This document provides an overview of otosclerosis, including:
- It is a primary metabolic bone disease affecting the bones of the middle ear that can cause conductive or sensorineural hearing loss.
- The pathophysiology involves abnormal bone remodeling leading to fixation of the ossicles or invasion of the inner ear.
- Treatment options include observation, hearing aids, medical management with drugs like sodium fluoride, and surgical procedures like stapedotomy or stapedectomy to restore hearing.
- Imaging with CT can help grade the severity of the disease and plan for surgical management when indicated based on the air-bone gap and progression of hearing loss.
Perilymph Fistula can be difficult to diagnose as a standalone condition. Post-trauma symptoms such as dizziness, headache, etc. can be linked to other conditions like a traumatic brain injury with a concussion.
otosclerosis....
stapedectomy vs stapedotomy
complication of otosclerotic surgery
management of otosclerotic surgery complications
techniques
latest trends
otosclerosis is also known as otospongiosis. otosclerosis is a condition causing bilateral progressive conductive hearing loss. it is characterized by cahart's notch in bone conduction PTA. treated by stapes surgery also known as stapedotomy/stapedectomy or fenestration surgery.
Eustachian tube is commonly overlooked even by many physicians as effect of chronic otitis media rather than a cause. this is a humble attempt to explain the role eustachian tube dysfunction and interventions to reduce the same
Perilymph Fistula can be difficult to diagnose as a standalone condition. Post-trauma symptoms such as dizziness, headache, etc. can be linked to other conditions like a traumatic brain injury with a concussion.
otosclerosis....
stapedectomy vs stapedotomy
complication of otosclerotic surgery
management of otosclerotic surgery complications
techniques
latest trends
otosclerosis is also known as otospongiosis. otosclerosis is a condition causing bilateral progressive conductive hearing loss. it is characterized by cahart's notch in bone conduction PTA. treated by stapes surgery also known as stapedotomy/stapedectomy or fenestration surgery.
Eustachian tube is commonly overlooked even by many physicians as effect of chronic otitis media rather than a cause. this is a humble attempt to explain the role eustachian tube dysfunction and interventions to reduce the same
Otosclerosis is defined as hereditary localized disease of bone derived from the otic capsule characterized by alternating phases of bone formation and resorption
The mature lamellar bone is resorbed and replaced by an immature woven bone of greater thickness, cellularity and vascularity
First described by Politzer in 1893
Types of Otosclerosis
Stapedial
Cochlear: Round window and Promontory
Mixed: Stapedial + cochlear
Malignant: Rapidly progressing cochlear lesion with severe sensori-neural deafness
Types of Stapedial otosclerosis
1. Anterior focus (commonest): 2 mm anterior to oval
window , fissula ante fenestrum, more unstable
2. Posterior focus: 2 mm behind oval window
3. Circumferential: involves footplate margin only
4. Biscuit type: footplate involved, margin is free
5. Obliterative : Obliterates the oval window completely
Slides prepared and compiled by highly experienced ENT teacher, Dr. Krishna Koirala from Nepal , for teaching undergraduate and postgraduate ENT students in the field of otorhinolaryngology.
A clear and concise explanation of the basic concepts in the subject matter concerned.
He is the Head of department with a sound knowledge in the field of ENT to teach both undergraduate and postgraduate ENT students
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
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- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
3. HISTORY
• Valsalva in 1704 - first to describe hearing loss due to
stapes fixation
• 140 yrs later, Meniere described hearing was temporarily
improved by tapping on the stapes with a small gold rod
• Toynbee – 1841 - described fixation of stapes to margins of
oval window
• Politzer - 1894 - the term coined and histologic features
of Otosclerosis
4. HISTORY OF THE PROCEDURE
1. Mobilization era
a) 1800 – kessel - attempted stapes mobilization without ossicular
chain reconstruction
b) Jack removed the stapes, leaving the oval window open
2. Fenestration era
a) Passow - 1897 - idea of 3rd window , created in promontory and
covered with TM
b) Holmgren – 1923 - created a fistula in HSC and sealed it
immediately with periosteum
c) Sourdille – 1930 - popularized the procedure with his 3-stage
technique
d) Lempert – 1938 - developed a 1-stage technique for HSC
fenestration
• Results, however, were short-lived because the fenestra often
resealed with bone.
