Differences in clinical features of cluster headache between drinkers and nondrinkers in Japan.

OBJECTIVE: Alcohol has been recognized as the main trigger for a cluster headache attack, but clinical features to distinguish between cluster headache in drinkers and nondrinkers are unclear. Thus, the present study aimed to investigate the differences in clinical features of cluster headache between drinkers and nondrinkers. METHODS: This retrospective, observational study compared the clinical features of cluster headache between drinkers and nondrinkers among patients who were diagnosed with cluster headache between November 2004 and April 2018 at the Japanese Red Cross Shizuoka Hospital. Demographic and clinical data were collected from medical records and/or by patient interview. RESULTS: Of 131 patients, 98 (75%) were drinkers, and 33 (25%) were nondrinkers. Compared with nondrinkers, drinkers had significantly more frequent conjunctival injection (43% vs. 21%, p = 0.037) but significantly less frequent nasal congestion (31% vs. 52%, p = 0.0037), vomiting (11% vs. 30%, p = 0.014), and photophobia (29% vs. 45%, p = 0.008). CONCLUSION: Among individuals with cluster headache, the frequencies of conjunctival injection, nasal congestion, vomiting, and photophobia were different between drinkers and nondrinkers. These results suggested that drinking might influence the responses of the cranial autonomic reflex with respect to conjunctival injection or nasal congestion.

[The role of vegetative tone in the pregnant women in the development of vasomotor rhinitis].

The objective of the present study was to evaluate the state of the vegetative nervous system in pregnant women both healthy and presenting with vasomotor rhinitis. The initial vegetative tone was determined based on the table for its instant diagnostics. The state of the vegetative nervous system was assessed in 116 pregnant women with vasomotor rhinitis (29 in the first trimester, 33 in the second trimester, and 54 in the third trimester) and in 48 healthy pregnant women (21 in the first trimester, 14 in the second trimester, and 13 in the third trimester). It was shown that the prevailing activity of the parasympathetic component of the vegetative nervous system appears to be the leading risk factor responsible for the development of vasomotor rhinitis in pregnant women in I, II, and III trimesters. It accounts for the occurrence of this disease in 85.2% of the women during the first trimester, in 72.7% and 70.4% during the second and third trimesters respectively).

Chapter 6: Nonallergic rhinitis.

Nonallergic rhinitis represents a non-IgE-mediated group of disorders that share the symptoms of nasal congestion, rhinorrhea, sneezing, and/or postnasal discharge but not pruritus that characterizes allergic rhinitis. Nonallergic rhinitis may be divided into two broad categories, inflammatory and noninflammatory etiologies. The inflammatory causes include postinfectious (viral and bacterial), rhinitis associated with nasal polyps, and nonallergic rhinitis with eosinophilia, where eosinophils are present in nasal smears but skin testing for aeroallergens is negative. The noninflammatory causes include idiopathic nonallergic rhinitis (formerly referred to as vasomotor rhinitis or colloquially as an "overreactive nose"); rhinitis medicamentosa, which is medication-induced rhinitis; hormone related (pregnancy); systemic disease related (severe hypothyroidism); and structural defect related (deviated septum, head trauma causing cerebrospinal fluid rhinorrhea). The classic symptoms of idiopathic nonallergic rhinitis are nasal congestion, postnasal drip, and sneezing triggered by irritant odors, perfumes, wine, and weather changes. The diagnosis of rhinitis begins with a directed history and physical exam. Examination of the nasal cavity with attention to appearance of the septum and inferior turbinates is recommended. Skin testing for seasonal and perennial aeroallergens is helpful in establishing the presence or absence of IgE antibodies and to help differentiate nonallergic from allergic rhinitis. Topical H(1)-receptor antagonist (antihistamine) nasal sprays, intranasal steroids, intranasal anticholinergics, and oral decongestants are options for pharmacotherapy. It is important to inquire about hypertension, arrhythmias, insomnia, prostate hypertrophy, or glaucoma to prevent undesirable side effects associated with the oral decongestant pseudoephedrine.

Sphenopalatine artery ligation with nerve resection in patients with vasomotor rhinitis and polyposis: a prospective, randomized, double-blind investigation.

