice is a direct result of increased fluid in the Reinke's space, which vibrates at a lower frequency than normal (females <130 Hz; males <110 Hz). Hoarseness is a common problem of many laryngeal diseases, such as laryngitis. It is described as a harsh and breathy tone of voice. Hoarseness is often seen alongside dysphonia, a condition in which the individual has difficulty speaking.

The swelling of the vocal cords and the lowering of the voice are warning signs that an individual has Reinke's edema. At the microscopic level, an examination of the vocal cords in patients with Reinke's edema will show lowered levels of collagen, elastin, and extracellular matrix proteins. These characteristics can be used to diagnose Reinke's edema. Reinke's edema is considered a benign polyp that may become precancerous if smoking is involved. An indicator of cancer is the development of leukoplakia, which manifests as white patches on the vocal folds.

Smoking, gastric reflux, and hypothyroidism are all risk factors for Reinke's edema. The symptoms of Reinke's edema are considered to be chronic symptoms because they develop gradually over time and depend on how long the individual is exposed to the risk factor. In the case of smoking, as long as the individual continues the habit of smoking, the Reinke's edema will continue to progress. This is true for other risk factors as well, such as untreated gastric reflux and overuse of the voice, which is common to professions such as singers and radio announcers.

Autophonia (self-hearing from inside, strongly amplified) seems to be a common symptom to all PET patients. Unfortunately, its presence also reveals an advanced degree of patency, requiring in most cases surgical management. Other symptoms of PET, such as tinnitus, fullness and ear blockage, can also be reported by patients suffering from obstructive ET dysfunction. This differential diagnosis problem unfortunately leads to some surgeries proposed by well-intentioned but inexperienced ENT surgeons. Some of these surgeries may make things worse.

At the beginning, patients hear their own voice "from inside". They describe it as being amplified and unpleasant. Patients frequently avoid speaking and retire in a rising solitude. Lying head down may help since it increases venous blood pressure and congestion of the mucosa.

With time patients may develop respiratory autophonia. At this stage, they hear "from inside”. They describe hearing their own respiration and sometimes other bodily functions, like heartbeat. Some patients may find this unbearable and depression is common. Psychological supervision may be indicated.

Symptoms are not specific; most patients report itching, burning, and soreness. A small subset of patients may be asymptomatic. Presence of vulvar pain, bleeding, and tumor formation are reported to be more common in patients affected by invasive disease.Signs and symptoms are skin lesions, often mistaken as eczema, that may be itchy or painful.

CNS involvement most often occurs as a chronic meningoencephalitis. Lesions tend to occur in the brainstem, the basal ganglia and deep hemispheric white matter and may resemble those of MS. Brainstem atrophy is seen in chronic cases.

Neurological involvements range from aseptic meningitis to vascular thrombosis such as dural sinus thrombosis and organic brain syndrome manifesting with confusion, seizures, and memory loss. Sudden hearing loss (Sensorineural) is often associated with it. They often appear late in the progression of the disease but are associated with a poor prognosis.

Arthralgia is seen in up to half of people, and is usually a non-erosive poly or oligoarthritis primarily of the large joints of the lower extremities.

Vulvar Paget disease presents as a variety of clinical lesions that may occur over a protracted course. Initially it is velvety, soft, and red or bright pink with scattered white islands of hyperkeratosis. (a strawberry and cream appearance) The lesions become erythematous, plaque like, and desquamating especially when located in dry areas. Rarely the appearance is ulcerated. The borders appear irregular, slightly elevated, and sharply demarcated. The visible borders of vulvar Paget disease are often misleading as Paget cells may spread along the basal layers of normal appearing skin with multicentric foci. Involvement may be extensive including the perianal region, genitocrural, and inguinal folds. Clinical examination should determine the presence of periurethral and perianal lesions. In these cases an involvement of the skin by a noncutaneous internal neoplasm may occur.

Reinke's edema is the swelling of the vocal cords due to fluid (edema) collected within the Reinke's space. First identified by the German anatomist Friedrich B. Reinke in 1895, the Reinke's space is a gelatinous layer of the vocal cord located underneath the outer cells of the vocal cord. When a person speaks, the Reinke's space vibrates to allow for sound to be produced (phonation). The Reinke's space is sometimes referred to as the superficial lamina propria.

Reinke's edema is characterized by the "sac-like" appearance of the fluid-filled vocal cords. The swelling of the vocal folds causes the voice to become deep and hoarse. Therefore, the major symptom of Reinke's edema is a hoarseness similar to laryngitis. The major cause associated with Reinke's edema is smoking. In fact, 97% of patient's diagnosed with Reinke's edema are habitual smokers. Other identified risk factors include overuse of the vocal cords, gastroesophageal reflux, and hypothyroidism. The disease is more often cited in women than in men, because lower voice changes are more noticeable in women.

