Pages — The pattern of inflammatory markers in nasal polyposis differentiates this disease from chronic rhinosinusitis.
A Th2 pattern predominates in nasal polyposis, characterized by IgE production, infiltration of eosinophils and upregulation of cytokines and mediators, including IL-5, ECP and eotaxin, that drive eosinophil response.
Nasal congestion can also occur secondary to structural causes, such as septal deviation, choanal atresia, concha bullosa, cleft palate, adenoid hypertrophy, and neoplasia. However, significant anatomic variance exists across individuals; anterior deflections affecting the nasal valve have the greatest impact on airflow, while those in the middle and inferior part of the nasal cavity have little effect on airflow resistance.
The recumbent position can influence both the perception of nasal obstruction and objective measurements of nasal volume and nasal cross-sectional area in normal subjects, as well as in patients with rhinitis. The perception of nasal obstruction induced by lying down seems to be greater in subjects with symptoms of rhinitis. Secondary inflammation may result from neurologic responses that involve a wide range of neurotransmitter systems. The nasal mucosa is invested with sensory, parasympathetic and sympathetic nerves, and they may all contribute to reflex activation of glands or neurogenic inflammation.
Sensory nerves generate sensations, including pruritus, and provide the afferent limb for motor reflexes, such as sneezing. Parasympathetic and sympathetic reflexes can affect both glandular and vascular function in the nose. Neural function can be chronically upregulated in the presence of mucosal inflammation. This may lead to neural hyperresponsiveness and neurogenic inflammation, which is thought to result from the release of peptides eg, substance P, calcitonin gene-related peptide [CGRP], neurokinin A from the peripheral terminals of nociceptive sensory nerve fibers.
The molecular mechanisms underlying hyperresponsiveness are not fully understood but are thought to involve actions of neurotrophins on sensory afferents. Generation of nasal symptoms through neural pathways. Sensory nerves can be stimulated by products of allergic reactions and by external physical and chemical irritants. Signals are transmitted to the central nervous system CNS , where they can trigger sensations pruritus and can further travel through secondary synapses to activate efferent motor sneezing and autonomic neurons.
Action potentials traveling through parasympathetic efferent nerves can lead to glandular activation and rhinorrhea, as well as to some vasodilatation. Suppression of sympathetic neural output, on the other hand, results in vasodilatation and nasal congestion. Antidromic stimulation of sensory nerves with release of tachykinins and other neuropeptides at the nasal mucosa contributes to symptom development with glandular activation, vasodilatation, and plasma extravasation.
Neuropeptide release can also lead to leukocyte recruitment and activation. The sensory nerves of the nose arise from the olfactory nerve, as well as from the ophthalmic and maxillary branches of the trigeminal nerve.
Nonolfactory sensory nerves consist of both myelinated and unmyelinated primarily nociceptive fibers. This effect is thought to be due to activation of cold receptors by menthol, and this cool sensation creates the impression of increased airflow. Specific symptoms of rhinitis are mediated by the actions of distinct neural pathways. Sensory axons can be classified according to size, conduction velocity, the neurotransmitters they release, and the different types of stimuli to which they are sensitive.
Small unmyelinated fibers C fibers conduct action potentials slowly and are generally responsive to noxious mechanical and chemical stimuli. Pruritus is a tactile sensation that is conveyed to the central nervous system via trigeminal fibers that have their cell bodies in the trigeminal ganglion. Trigeminal neuronal activation caused by mast cell mediators may also contribute to sneezing and itching. Calcitonin gene-related peptide CGRP , a potent vasodilator that may play a role in congestion, is also associated with trigeminal activation and is increased in nasal lavage fluids following allergen challenge.
Support for the role of trigeminal activation in the development of AR symptoms is seen in a recent study in which inhalation of CO 2 , a known inhibitor of both neuronal activation and CGRP release, significantly improved nasal allergy symptoms, including congestion. Abnormalities in parasympathetic reflex arcs may also contribute to the development of rhinorrhea and congestion.
Increased understanding of the neurotransmitters and other modulators released by different primary afferents has led to the realization that these neurons can also be classified on the basis of the molecules they use to communicate with other cells. Primary afferents can also be differentiated on the basis of the specific receptors they express and thus the substances to which they are sensitive.
A small subset of C fibers that express histamine H 1 , and perhaps also H 4 , receptors convey information that gives rise to the sensation of itch. Primary afferents expressing these receptors are thought to be involved in detection of painful heat stimuli. A growing body of evidence has indicated that the neurotransmitter phenotypes of primary afferent neurons are highly plastic and may change rapidly as a function of exposure to inflammatory stimuli.
This inflammatory neuroplasticity is the consequence of a combination of activity-dependent changes in the neurons and specific molecules that initiate particular signal transduction pathways. This suggestion is supported by the observation that nasal responsiveness to histamine and capsaicin a highly specific stimulus for C fibers is increased in subjects with allergic rhinitis.
These data support the view that alterations in sensory processing may play a role in the pathophysiology of congestion in some cases. Nasal obstruction or congestion is one of the most common symptoms encountered in primary care and specialist clinics, and it is the symptom that is most bothersome to patients. Mucosal inflammation is the primary pathophysiological mechanism leading to congestion in common upper respiratory diseases, such as allergic rhinitis, rhinosinusitis, and nasal polyposis.
