PUBLISHERS OTOLARYNGOLOGY ISSN 2470-4059 www.openventio.org Editor-in-Chief Arianna Di Stadio, PhD, MD Associate Editors Mohsen Naraghi, MD Mustafa Celik, PhD Sydney Correia Leao, MD Open Journal | September 2016 | Volume 2 | Issue 4 |
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PUBLISHERS
OTOLARYNGOLOGY
ISSN 2470-4059
www.openventio.org
Editor-in-ChiefArianna Di Stadio, PhD, MD
Associate EditorsMohsen Naraghi, MDMustafa Celik, PhD
Sydney Correia Leao, MD
Open Journal
| September 2016 | Volume 2 | Issue 4 |
OTOLARYNGOLOGY
Open Journal
Otolaryngol Open J
ISSN 2470-4059
– Arpit Saxena*, V. R. Sinha and D. K. Singh
2. Hot or Immediate Tonsillectomy: A Safe and Effective Method for Treatment of Acute Tonsillitis’ Complications
3. Loss of Consciousness: Can There Be Unexpected Otolaryngology Etiology?
4. Somatic Modulation of Tinnitus: A Review and Some Open Questions
5. Hearing Disorders in Turner’s Syndrome
– Katarzyna Amernik*, Krzysztof Sindrewicz and Ewa Jaworowska
– Massimo Ralli*, Giancarlo Altissimi, Rosaria Turchetta and Giancarlo Cianfrone
– Massimo Ralli*; Rosaria Turchetta and Giancarlo Cianfrone
Review
Mini Review
105-108
109-110
111-114
115-119
Table of Contents
1. The Effect of Adenotonsillectomy on Mean Platelet Volume and Neutrophil-to-Lymphocyte Ratio – Yakup Yegin, Mustafa Çelik*, Burak Olgun, Baver Maşallah Şimşek and Fatma Tülin Kayhan
Research
Research
Letter to The Editor
101-104
OTOLARYNGOLOGY
Open Journalhttp://dx.doi.org/10.17140/OTLOJ-2-122
Otolaryngol Open J
ISSN 2470-4059
Yakup Yegin, MD; Mustafa Çelik, MD*; Burak Olgun, MD; Baver Maşallah Şimşek, MD; Fatma Tülin Kayhan, MD
Departments of Otorhinolaryngology, Head and Neck Surgery, Bakırköy Dr. Sadi Konuk Training and Research Hospital, Istanbul, Turkey
*Corresponding authorMustafa Çelik, MD PhysicianDepartments of Otolaryngology Head and Neck SurgeryBakırköy Dr. Sadi Konuk Training and Research Hospital, Zuhuratbaba Mah. Tevfik Sağlam Cad. No: 11Bakırköy Istanbul, TurkeyTel. 090 (212) 4147282 E-mail: [email protected]
Article HistoryReceived: July 4th, 2016 Accepted: July 13th, 2016 Published: July 14th, 2016
CitationYegin Y, Çelik M, Olgun B, Şimşek BM, Kayhan FT. The effect of adenotonsil-lectomy on mean platelet volume and neutrophil-to-lymphocyte ratio. Otolar-yngol Open J. 2016; 2(4): 101-104. doi: 10.17140/OTLOJ-2-122
Copyright©2016 Çelik M. This is an open ac-cess article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Volume 2 : Issue 4Article Ref. #: 1000OTLOJ2122
The Effect of Adenotonsillectomy on Mean Platelet Volume and Neutrophil-to-Lymphocyte Ratio
Page 101
Research
ABSTRACT
Objectives: To explore the effect of adenotonsillectomy on mean platelet volume (MPV) lev-els and neutrophil to lymphocyte ratio (NLR) values in children with obstructive sleep apnea syndrome (OSAS).Subjects and Methods: In total, 127 children (69 males, 58 females; average age 10.20±8.96 years; range, 5-18 years) who underwent adenotonsillectomy with a diagnosis of OSAS were included in the study. Pre-operative MPV levels and NLR values were compared with measure-ments in the post-operative third month. A p-value <0.05 was considered to reflect statistical significance.Results: Mean pre-operative MPV values were 8.12±1.28 femtoliters (fL) and mean post-op-erative MPV values were 7.96±1.01 fL, respectively. Post-operative MPV values were signifi-cantly lower than pre-operative measurements (p=0,028, p<0.05). Mean pre-operative NLR levels were 1.46±0.82 and post-operative NLR values were 1.42±1.01, respectively. Post-oper-ative NLR values were significantly lower than pre-operative NLR values (p=0.032, p<0.05). Conclusion: We observed statistically significant lower MPV levels and NLR values after ad-enotonsillectomy in children with OSAS. Future randomized studies should explore the rela-tionship between the MPV levels, NLR values and parameters in polysomnography in larger numbers of patients with OSAS.
KEYWORDS: Mean platelet volume (MPV); Neutrophil to lymphocyte ratio (NLR); Adenoton-sillectomy; Obstructive sleep apnea syndrome (OSAS).
ABBREVIATIONS: MPV: Mean Platelet Volume; NLR: Neutrophil To Lymphocyte Ratio; OSAS: Obstructive Sleep Apnea Syndrome; QoL: Quality of Life; IEC: Institutional Eth-ics Committee; AH: Adenoid Hypertrophy; EDTA: Ethylene-diamine-tetracetic acid; NCSS: Number Cruncher Statistical System.
INTRODUCTION
Obstructive sleep apnea (OSA) caused by repetitive upper airway obstruction, is a syndrome characterized by recurrent episodes of sleep apnea and hypopnea. The incidence of OSA in children is reported lower than adult.1 Obstructive sleep apnea syndrome (OSAS) may inspire poor concentration, excessive daytime somnolence, morning headaches, metabolic, cardiopul-monary and cardiovascular diseases, and a lower quality of life (QoL).2 Polysomnography is utilized to diagnose and evaluate the severity of OSAS, and it is accepted as the gold standard diagnostic method for OSAS. The most common cause of OSAS in children is adenotonsillar hypertrophy.1,2
Mean platelet volume (MPV) is used as a parameter of platelet functions. Larger platelets are more reactive than platelets of normal platelets. Also, MPV is considered as a predictive value of aterosclerosis.3 In literature, increasing MPV levels have been associated
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with the prognosis of some diseases including such as hyperten-sion, unstable angina pectoris and OSA.4,5 The study of Sagit et al6 have shown that MPV levels are elevated in patients with marked septal deviation. They explained that the elevation in MPV levels of the patients with marked nasal septal deviation could be prevented by septoplasty.
Neutrophil to lymphocyte ratio (NLR) is recommended as a parameter of systemic inflammation.7 NLR can be easily determined by a simple complete blood count analysis and is a valuable parameter in diseases such as sudden hearing loss, some cancers, autoimmune and cardiovascular diseases.8,9 Neu-trophils and lymphocytes are essential for cytokine production in inflammatory disorders on acute and chronic process, respec-tively.10
In the present study, we explored the effect of adeno-tonsillectomy on MPV levels and NLR values in children with OSAS.