CONCLUSIONS: Sphenopalatine artery ligation relieves symptoms of rhinorrhea, sneezing, and nasal itching in patients with vasomotor rhinitis associated with nasal polyps. OBJECTIVES: Nasal polyps often arise in a setting of vasomotor rhinitis. Dysfunctions in nerve fiber activity of the sympathetic and parasympathetic systems are responsible for the accompanying symptoms of rhinorrhea, sneezing, and nasal itching. Sphenopalatine pedicle resection with autonomic denervation could potentially reduce related symptoms. METHODS: In a prospective, double-blind setting, 60 patients with vasomotor rhinitis and bilateral nasal polyps randomly assigned to functional endoscopic surgery either with (group A) or without (group B) sphenopalatine artery ligation completed a 3-year follow-up. Preoperative and postoperative (at 1 and 3 years) evaluations included symptom score, fiberendoscopy, and active anterior rhinomanometry. RESULTS: In both treatment groups nasal breathing had improved at 1-year and 3-year follow-up (p < 0.001), whereas an improvement in rhinorrhea (p < 0.001) and sneezing and itching (p < 0.01) was attained only in group A. The inter-group comparison showed that a statistically significant improvement in rhinorrhea and nasal itching (p = 0.002) and in sneezing (p < 0.001) was present in group A at both follow-up visits. Rhinomanometry improved in both treatment groups (p < 0.01). Inter-group comparison showed a significant difference only at the 3-year follow-up visit (p < 0.05).

Nonallergic rhinitis.

This article reviews a uniform way to describe nonallergic rhinitis in its various forms. The insights into its pathophysiology are briefly reviewed. A classification scheme for the different forms is provided. This is followed by descriptions of the diagnosis, evaluation, and management of nonallergic rhinitis.

Traumatic unilateral vasomotor rhinitis.

Vasomotor rhinitis (VMR) is a commonly encountered entity that may be difficult to diagnose. The classic symptoms are clear rhinorrhea and nasal congestion, commonly brought on by exercise, stress, heat, cold, and environmental irritants. The diagnosis is one of exclusion, and management usually involves avoidance of inciting agents and treatment with an anticholinergic nasal spray. We describe a case of VMR in a 22-year-old woman who presented with symptoms of clear, left-sided rhinorrhea and epiphora that had begun shortly after a motor vehicle accident approximately 1.5 years earlier, but which she had not reported at that time. The patient's left carotid canal had been fractured and the surrounding sympathetic plexus injured in the accident, resulting in an overactive parasympathetic system. Both exercise and heat exacerbated her symptoms. Allergy was excluded by negative allergy testing, and the patient did not respond to fluticasone nasal spray. Given the mechanism of injury, the unilaterality of symptoms, and the patient's lack of response to nasal steroids, it was thought that the VMR was due to the earlier traumatic injury, which had resulted in imbalance of the autonomic neural input. A trial of ipratropium was given to directly treat the parasympathetic overactivity. This treatment resulted in immediate improvement in both the nasal and lacrimal secretions.

Weather/temperature-sensitive vasomotor rhinitis may be refractory to intranasal corticosteroid treatment.

Vasomotor rhinitis (VMR) is a common but poorly understood disorder of which there are two major subgroups: VMR(w/t), triggered by weather/temperature and VMR(ir), triggered by airborne irritants. No specific biological pathways or specific treatments for VMR(w/t) or VMR(ir) have been identified. However, intranasal corticosteroids (INSs) are effective in treating many forms of nonallergic rhinitis that include these conditions. A recently introduced INS with established efficacy in allergic rhinitis and enhanced affinity, fluticasone furoate, may possess the potency and safety profile required to treat chronic VMR(w/t). Two replicate studies (FFR30006 and FFR30007) were conducted in six countries to evaluate the efficacy and safety of fluticasone furoate nasal spray in subjects with VMR(w/t). After a 7- to 14-day screening period, subjects (n = 699) with symptomatic VMR(w/t) received fluticasone furoate, 110 mug q.d. or placebo for 4 weeks in these two randomized, double-blind, parallel-group studies. Subjects rated their nasal symptoms (congestion, rhinorrhea, and postnasal drip) twice daily on a 4-point categorical scale and evaluated their overall response to treatment at study end. Fluticasone furoate did not significantly improve daily reflective total nasal symptom scores, the primary end point, versus placebo (p = 0.259) and there was no improvement in any other measure of efficacy. The active treatment was well tolerated. Fluticasone furoate was not effective in treating subjects with a newly defined condition, weather-sensitive VMR. These unexpected results suggest that VMR(w/t) is a distinct subgroup of VMR that is refractory to treatment with INSs. Additional study of other treatments for VMR(w/t) (including INSs) is warranted.

Vasomotor rhinitis update.

