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Author: admin | 29.08.2015 | Category: Homeopathic Treatment For Tinnitus

As an overview, low frequency (or tone) sensorineural hearing loss (LF SNHL or LT SNHL) is unusual, and mainly reported in Meniere's disease as well as related conditions such as low CSF pressure. Le Prell et al (2011) suggested that low frequency hearing loss was detected in 2.7% of normal college student's ears. Oishi et al (2010) suggested that about half of patients with LTSNHL developed high or flat hearing loss within 10 years of onset. The new international criteria for Meniere's disease require observation of a low-tone SNHL. Gatland et al (1991) reported fluctuation in hearing at low frequencies with dialysis was common, and suggested there might be treatment induced changes in fluid or electrolyte composition of endolymph (e.g. Although OAE's are generally obliterated in patients with hearing loss > 30 dB, for any mechanism other than neural, this is not always the case in the low-tone SNHL associated with Meniere's disease. The lack of universal correspondence between audios and OAE's in low-tone SNHL in at least some patients with Meniere's, suggests that the mechanism of hearing loss may not always be due to cochlear damage.
Of course, in a different clinical context, one might wonder if the patient with the discrepency between OAE and audiogram might be pretending to have hearing loss. Papers are easy to publish about genetic hearing loss conditions, so the literature is somewhat oversupplied with these. Bespalova et al (2001) reported that low frequency SNHL may be associated with Wolfram syndrome, an autosomal recessive genetic disorder (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness).
Bramhall et al (2008) a reported that "the majority of hereditary LFSNHL is associated with heterozygous mutations in the WFS1 gene (wolframin protein). Eckert et al(2013) suggested that cerebral white matter hyperintensities predict low frequency hearing in older adults.
Fukaya et al (1991) suggested that LFSN can be due to microinfarcts in the brainstem during surgery. Ito et al (1998) suggested that bilateral low-frequency SNHL suggested vertebrobasilar insufficiency.
Yurtsever et al (2015) reported low and mid-frequency hearing loss in a single patient with Susac syndrome.
There are an immense number of reports of LTSNHL after spinal anesthesia and related conditions with low CSF pressure. Fog et al (1990) reported low frequency hearing loss in patients undergoing spinal anesthesia where a larger needle was used. Waisted et al (1991) suggested that LFSNHL after spinal anesthesia was due to low perilymph pressure. Wang et al reported hearing reduction after prostate surgery with spinal anesthesia (1987).
We have encountered a patient, about 50 years old, with a low-tone sensorineural hearing loss that occured in the context of a herpes zoster infection (Ramsay-Hunt). LTSNHL is generally viewed as either a variant of Meniere's disease or a variant of sudden hearing loss, and the same medications are used. INTRODUCTIONEctodermal Dysplasia represents a complex group of pathologies containing over 170 clinical features (1,2), with an incidence of 7 out of 10,000 born-alive children (1). To us, this seems a little overly stringent, compared to the earlier 1995 AAO criteria that just required any kind of hearing loss, but criteria are better than no criteria. That being said, genetic conditions should not be your first thought when you encounter a patient with LTSNHL. One would think that diabetes insipidus is so rare that hearing loss is probably not the main reason these individuals are seeking attention.
These patients are extremely rare because there isn't much microsurgery done close to the brainstem. We are dubious about the conclusion of this paper because it is different than nearly every other paper in the literature. We are dubious that this has any applicability to humans and we have never seen a patient with lithium toxicity with any LFSNHL.
We have observed this occasionally ourselves, but of course, the usual pattern is a conductive hyperacusis.

We find this somewhat plausible as pregnancy and delivery might be associated with spinal anesthesia, with changes in collagen, and with gigantic changes in hormonal status. Ectodermal Dysplasia affects structures coming from the ectodermal, like the skin and its appendages and also affects other nonectodermal structures. There is a large literature about genetic causes, mainly in Wolfram's syndrome ( diabetes insipidus, diabetes mellitus, optic atrophy, and deafness), probably because it is relatively easier to publish articles about genetic problems. He defined LTSNH as that the sum of the three low frequencies (125, 250, 500) was more than 100 dB, and the sum of the 3 high frequencies (2, 4, 8) was less than 60 dB. In other words, Wolfram's is probably not diagnosed mainly by ENT's or audiologists, but rather by renal medicine doctors, as DI is exceedingly rare, while LTSNHL is not so rare in hearing tests.