MATERIALS AND METHODS
A retrospective review of data collected from January 2013 to January 2015 was performed at our hospital, by the Departments of Otolaryngology, Head and Neck Surgery. In total, 127 children who underwent adenotonsillectomy with a diagnosis of OSAS were included in the study. The OSAS was clinically defined by the occurrence of loud habitual snoring, witnessed apnea, and excessive daytime sleepiness at least one year due to parents observations. Patients with previous history of adenoidectomy, tonsillectomy, genetic syndromes, congenital malformations, cleft palate, nasal septal deviation, sinonasal infection, chronic diseases, hematological diseases were excluded from the study. Blood serum variables such as complete blood counts, glucose, cholesterol, triglyceride, and inflammatory markers including C-reactive protein (CRP) and erytrocyte sedimentation rate were evaluated to exclude hematological diseases, pre-operatively. No cardiovascular complaints and symptoms were determined in all of the patients. Also, electrocardiography was normal in all of the patients. All parents of the patients were informed about the study and a written consent was obtained from each parent of the patients. The study protocol was approved by the Institutional Ethics Committee (IEC). The study was conducted in accordance with the principles of Helsinki Declaration. All the patients had endoscopic examination of the oral cavity, nose and post-nasal space, pre-operatively. Adenoid tissue was clas-sified as follows; grade 1, adenoid tissue completes less than 25% of choana; grade 2, adenoid tissue completes 25-50% of choana; grade 3, adenoid tissue completes 50-75% of choana and grade 4, adenoid tissue completes 75-100% of choana. Ton-sil size was classified using Brodsky11 grading scale as +1, tonsil hypertrophy causing less than 25% upper airway obstruction, +2 it causing 25-50% upper airway obstruction, +3 it causing 50-75% upper airway obstruction and +4, it causing more than 75% upper airway obstruction. All patients had grade 3 and 4 adenoid hypertrophy (AH) and tonsil hypertrophy. All operations risks
and complications were explained to children’s parents. Ade-noidectomy was performed by using St. Clair-Thomsen® curatte under general anesthesia in supine position and haemostasis was secured by packing. Tonsillectomy was performed via cold-steel dissection approach. All the operations were performed by one of the surgeons in our department. All chidren were clinically no symptoms of infection at the time of adenotonsillectomy. Routine pre-operative blood samples were taken from the an-tecubital vein into tubes with ethylene-diamine-tetracetic acid (EDTA) by a nurse. Neutrophil, lymphocyte and MPV were measured by hematology analyzer machine. Normal values for MPV were accepted as 6.0-11.0 fL. NLR was calculated from the differential count by dividing the neutrophil measurement by the lymphocyte measurement. All of the patients were invited for control examinations at post-operative first week and third month. Blood samples were taken again in the post-operative third month, and the measurements were compared with pre-operative measurements.
Statistical Analysis
Number Cruncher Statistical System (NCSS) 2007 software (Kaysville, UT, USA) was used for all statistical analysis. De-scriptive statistics (means and standard deviation, medians with interquartile range) were derived. The significance of intergroup differences was analyzed using Student’s t-test, and the signifi-cance of the medians was analyzed with the Mann-Whitney U-test. A paired t-test was performed to test differences between preoperative and postoperative values of MPV and NLR. A p-value <0.05 was considered to reflect statistical significance.
RESULTS
We included 127 patients: 58(45.7%) females and 69(54.3%) males. Their average age was 10.20±8.96 years (range: 5-18 years). Mean pre-operative MPV values were 8.12±1.28 fL and mean post-operative MPV values were 7.96±1.01 fL, respective-ly. Post-operative MPV values were significantly lower than pre-operative measurements (p=0,028, p<0.05) (Figure 1). Mean pre-operative NLR levels were 1.46±0.82 and post-operative NLR values were 1.42±1.01, respectively. Post-operative NLR values were significantly lower than pre-operative NLR values (p=0.032, p<0.05, Figure 2) (Table 1).
DISCUSSION
Increased platelet activation may be related to an increase of cardiopulmonary risk in patients with OSAS. Also, MPV lev-els show indirectly the functions of platelets. MPV levels cor-relate with the cardiopulmonary risks and morbidity in several diseases. Patients with elevated MPV levels seem to have bad prognosis in some cardiovascular and neurological diseases such as unstable angina pectoris, myocardial infarction and stroke.3-5 In literature, previous studies explored the effect of OSAS on MPV levels. The study of Soyalıç et al12 have reported that MPV was higher in children with adenotonsillar hypertrophy and that
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adenotonsillectomy lowers MPV levels in such patients. In con-trast, the study of Cengiz et al13 have evaluated the associations between MPV levels and chronic tonsillitis-AH in children. They classified children into three groups. Group 1 consisted of patients who underwent adenoidectomy, whereas group 2 con-sisted of patients who underwent adenotonsillectomy and, group 3 consisted of healthy patients as control groups. MPV values (fL) in groups 1, 2 and 3 were 6.6±,0.8, 6.6±0.7 and 7.3±0.9, respectively, in their study. Also, they reported that MPV values in groups 1 and 2 were significiantly lower than control group and there was no significiant difference between group 1 and 2. These studies lead to new discussions. Overall, data on the effect of adenotonsillectomy on MPV levels remains sparse. In the present study, post-operative MPV levels reduced in children with OSAS. Therefore, we can not assert that adenotonsillec-tomy may reduce cardiovascular morbidity considering the lack of assessment of long-term outcomes. Confounding variables that were addressed include the study design, the study size and the characteristics of patients. To our knowledge, there is no re-ported study that focused on the effect of duration of OSAS on MPV levels in patients with OSAS. However, determination of the effect of duration of OSAS on MPV levels is objectively difficult. NLR is considered as an potential marker in identifica-tion of the disease severity in inflammatory disorders, including such as cardiovascular diseases, and auto-immune diseases.7-9 The adenoid tissues, like all lymphoid tissue, enlarge when in-fected. Although, lymphoid tissue does act to fight infection, sometimes bacteria and viruses can lodge within it and survive. Chronic infection, either viral or bacterial, can keep the pad of adenoid tissues enlarged for years, even into adulthood.14 In lit-
erature, there have been few studies of exploring the relationship between NLR levels and OSAS. The study of Köseoğlu et al7
have reported that mean NLR values of the OSAS group were 1.88±0.85 and NLR values of control group were 2.01±0.85 and they found no significiant difference between OSAS group and normal group in terms of NLR values. Also, they asserted that NLR may be used as a marker that indicates chronic intermittent hypoxia in patients with OSAS. To our knowledge, the present study provides the first report of exploring the relationships be-tween NLR and OSAS in children. In the present study, mean pre-operative NLR levels were 1.46±0.82 and post-operative NLR values were 1.42±1.01, respectively. We found that NLR values decreased by adenotonsillectomy.
Limitations of this study included a retrospective study design, the sample size, the lack of randomization and the lack of assessment of the polysomnography that is difficult procedure to be employed in children. If the study design was randomized study with performing polysomnography, the study may be more valuable. Future randomized studies should explore the relation-ship between the MPV levels, NLR values and parameters in polysomnography in larger numbers of patients with OSAS.
CONCLUSION
In conclusion, we observed statistically significant lower MPV levels and NLR values after adenotonsillectomy in children with OSAS. Overall, we cannot assert that adenotonsillectomy may reduce cardiovascular morbidity considering the lack of assess-ment of long-term outcomes.
Table 1: Comparison of pre- and post-operative MPV and NLR values of patients.
Figure 1: Mean Platelet Volume levels in pre- and post-operative terms.
Figure 2: Neutrophil to lymphocyte ratio levels in pre- and post-operative terms.
MPV levels(fL) NLR values
pre-operative 8.12±1.28 1.46±0.82
post-operative 7.96±1.01 1.42±1.01
*p p:0.028 p:0.032MPV: Mean platelet volume; NLR: Neutrophil-to-lymphocyte ratio.*p: Paired Samples t-test *p<0.05
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CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest.
FINANCIAL DISCLOSURE
The authors declare that this case has received no financial sup-port.