The first cases of Reinke's edema were recorded in 1891 by M. Hajek, followed by F. Reinke in 1895. In his investigations, Reinke injected a stained glue into the superficial lamina propria (Reinke's space) to mimic edema. Reinke's edema is considered to be a benign (non-cancercous) polyp (protrusion) that represents 10% of all benign laryngeal pathologies. Treatment of Reinke’s edema starts with the elimination of associated risk factors, such as smoking, gastric reflux, and hypothyroidism. Advanced cases may undergo phonosurgery to remove the fluid from the vocal cords.

Four cardinal symptoms have sometimes been used as diagnostic criteria:

1. painful, fatty lipomas (benign fatty tumors) across anatomy

2. obesity, frequently in menopausal age

3. weakness and fatigue

4. emotional instability, depression, epilepsy, confusion, and dementia.

There are also potential signs of the disease which are identified as the following:

However, as it is unclear which symptoms are cardinal and which symptoms are minor signs in Dercum's disease, it is unclear which should be used as diagnostic criteria. Researchers have proposed a 'minimal definition' based on symptoms most often part of Dercum's disease: 1) Generalized overweight or obesity. 2) Chronic pain in the adipose tissue. The associated symptoms in Dercum's disease include obesity, fatty deposits, easy bruisability, sleep disturbances, impaired memory, depression, difficulty concentrating, anxiety, rapid heartbeat, shortness of breath, diabetes, bloating, constipation, fatigue, weakness and joint and muscle aches. Regarding the associated symptoms in Dercum's disease, only case reports have been published. No study involving medical examinations has been performed in a large group of patients.

Kyrle disease symptoms are chronic and have an onset during adulthood between the ages of 30 and 50 years of age. However, there were reported cases of early onset as early as 5 years of age and late onset as late as 75 years of age. The main symptom is the development of small papules into painless lesions that are surrounded by silvery scales. The lesions are painless, however, there is a chance that the patient may experience extreme urges to itch them. In time, these lesions grow up to a radius of 0.75 inch and develop into red-brown nodules with a central plug of keratin. As more lesions develop, they can come together and form larger keratotic plaques. These lesions are usually observed on the lower extremities, however, can also develop on the upper extremities, such as, the arms, the head and the neck. The only parts of the body that Kyrle disease do not form are the palms, soles, and mucous membranes. Lesions may heal spontaneously without treatment, however, new ones will develop in its place.

Other symptoms that may be observed:

- Hyperkeratotic cone-shaped papular plugs

- Hyperkeratotic verrucous plaques

- Diabetes mellitus

- Hepatic insufficiency

- Presence of albumin in the urine

- Excess sugar in the urine

The most common presentation of Milroy Disease is bilateral lower extremity lymphedema, and may also be accompanied by hydrocele.

Persistent tinnitus may cause anxiety and depression. Tinnitus annoyance is more strongly associated with psychological condition than loudness or frequency range. Psychological problems such as depression, anxiety, sleep disturbances and concentration difficulties are common in those with strongly annoying tinnitus. 45% of people with tinnitus have an anxiety disorder at some time in their life.

Psychological research has looked at the tinnitus distress reaction (TDR) to account for differences in tinnitus severity. These findings suggest that at the initial perception of tinnitus, conditioning links tinnitus with negative emotions, such as fear and anxiety from unpleasant stimuli at the time. This enhances activity in the limbic system and autonomic nervous system, thus increasing tinnitus awareness and annoyance.

Due to variations in study designs, data on the course of tinnitus showed few consistent results. Generally the prevalence increased with age in adults, whereas the ratings of annoyance decreased with duration.

The histiocytosis of Rosai–Dorfman disease can occur in lymph nodes, causing lymphadenopathy, or can occur outside lymph nodes in extranodal disease.

Lymphadenopathy can occur in one or more groups of lymph nodes. Among 358 cases of Rosai–Dorfman disease that Rosai collected in a disease registry for which the location of lymphadenopathy was specified, 87.3% had cervical lymphadenopathy. Axillary, inguinal, and mediastinal lymphadenopathy are also found in Rosai–Dorfman disease.

Kyrle disease or hyperkeratosis follicularis et parafollicularis in cutem penetrans is identified as a form of an acquired perforating disease. Other major perforating diseases are elastosis perforans serpiginosa and reactive perforating collagenosis. Recently, however, there is a controversy on categorizing Kyrle disease with perforating dermatosis or a subtype of acquired perforating collagenosis.

Kyrle disease was first described by Josef Kyrle in 1916 when a diabetic woman presented generalized hyperkeratotic nodules. The disease is distinguished by large papules with central keratin plus on the skin, usually on the legs of the patient and is often in conjunction with hepatic, renal or diabetic disorders. It can affect both females and males with a 6:1 ratio. The papules usually show up on the patient with an average age of 30 years. Kyrle disease is a rare disease unless there is a high count of patients with chronic renal failure. The disease seems to be more prevalent in African Americans, which can be correlated to the high incidence of diabetes mellitus and renal failure in the population.

