title: Bronchial epilepsy or broncho-pulmonary hyper-excitability as a model of asthma pathogenesis.
abstract: Over the last 20 years, the prevalence of asthma has nearly doubled in industrialized countries. A similar increase has been predicted for the next two decades. Asthma is major illness in terms of morbidity and suffering, asthma is the leading cause of hospitalizations in children under 15 years of age. According to many top experts, asthma is correctly characterized as a syndrome rather than disease. This lack of definition for asthma makes the search for a cause, prevention and potential cure elusive. Episodic airway obstruction and reversible bronchial hyperresponsiveness to non-specific irritants are the major symptoms of asthma. Airway inflammation is now widely accepted as the key factor underlying the pathogenesis of asthma. However, many patients show no signs of inflammation, yet they still have severe airflow limitation and asthma symptoms. The primary clinical symptoms of asthma are attacks of shortness of breath, wheezing, and coughing resulting from excessive and inappropriate constriction of the airway smooth muscle. Our research suggests a possible epileptic or hyper-excitatory condition of bronchial system in asthma pathogenesis. The paroxysmal, spasmodic character of asthma attacks may be similar to seizures. We propose a unified pathogenetic mechanism of asthma as a syndrome of inducible or genetically predisposed membrane hyper-excitability (bronchial epilepsy).
authors.affiliation: Allergy Research Group, Immunology Research, 4010 Moorpark Avenue, Ste 119, San Jose, CA 95117, USA.
authors.forename: Ba X
authors.initials: BX
authors.lastname: Hoang
authors.forename: Stephen A
authors.initials: SA
authors.lastname: Levine
authors.forename: D
authors.initials: D
authors.lastname: Graeme Shaw
authors.forename: Phuong
authors.initials: P
authors.lastname: Pham
authors.forename: Cuong
authors.initials: C
authors.lastname: Hoang
mesh_terms: D000402:Airway Obstruction / Q000150:complications* / Q000175:diagnosis; D001249:Asthma / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D001980:Bronchi / Q000473:pathology*; D016535:Bronchial Hyperreactivity / Q000150:complications*; D002462:Cell Membrane / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D006985:Hyperventilation / Q000150:complications; D008012:Lidocaine / Q000627:therapeutic use; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D008954:Models, Biological; D018377:Neurotransmitter Agents / Q000502:physiology; D010672:Phenytoin / Q000627:therapeutic use; D012120:Respiration Disorders / Q000150:complications* / Q000175:diagnosis; D015222:Sodium Channels / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D018377:Neurotransmitter Agents; D015222:Sodium Channels; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D010672:Phenytoin; D008012:Lidocaine