5. 3. Stapedectomy era:
a) Rosen – 1952 – accedental stapes mobilization
b) Shea - 1955 - Stapedectomy - Removed the stapes, sealed
the oval window with an autograft vein wall, and then
reconstructed the sound-conducting mechanism with an
artificial prosthesis
4. Stepedotomy era
a) Mayers – 1970s - Stapedotomy using a piston prosthesis
b) Perkins – 1980s - Began using the laser for stapedotomy in a
procedure in which a small hole is made in the footplate
6. INTRODUICTION
Otosclerosis
Primary metabolic bone disease of the otic
capsule and ossicles
Results in fixation of the ossicles and
conductive hearing loss
May have sensorineural component if the
cochlea is involved
Genetically mediated
Autosomal dominant with incomplete
penetrance (40%) and variable expressivity
8. • TYPES:
– ‘Stapedial' otosclerosis: Involves the stapes and clinically
manifested by a CHL with normal TM, the tympanogram
was peaked with normal pressure, with an air-bone gap of
15 dB or more, over 0.5, 1 and 2 kHz
– 'Histologic' otosclerosis: Lesion that does not involve the
stapes, SV joint or cochlear endosteum, is consequently
asymptomatic and can be diagnosed only by post-mortem
examination of the temporal bone.
– 'Cochlear' otosclerosis is a term generally reserved for the
occurrence of pure SNHL due to involvement of cochlea
9. Types of stapedial otosclerosis.
(A) Anterior focus. (B) Posterior focus. (C) Circumferential.
(D) Biscuit type (thick plate). (E) Obliterative
10. EPIDEMIOLOGY
• 0.3 – 0.5% overall prevalence of clinical otosclerosis
% incidence of
Race otosclerosis
Caucasian 10%
Asian 5%
African descent 1%
Common in the Southern State of Tamil Nadu and North
Eastern part of the countries like Orissa, West Bengal &
Bangladesh
11. • Gender
– Histologic otosclerosis – 1:1 ratio
– Clinical otosclerosis – 2:1 (F:M) and 3:1(if AB Gap >30dB)
• 4:1 (in older age group 60 – 80yr)
• Increase progression during pregnancy (10%-17%)
• Bilaterality more common
• Age
– 15-45yr most comon age range of presentation
– 0.6% of individuals <5 yr old have foci of otosclerosis
12. PATHOPHYSIOLOGY
• An otosclerotic lesion consists of
– Areas of bone resorption
– New bone formation
– Connective tissue stroma
– Vascular proliferation
• Earliest histologic alterations is 'blue mantle'
• Blue mantles are areas of the otic capsule that stain more
basophilic than normal.
13. “Blue mantles of Manasseh”
Resorption of enchondral bone with enlargement of perivascular
spaces followed by deposition by immature (spongy) bone and a lot of
cement substance/connective tissue stroma which stains blue with
haematoxylin –eosin stain.
14. PATHOPHYSIOLOGY
• There is – Resorption of endochondral bone with
– Enlargement of the perivascular spaces followed by
– Deposition by immature (woven) bone & connective tissue
– Active resorption and remodelling occur continuously
– Production of more mature (lamellar) bone
– Proliferation of blood vessels in active otosclerotic foci
15. • Otosclerotic foci
– Contain a stroma made up of fibroblasts and histiocytes.
– Absence of acute inflammatory cells or PMN leukocytes.
– Focus is larger in volume than the bone, thus otosclerosis
causes thickening of the structures affected.
– Active or 'spongiotic' characterized by areas of increased
cellularity and vascularity as well as bone resorption and
new bone formation
– Inactive 'sclerotic' focus consisting of dense mineralized
bone.
16. • Expansion of otosclerotic foci can obliterate the oval and
round windows.
• Invasion of the labyrinthine spaces is rare and occurs only in
the most active lesions.
• Lumens of the IAC or facial canals are not invaded, even in the
most severe cases.
17. • Temporal bone section from a 68-year-old man showing
– Focus of active otosclerosis that has reached the endosteum of cochlea.
– There is atrophy and hyalinization of the spiral ligament.
– The organ of Corti is intact
– The stria vascularis appears normal.
18. • Temporal bone section in - 85yr old man with otosclerosis
– Focus of otosclerosis ant. to the OW, contains many vascular channels.
– Ankylosis of stapes footplate (ant. part) and has also pushed the footplate
posteriorly, resulting in narrowing of the posterior stapedio vestibular joint.
– The otosclerotic focus has also reached the endosteum of the basal turn of
the cochlea. Note that the sensory and neural elements of the cochlea are
intact, including the organ of Corti, stria vascularis and spiral ganglion cells.
