Interstitial cystitis is an extremely painful and distressing condition, characterized by severe suprapubic pain, which increases with bladder filling and is relieved by voiding. The daily frequency of micturition may approach 100 times, but no incontinence is observed. The symptoms persist throughout the night, which consequently affects sleep. The etiology of this condition is still unknown, but includes infection, autoimmune response, allergic reaction, neurogenic inflammation, epithelial dysfunction and inherited susceptibility. Herein, a case of interstitial cystitis, with severe symptoms, which was successfully treated with lumbar sympathetic block, is reported.
Autoimmunity ; Cystitis, Interstitial* ; Hypersensitivity ; Neurogenic Inflammation ; Urinary Bladder ; Urination

There is increasing recognition in medical fields of the importance of behavioral and psychosocial factors in the development of cardiovascular disease. Although the pathogenesis underlying stress-induced atherosclerosis is not well known, inflammation may play a key role. Activation of stress-induced neuroendocrine pathways, such as the hypothalamo-pituitary-adrenal axis, and the sympathetic nervous and renin angiotensin systems, direct neurogenic inflammation may also contribute to the development of stress-induced atherosclerosis.
Atherosclerosis* ; Axis, Cervical Vertebra ; Cardiovascular Diseases ; Inflammation ; Neurogenic Inflammation ; Psychology ; Renin-Angiotensin System

Prostatitis is a common disease that is confusing and frustrating for urologists. Chronic prostatitis/chronic pelvic pain syndrome(CP/CPPS) is the most common form of prostatitis. The etiology of CP/CPPS is unknown, but possibilities include infectious, autoimmune, neurological, endocrine and psychological causes. Clinical evaluation can aid in diagnosis and follow-up of the patient's response to therapy. Treatment for CP/CPPS is empiric and limited by a lack of randomized, placebo- controlled clinical trials. Antimicrobials are commonly used to treat patients with prostatitis. Other commonly used drugs include alpha-adrenoceptor antagonists, anti-inflammatory drugs, tricyclic antidepressants, and anticholinergic agents. Also, minimally invasive procedures are considered in patients with CP/CPPS and It is possible to treat intractable patients with invasive treatment. Although much progress has been made in therapy, there is no distinct treatment for patients with CP/CPPS. If the concept of neurogenic inflammation with pain is solved, it is possible to treat patients with CP/CPPS at future.
Antidepressive Agents, Tricyclic ; Cholinergic Antagonists ; Follow-Up Studies ; Humans ; Neurogenic Inflammation ; Pelvic Pain ; Prostatitis

It is often presumed that apical periodontitis follows total pulp necrosis, and consequently root canal treatment is commonly performed. Periapical lesion development is usually caused by bacteria and its byproduct which irritate pulp, develop pulpitis, and result in necrosis through an irreversible process. Afterwards, apical periodontitis occurs. This phenomenon is observed as an apical radiolucency in radiographic view. However, this unusual case presents a spontaneous healing of periapical lesion, which has developed without pulp necrosis in a vital tooth, through conservative treatment.
Bacteria ; Dental Pulp Cavity ; Dental Pulp Necrosis ; Necrosis ; Neurogenic Inflammation ; Periapical Periodontitis ; Pulpitis ; Tooth

Complex regional pain syndrome (CRPS) is a chronic painful, limb-confined condition with autonomic and inflammatory characteristics. Although the exact cause is still poorly understood, facilitated neurogenic inflammation, pathologic sympathetic-afferent coupling, and maladaptive neuroplasticity of CNS are suggested as major pathophysiology of CRPS. While acute CRPS may resolve with good prognosis, chronic CRPS is likely to continue painful condition, thus it is recommended to start early management with comprehensive, multidisciplinary intervention including physical and occupational therapy. It still lacks of studies regarding CRPS after stroke which applied new diagnostic criteria, although it was established in the year of 2004. Therefore, further researches are needed regarding the CRPS after stroke using new diagnostic criteria.
Chronic Pain ; Neuralgia ; Neurogenic Inflammation ; Neuronal Plasticity ; Occupational Therapy ; Prognosis ; Stroke*

