Paroxysmal sneezing in morning, especially in morning while getting out of the bed. Excessive rhinorrhea - watering discharge from the nose when patient bends forward. Nasal obstruction - bilateral nasal stuffiness alternates from one site to other; this is more marked at night, when the dependent side of nose is often blocked. Postnasal drip.

Nonallergic rhinitis is inflammation of the inner part of the nose that is not caused by an allergy. Nonallergic rhinitis involves symptoms including chronic sneezing or having a congested, drippy nose without an identified allergic reaction. Other common terms for nonallergic rhinitis are vasomotor rhinitis and perennial rhinitis. The prevalence of nonallergic rhinitis in otolaryngology is 40%. Allergic rhinitis is more common than nonallergic rhinitis; however, both conditions have similar presentation, manifestation and treatment. Nasal itching and paroxysmal sneezing are usually associated with nonallergic rhinitis in comparison to allergic rhinitis.

The various non-allergic NSAID hypersensitivity syndromes affect 0.5–1.9% of the general population, with AERD affecting about 7% of all asthmatics and about 14% of patients with severe asthma. AERD, which is more prevalent in women, usually begins in young adulthood (twenties and thirties are the most common onset times although children are afflicted with it and present a diagnostic problem in pediatrics) and may not include any other allergies. Most commonly the first symptom is rhinitis (inflammation or irritation of the nasal mucosa), which can manifest as sneezing, runny nose, or congestion. The disorder typically progresses to asthma, then nasal polyposis, with aspirin sensitivity coming last. Anosmia (lack of smell) is also common, as inflammation within the nose and sinuses likely reaches the olfactory receptors.

The respiratory reactions to aspirin vary in severity, ranging from mild nasal congestion and eye watering to lower respiratory symptoms including wheezing, coughing, an asthma attack, and in rare cases, anaphylaxis. In addition to the typical respiratory reactions, about 10% of patients with AERD manifest skin symptoms like urticaria and/or gastrointestinal symptoms such as abdominal pain or vomiting during their reactions to aspirin.

In addition to aspirin, patients usually also react to other NSAIDs such as ibuprofen, and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses is generally considered safe. NSAID that are highly selective in blocking COX-2 and do not block its closely related paralog, COX-1, such as the COX-2 inhibitors celecoxib and rofecoxib, are also regarded as safe. Nonetheless, recent studies do find that these types of drugs, e.g. acetaminophen and celecoxib, may trigger adverse reactions in these patients; caution is recommended in using any COX inhibitors. In addition to aspirin and NSAIDs, consumption of even small amounts of alcohol also produces uncomfortable respiratory reactions in many patients.

Aspirin-induced asthma, also termed Samter's triad, Samter's syndrome, aspirin-exacerbated respiratory disease (AERD), and recently by an appointed task force of the European Academy of Allergy and Clinical Immunology/World Allergy Organization (EAACI/WAO) Nonsteroidal anti-inflammatory drugs-exacerbated respiratory disease (N-ERD). is a medical condition initially defined as consisting of three key features: asthma, respiratory symptoms exacerbated by aspirin, and nasal/ethmoidal polyposis; however, the syndrome's symptoms are exacerbated by a large variety of other nonsteroidal anti-inflammatory drugs (NSAIDs) besides aspirin. The symptoms of respiratory reactions in this syndrome are hypersensitivity reactions to NSAIDs rather than the typically described true allergic reactions that trigger other common allergen-induced asthma, rhinitis, or hives. The NSAID-induced reactions do not appear to involve the common mediators of true allergic reactions, immunoglobulin E or T cells. Rather, AERD is a type of NSAID-induced hypersensitivity syndrome. EAACI/WHO classifies the syndrome as one of 5 types of NSAID hypersensitivity or NSAID hypersensitivity reactions.

Rhinorrhea is characterized by an excess amount of mucus produced by the mucous membranes that line the nasal cavities. The membranes create mucus faster than it can be processed, causing a backup of mucus in the nasal cavities. As the cavity fills up, it blocks off the air passageway, causing difficulty breathing through the nose. Air caught in nasal cavities, namely the sinus cavities, cannot be released and the resulting pressure may cause a headache or facial pain. If the sinus passage remains blocked, there is a chance that sinusitis may result. If the mucus backs up through the Eustachian tube, it may result in ear pain or an ear infection. Excess mucus accumulating in the throat or back of the nose may cause a post-nasal drip, resulting in a sore throat or coughing. Additional symptoms include sneezing, nosebleeds, and nasal discharge.

Rhinorrhea or rhinorrhoea is a condition where the nasal cavity is filled with a significant amount of mucus fluid. The condition, commonly known as a runny nose, occurs relatively frequently. Rhinorrhea is a common symptom of allergies (hay fever) or certain diseases, such as the common cold. It can be a side effect of crying, exposure to cold temperatures, cocaine abuse or withdrawal, such as from opioids like methadone. Treatment for rhinorrhea is not usually necessary, but there are a number of medical treatments and preventive techniques available.