19. • Distribution:
– Usually b/l – 70-90%
– Ant.to oval window – 80-95%
– Round window niche – 30%
– Medial wall of Cochlear labyrinth – 15%
– Foot plate – 12%
– Post.to oval window – 5-10%
– Other less frequent sites
• Walls of IAC
• Around vestibular and cochlear aqueducts
• Around SCC, malleus and incus
20. Pathology of CHL
• Involvement of the stapes – CHL - 5 to 60 dB.
• Expansion of focus
– Ant.to oval window – fibrous fixation of FP – upto 30dB
– Bony fixation of FP – 30 – 40dB
– Diffuse bony ankylosis of annular lig – CHL - >40dB
21. • Relationship b/w specific histologic changes at the stapes
footplate and magnitude of the air-bone gap
– CHL correlated highly with narrowing and impairment of
the annular ligament, especially at the posterior
stapediovestibular joint space
– Size of AB Gap determined by extent and degree of
narrowing
22. Pathology of SNHL
• Occurs when the focus reaches endosteum of cochlea
• Atrophy of spiral lig
with impairment of
fibrocytes and
replacement by
eosinophils –
hyalinisation of SL
23. • Fibrocytes – coupled, connected by gap jn, forms channel for
flow of ions and metabolites
– Contain enzymes, protein, cytokines are critical for
maintaining metabolic and ionic homeostasis of cochlea
• Cytokines released by the remodelling bone has reached
the ligament diffuse into the spiral ligament upset
the normal state of cytokine control In turn, this would
disrupt fluid and ion homeostasis within the cochlea lead
to a SNHL
24. Pathology of vestibular symptoms
• Degeneration of Scarpa's ganglion resulted from
– Soluble toxic substances liberated by otosclerotic bone (or)
– Changes in biochemistry of the inner ear fluids (or) both
• The incidence of vestibular symptoms correlated with the
degree of SNHL
25. Causes
• Genetic – AD, with incomplete penetration
– COL A1 gene
• Measles – measles RNA – Foot plate specimen
– Elevated levels of antimeasle antibodies in perilymph
– Incidence reduced after vaccine
• Pregnancy and lactation
26. Clinical presentation
• Hearing loss of gradual onset at 15 - 45 years
• Family history
• Slowly progressive course
• Usually bilateral
• Accelerates with pregnancy, estrogen therapy
• Tinnitus
• Paracusis Willisii
• Change of the speech pattern
• Vestibular symptoms
27. EXAMINATION
• Otomicroscopy
– Intact TM
– Schwartze’s sign
• Red vascular blush
seen
• Excessive vascularity
within the mucosa over
an otosclerotic focus
near the oval window
and promontory
– Imp: Can be a source of
unwanted bleeding during
stapes surgery.
31. Carhart’s notch
• Decrease in bone
conduction thresholds
• 05 dB at 500 Hz
• 15 dB at 1000 Hz
• 20 dB at 2000 Hz
• 05 dB at 4000 Hz
• Reverses following
successful surgery
33. CT
Axial cuts
Patient position – canthomeatal line perpendicular
to the table top
1 mm cuts
Top of sup. SCC to bottom of the cochlea
Coronal
Patient position – supine w/ head overextended
face turned 20 degrees ipsilateral
34. • Ref – bela Purohit, Robert Hermans, katya Op de beeck Imaging in
otosclerosis: A pectorial review insights imaging 2014 5:245- 252
35.
36.
37. CT grading system (Symons and Fanning):
• Grade 1
– Solely fenestral, either spongiotic or sclerotic lesions, evident as a
thickened stapes footplate, and decalcified, narrowed or enlarged
round or oval windows
• Grade 2
– Patchy localized cochlear disease (with or without fenestral
involvement)
• Grade 2A: basal cochlear turn involvement
• Grade 2B: middle / apical turns involvement
• Grade 2C: both the basal turn and the middle / apical turns
involvement
• Grade 3
– Diffuse confluent cochlear involvement of the otic capsule (with or
without fenestral involvement)
38. Axial CT images of the petrous bone in patients with otosclerosis.
. Lee TC1, Aviv RI, Chen JM, Nedzelski JM, Fox AJ, Symons SP. CT grading
of otosclerosis 2009 Aug;30(7):1435-9.
39. Pisa sign
• Evaluate the obliquity of stapes towards promontory and the
torsional effect of otosclerosis on the stapes and rest of the
ossicular chain by radiological imaging
• Torsional stresses on the stapes pulling the incus down is
believed to be responsible for Malleoincudal dislocation
40. Pisa sign
• Length
– A straight line was drawn to measure distance b/w the mid
horizontal segment of facial nerve and stapes head in
coronal sections
• Angle
– The angle measured between two lines, one from the oval
window to head of stapes and second line from the
promontory to stapes head
41. • Illustration showing the increase in length
from facial nerve to stapes head due to
obliquity of stapes in otosclerosis
• Illustration showing change in
angle due to obliquity of stapes
in otosclerosis (dotted line).
