Help For Hearing Loss Sufferers

Hearing Sense Recovery

This product was created by Mark after he had gone through an experienceof getting his wife's hearing back. He was contacted by one of the most brilliant researchers on the topic of getting one's hearing back and he was able to conduct a research with him in the African tribes in Kenya, the superfoods they have used have made them become the country with the least hearing loss in the world. They have made an experiment on Mark's wife who was able to get her hearing back in merely three weeks. After that, Mark has decided to put the information out to the world so they can help their hearing and the hearing of their loved ones to finally experience life as it truly should. He put the information into an easy step by step guide that walks you through every single phase you have to go through to improve the hearing. The method is very easy to attain and it does not need any technical knowledge, you can easily get this product and you will be able to get your hearing back in just three weeks. The method that is used is also natural and safe and it definitely works no matter how bad the hearing condition is, it will heal and strengthen the cells responsible for hearing. More here...

Hearing Sense Recovery Summary


4.7 stars out of 12 votes

Contents: Ebook
Author: Mark Allen
Official Website:
Price: $39.00

Access Now

My Hearing Sense Recovery Review

Highly Recommended

I've really worked on the chapters in this ebook and can only say that if you put in the time you will never revert back to your old methods.

Overall my first impression of this ebook is good. I think it was sincerely written and looks to be very helpful.

Improve Your Hearing Naturally

What You'll Find Inside Improve Your Hearing Naturally: What Supplements Vitamins and Herbs You Need To Be Taking Right Now To Stop Hearing Loss, Restore Your Hearing and Open Up Those Muffled Ears . In Fact If You Missing These Nutrients In Your Diet Your Hearing Will Continue To Decline. How To Unblock And Clean Out Years Of Built Up Toxins From Your Ears and Ear Canals Instantly Improving Your Hearing! No More Muffled Hearing, How Would You Like To Hear Out Of Both Ears Equally? - Most People Are Completely Shocked When They See What Comes Out Of Their Ear Canals. Learn The Best Natural Home Remedies For Ear Infections, Ear Blockage, Ear Aches, Ringing In The Ears (Tinnitus) And Other Ear Problems - Plus How To Properly Clean Your Ears, Safely With No Risk Of Damage. Discover What Common Drugs Every Home Has In Their Medicine Cabinet You May Be Taking That Can Permanently Damage Your Hearing - Doctors Don't Tell You This And You Need To STOP Immediately

Improve Your Hearing Naturally Summary

Official Website:

Tiziana Lazzarotto Maria Paola Landini

Purpura, hepatomegaly, splenomegaly, pneumonia and encephalitis. Mild clinical manifestations usually include liver problems with hepatosplenomegaly (60 of cases) and thrombocytopenia (53-77 of cases), and around half the babies present delayed intrauterine growth with low birth weight (Ramsay et al., 1991 Boppana et al., 1992). Structural abnormalities mainly affect the central nervous system (ventriculomegaly, intracranial calcifications and cerebral atrophy), whereas other organs are seldom involved. Associated visual impairment and hearing loss have also been reported and CMV has been implicated in non-immunological hydrops (Inoue et al., 2001). In addition 8-15 of asymptomatic newborns develop long-term sequelae, namely psychomotor delay and hearing loss (Fowler et al., 1997). CMV is the leading non-genetic cause of deafness in children more than half the babies born with symptomatic infection and 10 of asymptomatic newborns will develop mild-to-severe neurosensory hearing loss...

Mitochondria Aging and Human Disease

In 1988, Harding and colleagues (44) and Wallace et al. (45) reported the first mitochondrial mutations causing human disease. Since then, many other mi-tochondrial diseases caused by mitochondrial point mutations or multiple mito-chondrial deletions have been identified (46). There are a number of typical presentations of mitochondrial disease in humans, including (1) Kearns-Sayre syndrome, characterized by ptosis, ophthalmoplegia, retinitis pigmentosa, hearing loss, cardiac conduction defects, short stature, and elevated cerebrospinal fluid protein (2) mitochondrial encephalopathy with lactic acidosis and strokes (MELAS) (3) myoclonic epilepsy with ragged red fibers (MERRF) (4) Leber hereditary optic neuropathy (LHON) with sudden unilateral or bilateral painless central visual loss and (5) Leigh syndrome, or subacute necrotizing en-cephalomyopathy. The pleiotropic manifestations of mitochondrial disease may include, for example, diabetes mellitus, hearing loss, bone marrow aplasia,...