REFERENCES
1. Viana Ada C Jr, Thuler LC, Araújo-Melo MH. Drug-induced sleep endoscopy in the identification of obstruction sites in patients with obstructive sleep apnea: A systematic review. Braz J Otorhinolaryngol. 2015; 81: 439-446. doi: 10.1016/j.bjorl.2015.01.007
2. Izu SC, Itamoto CH, Pradella-Hallinan M, et al. Obstructi-ve sleep apnea syndrome (OSAS) in mouth breathing children. Braz J Otorhinolaryngol. 2010; 76(5): 552-556. doi: 10.1590/S1808-86942010000500003
3. Park Y, Schoene N, Harris W. Mean platelet volume as an indicator of platelet activation: Methodological issues. Platelets. 2002; 13: 301-306. doi: 10.1080/095371002220148332
4. Greisenegger S, Endler G, Hsieh K, Tentschert S, Mannhalter C, Lalouschek W. Is elevated mean platelet volume associated with a worse outcome in patients with acute ischemic cerebro-vascular events? Stroke. 2004; 35: 1688-1691. doi: 10.1161/01.STR.0000130512.81212.a2
5. Ulaşli SS, Ozyurek BA, Yilmaz EB, Ulubay G. Mean platelet volume: An inflammatory marker in acute exacerbation of chro-nic obstructive pulmonary disease. Pol Arch Med Wewn. 2012; 122(6): 284-290. Web site. http://pamw.pl/sites/default/files/PAMW_2012-06_Ulasil.pdf. Accessed July 4, 2016
6. Sagit M, Korkmaz F, Kavugudurmaz M, Somdas MA. Impact of septoplasty on mean platelet volume levels in patients with marked nasal septal deviation. J Craniofac Surg. 2012; 23: 974-976. doi: 10.1097/SCS.0b013e31824e2c08
7. Köseoğlu S, Özcan KM, Ikincioğlu A, Çetin MA, Yıldırım E, Dere H. Relationship between neutrophil to lymphocyte ratio, platelet to lymphocyte ratio and obstructive sleep apnea synd-rome. Adv Clin Exp Med. 2015; 24(4): 623-627. doi: 10.17219/acem/47735
8. Bhat T, Teli S, Rijal J, et al. Neutrophil to lymphocyte ratio and cardiovascular diseases: A review. Expert Rev Cardiovasc Ther. 2013; 11: 55-59. doi: 10.1586/erc.12.159
9. Proctor MJ, McMillan DC, Morrison DS, Fletcher CD, Hor-gan PG, Clarke SJ. A derived neutrophil to lymphocyte ratio pre-dicts survival in patients with cancer. Br J Cancer. 2012; 107:
695-699. doi: 10.1038/bjc.2012.292
10. Wang J, Arase H. Regulation of immune responses by neut-rophils. Ann N Y Acad Sci. 2014; 1319: 66-81. doi: 10.1111/nyas.12445
11. Brodsky L, Moore L, Stanievich JF. A comparison of tonsil-lar size and oropharyngeal dimensions in children with obstruc-tive adenotonsillar hypertrophy. Int J Pediatr Otorhinolaryngol. 1987; 13(2): 149-156. doi: 10.1016/0165-5876(87)90091-7
12. Soyalıç H, Somuk BT, Doğru S, Gürbüzler L, Göktaş G, Eyibilen A. Evaluation of mean platelet volume and its ratio over platelet count in children with obstructive sleep apnea sy-ndrome. Kulak Burun Bogaz Ihtis Derg. 2015; 25(1): 16-21. doi: 10.5606/kbbihtisas.2015.28863
13. Cengiz C, Erhan Y, Murat T, et al. Values of mean platelet volume in patients with chronic tonsillitis and adenoid hypert-rophy. Pak J Med Sci. 2013; 29(2): 569-572. Web site. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809227/. Accessed July 4, 2016
14. Shin SY, Choi SJ, Hur GY, et al. Local production of total IgE and specific antibodies to the house dust mite in adenoid tissue. Pediatr Allergy Immunol. 2009; 20(2): 134-141. doı: 10.1111/j.1399-3038.2008.00756.x
OTOLARYNGOLOGY
Open Journalhttp://dx.doi.org/10.17140/OTLOJ-2-123
Otolaryngol Open J
ISSN 2470-4059
Katarzyna Amernik, MD, PhD*; Krzysztof Sindrewicz, MD; Ewa Jaworowska, MD, PhD
Departments of Otolaryngology and Oncologic Laryngology, Pomeranian Medical University, Ul. Unii Lubelskiej 1, 71-252 Szczecin, Poland
*Corresponding authorKatarzyna Amernik, MD, PhD Departments of Otolaryngology and Oncologic LaryngologyPomeranian Medical UniversityUl. Unii Lubelskiej 1 71-252 Szczecin, Poland Tel. +48-91-425-32-89 Fax: +48-91-425-32-77 E-mail: [email protected]
Article HistoryReceived: June 24th, 2016 Accepted: July 19th, 2016 Published: July 20th, 2016
CitationAmernik K, Sindrewicz K, Jaworowska E. Hot or immediate tonsillectomy: A safe and effective method for treatment of acute tonsillitis’ complications. Oto-laryngol Open J. 2016; 2(4): 105-108. doi: 10.17140/OTLOJ-2-123
Copyright©2016 Amernik K. This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Volume 2 : Issue 4Article Ref. #: 1000OTLOJ2123
Hot or Immediate Tonsillectomy: A Safe and Effective Method for Treatment of Acute Tonsillitis’ Complications
Page 105
Research
ABSTRACT
Aim: The aim of this study was retrospective analysis of indications to hot tonsillectomy, its effectiveness and safety. Peritonsillar abscess (PTA) is one of the most common complications of acute tonsillitis and the cause of emergency laryngological counselling. In some cases, it is necessary to perform hot tonsillectomy. Material and Methods: In between 2009-2015, 21 patients (aged between 4 to 43 years old) with an initial diagnosis of peritonsillar abscess were admitted. Among them, 11 were women and 10 were men. All underwent hot tonsillectomy. Results: Most of the patients were between 20-40 years old. The most common symptoms were pain in the throat, trismus and dysphagia. In all cases incision of an abscess was made, in 9 patients purulent discharge was present. In all patients there was no relief of symptoms after in-cision and antibiotic therapy. In 12 cases without drainage after initial incision, pus was drained after tonsillectomy. In the remaining 9 cases there were additional reservoirs of pus, which were drained after surgery in 6 patients. In 8 patients there was more than one localization of an abscess. There were no problems with intubation and no complications in the early and late post-operative periods occurred. The average time of stay in hospital was 8 days (5-12 days). Conclusion: Lack of improvement after initial treatment of PTA is an indication to hot tonsil-lectomy. This procedure is not connected with an increased risk of complications. Evacuation of purulent content does not exclude presence of another abscess, unusual localization or para-pharyngeal space abscess.
KEYWORDS: Peritonsillar abscess (PTA); Tonsillectomy; Hot tonsillectomy; Acute tonsillitis; Complication; Parapharyngeal space abscess.
ABBREVIATIONS: PTA: Peritonsillar abscess; CRP: C-reactive protein.
INTRODUCTION
Peritonsillar abscess (PTA) is one of the most common complications of acute tonsillitis and cause of emergency laryngological counselling. It is also the most common deep neck infec-tion. The incidence is estimated to be 30 out of 100,000 people per year.1,2 Factors predisposing to the development of peritonsillar abscess described in the literature are bad periodontal status and smoking.2,3 Treatment is always connected with an abscess incision, drainage of purulent content, re-hydration4-10 with subsequent antibiotic therapy. In some cases, it is necessary to perform immediate tonsillectomy.5,9,11 Otherwise infection may spread into surrounding tissues such as parapharyngeal space. This procedure is potentially connected with an increased risk of complications, such as problems with intubation,8 intra- and post-operative haemorrhage and spread of the infection to surrounding tissues especially to the parapharyngeal space.4,10 Imme-diate tonsillectomy has also been reported in pediatric cases for airway obturation.12
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MATERIALS AND METHODS
Between 2009-2015 in The Clinic of Otolaryngology and On-cological Laryngology of Pomeranian Medical University 21 patients with an initial diagnosis of peritonsillar abscess were admitted, who underwent hot tonsillectomy. The ages of the patients ranged from 4 to 43 years old (middle 26 years), 11 women and 10 men.
Retrospective analysis of data from medical history, ac-cording to age, symptoms, signs and methods of treatment was made. Inclusion criteria were peritonsillar abscess recognized in clinical examination requiring tonsillectomy within 48 hours af-ter admission to the hospital. Symptoms were asymmetry of oral pharynx and palatoglossal arch, dislocation of the tonsil.13 Age, stay in the hospital, history of recurrent tonsillitis and peritonsil-lae abscesses, C-reactive protein (CRP) level and type of treat-ment were analyzed. The day of discharge from hospital was as-sumed as the end of treatment. Patients left hospital after healing of tonsillar niche and relief of local and general symptoms.
RESULTS
The age range of the patients is shown in Figure 1. The largest group of patients in this study were aged between 21 and 40 years.
The number of men and women in the study were simi-lar (M:W 57%/43%).
Symptoms reported by patients are shown in Table 1, the most common symptom was pain in the throat and problems with swallowing.
In the history of previous upper respiratory tract infec-tions more than half of the patients had at least 3 episodes of acute tonsilitis in the previous year and 13 had peritonsillar ab-scess in the past.
Upon admission to the hospital the patients were in good general condition. Following laryngological examination, swelling in the peritonsillar area and pain with enlargement of lymph nodes on the affected side were stated together with signs of acute tonsillitis.
Blood tests was performed in all patients on the days of admitting and discharges from the hospital. Results of the blood tests are shown in Table 2. In all patients, levels of inflammatory parameters decreased at the day of discharge.