PURPOSE OF REVIEW: This review was conducted to examine new data on vasomotor rhinitis, a common clinical problem. RECENT FINDINGS: Recent publications highlight advances in the study of the pathophysiology of vasomotor rhinitis. Electron microscopic and ultracytochemical evaluation of the nasal mucosa in vasomotor rhinitis demonstrates an emerging role of neuropeptides and nitric oxide in the pathogenesis of vasomotor rhinitis. Ozone, cigarette smoke, and other environmental factors may trigger neurogenic mechanisms that lead to vasomotor rhinitis. Objective tests have documented the presence of hypoactive sympathetic autonomic dysfunction. Such assessments also suggest autonomic dysfunction as a possible link between vasomotor rhinitis and gastroesophageal reflux disease. Recent publications propose nasal secretory protein analysis as a possible diagnostic tool. Evidence-based review of treatment outcomes shows topical sprays of azelastine, budesonide, and ipratropium to be of benefit in vasomotor rhinitis. SUMMARY: A better understanding of the role of nitric oxide and neuropeptides in the pathogenesis of vasomotor rhinitis has opened new avenues in research, diagnosis, and management. Clinical diagnosis may be aided by the analysis of nasal secretory proteins. Effective treatments include antihistamine, anticholinergics, and steroid nasal sprays.

Mechanisms of vasomotor rhinitis.

Nonallergic non-infectious perennial rhinitis (NANIPER) is a heterogeneous disorder comprising several pathophysiological entities. The etiology of some of these disorders (e.g. drug-induced rhinitis, nonallergic rhinitis with eosinophilia syndrome [NARES], occupational rhinitis, hormonal rhinitis, emotion-induced rhinitis, physical/chemical irritant-induced rhinitis) is well established. In contrast, the aetiology of idiopathic forms of rhinitis (also known as vasomotor rhinitis) is largely unknown. Mechanistic studies have suggested that non-IgE-mediated inflammatory and/or neurogenic processes may be involved. There is evidence that localized inflammation is the underlying cause of symptoms in drug-induced rhinitis and NARES, since eosinophilia is an important pathophysiological component in these conditions. In contrast, neurogenic reflex mechanisms initiated by environmental factors appear to be involved in idiopathic rhinitis. It has been suggested that there may be an imbalance of the sympathetic and parasympathetic nervous systems, with parasympathetic hyper-activity and sympathetic hypo-activity resulting in nasal congestion and rhinorrhoea. Indirect evidence suggests that C-fibres may also play an important role in the pathophysiology of idiopathic rhinitis.

Intrapharyngeal distribution of gastric acid refluxate.

OBJECTIVES/HYPOTHESIS: Determination of intrapharyngeal distribution of gastric acid refluxate is needed to better understand the pathogenesis of reflux-attributed aerodigestive tract disorders. The aims of the study were to determine intrapharyngeal distribution of gastric acid refluxate and to determine whether this distribution can better differentiate patients from control subjects compared with data obtained from a single hypopharyngeal site. METHODS: We prospectively studied 10 healthy volunteers, 12 patients with reflux laryngitis, and 15 patients with vasomotor rhinitis using a concurrent dual pharyngeal/dual esophageal pH recording technique. We determined the hypopharyngeal and oropharyngeal pH profile, including number, duration, and distribution of reflux events irrespective of and in correlation with intraesophageal pH profile using four different pH thresholds. RESULTS: Few drops in pharyngeal pH were found to be true reflux events based on their correlation with esophageal pH events. For the pharyngeal pH threshold criterion of a drop to 4.0 or less, 6 of 12 patients with reflux laryngitis, 5 of 15 patients with vasomotor rhinitis, and 2 of 10 normal control subjects exhibited a total of 25 (range, 1-5) distal pharyngeal acid reflux events. Overall, 34% of these events reached the oropharyngeal pH recording site. Between-group comparison for all levels of pH threshold criteria did not show any significant difference of reflux parameters in the hypopharyngeal or in the oropharyngeal sites among the studied groups. CONCLUSIONS: Reflux of gastric acid into the pharynx may extend to the region of the oropharynx in both patients and control subjects. Overall distribution of acid refluxate to the oropharynx is low but as groups is similar between healthy individuals and patients with reflux laryngitis and those with vasomotor rhinitis. Parameters of oropharyngeal acid reflux such as number and duration do not differentiate patients from control subjects.

Autonomic dysfunction, vasomotor rhinitis, and extraesophageal manifestations of gastroesophageal reflux.