That being said, it is very rare to encounter any substantial change in hearing after pregnancy. The most common clinical evidences are problems in the skin, hair, teeth, nails and sweat glands. It can be autossomic and X-linked - dominant or recessive and of sporadic transmission (1,2). Roughly speaking, the frequency patterns of hearing loss are divided up into: Low-frequency, mid-frequency, high-frequency, notches, and flat. Objective: Show the association of the early beginning Atrophic Rhinittis to Ectodermal Dysplasia and also other otolaryngological signs and symptoms that are found in Ectodermal Dysplasia in a 10 year-old child. Ectodermal Dysplasia holds clinical alteration which affects structures coming especially from ectoderm, such as skin and its appendages and also affects other non-ectodermal structures (4). Case Report: Patient showing nasal obstruction, crusts, maggots and nasal secretions since he was a new born child and also clinical alterations normally found in Ectodermal Dysplasia.
The most common clinical evidences are problems in the skin, hair, teeth, nails and sweat glands.Atrophic Rhinitis is one the situations related to Ectodermal Dysplasia (3,5-12).
Conclusion: For the fact that Atrofic Rhinittis has so many related complications as infections and for being the Patient?s major complain in the case reported, it has to be attended carefully by the otolaryngologists. Atrophic Rhinitis is a chronic inflammatory disease of the nose, producing crusts (6) due to imperfect movement of the nose hair. Besides being related to Ectodermal Dysplasia, it can be found at granulomatous diseases such as Tuberculosis and Hansen?s disease (5)TARGETTo first report a case of a child who developed Atrophic Rhinitis symptoms at one month year old and also to demonstrate the association of such pathology with Genetic Syndrome of Ectodermal Dysplasia.
Besides, to highlight the importance of Atrophic Rhinitis therapy by ENT doctors due to related complications.
CASE REPORTWe reported a case of a male patient at the age of 7 when he visited the doctor complaining of nasal obstruction and presence of crusts, mucopurulent rhinorrhea, nasal fetidness and breathing difficulties since his first month of life.During pregnancy, his mother reports having had threatened abortion at the third and sixth months. The first prenatal ultrasonography was performed at the seventh month, when hydrocephaly was diagnosed. She had a premature labor by Caeserian (32 to 33 weeks old), and the baby was kept in neonatal ICU for 22 days.
During first week after being delivered from hospital, mother noticed nasal obstruction followed by breathing difficulties with crusts formation, progressive bad smell and mucopurulent rhinorrhea.
Such symptoms remain up to now, and he had suffered 2 episodes of epistaxis so far.From 6 month years old, patient started with constant episodes of fever, which became worse when heat exposure, and had a fever convulsion at 8 month of age. Patient presents history of upper air pathway infections and recurrent othitis since he was 2 month years old. When he was four, myopia was diagnosed, presenting hypoacusis, occasional dysphonia, photophobia and a delay on psychomotor development.In the physical exam, presence of crusts and mucopurulent rhinorrhea with nasal obstruction at rhinoscopy were observed.
Yet, in the otoscopy there is presence of central perforation on the right tympanic membrane and retraction on the left one. Nose is sadlled-shape and face presents maxillary hypoplasia, inferior lip protusion, prominent front, periorbitary hyperpigmentation and low implanted ears. The audiometric exam showed bilateral conductive hearing loss and nasofibroscopy showed severe pereustachian tube area edema and ample nasal fossa with plentiful formation of crusts. Physical features pointed on the physical exam description can be seen on Pictures 1, 2 and 3Picture 1 - Occurrence of periorbitary hyperpigmentation and Partial Baldness, as well as presence of low implantation of pointed ears and saddled nose.Picture 2 - Image showing Lip, and thin Hair Protrusion.