Importantly, neurogenic mechanisms also contribute significantly to the pathophysiological changes underlying nasal congestion, and abnormal primary afferent signaling may give rise to the sensation of congestion even in the absence of inflammation and impaired airflow.
A greater understanding of the pathophysiological mechanisms underlying congestion, in particular the mucosal inflammation associated with common conditions such as allergic rhinitis and rhinosinusitis, has the potential to help clinicians and researchers optimize treatment with existing therapies and develop new treatments for these conditions. National Center for Biotechnology Information , U. Int J Gen Med. Published online Apr 8.
Author information Article notes Copyright and License information Disclaimer. Received Feb This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Nasal congestion is a common symptom in rhinitis both allergic and nonallergic , rhinosinusitis and nasal polyposis. Keywords: allergic rhinitis, congestion, obstruction, pathophysiology, rhinosinusitis.
Introduction Nasal congestion or obstruction is one of the most frequent symptoms encountered in primary care and specialist clinics, and it is often the predominant symptom in upper respiratory tract disorders, such as allergic rhinitis, rhinosinusitis, nonallergic rhinitis, and nasal polyposis. Open in a separate window. Figure 1. Rhinosinusitis Rhinosinusitis is now the accepted term for a group of disorders characterized by inflammation of the mucosa of the nasal passages and paranasal sinuses.
Figure 2. Figure 3. Nasal polyposis Nasal polyposis is a chronic inflammatory disease of the upper airway characterized histologically by the infiltration of inflammatory cells, most notably eosinophils. Figure 4. Structural problems Nasal congestion can also occur secondary to structural causes, such as septal deviation, choanal atresia, concha bullosa, cleft palate, adenoid hypertrophy, and neoplasia.
Figure 5. Modulation of sensory perception The sensory nerves of the nose arise from the olfactory nerve, as well as from the ophthalmic and maxillary branches of the trigeminal nerve. Minor illnesses are the most common causes of nasal congestion.
For instance, a cold, the flu , and sinus infections can all cause stuffy noses. Illness-related congestion usually improves within one week. Some explanations for long-term nasal congestion may be:. Nasal congestion may also occur during pregnancy, usually during the end of the first trimester.
Hormonal fluctuations and increased blood supply that occur during pregnancy may cause this nasal congestion. Humidifiers that add moisture to the air may help to break up mucus and soothe inflamed nasal passageways. However, if you have asthma , ask your doctor before using a humidifier.
In this case, medical treatment may be needed, especially if your condition is painful and interfering with your everyday activities. Nasal congestion can be more threatening in infants than in older children and adults. Symptoms can interfere with infant feedings and can even lead to fatal breathing problems. It may also prevent normal speech and hearing development. Your doctor can then work with you to find the best treatment options for your baby.
Kliegman RM, et al. Allergic rhinitis. In: Nelson Textbook of Pediatrics. Philadelphia, Pa. Peden D. An overview of rhinitis. King TE, et al. Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis Churg-Strauss.
Sexton DJ, et al. The common cold in adults: Diagnosis and clinical features. Nasal congestion and rhinorrhea. Merck Manual Professional Version. Cold versus flu. Centers for Disease Control and Prevention. Lemiere C, et al. Occupational asthma: Clinical features and diagnosis. Respiratory syncytial virus RSV infection pediatric. Rochester, Minn. Seller RH, et al. Colds, flu, and stuffy nose. In: Differential Diagnosis in Common Complaints. Accessed Jan. Nonallergic rhinitis. Walls RM, et al.
This swelling happens when blood vessels in your nasal tissues become dilated, to get the immune response cells to the nose to fight the virus that has entered the body. If your nasal congestion is from a cold or flu, it will likely last as long your cold or flu anywhere from five to 10 days or even longer. If your nasal congestion is the result of allergies, it may last longer, depending on your exposure to that particular allergen. When you have nasal congestion, it can stop you in your tracks.
Constant sniffling or mouth breathing may make it more difficult to focus on the day ahead of you. Many over-the-counter cold and flu medicines treat multiple symptoms. Since nasal congestion is the result of swollen nasal passages, so medicines that shrink the swollen tissues may help. Shrinking these tissues opens the airways, reducing resistance and improving airflow.
Sinex nasal sprays, like Sinex SEVERE Moisturizing Ultra Fine Mist , contain topical oxymetazoline that works in minutes to shrink swollen nasal membranes so you can breathe more freely, plus soothing aloe. It lasts for up to 12 hours to relieve nasal congestion from cold or upper respiratory allergies. If your nasal congestion is accompanied by common cold or flu symptoms like cough and chest congestion, consider a multi-symptom relief medicine, instead.
Sinex Saline Ultra Fine Nasal Mist instantly clears your nasal passages from allergens, dust, and irritants, and helps decongest your stuffy nose with purified saline.
Home treatment should focus on keeping your nasal passages and sinuses moist to prevent further irritation. Here are some ways to keep your nasal passages stay moist:. Use a humidifier or vaporizer. Adding moisture into the air can prevent your nose from drying out and stuffiness.
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