The term was coined in 1866 and is a combination of the Greek terms "rhino-" ("of the nose") and "-rhoia" ("discharge" or "flow").

Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose.

The characteristic presentation of RM involves nasal congestion without rhinorrhea, postnasal drip, or sneezing following several days of decongestant use. This condition typically occurs after 5–7 days of use of topical decongestants. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in permanent turbinate hyperplasia, which may block nasal breathing until surgically removed.

Nasal congestion is the blockage of the nasal passages usually due to membranes lining the nose becoming swollen from inflamed blood vessels.

Nasal decongestants target the discomfort directly. These come as nasal sprays, inhalers, and as oral pills.

Nasal congestion has many causes and can range from a mild annoyance to a life-threatening condition. Most people prefer to breathe through the nose (historically referred to as "obligate nasal breathers"). Nasal congestion in an infant in the first few months of life can interfere with breastfeeding and cause life-threatening respiratory distress; in older children and adolescents it is often just an annoyance but can cause other difficulties.

Nasal congestion can interfere with the hearing and speech. Significant congestion may interfere with sleep, cause snoring, and can be associated with sleep apnea. In children, nasal congestion from enlarged adenoids has caused chronic sleep apnea with insufficient oxygen levels and hypoxia, as well as right-sided heart failure. The problem usually resolves after surgery to remove the adenoids and tonsils, however the problem often relapses later in life due to craniofacial alterations from chronic nasal congestion.

Nasal congestion can also cause mild facial and head pain, and a degree of discomfort, often from allergies or the common cold.

Nasal obstruction characterized by insufficient airflow through the nose can be a subjective sensation or the result of objective pathology. It is difficult to quantify by subjective complaints or clinical examinations alone, hence both clinicians and researchers depend both on concurrent subjective assessment and on objective measurement of the nasal airway. Often a doctor's assessment of a perfectly patent nasal airway might differ with a patient's complaint of an obstructed nose.

Headache/facial pain or pressure of a dull, constant, or aching sort over the affected sinuses is common with both acute and chronic stages of sinusitis. This pain is typically localized to the involved sinus and may worsen when the affected person bends over or when lying down. Pain often starts on one side of the head and progresses to both sides.

Acute sinusitis may be accompanied by thick nasal discharge that is usually green in color and may contain pus (purulent) and/or blood. Often a localized headache or toothache is present, and it is these symptoms that distinguish a sinus-related headache from other types of headaches, such as tension and migraine headaches. Another way to distinguish between toothache and sinusitis is that the pain in sinusitis is usually worsened by tilting the head forwards and with valsalva maneuvers.

Infection of the eye socket is possible, which may result in the loss of sight and is accompanied by fever and severe illness. Another possible complication is the infection of the bones (osteomyelitis) of the forehead and other facial bones – Pott's puffy tumor.

Sinus infections can also cause middle ear problems due to the congestion of the nasal passages. This can be demonstrated by dizziness, "a pressurized or heavy head", or vibrating sensations in the head. Post-nasal drip is also a symptom of chronic rhinosinusitis.

Halitosis (bad breath) is often stated to be a symptom of chronic rhinosinusitis; however, gold standard breath analysis techniques have not been applied. Theoretically, there are several possible mechanisms of both objective and subjective halitosis that may be involved.

A 2004 study suggested that up to 90% of "sinus headaches" are actually migraines. The confusion occurs in part because migraine involves activation of the trigeminal nerves, which innervate both the sinus region and the meninges surrounding the brain. As a result, it is difficult to accurately determine the site from which the pain originates. People with migraines do not typically have the thick nasal discharge that is a common symptom of a sinus infection.

Sinusitis (or rhinosinusitis) is defined as an inflammation of the mucous membrane that lines the paranasal sinuses and is classified chronologically into several categories:

- Acute rhinosinusitis – A new infection that may last up to four weeks and can be subdivided symptomatically into severe and non-severe. Some use definitions up to 12 weeks.

- Recurrent acute rhinosinusitis – Four or more full episodes of acute sinusitis that occur within one year

- Subacute rhinosinusitis – An infection that lasts between four and 12 weeks, and represents a transition between acute and chronic infection

- Chronic rhinosinusitis – When the signs and symptoms last for more than 12 weeks.

- Acute exacerbation of chronic rhinosinusitis – When the signs and symptoms of chronic rhinosinusitis exacerbate, but return to baseline after treatment

All these types of sinusitis have similar symptoms, and are thus often difficult to distinguish. Acute sinusitis is very common. Roughly ninety percent of adults have had sinusitis at some point in their life.

Individuals with the condition of fungal sinusitis mostly present with features that include facial pain and pain around the eyes, nasal congestion, rhinorrhea(running nose), headache, later there may be ophthalmoplegia (paralysis of ocular muscles).

The types of fungal sinusitis are based on "invasive" and "non-invasive" as follows:

- Invasive

- Non Invasive

Permanent loss of smell and impairment of taste may also be a result of this disease, even after the symptoms are cured.

Extreme deviation of nasal septum may be accompanied by atrophic rhinitis on the wider side.

