Vasomotor Rhinitis

Continuing Education Activity

Vasomotor rhinitis affects millions of Americans and costs billions of dollars annually in healthcare costs. Vasomotor rhinitis is the most common form of nonallergic rhinitis and is a diagnosis of exclusion. Avoidance of triggers combined with topical nasal medications is the foundation of treatment. This activity reviews the evaluation and treatment of vasomotor rhinitis and highlights the role of the healthcare team in evaluating and treating patients with this condition.


  • Identify the etiology of vasomotor rhinitis.
  • Review the evaluation of vasomotor rhinitis.
  • Outline the treatment and management options available for vasomotor rhinitis.
  • Summarize interprofessional team strategies for improving care coordination and communication to advance vasomotor rhinitis and improve outcomes.


Nonallergic rhinitis (NAR) describes a syndrome of chronic symptoms of nasal congestion and rhinorrhea, unrelated to a specific allergen. Nonallergic rhinitis can subdivide into numerous different subtypes with vasomotor rhinitis (VMR) being the most common type. Vasomotor rhinitis is a term often used to describe rhinitis symptoms associated with nonallergic, noninfectious triggers with no clear etiology after the conclusion of an exhaustive search for a diagnosis. The pathophysiology of nonallergic rhinitis is complex, with still much to be discovered. It is partly due to an imbalance between parasympathetic and sympathetic inputs on the nasal mucosa.[1] The most critical factor in attaining a proper diagnosis of vasomotor rhinitis is a comprehensive history and physical. The best overall treatment is the avoidance of the known trigger with medical therapy as an adjunct. When all other options fail, surgical intervention becomes a viable therapy.


Although the etiology of vasomotor rhinitis is not well understood, it is thought to be associated with the dysregulation of sympathetic, parasympathetic, and nociceptive nerves innervating the nasal mucosa.[1] The imbalance among mediators results in increased vascular permeability and mucus secretion from the submucosal nasal glands.[2][3]  Mucous secretion is regulated primarily by the parasympathetic nervous system, whereas the sympathetic nervous system controls vascular tone.[4] Acetylcholine is the primary parasympathetic neurotransmitter that regulates mucus secretion and rhinorrhea. Norepinephrine and neuropeptide Y are sympathetic neurotransmitters that control the vascular tone of vessels in the nasal mucosa and modulate the parasympathetic system initiated secretions.[5] Sensory neuropeptides and nociceptive type C fibers of the trigeminal nerve contribute to mast cell degranulation as well as the itching/sneezing reflexes.[1] 


Rhinitis, whether allergic or nonallergic, affects roughly 20% of the population in industrialized countries.[6] An estimated 20 to 40 million people are affected by allergic rhinitis, costing over $1.9 billion annually.[1] An estimated 17 to 19 million Americans experience nonallergic rhinitis.[7] Nonallergic rhinitis presents later in life, with patients developing symptoms most commonly between the ages of 30 and 60.[6] Females are more affected by nonallergic rhinitis than men. 70% of women aged 50 to 64 experience some form of nonallergic rhinitis in any given year.[8]

History and Physical

Vasomotor rhinitis is clinically diagnosed. An exhaustive history, complete head and neck examination, and diagnostic testing will rule out infections, allergic, and inflammatory causes.[9] Headache, facial pressure, postnasal drip, coughing, and throat clearing are common symptoms among both allergic and nonallergic rhinitis.[10]  Vasomotor rhinitis patients tend to categorize into two groups depending on predominant symptomatology: “blockers” with congestion and “runners” with rhinorrhea.  Patients with rhinorrhea tend to have an enhanced cholinergic response. Those with nasal obstruction tend to have nociceptive neurons with a heightened response to harmless stimuli.[9][10] Vasomotor rhinitis is generally perennial. However, seasonal exacerbation of vasomotor rhinitis from shifts in barometric pressure, temperature, and humidity may get misconstrued as allergic rhinitis.   Environmental triggers that affect vasomotor rhinitis patients may include strong odors, cold air exposure, alcohol ingestion, and/or spicy foods. Physical exam often reveals boggy edematous mucosa with clear mucoid secretions. Mucosal injection and lymphoid hyperplasia involving the tonsils, adenoids, and lingual tonsils may be present. There are reports of an area of blanched mucosa surrounds prominent vessels in chemical sensitivities.[11]  Examination of the nasal cavity and nasopharynx may help to identify primary or secondary causes of rhinitis. An example: the presence of purulent drainage from the middle meatus on nasal endoscopy would indicate an infectious process essentially ruling out vasomotor rhinitis. 


