Cybermedlife - Therapeutic Actions Humming

Strong humming for one hour daily to terminate chronic rhinosinusitis in four days: a case report and hypothesis for action by stimulation of endogenous nasal nitric oxide production.

Abstract Title: Strong humming for one hour daily to terminate chronic rhinosinusitis in four days: a case report and hypothesis for action by stimulation of endogenous nasal nitric oxide production. Abstract Source: Med Hypotheses. 2006;66(4):851-4. Epub 2006 Jan 10. PMID: 16406689 Abstract Author(s): George A Eby Abstract: Rhinosinusitis is an inflammation or infection of the nose and air pockets (sinuses) above, below and between the eyes which connect with the back of the nose through tiny openings (ostia). Rhinosinusitis can be caused by bacteria, viruses, fungi (molds) and possibly by allergies. Chronic rhinosinusitis (CRS) is an immune disorder caused by fungi. The immune response produced by eosinophils causes the fungi to be attacked, which leads to damage of the sinus membranes, resulting in full-blown rhinosinusitis symptoms. Gaseous nitric oxide (NO) is naturally released in the human respiratory tract. The major part of NO found in exhaled air originates in the nasal airways, although significant production of NO also takes place in the paranasal sinuses. Proper ventilation is essential for maintenance of sinus integrity, and blockage of the ostium is a central event in pathogenesis of sinusitis. Concentrations of NO in the healthy sinuses are high. Nasal NO is known to be increased 15- to 20-fold by humming compared with quiet exhalation. NO is known to be broadly antifungal, antiviral and antibacterial. This case report shows that a subject hummed strongly at a low pitch ( approximately 130 Hz) for 1h (18 hums per minute) at bedtime the first night, and hummed 60-120 times 4 times a day for the following 4 days as treatment for severe CRS. The humming technique was described as being one that maximally increased intranasal vibrations, but less than that required to produce dizziness. The morning after the first 1-h humming session, the subject awoke with a clear nose and found himself breathing easily through his nose for the first time in over 1 month. During the following 4 days, CRS symptoms slightly reoccurred, but with much less intensity each day. By humming 60-120 times four times per day (with a session at bedtime), CRS symptoms were essentially eliminated in 4 days. Coincidentally, the subject's cardiac arrhythmias (PACs) were greatly lessened. It is hypothesized that strong, prolonged humming increased endogenous nasal NO production, thus eliminating CRS by antifungal means. Article Published Date : Jan 01, 2006
Therapeutic Actions Humming

NCBI pubmed


Related Articles GeneReviews® Book. 1993 Authors: Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, Amemiya A Abstract CLINICAL CHARACTERISTICS: Autosomal dominant epilepsy with auditory features (ADEAF) is a focal epilepsy syndrome with auditory symptoms and/or receptive aphasia as prominent ictal manifestations. The most common auditory symptoms are simple unformed sounds including humming, buzzing, or ringing; less common forms are distortions (e.g., volume changes) or complex sounds (e.g., specific songs or voices). Ictal receptive aphasia consists of a sudden onset of inability to understand language in the absence of general confusion. Less commonly, other ictal symptoms may occur, including sensory symptoms (visual, olfactory, vertiginous, or cephalic) or motor, psychic, and autonomic symptoms. Most affected individuals have focal to bilateral tonic-clonic seizures, usually accompanied by "focal aware" and "focal impaired-awareness" seizures, with auditory symptoms as a major focal aware seizure manifestation. Some persons have seizures precipitated by sounds such as a ringing telephone. Age at onset is usually in adolescence or early adulthood (range: age 4-50 years). The clinical course of ADEAF is benign. Seizures are usually well controlled after initiation of medical therapy. DIAGNOSIS/TESTING: The clinical diagnosis of ADEAF is established in a proband with characteristic clinical features, normal brain imaging (MRI or CT), and family history consistent with autosomal dominant inheritance. Identification of a heterozygous pathogenic variant in LGI1, MICAL1, or RELN by molecular genetic testing establishes the diagnosis if other findings are inconclusive. MANAGEMENT: Treatment of manifestations: Seizure control is usually readily achieved with antiepileptic drugs used routinely in clinical practice (including but not limited to carbamazepine, phenytoin, valproate, and levetiracetam). Evaluation of relatives at risk: Interviewing relatives at risk to identify those with suggestive findings may enable early treatment in those who develop seizures. GENETIC COUNSELING: ADEAF is inherited in an autosomal dominant manner. Most individuals with ADEAF have an affected parent; the proportion of cases caused by a de novo pathogenic variant is believed to be very low. Each child of an individual with ADEAF has a 50% chance of inheriting the pathogenic variant. The chance that the offspring who inherits the pathogenic variant will manifest ADEAF is between 55% and 78%, depending on the penetrance. While prenatal diagnosis for pregnancies at increased risk and preimplantation genetic diagnosis are possible if the pathogenic variant in the family is known, prenatal testing and preimplantation genetic diagnosis are rarely requested for conditions that (like ADEAF) do not affect intellect and are usually easily treated. PMID: 20301709
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