Stomatitis is inflammation of the mouth and lips. It refers to any inflammatory process affecting the mucous membranes of the mouth and lips, with or without oral ulceration.

In its widest meaning, stomatitis can have a multitude of different causes and appearances. Common causes include infections, nutritional deficiencies, allergic reactions, radiotherapy, and many others.

When inflammation of the gums and the mouth generally presents itself, sometimes the term "gingivostomatitis" is used, though this is also sometimes used as a synonym for herpetic gingivostomatitis.

The term is derived from the Greek "stoma" (), meaning "mouth", and the suffix "-itis" (), meaning "inflammation."

The symptoms can be mild or severe and may include:

- Not able to chew or swallow

- Sores on the inside of the cheeks or gums

- Fever

- General discomfort, uneasiness, or ill feeling

- Very sore mouth with no desire to eat

- Halitosis (bad breath)

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).

Inflammation of the corners (angles) of the lips is termed angular stomatitis or angular cheilitis. In children a frequent cause is repeated lip-licking, and in adults it may be a sign of underlying iron deficiency anemia, or vitamin B deficiencies ("e.g.", B-riboflavin, B-folate, or B-cobalamin, which in turn may be evidence of poor diets or malnutrition such as celiac disease).

Also, angular cheilitis can be caused by a patient's jaws at rest being 'overclosed' due to edentulousness or tooth wear, causing the jaws to come to rest closer together than if the complete/unaffected dentition were present. This causes skin folds around the angle of the mouth which are kept moist by saliva, which in turn favours infection; mostly by "Candida albicans" or similar species. Treatment usually involves the administration of topical nystatin or similar antifungal agents. Another treatment can be to correct the jaw relationship with dental treatment ("e.g.", dentures or occlusal adjustment).

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.

Gingivostomatitis (also known as primary herpetic gingivostomatitis or orolabial herpes) is a combination of gingivitis and stomatitis, or an inflammation of the oral mucosa and gingiva. Herpetic gingivostomatitis is often the initial presentation during the first ("primary") herpes simplex infection. It is of greater severity than herpes labialis (cold sores) which is often the subsequent presentations. Primary herpetic gingivostomatitis is the most common viral infection of the mouth.

Primary herpetic gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes simplex virus (HSV) infection, since the vast majority of other primary infections are symptomless. PHGS is caused predominantly by HSV-1 and affects mainly children. Prodromal symptoms, such as fever, anorexia, irritability, malaise and headache, may occur in advance of disease. The disease presents as numerous pin-head vesicles, which rupture rapidly to form painful irregular ulcerations covered by yellow–grey membranes. Sub-mandibular lymphadenitis, halitosis and refusal to drink are usual concomitant findings.

The Newton classification divides denture-related stomatitis into three types based on severity. Type one may represent an early stage of the condition, whilst type two is the most common and type three is uncommon.

- Type 1 - Localized inflammation or pinpoint hyperemia

- Type 2 - More diffuse erythema (redness) involving part or all of the mucosa which is covered by the denture

- Type 3 - Inflammatory nodular/papillary hyperplasia usually on the central hard palate and the alveolar ridge

Signs and symptoms may include:

- Persistent or recurrent enlargement of the lips, causing them to protrude. If recurrent, the interval during which the lips are enlarged may be weeks or months. The enlargement can cause midline fissuring of the lip ("median cheilitis") or angular cheilitis (sores at the corner of the mouth). The swelling is non-pitting (c.f. pitting edema) and feels soft or rubbery on palpation. The mucous membrane of the lip may be erythemaous (red) and granular. One or both lips may be affected.

- Oral ulceration (mouth ulcers) which may be aphthous like, or be more chronic and deep with raised margins. Alternatively, lesions similar to pyostomatitis vegetans may occur in OFG, but this is uncommon.

- "Full width" gingivitis (compare with marginal gingivitis).

- Gingival enlargement (swelling of the gums).

- Fissured tongue (grooves in the tongue).

- Enlargement of the mucous membrane of the mouth, which may be associated with cobblestoning and mucosal tags (similar lesions often occur on the intestinal mucosa in Crohn's disease).

- Enlargement of the perioral and periorbital soft tissues (the tissues of the face around the mouth and the eyes). The facial skin may be dry, exfoliative (flaking) or erythematous.

- Cervical lymphadenopathy (enlarged lymph nodes in the neck).

- Facial palsy (weakness and altered sensation of the face).

The enlargement of the tissues of the mouth, lips and face seen in OFG is painless. Melkersson-Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve. The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression.

Despite the alternative name for this condition, "denture sore mouth", it is usually painless and asymptomatic. The appearance of the involved mucosa is erythematous (red) and edematous (swollen), sometimes

with petechial hemorrhage (pin-points of bleeding). This usually occurs beneath an upper denture. Sometimes angular cheilitis can coexist, which is inflammation of the corners of the mouth, also often associated with "Candida albicans". Stomatitis rarely develops under a lower denture. The affected mucosa is often sharply defined, in the shape of the covering denture.