The workup for vasomotor rhinitis should include skin testing and/or serum specific IgE antibodies. As a diagnosis of exclusion, vasomotor rhinitis will typically have a negative skin test and serum antibodies for relevant allergens. Nasal cytology can provide information about cell types composing the mucosa and helps to identify the presence of inflammatory markers. Scrapings from the inferior turbinate, nasal lavage or nose blowing can provide epithelial cells for analysis. The presence of eosinophils 5 to 25 in high-powered fields is compatible with the diagnosis of nonallergic rhinitis with eosinophilia syndrome (NARES), a subset of nonallergic rhinitis.[12] Brandt and Bernstein developed a validated questionnaire to aid in the diagnosis of vasomotor rhinitis through a series of questions. Their results revealed that patients with onset of symptoms after the age of 35 years, a negative family history of allergies or atopy, no outdoor or cat-related symptoms, and symptoms associated with exposure to perfumes and fragrances; had a 96% likelihood of having vasomotor rhinitis.[13]  Nasal provocation testing has become standardized via commercially available products. Provocation testing involves exposing a patient to a respective allergen, assessing the clinical response, and collecting objective data with rhinomanometry and acoustic rhinometry.[14]  A computer tomography scan of the paranasal sinuses is a diagnostic option for patients with suspected sinus disease, and magnetic resonance imaging can assist with suspected mass lesions of the head and neck.  However, in cases of vasomotor rhinitis, imaging will rarely reveal pathology and is not particularly useful.

Distinguishing vasomotor rhinitis from allergic rhinitis can be challenging.  Symptomatology and physical exam findings are often very similar.  Allergic rhinitis is a nasal disorder associated with an allergen exposure that induces an IgE-mediated inflammatory response. The timing symptoms provide clues into differentiating between nonallergic rhinitis and allergic rhinitis. Seasonal peaks of pollen, places with pet dander and/or mold spores, geographical relocation leading to symptoms can point to a diagnosis of allergic rhinitis. The patient’s history provides essential information for diagnosis. Allergy testing a clinically useful tool to identify a specific allergen and treat the condition. Allergy testing alone can be nonspecific, but in conjunction with a thorough history and physical exam is valuable in distinguishing between vasomotor rhinitis and allergic rhinitis.[15]  

A detailed history will often elucidate an infectious process from an allergic or nonallergic one. Infectious rhinitis also presents with similar symptomatology to nonallergic rhinitis: nasal purulence, postnasal drip, facial pressure and pain, fever, sore throat, etc.  The three cardinal symptoms of infectious rhinitis include purulent nasal discharge, nasal obstruction, and facial pressure, and are often present for ten days or longer. A fever may or may not be present depending on the acuity of the infection, and is only 50% sensitive and specific.[16] A physical exam will often reveal purulence in the region of the middle meatus with hyperemia, edema, or crusting along the middle turbinate.

Treatment / Management

Upon determining a diagnosis of vasomotor rhinitis, educating the patient on avoiding environmental triggers is critical.[10] Evading or limiting exposure to inciting factors such as perfumes, tobacco smoke, and cleaning supplies can significantly reduce symptoms. Avoidance of triggers is generally not very difficult. However, when inciting exposures are unavoidable, medications are an option.[1] 

A stepwise pharmacologic approach is often implemented, with the initial intervention targeted toward the predominant symptom.[10]  Topical nasal corticosteroids are considered first-line in vasomotor rhinitis, especially for congestion and obstructive symptoms. Topical steroids work on the nasal mucosa resulting in decreased neutrophil and eosinophil chemotaxis, reduced mast cell and basophil mediator release, and ultimately decreased edema and inflammation.[17] Topical steroids are generally well-tolerated, and side effects are infrequent. The most commonly reported side effects are nasal dryness, crusting, and septal irritation.[18] Multiple studies have shown the effectiveness of topical nasal steroids in the treatment of vasomotor rhinitis.  Integrated analysis of three double-blinded randomized controlled trials demonstrated that fluticasone 200 or 400 mcg was significantly more effective than a placebo.[19] Fluticasone propionate and beclomethasone are currently the only topical steroid preparations approved by the FDA for vasomotor rhinitis.[1][19][20] Budesonide has also shown to be efficacious and is currently the only topical steroid agent with a pregnancy category B rating.[21][22]