Other Hereditary Optic Neuropathies

Other heredofamilial optic neuropathies are very uncommon. They are encountered primarily in cases in which additional, and unexpected, deficits develop. Behr's recessive optic atrophy affects young males under 10 years of age, accompanied by mild cognitive impairment, spasticity, ataxia, and muscular hypertonicity. A rare form of reces-sively inherited optic neuropathy is found accompanied by type I diabetes, deafness, and diabetes insipidus (hence DIDMOAD diabetes insipidus, diabetes mellitus, optic atrophy, and deafness - or Wolfram's syndrome). Optic atrophy also commonly develops in conjunction with various forms of spino- or olivocerebellar degenerations, such as Friedreich's ataxia.

Friedreichs Ataxia Clinical Features

Joint position and vibration, and loss of tendon reflexes. During the course of the disease, which averages from 20 to 25 years, optic atrophy, sensorineural hearing impairment, weakness and spasticity in lower extremities, Babinski sign, and dysarthria develop. Characteristic systemic manifestations include skeletal anomalies with scoliosis and pes cavus, hypertrophic cardiomyop-athy, and occasional diabetes mellitus. FA, an autosomal recessive disease, is caused by an expansion of guanine-adenine-adenine (GAA) repeats in the frataxin gene on chromosome 9. Expansion of the repeats is from 90 to more than 100. The normal number of repeats is 6 to 27.

Risk Of Congenital Infection

For infants with congenital infection, the risk of congenital anomalies is also closely associated with the gestational age of the fetus at the time of maternal infection. The risk for defects in neonates infected during the first trimester of pregnancy is very high. As many as 85 of neonates of mothers with infection during the first 4 weeks of gestation have congenital anomalies, but the risk falls to 20-30 during the second month of gestation and 5 during the third month (13). Infection after the 16th week of gestation rarely results in congenital defects in the infant that are detectable at birth (3). A number of abnormalities may not be present or not detected at birth but can present months to years later (10). These include deafness, ocular abnormalities, endocrinopa-thies, and central nervous system disease.

Differential Diagnosis

These disorders are distinguished from each other by the presence or absence of receptive problems. Children with autism may have any or all of the characteristics of the language disorders. However, they have many additional problems including the use of language in a restricted and often stereotypic fashion rather than for communicative purposes. They also have difficulties with a wider range of interactions with persons and objects in their environment, and exhibit a restricted range of behaviors. The language impairments of mental retardation, oral-motor deficits, or environmental deprivation are not diagnosed in this category unless they are well in excess of what is expected. Language impairment due to environmental deprivation tends to improve dramatically with environmental improvement. Sensory deficits, especially hearing impairment, may restrict language development. Any indication of potential hearing impairment, no matter how tenuous, should prompt a referral for an...

Stellate Ganglion Block

Stellate ganglion blocks have been used for the treatment of many conditions, from hay fever, angina, headache, deafness and vasospasm in peripheral vessels to persistent pain in the upper limb. There is no evidence to support the long- term use of stellate ganglion block with local anesthetics in upper limb pain In skilled hands it is a safe procedure, but the side effects can be significant and the patient should be warned regarding the potential for rare but serious or catastrophic consequences 32 .

Childhood Juvenile and Adult Adrenoleukodystrophies

Childhood, juvenile, and adult adrenoleukodystrophies are characterized by mental regression progressing to dementia, motor disorders, visual and sensorineuronal hearing loss, and seizures culminating in a terminal vegetative state. Death occurs 2 to 3 years after onset in childhood cases. The clinical course is longer in juvenile and adult cases.

Adult Refsums Disease

This disease presents in adulthood, but earlier onsets are not uncommon. Cardinal clinical features are slowly progressive sensorimotor neuropathy, retinitis pigmentosa, optic atrophy, ichthyosis of the skin and, later in the course, cerebellar ataxia. Additional features are cardiomyopathy, anosmia, and neuronal hearing impairment. Skeletal anomalies and cutaneous changes may occur.