Clinical appearance of the disease includes depression, a serous nasal discharge, and sporadically minor facial inflammation in mild form of the disease. In severe form, there is severe inflammation of one or both infraorbital sinuses with edema of the surrounding tissue. The swelling can cause closure of one eye or both of them. Intermandibular space and wattles of corks do swell as a course of the disease .

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

Although the dermatological changes are the most obvious symptoms of Urbach–Wiethe disease, many patients also have neurological symptoms. About 50–75% of the diagnosed cases of Urbach–Wiethe disease also show bilateral symmetrical calcifications on the medial temporal lobes. These calcifications often affect the amygdala and the periamygdaloid gyri. The amygdala is thought to be involved in processing biologically relevant stimuli and in emotional long term memory, particularly those associated with fear, and both PET and MRI scans have shown a correlation between amygdala activation and episodic memory for strongly emotional stimuli. Therefore, Urbach–Wiethe disease patients with calcifications and lesions in these regions may suffer impairments in these systems. These calcifications are the result of a buildup of calcium deposits in the blood vessels within this brain region. Over time, these vessels harden and the tissue they are a part of dies, causing lesions. The amount of calcification is often related to disease duration. The true prevalence of these calcifications is difficult to accurately state as not all patients undergo brain imaging. Some patients also exhibit epilepsy and neuropsychiatric abnormalities. Epilepsy symptoms could begin with light anxiety attacks and it can be controlled with "Epilum" (Epilepsy Medicine) Other patients present with symptoms similar to schizophrenia while some suffer from mood, anxiety, and psychotic disorders.

Adiposis dolorosa, also known as Dercum's disease or Anders disease, is a rare condition characterized by generalized obesity and fatty tumors in the adipose tissue. The tumors are normally painful and found in multiples on the extremities. The cause and mechanism of Dercum's disease remains unknown. Possible causes include nervous system dysfunction, mechanical pressure on nerves, adipose tissue dysfunction, and trauma.

Dercum's disease was first described at Jefferson Medical College by neurologist Francis Xavier Dercum in 1892.

Signs and symptoms are variable and depend largely upon whether the obstruction of the duct is complete or partial, and how much resultant pressure is created within the gland. The development of infection in the gland also influences the signs and symptoms.

- Pain, which is intermittent, and may suddenly get worse before mealtimes, and then slowly get better (partial obstruction).

- Swelling of the gland, also usually intermittent, often suddenly appearing or increasing before mealtimes, and then slowly going down (partial obstruction).

- Tenderness of the involved gland.

- Palpable hard lump, if the stone is located near the end of the duct. If the stone is near the submandibular duct orifice, the lump may be felt under the tongue.

- Lack of saliva coming from the duct (total obstruction).

- Erythema (redness) of the floor of the mouth (infection).

- Pus discharging from the duct (infection).

- Cervical lymphadenitis (infection).

- Bad Breath.

Rarely, when stones form in the minor salivary glands, there is usually only slight local swelling in the form of a small nodule and tenderness.

Although symptoms can vary greatly between affected individuals, even those within the same family, symptoms normally begin in infancy and are typically a result of thickening skin and mucous membranes. The first symptom is often a weak cry or a hoarse voice due to a thickening of the vocal cords. The hoarse voice can be one of the most striking clinical manifestations of the disease. Lesions and scars also appear on the skin, usually the face and the distal parts of the limbs. This is often the result of poor wound healing and the scarring continues to increase as the patient ages, leaving the skin with a waxy appearance. Skin may be easily damaged as a result of only a minor trauma or injury, leaving many blisters and additional scars. The skin is also usually very dry and wrinkly. White or yellow infiltrates form on the lips, buccal mucosa, tonsils, uvula, epiglottis and frenulum of the tongue. This can lead to upper respiratory tract infection and sometimes requires tracheostomy to relieve the symptom. Too much thickening of the frenulum can restrict tongue movement and may result in speech impediments. Beading of the papules around the eyelids is a very common symptom and is often used as part of a diagnosis of the disease. Some other dermatological symptoms that are sometimes seen but less common include hair loss, parotitis and other dental abnormalities, corneal ulceration, and focal degeneration of the macula.

Milroy's disease (MD) is a familial disease characterized by lymphedema, commonly in the legs, caused by congenital abnormalities in the lymphatic system. Disruption of the normal drainage of lymph leads to fluid accumulation and hypertrophy of soft tissues. It is also known as Milroy disease, Nonne-Milroy-Meige syndrome and hereditary lymphedema.

It was named by Sir William Osler for William Milroy, a Canadian physician, who described a case in 1892, though it was first described by Rudolf Virchow in 1863.