Anticholinergic medications can provide relief from unrelenting rhinorrhea. However, the oral preparations have disturbing systemic side effects such as blurred vision, dry mouth, and thickened secretions.  A topical anticholinergic like ipratropium bromide is the first choice for rhinorrhea. Two separate randomized controlled trials demonstrated the effectiveness of ipratropium bromide in controlling rhinorrhea.[23][24] Topical anticholinergics act locally and block parasympathetic input to the nasal mucosa glands only.[23] Systemic side effects are uncommon. Epistaxis and nasal dryness may occur.[24]  Ipratropium bromide also carries a pregnancy category B rating and can be used in children as young as six.

Oral antihistamines have a limited role in vasomotor rhinitis, with no specific formulation approved. They tend only to benefit those patients with a sneezing and itching component. Topical antihistamines such as azelastine have approval for both allergic and nonallergic rhinitis. Azelastine is helpful in patients with rhinorrhea and nasal congestion. Azelastine is an H1-receptor antagonist. It also inhibits the synthesis of leukotrienes, kinins, cytokines, and adhesion molecule expression, while providing anti-inflammatory effects unrelated to histamine.[25][26] This characteristic makes it effective in vasomotor rhinitis. Azelastine provides a significant reduction in vasomotor symptomatology, including nasal obstruction, rhinorrhea, and nasal edema, as demonstrated in two randomized control trials.[27][28] These trials demonstrated significant improvement in all symptoms within the first week of treatment. Azelastine is well tolerated with low cessation rates.[27][28] Patients with chronic vasomotor rhinitis are generally less responsive to pharmacologic therapy than those with allergic rhinitis.  The combination of intranasal steroids and topical antihistamines have been effective in treating the symptomatology of chronic nonallergic rhinitis.[29] Topical capsaicin has also demonstrated efficacy as an adjunct therapy for those with rhinorrhea and nasal congestion.[30]  The mechanism is thought to center around modulation of the C fibers associated with nociceptive neurons. Capsaicin targets transient receptor potential vanilloid type 1 (TRPV1), an ion channel that present on epithelial cells, submucosal glands, and nerves in the human nasal mucosa and assists in regulating nasal secretions and congestion. Repeated intranasal applications of capsaicin can desensitize TRPV1 make it less sensitive to physical and chemical nociceptive stimuli.  However, the limiting factor with capsaicin use is a person’s ability to tolerate its irritant quality.[31]

Sympathomimetic medications, specifically topical decongestants, can provide short term symptomatic relief.  Topical decongestants work primarily by stimulating alpha-1 and alpha-2 adrenoreceptors on the vasculature of the nasal mucosa. This action leads to vasoconstriction, decreased blood flow, and subsequently decreased congestion and rhinorrhea of the nasal cavity. To date, no study has determined the effectiveness of topical decongestants on chronic non-allergic rhinitis.  Long term use of topical decongestants can lead to rebound vasodilation and increased congestion. This condition is termed rhinitis medicamentosa, a form of drug-induced rhinitis. By limiting the use of nasal decongestant to five days and not exceeding the recommended dosing, rhinitis medicamentosa and addiction are avoidable.[32]

Botulinum toxin has also demonstrated a potential role in the treatment of vasomotor rhinitis through its anticholinergic effects.[4] Botulinum toxin (BTX) inhibits acetylcholine release from the presynaptic nerve terminal. Injecting BTX into the inferior and middle turbinates decreases rhinorrhea and nasal mucous gland secretion in patients with vasomotor rhinitis. The improvement is usually short-lived, lasting roughly four weeks.[33] BTX is considered a safe treatment without significant side effects. However, temporary symptom relief may not be a practical option for most patients.[5]

When medical management alone does not adequately control vasomotor rhinitis symptoms, surgical interventions may be employed.  Mucosal sparing inferior turbinate reduction surgery improves obstruction symptoms and acts synergistically with medical therapies.[34] By improving the nasal airway, decreasing mucosal edema, and preserving turbinate function, and reducing obstructive nasal symptoms, which also allows for topical steroids and histamines to reach further into the nasal cavity, and greater reduce symptoms.[1]