Multiple Sulfatase Deficiency MSD

The disease affects neonates, infants, and juveniles. Coarse facial features and skeletal anomalies resembling mucopolysaccharidosis, corneal opacity, deafness, and mental retardation are characteristic clinical features. The pathology combines the features of metachromatic leukodystrophy with those of mucopolysaccharidosis.

Otoacoustic Emissions or Ear Sounds

Did you know that your ear not only hears but also produces sound These sounds are called otoacoustic emissions. They were accidentally discovered in 1978 by David Kemp, who was trying to build an improved tiny microphone to measure how much sound bounces off an eardrum. Using a signal averaging technique, he identified a new auditory phenomenon in the acoustic impulse response of the human ear. Kemp found that when a brief sound, such as a click, is presented to the ear, a very weak sound similar in form is emitted by the ear after a slight delay (about of 5 ms). The slowly decaying response component was present in all normal ears tested, but was not present in ears with cochlear deafness. Therefore, the otoacoustic emissions are thought to be sounds produced by healthy ears in response to acoustic stimulation. Although Kemp's observations were greeted with skepticism, the otoacoustic emissions have since been reliably confirmed. The otoacoustic emissions by the cochlea and the...

What Is a Cochlear Implant

A cochlear implant is an electronic device designed to provide sound information for adults and children who have a sensorineural hearing loss in both ears and obtain limited benefit from appropriate binaural hearing aids. The first research on cochlear implants was conducted in France over thirty years ago. Since then, cochlear implant technology has evolved from a device with a single electrode (or channel) to systems that transmit more sound information through multiple electrodes (or channels). Those who used the cochlear implants confirm that the implants restored the hearing to a practically full extent, except in those who were born deaf. By now more than 15,000 people worldwide have received cochlear implants.

Myoclonus Epilepsy with Ragged Red Fibers

Myoclonus epilepsy with ragged red fibers (MERRF) affects children and adults. Cardinal clinical manifestations include short stature, seizures, polymyoclonus, optic atrophy, sensory-neuronal hearing loss, cerebellar ataxia, peripheral neuropathy, and myopathy. The disease is maternally transmitted and is associated with point mutations in tRNA gene.

Lafora Disease with Myoclonic Epilepsy

Lafora disease with myoclonic epilepsy, a rare autosomal recessive disorder of juveniles, is caused by mutations in the gene EPM2A, located on chromosome 6. The disease presents with tonic-clonic seizures, widespread stimulus-induced myoclonic jerks, hearing impairment, ataxia, and mental regression. Over several years, the disease progresses to total disability. Death usually occurs in the third decade of life.

It is apparent that spoken language development occurs spontaneously in the presence of normal hearing from birth given

That occurs with prelingual hearing loss. Before hearing aids were widely available, deaf children missed many of the speech sounds that occurred in everyday life, and teaching them to use and understand spoken language relied largely on visual, kinesthetic and tactile cues. The advent of the wearable electronic hearing aid more than 50 years ago had a dramatic effect on the spoken language development of these children. Teachers soon realized that more normal speech development could be encouraged in deaf children by maximizing use of their limited residual hearing 1, 2 . This auditory approach, combined with an emphasis on early intervention, formed the basis for auditory-oral education of deaf children, as we know it today. New developments in hearing aids and ear molds permitted even severely hard of hearing children to detect most speech sounds, including the low intensity, high frequency sounds of speech, such as the s and t . When hearing aids were fitted early in life, and...

Psychotic Disorder Due to a General Medical Condition

That do not necessarily cause dementia (multi-infarct disease) are associated with late-life onset of schizophrenia. Whether this syndrome should be thought of as a psychotic disorder secondary to a general medical condition or as late-onset schizophrenia cannot be determined from the available data. Some specific delusion-like false beliefs also have been observed in patients with damage to the occipital lobe (denial of blindness) and parietal lobe (denial of hemipare-sis). Blindness and deafness have been associated with visual and auditory hallucinations, and complex partial seizures have been associated with olfactory hallucinations and delusions. Psychosis has been reported as a consequence of vitamin B12 deficiency, meningioma, and antiretroviral therapy. Alcoholic hallucinosis is a specific syndrome that occurs within 2-3 days after termination of drinking. In this syndrome, frightening auditory or visual, sometimes tactile, hallucinations occur in an otherwise clear sensorium...