OBJECTIVE: Several recent reports suggest there may be a relationship between chronic rhinitis and extraesophageal manifestations of gastroesophageal reflux (EER). It is hypothesized that this relationship is a result of autonomic nervous system (ANS) dysfunction. STUDY DESIGN: Patients with isolated vasomotor rhinitis (VR), both VR and EER, and a control group were studied by a battery of tests designed to objectively evaluate ANS function. In addition all 3 groups underwent barium esophagogram and 4-site (proximal pharynx, distal pharynx, proximal esophagus, and distal esophagus) ambulatory pH monitoring. Adult patients fulfilling diagnostic criteria for VR, and with both VR and EER underwent objective ANS testing in a recently developed ANS testing laboratory. The control group consisted of age- and sex-matched adults without diagnostic criteria for VR or EER. RESULTS: In patients with VR only (n = 9), 2 patients had a positive esophagogram, whereas a positive pharyngeal reflux probe was found in 1 and an abnormal composite autonomic scoring scale (CASS) was found in 8 (mean VR CASS = 1.750 vs control CASS 0.556, P =.02). The group with VR and EER (n = 12) had a positive esophagogram in 10 patients, positive pharyngeal reflux by probe in 9, and all 12 had an abnormal CASS (mean CASS VR/EER = 2.909 vs CASS control = 0.556, P =.001 and vs VR CASS = 1.750, P =.05). The control patients (n = 9) had normal transesophageal gastroduodenoscopy in 8, 1 had a positive pharyngeal probe study, and all 9 had a normal CASS. In addition ANS testing in patients with diagnostic criteria for both VR/EER revealed statistically significant evidence of an adrenergic deficit as compared with control patients on the basis of mean phase II blood pressure response to Valsalva maneuver (mean phase II VR/EER = -16.730 vs control = -7.780, P =.05). In the VR only group, the phase II blood pressure decrease was greater than in control patients, but did not reach statistical significance (mean phase II VR = -9.370 vs control = -7.780, P = 0.672). CONCLUSION: Patients with VR and VR/EER have objective evidence of ANS dysfunction when compared with a group of age- and sex-matched control patients. Patients with both VR/EER demonstrate a significantly greater degree of ANS dysfunction than patients with isolated VR. The mechanism by which VR and EER interact is not entirely clear, but ANS dysfunction is objectively associated with both disorders. In addition, patients with VR/EER seem to demonstrate hypofunction of the adrenergic component of the ANS, in contrast to the generally held hypothesis that VR results from increased cholinergic activity. Further characterization of the type of ANS abnormality may allow the development of novel pharmacologic therapies for these disorders.

Autonomic nervous system evaluation of patients with vasomotor rhinitis.

OBJECTIVE: To demonstrate the utility of quantitative neurological laboratory testing of autonomic nervous system dysfunction and to apply this methodology to further study the relation of chronic vasomotor (nonallergic) rhinitis to the autonomic nervous system. METHODS: It has been suspected that vasomotor rhinitis is due either to a hyperactive parasympathetic nervous system or an imbalance between it and the sympathetic nervous system. The exact relation has not been determined. Recently neurological laboratories have been developed in which a battery of tests can be performed to determine reactivity of the autonomic nervous system. RESULTS: Autonomic nervous system testing was performed on 19 patients with symptoms fulfilling the diagnostic criteria for vasomotor rhinitis and the results were compared with 75 sex- and age-matched control subjects. Patients with vasomotor rhinitis had significant abnormalities of their sudomotor, cardiovagal, and adrenergic subscores. Their composite autonomic scale score was significantly impaired at 2.43, as compared with 0.11 for controls (P < .005). CONCLUSION: Autonomic nervous system dysfunction is significant in patients with vasomotor rhinitis. Possible factors that trigger this dysfunction including nasal trauma and extraesophageal manifestations of gastroesophageal reflux are discussed.

[Vasomotor rhinitis following endoscopic sinus surgery: 5 cases report].

OBJECTIVE: To investigate the possibility of endoscopic sinus surgery causing vasomotor rhinitis. METHOD: A retrospective study of 300 patients who received endoscopic sinus surgery. 5 cases out of 300 suffered from vasomotor rhinitis 1-3 weeks following endoscopic sinus surgery. Radio frequency cautery of agger nasi mucous was applied to all 5 patients. RESULT: After 4-6 months of follow-up, 4 cases out of 5 with vasomotor rhinitis were effective and 1 improved. CONCLUSION: Endoscopic sinus surgery may be causative factor for vasomotor rhinitis.

Vasomotor rhinitis following trauma to the nose.

Complaints of nasal obstruction following nasal trauma without any deformation have been noticed by rhinologists for many years. However, neither an epidemiologic nor a pathophysiologic connection has ever been established. The complaints and physical examination findings of these patients resemble those of vasomotor rhinitis. Only very few articles suggesting nasal trauma as a possible cause for vasomotor rhinitis have ever been published. We present a retrospective study that found 87 of 802 patients to suffer from vasomotor rhinitis following nasal trauma. No other factors known to cause vasomotor rhinitis were present in these patients. None had any previous nasal problems. We therefore suggest that nasal trauma was the causative factor in their vasomotor rhinitis.

The differential diagnosis of rhinorrhea.

Rhinorrhea disrupts the quality of life of a large segment of the population. The first step to treating it properly is to make an accurate diagnosis of its underlying cause. This is not always a simple proposition, however, because rhinorrhea has many causes that can easily be confused in clinical practice. Diagnosis has come to rely increasingly on testing, but test costs add significantly to the health-care burden. This article reviews the use of medical logic in the differential diagnosis of rhinorrhea and describes the relative usefulness of various testing methods.