The therapeutic transection of the vidian nerve is a well-known surgical option for vasomotor rhinitis.  The technique aims to disrupt the autonomic nerve supply of the nasal cavity, thus decreasing nasal secretions.[1] The vidian nerve forms from the confluence of the greater superficial petrosal and deep petrosal nerves. The deep petrosal contains sympathetic fibers. The greater superficial petrosal nerve contains preganglionic parasympathetic secretomotor fibers for the lacrimal, palatine, and nasal mucus glands, as well as the nerves responsible for vasodilating the vessels of the nasal mucosa.[35] The first vidian neurectomy was described by Golding-Wood in 1961 using a transantral approach and carried significant morbidity due to facial numbness, postoperative bleeding, and ocular injuries.[36][37] With the advent of endoscopic techniques, improved visualization of the pterygopalatine fossa has decreased complications associated with neurectomy. Rates of successful control of rhinitis and patient satisfaction following endoscopic vidian neurectomy have been reported as high as 91%.[38] A systematic review performed by Marshak et al. reported that all published case series associated with vidian neurectomy improved rhinorrhea and nasal congestion.[35] The most notable complication associated with neurectomy includes postoperative dry eyes from decreased lacrimation with a reported aggregate rate of 48%, dysesthesia, and mucosal engorgement when supine.[3][37]  Most symptoms were temporary, with dry eyes resolving in 1 to 6 months.[1][35]

Treating nonallergic rhinitis in pregnancy and the pediatric population presents its own challenges. Management should center around conservative therapy first. Nasal saline irrigations have essentially no risk and may be helpful. If medications are necessary, several options exist. Diphenhydramine may be an option when needed, although with caution in children less than two and in the first trimester. Ipratropium bromide carries a category B rating and is safe in children as young as six. As discussed above, budesonide is the only topical nasal steroid with a category B rating. Fluticasone is safe to use in patients as young as four years of age. Topical decongestants can be used on a limited basis in children as young as 6. Oxymetazoline is the decongestant of choice in both pregnancy and pediatric population.[39][40]

Differential Diagnosis

Primary and secondary causes of nonallergic rhinitis exist. Primary causes include eight subtypes: drug-induced rhinitis; gustatory rhinitis; hormonal induced rhinitis; nonallergic rhinitis with eosinophilia syndrome; senile rhinitis; atrophic rhinitis; cerebral spinal fluid leak; and idiopathic nonallergic rhinitis.[9] Secondary causes include Wegner granulomatosis; Churg-Strauss syndrome, relapsing polychondritis, systemic lupus erythematosus, Sjogren syndrome, autoimmune rhinitis, hypothyroidism, pregnancy, acromegaly, metabolic syndromes, cystic fibrosis, Kartagener syndrome, sarcoidosis, immunodeficiency, amyloidosis, laryngopharyngeal reflux, and chronic fatigue syndrome.[41] 

Drug-induced rhinitis is often further divided into three categories: neurogenic, inflammatory, and idiopathic. Numerous medications list rhinitis as a side effect. The most notable offenders are antihypertensive medications, erectile dysfunction medications, and some psychiatric medications. Overuse of topical decongestants leads to rhinitis medicamentosa by a different mechanism. Systemic anti-hypertensive drugs cause rhinitis through neurogenic mechanisms. They induce a parasympathetic dominance of the nasal mucosa by inhibiting norepinephrine release, which leads to congestion and rhinorrhea.[42]

Hormone-induced rhinitis is associated with nasal congestion secondary to elevated estrogen and progesterone. Up to 65% of women self-report nasal congestion at some time during their pregnancy.[43] The mechanism is still under investigation. It appears that a cyclic hormonal pattern or slowly increasing plasma levels can affect the nasal mucosa. The decrease in estrogen and progesterone after delivers correlates with a rapid resolution of rhinitis symptoms postpartum.[44]

Occupational rhinitis is a nasal irritation and inflammation that occurs from workplace exposures. Causes of rhinitis in the workplace can classify as either allergic, irritant, or a combination. Occupational rhinitis causes often get subdivided into high molecular weight compounds such as plant or animal-derived proteins and low molecular weight compounds, which are often hapten associated. Certain occupations are at an increased risk: bakers, livestock breeders, industry workers, veterinarians, etc.[45] The diagnosis of OR requires both documentation of rhinitis and causation related to workplace exposure. IgE specific antibodies are often seen in the high molecular weight compound exposures but are less sensitive in the low molecular weight compounds. Reproduction of nasal symptoms from nasal provocation challenge testing remains the standard of care in diagnosing occupational rhinitis.[46]