ADA Deficiency and Other Forms of SCID Caused by Defects in Nucleotide Metabolism

The most common cause of autosomal recessive SCID is deficiency of an enzyme called adenosine deaminase (ADA) due to mutations in the ADA gene. ADA functions in the salvage pathway of purine synthesis and catalyzes the irreversible deamination of adenosine and 2'-deoxy-adenosine to inosine and 2'-deoxyinosine, respectively. Deficiency of the enzyme leads to the accumulation of deoxyadenosine and its precursors S-adenosyl-homocysteine and deoxyadenosine triphosphate (dATP). These byproducts have many toxic effects, including inhibition of DNA synthesis. Although ADA is present in most cells, developing lymphocytes are less efficient than most other cell types at degrading dATP into 2'-deoxy-adenosine, and therefore lymphocyte maturation is particularly sensitive to ADA deficiency. Other features of the disease can include deafness, costochondral abnormalities, liver damage, and behavioral problems. ADA deficiency leads to reduced numbers of B and T cells lymphocyte cell numbers are...

Mitochondrial Inheritance

Mitochondria are the only organelles of the cell besides the nucleus that contain their own DNA. They also have their own machinery for synthesising RNA and proteins. Instead of individual chromosomes, mitochondria contain circular DNA similar to bacteria (from which they are thought to be derived). Mitochondrial DNA contains 37 genes,predominately encoding the enzymes necessary for the respiratory chain. All mitochondria in the zygote are derived from the ovum therefore, a mother carrying a mitochondrial DNA mutation will pass it on to all of her children (maternal inheritance) but only her daughters will pass it on to their children. Mito-chondrial DNA mutations are usually manifest clinically in tissues with a high metabolic demand, for example brain, nerve, retina, muscle and renal tubule. Examples of ophthalmic diseases caused by mitochondrial DNA mutations include Leber's hereditary optic neuropathy, chronic progressive external ophthal-moplegia, maternally inherited diabetes...

Agnogenic Myeloid Metaplasia Ammmyelofibrosis With Myeloid Metaplasia

AMM occurs primarily in older patients. Nearly two thirds of the cases occur between the ages of 50 and 70, about equally in men and in women. Symptoms and signs depend upon the stage of disease when the patient is first encountered. Most often, symptoms are related to anemia and or an enlarged spleen. Otosclerosis, which can be a presenting symptom in advanced cases, causes deafness in about 10 of patients.

Exudative Retinal Detachment

Retinal detachments secondary to inflammatory exudates are not common. One example is Harada's disease, which is the constellation of exudative uveitis with retinal detachment, patchy depigmentation of the skin, meningitis and deafness. Its cause is unknown. Exudative detachments do not require surgery but treatment of the underlying cause.

Aage R Moller

Includes bibliographical references and index. ISBN 3-8055-8157-2 (hard cover alk. paper) 1. Cochlear implants. I. M0ller, Aage R. II. Series. DNLM 1. Auditory Brain Stem Implants. 2. Cochlear Implants. 3. Auditory Brain Stem Implantation. 4. Cochlear Implantation. 5. Hearing Loss-rehabilitation. 6. Hearing Loss-surgery. W1 AD701 v.64 2006 WV 274 C6588 2006 RF305.C59 2006 617.8'82-dc22

Alports syndrome

This syndrome is defined by the association of progressive haematuric nephritis and sensorineural hearing loss. Eye abnormalities (bilateral anterior lenticonus, retinal macular and perimacular flecks, and, occasionally, recurrent corneal erosions) are found in 35 of patients. Alport's syndrome is a disease of type IV collagen, a major component of the basement membranes 8 . In fact, it includes at least two diseases the first is X-linked dominant, due to mutations involving COL4A5, the gene coding for the a5 chain of type IV collagen (a5 IV ). Affected males are hemizygotes and all of them progress to end-stage renal disease, (ESRD). Hearing defects are absent in some families. Carrier females are heterozygous and often have only slight or intermittent microhaematuria. However, 15 of the female heterozygotes progress to renal failure, usually later than males 9 . The second disease is autosomal recessive, due to mutations in the genes encoding a3(IV) or a4(IV). The phenotypic...