All patients at the day of admission had undergone inci-sion of PTA. In 9 there was purulent drainage (43%). The algo-rithm of treatment is show in Figure 2.
In all patients indication for surgery, hot tonsillectomy, was lack of improvement within the following 48 hours, inde-pendent of purulent drainage after initial incision.
All 21 patients had immediate/hot tonsillectomy. In 11 it was on one side and in 10 bilateral. Indications for bilateral tonsillectomy were recurrent acute tonsillitis and history of PTA in the previous year (7 cases) and signs of chronic tonsillitis (3 cases). During surgery in 86% of patients purulent content was drained and among those cases half of them were parapharyn-geal space abscesses. Table 3 gives detailed information about
Symptom Number of patients Percentage
Fever 9 43%
Trismus 19 90%
Pain in the throat 21 100%
Dysphagia 13 62%
Ear pain 2 9,5%
≥3 acute tonsilitis in the previous 1 year 10/21 48%
1-2 acute tonsilitis in the previous 1 year 2/21 10%
Peritonsillar abscess (previous year) 13(10) 62% (47%)
Min Max Average Standard deviation
CRP (C reactive protein) 82 241 123 67.7
WBC 10.34 21.03 15.7 3.63
RBC 3.99 5.48 5.01 0.38
CRP controls 5 69 35 20.03
WBC controls 7.05 11.34 9.56 1.24
RBC controls 3.75 5.15 4.57 0.34
Figure 1: Age groups of patients.
Figure 2: Algorithm of treatment for patients with PTA.
Table 1: Symptoms reported by patients.
Table 2: Blood tests results.
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recognized abscesses during surgery.
Among all patients with parapharyngeal space abscess only in 2 cases on initial incision drainage of pus was present. In 8 patients there was more than one localization of an abscess. In 4 patients PTA in antero–superior area and parapharyngeal space abscess were found and in 4 posterior PTA and parapharyngeal space were found simultaneously.
Loss of blood was on average 150 ml. The average time of surgery was 100 minutes.
There were no problems with intubation, no complica-tions in the early and late post-operative period occurred.
Patients were treated with antibiotics and it was usually intravenous amoxycylin with clavulanic acid (3 times daily, 1,2 g in 19 out of 21 patients), in one case cefurixime with metroni-dazole was used and in another case cefotaxim with clindamycin was used.
The average time of stay in hospital was 8 days (5-12 days). None of the described patients required treatment on our clinic again.
DISCUSSION
PTA is a purulent reservoir localized between the superior pha-ryngeal sphincter and a tonsil which is a complication of acute tonsillitis.3,12,14 This diagnosis requires immediate treatment be-cause of the possibility of infection spread to the parapharyngeal space, retropharyngeal space and floor of the mouth.15 Continu-ation of disease leads to the involvement of deep neck spaces and mediastinum, which is a life threatening condition.14,15 Ac-cording to the literature progression of infection from throat to deep neck space occurs in 1.8% patients and from those spaces to mediastinum in 10%.16 Mortality in acute mediastinitis is still high and ranges from 30% to 40%.14,16
In the group of patients analyzed in the study, most patients were young adults aged from 21 to 40 years old who are professionally active people. These data are consistent with those from the literature2,3,5-7,12 and that makes problem of PTA treatment economically important. The symptoms reported by patients were typical for throat infections.
Out of the whole group in 8, patients abscesses were present in more than one localization, for example PTA with abscess of parapharyngeal space. This means that even initial incision with drainage of pus from the peritonsillar area requires subsequent controls, especially in situations when there is no ex-
pected improvement in patient’s clinical status or recurrence of symptoms after initial improvement. There are data in the litera-ture concerning the spread of infection from peritonsillar area to deep neck spaces in similar cases.14-17
Fine needle aspiration of PTA or incision with drain-age of pus with subsequent antibiotic therapy is the treatment of choice.2 Although, when there is a lack of expected improvement the next step that should be considered is hot tonsillectomy. This procedure is also called tonsillectomy “a chaud” or urgent ton-sillectomy and was described at the beginning of 20th century as typical treatment of PTA.5 Potentially increased risk of the procedure and intra-operative and post-operative complications led to the abandonment of this procedure by surgeons. However, on the basis of the results presented here, along with data from the literature we can suggest that this procedure is not connected with increased risk of complications such as haemorrhage during surgery or delayed haemorrhage.5-7,9-11,18 Albertz et al13 reported that describing their 10 years experience. The authors had cases of bleeding (3.6%) and single cases of edema, diarrhea, persisted odynophagia, panic attack, cutaneous rash.12 No problems with intubation or complications such as haemorrhaging occurred in any of our patients. These results confirm information from the literature according to Berry et al5 who estimated hot tonsillecto-my to be easier than delayed tonsillectomy, especially on the side of PTA. Johnson6 suggested that if there is delayed tonsillectomy following abscess, this may be connected with higher costs of treatment as it may require another hospitalization and absence at work. The same author recommends hot tonsillectomy in all patients with recurrent PTA,6,7 as it may prevent recurrences.2,12 It is still controversial if this tonsillectomy should be performed on one side only or if it should be performed bilaterally. In our material bilateral tonsillectomy was made in all patients who had indications for tonsillectomy, independent from PTA. Ac-cording to the literature it seems to be the most common practice in another centres.11 However, Albertz et al13 recommend bilat-eral tonsillectomy in all cases as a prevention of recurrences, on the basis of their study. Immediate tonsillectomy is especially effective in cases of intratonsillar and posterior abscess,12 which was confirmed in our study.
It is recommended to administer antibiotics intrave-nously before hot tonsillectomy and to avoid analgesic drugs which inhibit aggregation of blood platelets and may influence blood coagulation.5,19
In all of our patients improvement was achieved after surgery and antibiotic therapy with amoxicillin with clavulan-ic acid. Diagnostic imaging may include computer tomogra-phy11,17,20 but it seems that the main indication for hot tonsillec-tomy is lack of expected clinical improvement in spite of proper treatment. Diagnostic imaging may be useful in case of doubts.
CONCLUSION
Lack of improvement after initial treatment of PTA should make a consideration of performing hot tonsillectomy as an emer-
Number Percentage
antero-superior PTA 14 66%
Posterior PTA 6 29%
Parapharyngeal space abscess 9 43%
Table 3: Postoperative diagnosis.
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gency. This procedure is not connected with increased risk of complications and postponing the decision may lead to infection spread into surrounding tissues. Evacuation of purulent content does not exclude the presence of another abscess in close, un-usual localization or parapharyngeal space abscess.
ACKNOWLEDgEMENTS
The author wishes to thank Ms. Ruth Danielski for help in prepa-ration of the manuscript and editorial assistance.
CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest.
CONSENT
As the article is a retrospective study and did not publish any personal photo or information regarding any of the patients in the manuscript. Thus, the consent is not required for the article publication.
REFERENCES
1. Zagólski O, Gajda M. The role of anaerobic flora in formation of peritonsillar abscess. Pol Merk Lek. 2008; 24: 140-146.