Nonallergic rhinitis is a persistent condition that is usually present lifelong.  One study by Rondon and colleagues,[47]  reexamined 180 patients with nonallergic rhinitis 3 to 7 years after initial diagnosis. As high as 52% of patients experienced worsening disease, with a 12% increase in persistence, and a 9% increase in the severity of nasal symptoms. Additionally, patients with nonallergic rhinitis went on to develop new comorbidities, with the most common being asthma. The development of chronic sinusitis also increased.[48]


Chronic vasomotor rhinitis symptoms often interfere with work performance and school attendance due to loss of productivity and frequent doctor visits. Chronic nonallergic rhinitis places considerable physical and economic burdens on sufferers. In a survey of rhinitis patients, 25% endorsed limiting their choice of occupation or place of residence to reduce rhinitis symptoms.[49]  Also, medical treatments to control symptoms may prompt undesirable side effects such as nasal dryness, palpitations, epistaxis, and drowsiness. These side effects compound the negative impact of nonallergic rhinitis on patients.[50] Chronic nonallergic rhinitis is often associated with other conditions such as headaches, eustachian tube dysfunction, nasal polyps, obstructive sleep apnea, and chronic cough. These symptoms can significantly complicate management and impair quality of life.[41]

Deterrence and Patient Education

Patient education is critical in managing vasomotor rhinitis. Patients with known environmental, non-immunologic, and irritant triggers should be reminded to avoid exposure to these offending agents. Avoidance of irritating stimuli is the mainstay of treatment. Avoidance measures and medical therapy are often enough to decrease most of the symptomatology and mucosal disease associated with nonallergic rhinitis. If stimuli are unavoidable, educating the patient on pretreating with topical nasal steroids or histamines can limit symptoms.[1][10]

Enhancing Healthcare Team Outcomes

Vasomotor rhinitis is a diagnosis of exclusion after performing an exhaustive investigation into a patient’s history. Vasomotor rhinitis is the most commonly diagnosed nonallergic rhinitis, not because of high prevalence, but often from healthcare professionals resorting to diagnosis without performing an extensive workup. Allergic rhinitis and nonallergic rhinitis have very similar symptomatology, such as congestion, rhinorrhea, facial pressure, and headache. They are often differentiated by whether an immunoglobulin E (IgE) response assessment is positive. However, not all allergic rhinitis patients are affected by an IgE inflammatory process. Skin and serum allergy tests are often inadequate in their ability to describe local allergic rhinitis.

Physicians are almost always involved in the care of patients with allergic and nonallergic rhinitis. Whether its an allergist, otolaryngologist, and/or family physician, rhinitis is very common with most physicians encountering the disease in their practice. When the diagnosis becomes more complex, consultation with a rhinologist or specialist may be warranted. As will all aspects of healthcare, interprofessional coordination is critical for the effective management of patients with nonallergic and allergic rhinitis. The laboratory technicians collect serum samples for IgE testing and analyze the results. The allergy technicians perform the appropriate allergen skin testing and interpret results. The nurses are a vital member of the interprofessional group as they monitor the patient's vital signs, review patients’ medications, assess therapeutic effectiveness, and triage symptom severity. The pharmacists ensure proper dosing for intranasal steroids and histamines and other medical management of rhinitis while screening for interactions amongst medications. Pharmacists can also discuss alternative agents with the prescriber in the event of inadequate therapeutic response or adverse events. The radiologists also play a vital role in analyzing nasal anatomic obstructions on imaging. As with any condition, an interprofessional team approach to diagnosis and management ensures the best potential for positive results for the patient. [Level V]

Patients with negative systemic allergy assessments and negative imaging are often categorized into a nonallergic rhinitis subtype but have a clinical picture congruent with local allergic rhinitis. A recent cross-sectional study was performed to assess the clinical characteristics of patients with nonallergic rhinitis. Older patients denied a history of asthma and lacked an inhalant allergy trigger were more likely to have true nonallergic rhinitis. Environmental triggers were not considered a distinguishing feature between local allergic rhinitis and nonallergic rhinitis. The results of this research study may help guide differentiation between truly nonallergic etiologies and those with falsely negative systemic allergy testing.[51] [Level 4]

Article Details

Article Author

Preston Leader

Article Editor:

Zachary Geiger


8/16/2020 3:06:41 AM

PubMed Link:

Vasomotor Rhinitis



Surgical Management of Nonallergic Rhinitis., Yan CH,Hwang PH,, Otolaryngologic clinics of North America, 2018 Jun 21     [PubMed PMID: 29937065]


Bernstein JA, Nonallergic rhinitis: therapeutic options. Current opinion in allergy and clinical immunology. 2013 Aug;     [PubMed PMID: 23756873]


Joe SA, Nonallergic rhinitis. Facial plastic surgery clinics of North America. 2012 Feb;     [PubMed PMID: 22099614]


Shaari CM,Sanders I,Wu BL,Biller HF, Rhinorrhea is decreased in dogs after nasal application of botulinum toxin. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery. 1995 Apr;     [PubMed PMID: 7700663]


Ozcan C,Ismi O, Botulinum Toxin for Rhinitis. Current allergy and asthma reports. 2016 Aug;     [PubMed PMID: 27461136]


Settipane RA,Charnock DR, Epidemiology of rhinitis: allergic and nonallergic. Clinical allergy and immunology. 2007;     [PubMed PMID: 17153005]


Settipane RA,Lieberman P, Update on nonallergic rhinitis. Annals of allergy, asthma     [PubMed PMID: 11379801]


Lund VJ,Preziosi P,Hercberg S,Hamoir M,Dubreuil C,Pessey JJ,Stoll D,Zanaret M,Gehanno P, Yearly incidence of rhinitis, nasal bleeding, and other nasal symptoms in mature women. Rhinology. 2006 Mar;     [PubMed PMID: 16550946]


Kaliner MA, Classification of Nonallergic Rhinitis Syndromes With a Focus on Vasomotor Rhinitis, Proposed to be Known henceforth as Nonallergic Rhinopathy. The World Allergy Organization journal. 2009 Jun 15;     [PubMed PMID: 24229372]


Pattanaik D,Lieberman P, Vasomotor rhinitis. Current allergy and asthma reports. 2010 Mar;     [PubMed PMID: 20425499]


Meggs WJ,Cleveland CH Jr, Rhinolaryngoscopic examination of patients with the multiple chemical sensitivity syndrome. Archives of environmental health. 1993 Jan-Feb;     [PubMed PMID: 8452394]


Greiner AN,Meltzer EO, Pharmacologic rationale for treating allergic and nonallergic rhinitis. The Journal of allergy and clinical immunology. 2006 Nov;     [PubMed PMID: 17088121]


Brandt D,Bernstein JA, Questionnaire evaluation and risk factor identification for nonallergic vasomotor rhinitis. Annals of allergy, asthma     [PubMed PMID: 16680922]


Gosepath J,Amedee RG,Mann WJ, Nasal provocation testing as an international standard for evaluation of allergic and nonallergic rhinitis. The Laryngoscope. 2005 Mar;     [PubMed PMID: 15744168]


Bousquet J,Khaltaev N,Cruz AA,Denburg J,Fokkens WJ,Togias A,Zuberbier T,Baena-Cagnani CE,Canonica GW,van Weel C,Agache I,Aït-Khaled N,Bachert C,Blaiss MS,Bonini S,Boulet LP,Bousquet PJ,Camargos P,Carlsen KH,Chen Y,Custovic A,Dahl R,Demoly P,Douagui H,Durham SR,van Wijk RG,Kalayci O,Kaliner MA,Kim YY,Kowalski ML,Kuna P,Le LT,Lemiere C,Li J,Lockey RF,Mavale-Manuel S,Meltzer EO,Mohammad Y,Mullol J,Naclerio R,O'Hehir RE,Ohta K,Ouedraogo S,Palkonen S,Papadopoulos N,Passalacqua G,Pawankar R,Popov TA,Rabe KF,Rosado-Pinto J,Scadding GK,Simons FE,Toskala E,Valovirta E,van Cauwenberge P,Wang DY,Wickman M,Yawn BP,Yorgancioglu A,Yusuf OM,Zar H,Annesi-Maesano I,Bateman ED,Ben Kheder A,Boakye DA,Bouchard J,Burney P,Busse WW,Chan-Yeung M,Chavannes NH,Chuchalin A,Dolen WK,Emuzyte R,Grouse L,Humbert M,Jackson C,Johnston SL,Keith PK,Kemp JP,Klossek JM,Larenas-Linnemann D,Lipworth B,Malo JL,Marshall GD,Naspitz C,Nekam K,Niggemann B,Nizankowska-Mogilnicka E,Okamoto Y,Orru MP,Potter P,Price D,Stoloff SW,Vandenplas O,Viegi G,Williams D, Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen). Allergy. 2008 Apr     [PubMed PMID: 18331513]