Prenatal Diagnosis

In addition, erroneous assumptions about the significance of IgG and IgM antibody levels could lead to provision of incorrect information regarding risk to the fetus. Even when a prenatal diagnosis of congenital CMV infection is accomplished, the only possible clinical recourse involves the decision of whether to terminate the pregnancy. Although CMV is a leading cause of brain disease and hearing loss in the United States, the outcome of congenital CMV infection is highly variable, thus limiting the value of prenatal diagnosis.

Congenital Factors

Many of the cases of congenital cataract seen in ophthalmic practice are inherited. Sometimes there is a dominant family history and there are many other possible associated defects, some of which fit into named syndromes. Acquired congenital cataract can result from maternal rubella infection during the first trimester of pregnancy. The association of deafness, congenital heart lesions and cataract must always be borne in mind. The ophthalmic house surgeon must take special care when examining the congenital cataract case preoperatively and likewise, the paediatric house surgeon must bear in mind that congenital cataracts might be overlooked, especially if they are not severe. Sometimes the cataracts can be slight at birth and gradually progress subsequently, or sometimes they can remain stationary until later years.


This is a crucial part of the evaluation and needs to be done in a systematic and comprehensive and non-threatening manner. The initial aspects have to do with observation as described above in the section on general appearance, manner, andattitude,observingfor level of alertness, consciousness, confusion, fluctuation, somnolence, or stupor. Careful observation may reveal perseveration on words, numbers, or actions. Perseveration may be evident in the absence of hearing impairment when the patient responds to a prior question more than one time as if he or she had not heard the following question. Specific questions as to orientation can be approached in an ego-supportive manner and can be asked as part of the routine. Memory is best tested by observing the patient's ability to provide his or her medical history in an organized manner and asking direct and specific questions about onset, course, and treatments. If a patient spontaneously reveals that memory is a problem, this lead can...

Late effects

Ototoxicity is related to the total dose of cisplatin, is permanent, and occurs in 20-40 of patients. It begins as a high-frequency loss and progresses to involve frequencies in the speech range with continued exposure to the drug. The concurrent exposure to ototoxic environmental factors (e.g., rock concerts, airplanes, jack hammers) by adolescents and young adults may increase their risk of hearing loss. Appropriate anticipatory guidance and monitoring of audiograms may lessen the impact of ototoxicity. The delivery of only three cycles of cisplatin, when appropriate, will decrease the incidence of severe toxicity.


One of the most widely used classes of diuretic drugs, the loop diuretics, markedly inhibit salt reabsorption by the kidney tubules. They are very effective, even in severe kidney failure, even though it may be necessary to increase the dose substantially beyond the usually recommended doses. Fortunately these drugs have very low toxicity. One of the most commonly used drugs of this class is furosemide. It is best given twice a day, because with a single dose there is rebound salt retention in the other 12 hours of the day. Giving it at night probably will increase nocturnal voiding, but this is a price that must be paid. The usual starting dose is 20 to 40 mg twice a day. It can be increased safely to at least 200 mg twice a day in cases of severe kidney failure. Occasionally hearing may become impaired at higher doses. If the drug is stopped, hearing generally returns to normal, but a very small number of patients develop permanent partial or even complete hearing loss. Large doses...


This group of rare lysosomal disorders results from deficiencies of enzymes involved in glycoprotein degradation. Glycoproteins consist of oligosaccharide chains attached to a protein core. Defective degradation of glycoproteins leads to the neurovisceral storage of oli-gosaccharides, glycopeptides, and glycolipids, and the urinary excretion of abnormal oligosaccharides. The group encompasses the mannosidosis, the fucosidoses, aspartyl-glycosaminuria, and Schindler's disease. The diseases affect neonates, infants, and young children, but juvenile and adult forms also occur. The clinical expression, except for the Schindler's disease, resembles that of Hurler's disease psychomotor retardation, facial and skeletal abnormalities, corneal opacity, deafness,


LCMV infection should be considered as a potential etiology of congenital infection in babies with CNS disease (micro- or macrocephaly, hydrocephalus) and chorioretini-tis. The disease most closely resembles congenital toxoplasmosis or CMV infection in babies with the exception that LCMV-infected newborns rarely exhibit hepatosple-nomegaly or hearing loss. Diagnosis of congenital LCMV infection is based on compatible clinical findings, serologic evidence of LCMV infection (IgM and IgG against LCMV), and negative diagnostic studies for other congenital infections (CMV culture, toxoplasmosis serology, syphilis, enterovirus, rubella, and herpes simplex virus).