2. Shaul C, Koslowsky B, Rodriguez M, et al. Is needle aspira-tion for peritonsillar abscess still as good as we think? A long-term follow-up. Ann Otol Rhinol Laryngol. 2015; 124(4): 299-304. doi: 10.1177/0003489414556083
3. Lepelletier D, Pinaud V, Le Conte P, et al. Peritonsillar ab-scess (PTA): Clinical characteristics, microbiology, drug expo-sures and outcomes of a large multicenter cohort survey of 412 patients hospitalized in 13 French university hospitals. Eur J Clin Microbiol Infect Dis. 2016; 35(5): 867-873. doi: 10.1007/s10096-016-2609-9
4. Herzon FS, Martin AD. Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses. Curr Infect Dis Rep. 2006; 8: 196-202. doi: 10.1007/s11908-006-0059-8
5. Berry S, Pascal I, Whittet HB. Tonsillectomy à chaud for quinsy: Revisited. Eur Arch Otorhinolaryngol. 2008; 265: 31-33. doi: 10.1007/s00405-007-0498-3
6. Johnson RF, Stewart MG, Wright CC. An evidence based re-view of the treatment of peritonsillar abscess. Otolaryngol Head Neck Surg. 2003; 128: 332-343. doi: 10.1067/mhn.2003.93
7. Page C, Chassery G, Boute P, Obongo R, Strunski V. Immedi-ate tonsillectomy: Indications for use as first-line surgical man-agement of peritonsillar abscess (quinsy) and parapharyngeal abscess. J Laryngol Otol. 2010; 124: 1085-1090. doi: 10.1017/S0022215110000903
8. Steyer TE. Peritonsillar abscess: Diagnosis and treatment. Am Fam Physician. 2002; 65: 93-96. Web site. http://www.aafp.org/afp/2002/0101/p93.html. Accessed June 23, 2016
9. Suzuki M, Ueyama T, Mogi G. Immediate tonsillectomy for peritonsillar abscess. Auris Nasus Larynx. 1999; 26: 299-304. doi: 10.1016/S0385-8146(98)00070-4
10. Windfuhr JP, Chen YS. Immediate abscess tonsillectomy--a safe procedure? Auris Nasus Larynx. 2001; 28: 323-327. doi: 10.1016/S0385-8146(01)00098-0
11. Page C, Biet A, Zaatar R, Strunski V. Parapharyngeal ab-scess: Diagnosis and treatment. Eur Arch Otorhinolaryngol. 2008; 265: 681-686. doi: 10.1007/s00405-007-0524-5
12. Coyle P, Marzouk SD, Gerolympou M, Marais J. Hot tonsil-lectomy for pediatric obstructive sleep apnoea. BMJ Case Rep. 2014. doi: 10.1136/bcr-2013-203378
13. Albertz N, Nazar G. Peritonsillar abscess: Treatment with im-mediate tonsillectomy - 10 years of experience. Acta Otolaryngol. 2012; 132(10): 1102-1107. doi: 10.3109/00016489.2012.684399
14. Machała W, Śmiechowicz K, Gaszyński T. Sepsis caused by descending mediastinitis as peritonsillar abscess complica-tion. Case report. Otolaryngol Pol. 2006; 60: 211-215. Web site. http://www.ncbi.nlm.nih.gov/pubmed/16903340. Accessed June 23, 2016
15. Nowak K, Błaszyk M, Szyfter W. Fatal necrotic mediasti-nitis as a complicaion of peritonsillar abscess. Otolaryngol Pol. 2005; 59: 751-754. Web site. http://www.ncbi.nlm.nih.gov/pubmed/16471196. Accessed June 23, 2016
16. Collin J, Beasley N. Tonsillitis to mediastinitis. J Laryngol Otol. 2006; 120: 963-966. doi: 10.1017/S0022215106001940
17. Thapar A, Tassone P, Bhat N, Pfleiderer A. Parapharyngeal abscess. A life threatening complication of quinsy. Clin Anat. 2008; 21: 23-26. doi: 10.1002/ca.20569
18. Watanabe T, Arita M, Suzuki M, Mogi G. Immediate ton-sillectomy for peritonsillar abscess. Int Congress Series. 2003; 1257: 199-203.
19. Giger R, Landis BN, Dulguerov P. Hemorrhage risk af-ter quinsy tonsillectomy. Otolaryngol Head Neck Surg. 2005; 133(5): 729-734. doi: 10.1016/j.otohns.2005.07.013
20. Kawabata M, Umakoshi M, Makise T, et al. Clinical clas-sification of peritonsillar abscess based on CT and indications for immediate abscess tonsillectomy. Auris Nasus Larynx. 2016; 43(2): 182-186. doi: 10.1016/j.anl.2015.09.014
OTOLARYNGOLOGY
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Otolaryngol Open J
ISSN 2470-4059
Arpit Saxena, MS (ENT)*; V. R. Sinha, MS (ENT), DNB; D. K. Singh, MS (ENT)
Department of Otolaryngology, Command Hospital (CC), Lucknow, UP, India
*Corresponding authorArpit Saxena, MS (ENT) Department of OtolaryngologyCommand Hospital (CC)Lucknow, UP, IndiaTel. +91-9532306179 E-mail: [email protected]
Article HistoryReceived: August 12th, 2016 Accepted: August 24th, 2016 Published: August 24th, 2016
CitationSaxena A, Sinha VR, Singh DK. Loss of consciousness: Can there be unex-pected otolaryngology etiology? Otolar-yngol Open J. 2016; 2(4): 109-110. doi: 10.17140/OTLOJ-2-124
Copyright©2016 Saxena A. This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Volume 2 : Issue 4Article Ref. #: 1000OTLOJ2124
Loss of Consciousness: Can There Be Unexpected Otolaryngology Etiology?
Page 109
Letter to The Editor
I am honoured and enthusiastic to be a part of Otolaryngology-Open Access Journal. I will like to discuss a case of academic interest.
Thirty-four-years old male, soldier by occupation had complains of three episodes of loss of consciousness lasting for 3-4 seconds for last one year. There was no history of giddi-ness, ear discharge, aural fullness, autotoxin medication, tinnitus etc. His examination revealed bilateral normal tympanic membrane and tuning fork tests were suggestive of left sided Sensor Neural Hearing Loss (SNHL). Patient was unaware of hearing loss. Fistula test was negative and caloric test demonstrated left canal paresis. Rest neurotological examination was normal. Audiomertry presented left sided moderate severe SNHL. Cardiologist and neurologist evalua-tion was normal. MRI brain was also normal.
In view of left sided ear hearing loss and canal paresis on caloric test, high resolution CT temporal bone was performed and it clinched the diagnosis of left Superior Semicircular Canal Dehiscence (SSCD) (Figure 1). The patient was taken up for surgical closure of SSCD by middle cranial fossa approach. The defect was closed by fat and tissue glue. Presently, patient is asymptomatic for two years.
Figure 1: HRCT Temporal Bone showing coronal cuts. Yellow encircled region shows superior semicircular canal of both sides. Red pointing arrow shows dehiscence in left superior semicircular canal.
The true incidence of SSCD is unknown due its rare presentation. The etiology of this syndrome was localized to a dehiscence of the bone covering the superior semicircular canal. The abnormal communication between the superior semicircular canal and the brain can result in vertigo and oscillopsia induced by loud sounds (Tullio phenomenon), by changes in pressure in the ear canal that are transmitted to the middle ear (Hennebert sign), or by Valsalva maneuvers.1-3 Our patient was not having any such presentation as described making it atypical. Our case of young adult soldier with episodes of loss of consciousness with unilateral SNHL is being reported to emphasize on complete neurotological examination and thorough workup on such patients as diseases can have unusual presentation.
CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest.
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REFERENCES
1. Minor LB, Solomon D, Zinreich JS, Zee DS. Sound- and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal. Arch Otolaryngol Head Neck Surg. 1998; 124(3): 249-258. doi: 10.1001/archotol.124.3.249
2. Minor LB. Superior canal dehiscence syndrome. Am J Otol. 2000; 21(1): 9-19. Web site. http://journals.lww.com/otology-neu-rotology/Abstract/2000/01000/Superior_Canal_Dehiscence_Syndrome.4.aspx. Accessed August 11, 2016
3. Minor LB, Cremer PD, Carey JP, et al. Symptoms and signs in superior canal dehiscence syndrome. Ann NY Acad Sci. 2001; 942: 259-273. doi: 10.1111/j.1749-6632.2001.tb03751.x
OTOLARYNGOLOGY
Open Journalhttp://dx.doi.org/10.17140/OTLOJ-2-125
Otolaryngol Open J
ISSN 2470-4059
Massimo Ralli, MD,PhD1*; Giancarlo Altissimi, MD2; Rosaria Turchetta, MD2; Giancarlo Cianfrone, MD2
1Department of Oral and Maxillofacial Sciences, Sapienza University of Rome, Rome, Italy2Department of Otorhinolayngology, Audiology and Ophtalmology, Sapienza University of Rome, Rome, Italy
*Corresponding authorMassimo Ralli, MD, PhD Department of Oral and Maxillofacial SciencesSapienza University of RomeViale del Policlinico 15500186 Rome, ItalyTel. +39 333 8200853 E-mail: [email protected]
Article HistoryReceived: August 18th, 2016 Accepted: August 24th, 2016 Published: August 24th, 2016
CitationRalli M, Altissimi G, Turchetta R, Cian-frone G. Somatic modulation of tinni-tus: a review and some open questions. Otolaryngol Open J. 2016; 2(4): 111-114. doi: 10.17140/OTLOJ-2-125
Copyright©2016 Ralli M. This is an open ac-cess article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Volume 2 : Issue 4Article Ref. #: 1000OTLOJ2125
Somatic Modulation of Tinnitus: A Review and Some Open Questions
Page 111
Review
ABSTRACT
Tinnitus modulation by movements of the temporomandibular joint, head and neck musculo-skeletal structures and the eye can be found in one to two thirds of tinnitus sufferers; unfortu-nately this condition is often overlooked by otolaryngologists. Although somatic modulation has been initially hypothesized as a fundamental characteristic of tinnitus, there is increasing evidence of a tight connection with disorders of non-auditory regions. The structure that mostly modulates tinnitus is the temporomandibular joint, which mainly causes an increase in tinnitus loudness, followed by head and neck movements that may result in an increase or decrease of loudness and eye movements (gaze-evoked tinnitus). Besides loudness, somatic movements can also modulate tinnitus pitch and localization. Somatosensory tinnitus is a relatively new finding that leaves several open questions: are there individual predisposing factors to somatic modulation? How strong is the association between the capability to somatically modulate tin-nitus and an underlying non-auditory disorder? Why patients that have concomitant hyperacu-sis also have higher chances of tinnitus modulation? Further basic science and clinical research is required to address these and many other questions about somatosensory tinnitus.