Rosenfeld RM, CLINICAL PRACTICE. Acute Sinusitis in Adults. The New England journal of medicine. 2016 Sep 8     [PubMed PMID: 27602668]


Pipkorn U,Proud D,Lichtenstein LM,Kagey-Sobotka A,Norman PS,Naclerio RM, Inhibition of mediator release in allergic rhinitis by pretreatment with topical glucocorticosteroids. The New England journal of medicine. 1987 Jun 11;     [PubMed PMID: 2438553]


Cervin A,Andersson M, Intranasal steroids and septum perforation--an overlooked complication? A description of the course of events and a discussion of the causes. Rhinology. 1998 Sep;     [PubMed PMID: 9830677]


Webb DR,Meltzer EO,Finn AF Jr,Rickard KA,Pepsin PJ,Westlund R,Cook CK, Intranasal fluticasone propionate is effective for perennial nonallergic rhinitis with or without eosinophilia. Annals of allergy, asthma     [PubMed PMID: 11995670]


Synnerstad B,Lindqvist N, A clinical comparison of intranasal budesonide with beclomethasone dipropionate for perennial non-allergic rhinitis: a 12 month study. The British journal of clinical practice. 1996 Oct-Nov;     [PubMed PMID: 9015907]


Creticos P,Fireman P,Settipane G,Bernstein D,Casale T,Schwartz H, Intranasal budesonide aqueous pump spray (Rhinocort Aqua) for the treatment of seasonal allergic rhinitis. Rhinocort Aqua Study Group. Allergy and asthma proceedings. 1998 Sep-Oct;     [PubMed PMID: 9801742]


Wight RG,Jones AS,Beckingham E,Andersson B,Ek L, A double blind comparison of intranasal budesonide 400 micrograms and 800 micrograms in perennial rhinitis. Clinical otolaryngology and allied sciences. 1992 Aug;     [PubMed PMID: 1526057]


Grossman J,Banov C,Boggs P,Bronsky EA,Dockhorn RJ,Druce H,Findlay SR,Georgitis JW,Hampel FC,Kaiser H, Use of ipratropium bromide nasal spray in chronic treatment of nonallergic perennial rhinitis, alone and in combination with other perennial rhinitis medications. The Journal of allergy and clinical immunology. 1995 May;     [PubMed PMID: 7538520]


Bronsky EA,Druce H,Findlay SR,Hampel FC,Kaiser H,Ratner P,Valentine MD,Wood CC, A clinical trial of ipratropium bromide nasal spray in patients with perennial nonallergic rhinitis. The Journal of allergy and clinical immunology. 1995 May;     [PubMed PMID: 7751528]


Lieberman PL,Settipane RA, Azelastine nasal spray: a review of pharmacology and clinical efficacy in allergic and nonallergic rhinitis. Allergy and asthma proceedings. 2003 Mar-Apr;     [PubMed PMID: 12776442]


Lieberman P, Intranasal antihistamines for allergic rhinitis: mechanism of action. Allergy and asthma proceedings. 2009 Jul-Aug;     [PubMed PMID: 19772756]


Banov CH,Lieberman P, Efficacy of azelastine nasal spray in the treatment of vasomotor (perennial nonallergic) rhinitis. Annals of allergy, asthma     [PubMed PMID: 11206234]


Lieberman P,Kaliner MA,Wheeler WJ, Open-label evaluation of azelastine nasal spray in patients with seasonal allergic rhinitis and nonallergic vasomotor rhinitis. Current medical research and opinion. 2005 Apr;     [PubMed PMID: 15899111]


Luo X,Ma R,Wu X,Xian D,Li J,Mou Z,Li H, Azelastine enhances the clinical efficacy of glucocorticoid by modulating MKP-1 expression in allergic rhinitis. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery. 2015 May;     [PubMed PMID: 25060977]


Fokkens W,Hellings P,Segboer C, Capsaicin for Rhinitis. Current allergy and asthma reports. 2016 Aug;     [PubMed PMID: 27485456]


Gevorgyan A,Segboer C,Gorissen R,van Drunen CM,Fokkens W, Capsaicin for non-allergic rhinitis. The Cochrane database of systematic reviews. 2015 Jul 14;     [PubMed PMID: 26171907]