Kearns Sayre Syndrome

Kearns-Sayre Syndrome (KSS), with onset in adolescence, is distinguished by progressive external ophthal-moplegia, pigmentary retinopathy, sensorineuronal hearing loss, cerebellar ataxia, heart block, mental regression, myopathy, and elevated CSF protein. Neuro-imaging shows white matter hyperintensities on T2-weighted MRI and calcifications in the basal ganglia

Risk Factors

Risk factors for development of VLOSLP include age (the incidence increases by 11 with each 5-year increase in age van Os et al. 1995 ), female gender, and ethnic minority immigrant status. British investigators found that the incidence of VLOSLP was significantly higher in African- and Caribbean-born elders than in indigenous elders (Reeves et al. 2001). Compared with early-onset schizophrenia patients, patients with VLOSLP are less likely to have a family history of schizophrenia, more commonly have sensory deficits (particularly conductive hearing loss), and less commonly have negative symptoms. Rodriguez-Ferrera et al. (2004) and Barak et al. (2002) found that patients with VLOSLP had higher levels of education and were more likely to be married than were members of a comparison group of early-onset schizophrenia patients. Despite the age association, VLOSLP appears to be a stable entity and not merely the harbinger of a progressive dementing condition, as indicated by follow-up...


In congenital syphilis, other possible features occur such as deafness and corneal scarring from previous interstitial keratitis. The scattered pigmentation in the fundus might suggest an inherited retinal degeneration but a careful family history together with electrodiagnostic testing of the eyes usually enables one to distinguish the two conditions. It is also important to

Clinical Aspects

The most frequent and common form of KD is the infantile form, which begins in the first 6 mo of life and rapidly progresses leading to death before the child reaches the age of 2. Children with KD present rapid psychomotor regression, generalized rigidity, and peripheral neuropathy they subsequently develop optic atrophy, deafness, and cachexia. Increased proteins in the cerebrospinal fluid is a constant finding cell count is usually normal. Nerve conduction velocity is always abnormal.

Organic Aciduria

By the second year of life, hypotonia has given way to spas-ticity with tonic extensor spasms. Cortical blindness and optic atrophy develop. Sensorineural hearing loss may be present with developmental malformations of the organ of Corti (116). Macrocephaly is a prominent finding at this stage. The patient may have myoclonic or other seizures and choreoathetosis. Autonomic crises may occur with vomiting, temperature instability and vasomotor disturbances. A vegetative state develops and affected infants generally die in early childhood.

Congenital Cataract

The lens can be partially or completely opaque at birth. Congenital cataract is often inherited and can be seen appearing in a dominant manner together with a number of other congenital abnormalities elsewhere in the body. The condition might also be acquired in utero, the best known example of this being the cataract caused by rubella infection during the first trimester of pregnancy remember the triad of congenital heart disease, cataract and deafness in this respect. Minor degrees of congenital cataract are sometimes seen as an incidental finding in an otherwise normal and symptom-less eye. The nature of the cataract usually helps with the diagnosis. The lens fibres are laid down from the outside of the lens throughout life. If the opaque lens fibres are laid down in utero, this opaque region can remain in the centre of the lens. Only when the cataract is thick does it present as a white appearance in the pupil and often it is difficult to detect it. It is important to examine the...

Cockayne Syndrome

Cockayne syndrome, a rare autosomal recessive disorder, is caused by mutations in either the CSA or CSB gene. The disease manifests with dwarfism microcephaly facial dysmorphism with prognathism, malformed large ears, enophthalmos, and beaked nose long extremities and sensitivity to sunlight. Neurologic abnormalities are mental retardation, sensorineuronal hearing impairment, optic atrophy and pigmentary retinal degeneration, myoclonus, and pyramidal and extrapyramidal symptoms and signs.

Hearing Aids Inside Out

Hearing Aids Inside Out

Have you recently experienced hearing loss? Most probably you need hearing aids, but don't know much about them. To learn everything you need to know about hearing aids, read the eBook, Hearing Aids Inside Out. The book comprises 113 pages of excellent content utterly free of technical jargon, written in simple language, and in a flowing style that can easily be read and understood by all.

Get My Free Ebook