KEYWORDS: Somatic modulation of tinnitus; Temporomandibular joint disorder; Somatosen-sory tinnitus.
INTRODUCTION
Tinnitus is a widely spread symptom affecting over 16 million subjects in the US with conse-quences, sometimes severe,1 on the overall quality of life of affected individuals.2,3 Estimated prevalence ranges between 12 and 16%.4 Tinnitus can derive from age-related or hereditary hearing loss,5 acute or chronic acoustic trauma,6-8 ototoxic drugs including aminoglycosides, cisplatin and high doses of salicylate,9,10 other hearing disorders as well as from psychological factors such as depression, anxiety, obsessive compulsive, mood, conversion, somatoform and other psychiatric disorders.11,12
The pitch and loudness of tinnitus can be modulated and even evoked or silenced for a short time in some individuals by movements of the temporomandibular joint, head and neck muscles and the eyes due to interactions between the auditory and the somatosensory systems. This type of tinnitus, called somatosensory tinnitus, could be a direct consequence of a disorder of non-auditory musculoskeletal structures, a fundamental characteristic of tinnitus as hypothesized by Levine13 or, most probably, an attribute of tinnitus favored by an underlying somatic disorder that triggers existing neural connections between somatosensory and auditory pathways. So far, even if clinical experience suggests a direct connection, there is a lack of studies that prove an association between modulation and a somatic disorder and, to date, no statistically significant association between somatic disorders and higher prevalence of tinnitus modulation following somatic maneuvers has been described.14,15
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The knowledge of the pathophysiologic basis of so-matosensory tinnitus is constantly increasing thanks to basic research studies on animal models. Data from animal studies indicates the relay of afferent somatosensory information by the trigeminal and dorsal root ganglia; somatosensory input causes changes in the firing rate and synchrony in dorsal cochlear nu-cleus neurons that may be at the base of somatic tinnitus.16,17
The modulation of tinnitus by somatic movements is widely diffused among acute and chronic tinnitus sufferers and has been reported to involve one to two-thirds of them with dif-ferent patient series ranging between 65% and 83%.18-22 Several authors have developed sets of maneuvers to modulate tinnitus; a detailed description of these maneuvers has been published by Won in 2013 comparing the prevalence and characteristics of somatic modulation found in six previous studies.22
SOMATIC MODULATION OF TINNITUS
Temporomandibular Joint
The temporomandibular joint appears to be the region that mostly modulate tinnitus. Several authors reported a prevalent increase of tinnitus loudness following jaw maneuvers14,18-20; this could be explained by the mainly excitatory input of trigeminal nerve stimulated by temporomandibular movements. Rubinstein reported modulation of tinnitus in one-third of studied subjects following jaw movements or pressure on the temporomandibular joint.23 In 2003, Levine reported that up to 80% of the subjects could somatically modulate tinnitus, mainly with jaw maneu-vers.19 In a following study by Simmons, the authors investi-gated patients who could modulate tinnitus by movements of the jaw: 90% indicated that their tinnitus became louder with a jaw clench, 41% reported that clenching caused their tinnitus loud-ness to double, 26% to triple. In the same patient series, a large portion of the subjects reported that jaw movements could also alter the pitch of the tinnitus, mainly increasing it to a higher fre-quency (91%).21 In a smaller sample, Kapoula report that 61% of the examined patients (14/23 subjects) could modulate tinnitus with jaw movements.24 In a recent analysis of 163 patients at the National University of Seoul, South Korea, Won reported that all jaw maneuvers, especially clenching of teeth and opening of the jaw with or without pressure increased tinnitus loudness.22
Head and Neck Musculoskeletal System
Daily fluctuations in perception of tinnitus have been reported, with some patients describing louder tinnitus upon awakening in the morning, while others reported absence of tinnitus in the morning, which returns during the day. Also, some tinnitus suf-ferers have reported experiencing louder tinnitus upon awaken-ing from a nap in the sitting position; this could be explained by somatic factors like cervical spine muscle relaxation during the night or stretching of the neck muscles when the head passively falls forward while sleeping in a sitting position.25
Levine conducted a study on 70 patients and reported that 68% of the subjects could somatically modulate their tinni-tus with head or neck maneuvers.13 This finding was confirmed by Sanchez and colleagues with similar results (65%).18 Kapoula reported that 10 patients out of 23 (43%) were able to modulate their tinnitus with head movements, 9 (39%) with muscle pres-sure.24
Discordant results in terms of increase or decrease of tinnitus loudness have been reported following head and neck maneuvers: Levine reported that 41% of the subjects could in-crease their tinnitus, 17% could decrease tinnitus loudness and 10% could either increase or decrease tinnitus loudness depen-ding upon the maneuver.13 On the contrary, Won reported a con-sistent increase in all jaw maneuvers and a consistent decrease in all head and neck maneuvers.21
Eye (Gaze-Evoked Tinnitus)
Movements of the eye have often been reported inducing a chan-ge in tinnitus pitch and loudness (gaze-evoked tinnitus). This was initially reported by Whittaker in 1982 in a patient experien-cing tinnitus shifting eye gaze from straight to side gaze in right and left directions as a complication of acoustic neuroma sur-gery.26 Simmons found that 77% of patients who had undergone acoustic neuroma surgery developed gaze-evoked tinnitus. In most cases tumor removal resulted in total loss of hearing in the affected ear; patients could hear tinnitus in the side of the acous-tic neuroma. Interestingly, pre-existing tinnitus was a major risk factor associated with the development of gaze-evoked tinnitus in patients who had undergone acoustic neuroma resection.21
Other Structures
Besides temporomandibular joint, cranio-cervical muscle and eye movements, other structures have been also reported modu-lating tinnitus. They include limb,13,18-20 cutaneous stimulation of the hand and face,27,28 finger movements,29 thrusting of the ton-gue in the midline, to the left, and to the right, and movements of facial expression such as eye closure, eyebrow raise, puffing the cheeks, baring the teeth, and pursing the lips.21
DISCUSSION
Tinnitus modulation by somatic movements is a relatively new finding that still requires basic science and human studies to better understand its pathophysiologic basis and clinical corre-lations. However, it has been reported that up to two-thirds of subjects with tinnitus have some form of somatic modulation; therefore this type of tinnitus certainly needs to be taken into ac-count in future research directions.30 Also, under a clinical point of view, somatosensory tinnitus is still widely overlooked by otolaryngologists when approaching tinnitus patients, missing the opportunity to highlight the presence of a disorder external to the auditory pathways that if correctly identified and treated
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could help in obtaining satisfactory results.
To date, there are several open questions about somatosensory tinnitus to be addressed:
1. Modulation of tinnitus is present in some subjects and is ab-sent in others; are there predisposing factors to it? The iden-tification of possible factors, such as gender, age, Tinnitus Handicap Index score, type of sound and tinnitus age, that increase the chance of tinnitus modulation could be an inte-resting information to facilitate patient selection for further somatic testing. Studies on larger patient series are required to address this question.