Picture 3 - Presence of hypodontia and prominent front.DISCUSSIONAmong the 30 types of Ectodermal Dysplasia in which their clinical alteration, Genetic and molecular causes (1,4) are known, the most common one is Hypohidrotic, also called as Anhidrotic Ectodermal Dysplasia or Christ-Siemens-Touraine`s syndrome (6).

This one is related to alterations on X-linked recessive genes, or rarely to alteration on autossomal recessive and dominant genes (1, 2, 13).
Such gene is responsible for coding 2 isoforms of ectodysplasin, a transmembrane protein of collagen which is similar to proteins that join Tumor Necrosis Factor. The alteration on homologous domain to the TNF ligand ones shows that this protein area is fundamental to its functioning (1).
The two isoforms of Ectodysplasin are ED1-A1 and EDA-A2, which are respectively connected to the EDAR and XEDAR receptors. Both are responsible for the activation of signs to Epidermal Growth Factor job, which differ epiderm from its appendages (1,2,13). So, one might conclude that Ectodysplasin works on cell surviving, communication and growth (1).Another alteration, besides this one, is the DL gene one, which is responsible for EDAR receptor.
This causes recessive or dominant autossomic Ectodermal Dysplasia (1).The most common manifestation of Hypohidrotic Ectodermal Dysplasia is the reduction or complete absence of eccrine, sweat and lacrimal glands. However, apocrine glands are in normal condition (1-3,6,13).One of the consequences of gland alteration is the impossibility to sweat, what happens due to body temperature, hyperthermia crisis and fever convulsions (3,13). Teeth are small and conical shaped (1-3,6,13).Hypotrichosis is frequent and it can many times be associated with baldness. Among nail abnormalities, it can be found hyperconvexed, hypertrophic dystrophic, keratinized nails and even the absence of them. It is constant the occurrence of infections of superior air pathways and repetition otitis - medium, external and eczematous one - many times followed by sensorineural hypoacusis. Patient can present chronic conditions such as pharyngitis, laryngitis, dysphonia and odinophagy as well as atrophic rhinitis followed by epistaxis and catarrh (3).The occurrence of Atrophic Rhinitis is related to secretion disorder of mucosal gland, and also to inherited association with Ectodermal Dysplasia (4,5,7). Together with drainage and deficient ciliary movement, there is secretion retention with late development of crusts and fetid smell. Mucosa is bleeding and ulcer-like (4).Atrophic Rhinitis is a type of disease that normally develops during late childhood (3,6) or young adult age (4), as mentioned in the literature (3,15).
However, in the current case, its clinical condition appeared soon after birth, and it was diagnosed when patient was 7 years old. This occurs due to severe inflammatory reaction in Atrophic Rhinitis (6).After describing signs and symptoms found in Ectodermal Dysplasia, it is possible to observe that the current patient has many of them, what characterizes a peculiar case as the disease appears in different ways in different people (2).
Humidification and often nose washing are used in order to prevent smell and crusts formation (3). CONCLUSIONAtrophic Rhinitis is a type of disease associated with Genetic and molecular alterations of Ectodermal Dysplasia. Although it does not exist in all cases of Ectodermal Dysplasia, it is considered as a predominant complaint from patient. For this reason, it should be followed up and treated carefully by ENT doctors as it is related to different cases of infectious complications. Sinha V, Sinha S, Anhidrotic Ectodermal Dysplasia Presenting as Atrophic Rhinitis and Maggots. Ozena as presenting symptom of a rare and severe genetic disease: hypohidrotic ectodermal dysplasia. Gun Yoen Na, Do Won Kim, Seok Jong Lee, Sang Lip Chung, Dong Jae Park, Jung Chul Kim, Moon Kyu Kim.
Mutation in the ED1 Gene, Ala349Thr, in a Korean Patient with X-linked Hypohidrotic Ectodermal Dysplasia Developing de novo. Rafiq M.A, Faiyaz-ul-Haque M, Amin ud Din M, Malik S, Sohail M, Anwar M, Haque S, Paterson A, Tsui L, Ahmad W.

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