The purpose of this study was to investigate the influence of NK1 receptor antagonists on the pulpal blood flow (PBF) when applied iontophoretically through the dentinal cavity of the teeth in order to understand whether iontophoretically applied NK1 receptor antagonists can control the pulpal inflammation. Eleven cats were anesthetized with alpha-chloralose and urethane, and substance P (SP) was administered to the dental pulp through the catheterized lingual artery in doses that caused PBF change without the influence of systemic blood pressure. NK1 receptor antagonists were applied iontophoretically to the prepared dentinal cavity of ipsilateral canine teeth of the drug administration, and PBF was monitored. Data were analyzed statistically with paired t-test. PBF increase after iontophoretic application of the NK1 receptor antagonists followed by the intra-arterial administration of SP was significantly less than PBF increase after iontophoretic application of the 0.9% saline followed by the intra-arterial administration of SP as a control (p < 0.05). Iontophoretic application of the NK1 receptor antagonists (0.2~3.4 mM) following the intra-arterial administration of SP resulted in less increase of PBF than the iontophoretic application of the 0.9% saline following the intra-arterial administration of SP as a control (p < 0.05). Therefore, the results of the present study provide evidences that the iontophoretic application is an effective method to deliver drugs to the dental pulp, and that iontophoretically applied NK1 receptor antagonists block SP-induced vasodilation effectively. The above results show the possibility that the iontophoretical application of NK1 receptor antagonists can control the neurogenic inflammation in the dental pulp.
Animals ; Arteries ; Blood Pressure ; Catheters ; Cats* ; Chloralose ; Cuspid ; Dental Pulp ; Dentin ; Inflammation ; Iontophoresis ; Neurogenic Inflammation ; Substance P ; Tooth ; Urethane ; Vasodilation

The primary headaches include migraine, tension-type headache(TTH), cluster headache, and other primary headaches. An understanding of the basic pathophysiology facilitates the assessment and management of patients with headache. There have been remarkable advances in the last decade in unraveling the mystery of primary headaches. The vascular theory has been superseded by the neurovascular phenomenon, which seems to be the permissive triggering factor in migraine and cluster headache. Calcitonin gene-related peptide(CGRP) is one of the main neuropetides involved in the neurogenic inflammation, which is important in the generation of migraine. The serotonin also appears to have a pivotal role in some aspects of migraine pathogenesis. Cortical spreading depression(CSD) seems to be an important phenomenon explaining migraine with aura. The brain stem nuclei(raphe and locus coeruleus) and cortical hyperexcitability may well have a important role in generating CSD. These have been achieved through new imaging modalities such as positron emission tomography(PET) and functional magnetic resonance imaging(fMRI). In migraine, the throbbing pain is mediated by the sensitization of the meningeal nociceptor of trigeminovascular neurons. The sustained sensitization of peripheral trigeminal neurons eventually leads to subsequent sensitization of central trigeminovascular neurons, which can be manifested as cutaneous allodynia. TTH and migraine belong to the same physiological spectrum. However, they are genetically most likely multifactorial.
Brain Stem ; Calcitonin ; Cluster Headache ; Electrons ; Headache* ; Humans ; Hyperalgesia ; Migraine Disorders ; Migraine with Aura ; Neurogenic Inflammation ; Neurons ; Nociceptors ; Serotonin

BACKGROUND: There have been many debates about the effects of nitric oxide on the neurogenic inflammation. The role of nitric oxide in the neurogenic inflammation of airways will be required a better understanding of the localization and types of nitirc oxide synthase(NOS) activity in the neurogenic inflammation of airways. METHOD: To investigate the role of nitric oxide in airway neurogenic inflammation, 1) the effects of neurokinin receptor antagonist (FK224) and nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine (L-NNA) on plasma extravastion were evaluated in four groups of Sprague-Dawley rats ; sham operation group(sham NANC group), electrical vagal stimulation group(NANC2 group), intravenous pretreatment groups with FK224 (1mg/kg ; FK224 group), and L-NNA(1mg/kg ; L-NNA group) 15 minutes before vagal NANC stimulation 2) NOS activity in trachea with neurogenic inflammation was localized by immunohistochemical stain. Immunohistochemical stain was performed by antibodies specific for inflammatory cells (iNOS), brain (bNOS), and endothelium (eNOS) on trachea obtained from sham NANC, NANC2, and FK224 groups. RESULTS: The results are that plasma extravsation in neurogenic inflammation of rat airways was inhibited by FK224, but enhanced by L-NNA pretreatment (P<0.05). There was significantly increased infiltration of inflammatory cells in subepithelium of neurogenic inflammatory trachea, but the reduction of subepithelial infiltration of inflammatory cells was observed after pretreatment with FK224 (P<0.05). Immunostaining with anti-iNOS antibody showed strong reactivity only in infiltrated inflammatory cells in neurogenic rat trachea, and these iNOS reactivity was reduced by pretreatment with FK224. bNOS immunoreactivity was significantly increased only in the nerves both of neurogenic inflammatory and FK224 pretreated trachea compared with sham NANC trachea(p<0.05). eNOS immunoreactivity was not significant change in endothelium in neurogenic inflammation of rat trachea. CONCLUSION: These results suggest that nitric oxide released from iNOS in infiltrated inflammatory cells has main role in neurogenic inflammation of rat trachea. The presence of bNOS immunoreactivity in the nerves indicates that nitric oxide may be released from the nerves in rat trachea with neurogenic inflammation.
Animals ; Antibodies ; Brain ; Endothelium ; Neurogenic Inflammation* ; Nitric Oxide Synthase ; Nitric Oxide* ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Trachea