2. Is there, and how strong it is, an association between the ca-pability to modulate tinnitus and an underlying pathological disorder of the involved region? Modulation seems to be fa-vored when a musculoskeletal disorder is present,31 but can also happen in its absence. The identification of a possible relationship between higher prevalence of positive tinnitus modulation following somatic maneuvers and a disorder of the corresponding region (mainly for temporomandibular joint and cranio-cervical regions) could facilitate the diag-nosis of potentially overlooked temporomandibular joint or cranio-cervical dysfunctions responsible for the somatic ori-gin of the tinnitus and therefore indicate a treatment of these disorders increasing chances of tinnitus improvement.
3. Changes that occur after somatic maneuvers are in most cas-es transitory and last for the time the maneuver is performed or for a short-time afterwards. However, some patients re-ported that tinnitus changes experienced during the maneu-ver, especially in loudness, last for longer periods of time af-ter manipulation. This is consistent with patients who report tinnitus disappearance after a nap or in the morning, mainly linked to head and neck positions, and could represent a basis for a long-lasting effect of manual therapies.
4. Hyperacusis has been recently associated to higher modu-lation of tinnitus with somatic maneuvers of temporoman-dibular joint and head and neck. In a large retrospective analysis, Schecklmann reported that 27% of tinnitus patients were positive to somatic modulation, compared to 38% of patients with tinnitus and hyperacusis.32 This could be linked to a higher sensitivity to somatic input in tinnitus patients with hyperacusis that could follow a generally increased sen-sitivity to sensory input. It would be certainly interesting to further explore this and highlight the basis of such potential hypersensitivity that could be useful for future therapeutic approaches.
In the authors opinion, tinnitus modulation should always be investigated when approaching tinnitus patients. In positive cases, a multidisciplinary approach aimed to identify underlying non-auditory disorders should always be sought to increase chances of tinnitus improvement. Clinical research to
investigate the strength of the connection between modulation and somatic disorder, as well as possible predisposing factors is certainly needed. Further understanding of the pathophysiologic basis of somatic modulation of tinnitus and, especially, more studies on larger patients series are required to address these and many other questions about somatosensory tinnitus.
CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest.
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18. Sanchez TG, Guerra GCY, Lorenzi MC, Brandao AL, Ben-to RF. The influence of voluntary muscle contractions upon the onset and modulation of tinnitus. Audiol Neurotol. 2002; 7: 370-375. doi: 10.1159/000066155
19. Levine RA, Abel M, Cheng H. CNS somatosensory-auditory interactions elicit or modulate tinnitus. Exp Brain Res. 2003; 153(4): 643-648. doi: 10.1007/s00221-003-1747-3
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21. Simmons R, Dambra C, Lobarinas E, Stocking C, Salvi R. Head, neck, and eye movements that modulate tinnitus. Semin Hear. 2008; 29: 361-370.
22. Won JY, Yoo S, Lee SK, et al. Prevalence and factors asso-ciated with neck and jaw muscle modulation of tinnitus. Audiol Neurootol. 2013; 18(4): 261-273. doi: 10.1159/000351685
23. Rubinstein B. Tinnitus and craniomandibular disorders is there a link? Swed Dent J Suppl. 1993; 95: 1-46.
24. Kapoula Z, Yang Q, Lê TT, et al. Medio-lateral postural in-stability in subjects with tinnitus. Front Neurol. 2011; 2: 35. doi: 10.3389/fneur.2011.00035
25. Levine RA. Somatic tinnitus in tinnitus: Theory and manage-ment. BC Decker. 2004; 108-124.
26. Whittaker CK. Tinnitus and eye movement. Am J Otol. 1982; 4(2): 188.
27. Cacace AT, Cousins JP, Parnes SM, et al. Cutaneous-evoked tinnitus. II. Review Of neuroanatomical, physiological and fun-ctional imaging studies. Audiol Neurootol. 1999; 4(5): 258-268. doi: 10.1159/000013849
28. Sanchez TG, Marcondes RA, Kii MA, Lima AS, Rocha CAB, Ono CR. A different case of tinnitus modulation by tactile stimuli in a patient with pulsatile tinnitus. Presented at the Se-cond Meeting of the Tinnitus Research Initiative. Monaco, Eu-rope; 2007: 21-23.
29. Cullington H. Tinnitus evoked by finger movement: Brain plasticity after peripheral deafferentation. Neurology. 2001; 56(7): 978. doi: 10. 1212/ WNL. 56. 7. 978
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OTOLARYNGOLOGY
Open Journalhttp://dx.doi.org/10.17140/OTLOJ-2-126
Otolaryngol Open J
ISSN 2470-4059
Massimo Ralli, MD, PhD1*; Rosaria Turchetta, MD2; Giancarlo Cianfrone, MD2
1Department of Oral and Maxillofacial Sciences, Sapienza University of Rome, Rome, Italy2Department of Otorhinolayngology, Audiology and Ophtalmology, Sapienza University of Rome, Rome, Italy
*Corresponding authorMassimo Ralli, MD, PhD Department of Oral and Maxillofacial SciencesSapienza University of RomeViale del Policlinico 15500186 Rome, ItalyTel. +39 333 8200853 E-mail: [email protected]
Article HistoryReceived: August 26th, 2016 Accepted: September 12th, 2016 Published: September 12th, 2016
CitationRalli M, Turchetta R, Cianfrone G. Hearing disorders in Turner’s syn-drome. Otolaryngol Open J. 2016; 2(4): 115-119. doi: 10.17140/OT-LOJ-2-126
Copyright©2016 Ralli M. This is an open ac-cess article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Volume 2 : Issue 4Article Ref. #: 1000OTLOJ2126
Hearing Disorders in Turner’s Syndrome
Page 115
Mini Review
ABSTRACT
Introduction: Turner’s Syndrome (TS) is associated with hearing disorders in about 20 to 50% of affected individuals. The most common hearing disorders include congenital auricular mal-formations, recurrent otitis media and sensorineural hearing loss, although altered vestibular function and tinnitus have also been reported. Objectives: The aim of this paper is to provide an up-to-date overview of the principal findings and research perspectives about the association between TS and hearing disorders.Review: Middle ear disorders, found in a range between 21 and 91% of subjects, are a conse-quence of morphological cranio-facial alterations resulting in middle ear ventilation dysfunc-tion. Sensorineural hearing loss follows 2 main audiological profiles: a bilateral symmetrical mid-frequency dip and a high frequency down-sloping curve. Although the pathophysiologic basis of sensorineural hearing loss in TS patients are still unclear, several hypothesis have been made so far and are reviewed in this paper.Conclusion: Literature confirms that hearing disorders, although not the most relevant clinical problem in these patients, have a high incidence in patients with TS and should therefore un-dergo early evaluation and monitoring over time.
KEYWORDS: Turner’s Syndrome (TS); Hearing disorders; Hearing loss; Tinnitus.
ABBREVIATIONS: TS: Turner’s Syndrome; SNHL: Sensorineural hearing loss; ABR: Auditory Brainstem Responses.