Lockey RF, Rhinitis medicamentosa and the stuffy nose. The Journal of allergy and clinical immunology. 2006 Nov     [PubMed PMID: 17088123]


Braun T,Gürkov R,Kramer MF,Krause E, Septal injection of botulinum neurotoxin A for idiopathic rhinitis: a pilot study. American journal of otolaryngology. 2012 Jan-Feb;     [PubMed PMID: 21419514]


Passàli D,Passàli FM,Damiani V,Passàli GC,Bellussi L, Treatment of inferior turbinate hypertrophy: a randomized clinical trial. The Annals of otology, rhinology, and laryngology. 2003 Aug;     [PubMed PMID: 12940665]


Marshak T,Yun WK,Hazout C,Sacks R,Harvey RJ, A systematic review of the evidence base for vidian neurectomy in managing rhinitis. The Journal of laryngology and otology. 2016 Jul;     [PubMed PMID: 27488341]


GOLDING-WOOD PH, Observations on petrosal and vidian neurectomy in chronic vasomotor rhinitis. The Journal of laryngology and otology. 1961 Mar;     [PubMed PMID: 13706533]


Halderman A,Sindwani R, Surgical management of vasomotor rhinitis: a systematic review. American journal of rhinology     [PubMed PMID: 25785754]


Ma Y,Tan G,Zhao Z,Li W,Huang L,Liu G, Therapeutic effectiveness of endoscopic vidian neurectomy for the treatment of vasomotor rhinitis. Acta oto-laryngologica. 2014 Mar;     [PubMed PMID: 24433056]


Ellegård EK,Karlsson NG,Ellegård LH, Rhinitis in the menstrual cycle, pregnancy, and some endocrine disorders. Clinical allergy and immunology. 2007     [PubMed PMID: 17153022]


Berger WE,Schonfeld JE, Nonallergic rhinitis in children. Current allergy and asthma reports. 2007 May     [PubMed PMID: 17437681]


Greiwe J,Bernstein JA, Nonallergic Rhinitis: Diagnosis. Immunology and allergy clinics of North America. 2016 May;     [PubMed PMID: 27083103]


Fokkens WJ, Thoughts on the pathophysiology of nonallergic rhinitis. Current allergy and asthma reports. 2002 May     [PubMed PMID: 11918861]


Ellegård EK, Pregnancy rhinitis. Immunology and allergy clinics of North America. 2006 Feb     [PubMed PMID: 16443147]


Philpott CM,Robinson AM,Murty GE, Nasal pathophysiology and its relationship to the female ovarian hormones. Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale. 2008 Aug     [PubMed PMID: 19128590]


Hytönen M,Kanerva L,Malmberg H,Martikainen R,Mutanen P,Toikkanen J, The risk of occupational rhinitis. International archives of occupational and environmental health. 1997     [PubMed PMID: 9215937]


Pałczyński C,Walusiak J,Krakowiak A,Szymczak W,Wittczak T,Ruta U,Górski P, Nasal lavage fluid examination in diagnostics of occupational allergy to chloramine. International journal of occupational medicine and environmental health. 2003     [PubMed PMID: 14587536]


Rondón C,Doña I,Torres MJ,Campo P,Blanca M, Evolution of patients with nonallergic rhinitis supports conversion to allergic rhinitis. The Journal of allergy and clinical immunology. 2009 May;     [PubMed PMID: 19361848]


Lieberman PL,Smith P, Nonallergic Rhinitis: Treatment. Immunology and allergy clinics of North America. 2016 May;     [PubMed PMID: 27083104]


Rydén O,Andersson B,Andersson M, Disease perception and social behaviour in persistent rhinitis: a comparison between patients with allergic and nonallergic rhinitis. Allergy. 2004 Apr;     [PubMed PMID: 15005772]


Levenson T,Greenberger PA, Pathophysiology and therapy for allergic and nonallergic rhinitis: an updated review. Allergy and asthma proceedings. 1997 Jul-Aug;     [PubMed PMID: 9270882]


Hamizan AW,Azer M,Alvarado R,Earls P,Barham HP,Tattersall J,Rimmer J,Kalish L,Sewell WA,Harvey R, The Distinguishing Clinical Features of Nonallergic Rhinitis Patients. American journal of rhinology     [PubMed PMID: 31106562]