The aims of the study were to evaluate the effect of epinephrine-containing local anesthetics on pulpal blood flow (PBF) and to investigate its effect on cavity preparation-induced PBF change. PBF was recorded using a laser Doppler flowmeter (Perimed Co., Sweden) from canines of nine cats under general anesthesia before and after injection of local anesthetics and after cavity preparation. 2% lidocaine hydrochloride with 1 : 100,000 epinephrine was administered by local infiltration given apical to the mandibular canine at the vestibular area and the same volume of isotonic saline was injected on the contralateral tooth as a control. A round carbide bur was operated at slow speed with isotonic saline flushing to grind spherical cavities with increasing depth through the enamel and into the dentin on both teeth. The obtained data was analyzed with paired t-test. Cavity preparation caused significant increase of PBF (n = 9, p < 0.05). Local infiltration of lidocaine with epinephrine resulted in decreases of PBF (n = 9, p < 0.05), whereas there was no significant change of PBF with the physiologic saline as a control. Cavity preparation on tooth anesthetized with lidocaine with epinephrine caused significantly less increase of PBF than in control tooth (p < 0.05). Therefore, the result of the present study demonstrates that local infiltration of 2% lidocaine with 1 : 100,000 epinephrine effectively reduces PBF increase caused by cavity preparation.
Anesthesia, General ; Anesthesia, Local* ; Anesthetics, Local ; Animals ; Cats ; Dental Enamel ; Dentin ; Epinephrine ; Flowmeters ; Flushing ; Lidocaine ; Neurogenic Inflammation ; Tooth*

It has been suggested that the role of neurogenic inflammation is to protect the airway from various noxious irritants in inhaled air. Repeated exposure to various irritating stimuli has become very common in daily life. However, the process that occurs in neurogenic inflammation after repeated exposure to irritating stimuli is not yet clearly understood. The aim of this study was to investigate the changes of microvascular leakage in the airways after re-exposure to capsaicin in an experiment using a rat model challenged/rechallenged with capsaicin. Twenty-four Sprague-Dawley rats were divided into four groups : a capsaicin-challenged group (10 microgram/kg of capsaicin, intravenous, n=6) and three capsaicin-rechallenged groups (10 microgram/kg of capsaicin, intravenous, n=6 in each group) corresponding to time intervals of 1, 3, or 6 hours after capsaicin-challenge. The amount of microvascular leakage in the nasal mucosa and trachea of the animal in each group was measured with extravasation of Evans blue dye (30 mg/kg, intravenous) using a spectrophotometer. In the nasal mucosa, a significant enhancement of microvascular leakage with capsaicin-rechallenge was observed at 3 hours after capsaicin-challenge (AVOVAR, * : p<0.01). However, there was no significant changes in the trachea. In conclusion, the protective mechanisms against repeated irritating stimuli in the nasal mucosa and trachea are different. After exposure to a noxious irritant, the airway defense mechanism mediated by an axon reflex in the nose may be up- regulated, while that in the trachea may not be changed.
Animals ; Axons ; Capsaicin* ; Evans Blue ; Irritants ; Models, Animal* ; Nasal Mucosa* ; Neurogenic Inflammation ; Nose ; Rats* ; Rats, Sprague-Dawley ; Reflex ; Trachea