INTRODUCTION
Turner’s Syndrome (TS), a common chromosomal condition with an estimated incidence of 1 per 2,000 women,1 is associated with hearing disorders in about 20 to 40% of affected individu-als. TS, also known as 45,X, is caused by a complete or partial deletion of one of X chromo-somes; affected subjects are characterized by short stature, typical dysmorphic features, cardiac abnormalities, gonadal dysgenesis, congenital lymphoedema, renal malformations, obesity, diabetes and other minor somatic anomalies described by the Turner’s Syndrome Association.2 Intelligence is usually within normal range, minor problems with non-verbal, social and psy-chomotor skills may be present.3
The most common hearing disorders found in patients with TS include congenital auricular malformations, recurrent otitis media and sensorineural hearing loss.4 Current stud-ies available in the literature report an incidence of hearing loss in about 50% of patients with TS: 60% for sensorineural hearing loss, 25% for conductive hearing loss, and 15% for mixed hearing loss.4-7 Asymptomatic vestibular dysfunction and tinnitus have also been reported, but only in the form of case reports; the first could be due to the impact of estrogen on the vestibule, while the second could be a consequence of hearing deafferentation (Table 1).8
Conductive hearing loss may be a consequence of lymphatic hypoplasia, common in TS, with lymphatic effusion in the middle ear predisposing to adhesions and impaired aeration and drainage, as well as of morphological alterations of the eustachian tube and middle ear following cranio-facial alterations in TS patients, probably the shortening of longitudinal skull
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dimension, and causing inadequate ventilation of the middle ear. The most common alterations include cylindrical shape of the tympanic ostium of the tube, hypotonia of tensor veli pala-tini muscle and mastoid hypocellularity. This results in chronic ventilation dysfunction often followed by chronic otitis media sometimes associated to cholesteatoma.9
Sensorineural hearing loss (SNHL) in TS represents a relatively recent finding and seems to be independent from mid-dle ear diseases; several hypothesis about the pathophysiologic basis have been made so far, but still remain unclear. The most common sensorineural audiological finding in TS patients con-sists in a bilateral symmetrical mid-frequency dip, mainly at 2 kHz, probably correlated to karyotype.10 In some patients, high frequency down-sloping SNHL can also be present. SNHL in TS patients can have an early onset, starting during the first decade of life or, most commonly, during the second and third decades, with a tendency to worsen over time. Studies have attributed the mid-frequency dip to cell cycle delay that is more evident in the middle turn of the cochlea where hair cells have the highest concentration per millimeter length of the organ of Corti.11,12 The early onset of the high-frequency hearing loss may instead be a consequence of a faster apoptotic process of hair cells in the basal turn. Estrogen deficiency could play an important role in
these processes through its action on estrogen receptors in the inner ear.10,13 It is also important to mention that different altera-tions of auditory brainstem responses (ABR) have been reported in TS, revealing possibly impaired cochlear nerve function to the level of brainstem.
OBJECTIVES
Although several papers have been published about the associa-tion between Turner’s Syndrome and hearing disorders, some aspects, especially for patients with sensorineural hearing loss, are still debated and certainly need more clinical and basic re-search studies.14 The purpose of this review paper is to provide an up-to-date overview of the principal findings and research perspectives about such association.
REVIEW OF THE LITERATURE
Several studies have focused on the hearing function in patients with TS. From a literature research, 26 studies that focused on hearing disorders in patients with TS have been found (Table 2). Studies have been published between 1988 and 2015, with an average of 0.89/year (Figure 1). The most relevant are reported in the following paragraph.
Conductive/mixed hearing loss Frequency
Acute otitis media Common
Recurrent acute otitis media Common
Otitis media with effusion Uncommon
Cholesteatoma Rare
Retraction pocket Common
Perforation of the tympanic membrane Uncommon
Sensorineural hearing loss
Bilateral high frequencies hearing loss Common
Bilateral mid frequencies hearing loss Common
Profound hearing loss (>85 dBHL) Very Rare
Other
Tinnitus Case Report
Asymptomatic vestibular dysfunction Case ReportTable 1: Audiological findings reported in patients with Turner’s Syndrome with re-lated frequency.
Figure 1: Frequency of studies reporting audiological findings in patients with Turner’s Syndrome from 1988 to 2016.
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In 2003, Hultcrantz10 performed audiometric and karyo-type exams in 325 women with TS, finding otitis media in 61% and SNHL in 80% of the individuals studied, most of them hav-ing the 45XO or 45XO/46Xi(Xq) karyotype. In 2005, Dhooge23 published a prospective study with a questionnaire and audiolog-ic evaluation in 41 patients with TS (median age: 24 years), find-ing pure sensorineural hearing loss in one-third of the patients (38.8%) and pure conductive losses in one-fifth (21.3%). The remaining 60.1% had normal hearing. One year later, Morimo-to24 studied 33 TS patients with age ranging between 8 and 40 years; 20 subjects showed high-frequency SNHL (60.1%) with a statistically significant correlation between hearing loss, age and body height (p<.001). Also, age-dependent hearing loss was more apparent in patients with monosomic 45,X kariotype than in those with the mosaic type. This was confirmed in a later study published in 2013 by Oliveira30 who reported a large prevalence of high frequency hearing loss in TS patients; those with a 45,X karyotype and isochromosomes with loss of the p-arm of the X chromosome had a greater risk of developing hearing loss than patients with mosaicism. Furthermore, the authors described a linear association between hearing loss and age in these pa-tients. In 2008, Gawron25 studied 51 TS patients (median age: 14.3 years), reporting recurrent acute otitis media in 19.6% of subjects, conductive hearing loss in 11.7%, mixed hearing loss
in 5.9% and a moderate sensorineural hearing loss in 18.6%. The authors also reported altered ABR in 52% of the patients revealing a possible retrocochlear involvement. In the same year, a large study by Bergamaschi and colleagues26 was performed in 173 TS patients (median age: 12 years). Conductive hearing loss was found in 38.7% of patients: persistent secretory otitis media in 55.2%, chronic otitis media in 10.4%, pars flaccida re-traction pocket in 19.4%, chronic otitis media with cholestea-toma in 15% of the subjects. Sensorineural hearing loss occurred in 15.6% of the subjects, mostly bilateral (93%) for both high (42%) and mid (58%) frequencies. In a different paper, Parkin and Walker27 focused on 23 children with TS (median age: 10.4 years), finding middle ear disease in 91% of subjects and SNHL in 9%. In 2009, Hederstierna28 conducted a longitudinal study of hearing decline in women with Turner syndrome, confirming that young and middle-aged women with TS have a progressive type of hearing impairment, deteriorating rapidly in adult age.
The group of Verver of the Radboud University Nijmegen Medi-cal Centre, Netherlands, published 2 studies on hearing function and TS. In the first, the authors studied a group of 60 children with TS and correlated their findings to karyotype, supporting the hypothesis that hearing can be affected by loss of the p-arm of the X-chromosome.29 In the second paper, published in 2014, the authors studied 65 TS patients finding a higher prevalence of
Authors No. of patients Year of Publication
Leheupet al15 60 1988
Watkin et al16 24 1989
Sculerati et al9 22 1990
Hultcrantz et al17 44 1994
Sculerati et al18 24 1996
Hultcrantz et al19 40 1997
Benazzo et al6 62 1997
Stenberg et al7 56 1998
Barrenas et al20 115 1999
Barrenas et al21 119 2000
Gungo R et al12 38 2000
Serra et al4 21 2003
Hultcrantz10 325 2003
Beckam et al5 113 2004
Ostberg et al22 138 2004
Dhooge et al23 41 2005
Morimoto et al24 33 2006
Gawron et al25 51 2008
Bergamaschi et al26 153 2008
Parkin et al27 23 2008
Hederstierna et al28 69 2009
Verver et al29 60 2011
Oliveira et al30 52 2013
Ros et al31 31 2014
Verver et al32 65 2014
Bakhshaee et al33 24 2015
Table 2: Previous studies reporting audiological findings in patients with Turner’s Syn-drome (literature review).
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hearing disorders in patients with monosomy 45,X or isochro-mosome 46,X,i(Xq), thus confirming the results of their previ-ous study.32 In the same year, Ros compared 31 adult patients with TS to 15 women with other congenital hypogonadims and 41 healthy age-matched women. Their findings confirmed that more than a half of TS females presented HL; SNHL was the most frequent pattern among middle-aged women with TS and old age, karyotype and recurrent otitis were predisposing factors to induce HL.31
CONCLUSION
In conclusion, literature confirms that hearing disorders, al-though not the most relevant clinical problem in these patients, have a high incidence in individuals with TS. They can be both conductive due to morphological alterations common to other conditions with similar cranio-facial alterations, and sensorineu-ral with a chronic worsening trend over time. Also, sensorineural hearing loss may not be clinically noticeable in most cases, espe-cially at its onset and during the first decades of life. Therefore, it is always recommended investigating the hearing function in TS patients with subjective and objective techniques includ-ing audiometry, otoacoustic emissions and auditory brainstem responses; both early hearing evaluation and monitoring over time are necessary. Because patients with TS can present with different manifestations affecting multiple systems, the otolar-yngologist should be aware of TS and its association with hear-ing disorders. Further studies are required to better understand the pathophysiologic basis of SNHL in patients with TS, while an increased clinical attention to conductive hearing loss in the recent years has contributed to a substantial decrease in chroni-cization of hearing loss and its consequences.
CONFLICTS OF INTEREST
The authors declare that they have no conflicts of interest.
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