* Veluswamy Anand, H. N. Udayabhanu, B. Siva Subramaniam: Obliquity of the Stapes in
Otosclerosis: A New Radiological Sign Int Arch Otorhinolaryngoly :2016;20:94–98.
LENGTH ANGLE
42. Length in otosclerotic pt - 2.49 mm +/- 0.24 mm SD
in non-otosclerotic pt - 1.46 mm +/- 0.16 mm SD
Mean angle In otosclerosis pts - 64.55° +/- 7.19° SD
in non-otosclerotic pts - 99.70° +/- 4° SD.
showing length and angle
measured in Otosclerotic patient.
length measured in non-otosclerotic
patient
angle measured in non-otosclerotic
patient..
43. • MRI
– MRI has a limited role.
– Lesions in the lateral wall of the labyrinth
– In retro-fenestral otosclerosis, pericochlear and
perilabyrinthine soft tissue intensity signal on T1 with
contrast enhancement may be demonstrated.
46. Hearing aid
• As a primary treatment in CHL
• In combination with surgery
– Useful in far advanced otosclerosis
– Avoid need for CI
• Post-stapedectomy rehabilitation with hearing aids it is likely
to be the sensorineural rather than CHL
• As a rescue treatment many years after surgery
• BAHA – benefit – do not produce risk of dead ear
– Only hearing ear with otosclerosis
– Post fenestration cavity
47. Medical management
• Aim
– Stabilize the disease by reduction of the osteoclastic bone
resorption and increase osteoblastic bone formation
• Indications
– Cochlear otosclerosis
– Patients with confirmed otosclerosis but having
progressive SNHL disproportionate to age
48. • Drug
– Sodium fluoride: 8mg TID, until hearing loss stabilizes.
– Bisphosphonates eg: itodronate
• Contraindications
– Chronic nephritis
– Rheumatoid arthritis
– Pregnancy and lactation
– Children
49. • Sodium floride
• Idea comes from high incidence in low-fluoride areas
– Antienzymatic activity against proteolytic enzymes
– Reduction of bone resorption
– Changing otospongiotic active lesions to more dense
inactive lesions
– Increase of new bone formation
• The adverse reactions include synovitis, plantar faciitis, peptic
ulcer, anemia, and increased skeletal fragility
50. SURGICAL TREATMENT
• Patient selection
– Socially unacceptable conductive or mixed hearing loss
– Good speech discrimination
– Age
– Lifestyle and occupation
• Flying restrictions – 01 – 24 wk
• Scuba diving restriction - 35% recommended– 01 – 6 months
- >50% recommended - permanent
• Post op test – apply 400mm of H2O – nystagmus
– A-B gap > 20dB
51. • Absolute contraindication of surgery
– The only functioning ear
– Pregnancy
– Active middle or external ear disease
• Other contraindications
– Patients experience frequent changes in barometric
pressure
– Endolymphatic hydrops (constraints for sx – 35dBHL at
500Hz & no high frequency loss)
– TM perforation
59. Lasers in stapes surgery
• Reduce the incidence of intraoperative floating footplate and
incus dislocation.
• As effective as traditional techniques for closure of the air-
bone gap.
• Lasers – Argon
– KTP
– CO2 – decreased inner ear trauma,
• Risk of perilymph heating - reduced by pulsating the
beam, (micropips)
– Er:YAG laser – limited thermal effect
• The newly introduced CO2 laser hand piece is safe and
effective and laser of choice for stapedotomy.
60. Stapedectomy
• The operation is unavoidable in
– Comminuted fracture of the footplate
– Floating footplate
– Revision surgery
• More traumatic to the inner ear
– Increased post-op vestibular symptoms
– Higher incidence of postoperative SNHL
62. STAMP ( stapedotomy minus prosthesis)
• By Silverstein in 1998
• Lesion Ant.part of footplate
• Preservation of the stapedius tendon
– Better speech discrimination in noisy environments
– Increased tolerance for high-amplitude sounds
• No prosthesis complications
64. Outcome of stapes surgery
• After stapes surgery, the biologically remodeled incus would
revert back to its original position due to the absence of
torsional forces of otosclerosis and subsequent pull by the
superior incudal ligament
• Closure of A-B gap <10 dB in > 90% cases
• Persistent benefit > 90% cases
• Profound postoperative SNHL < 1% cases.
65. OPERATIVE PROBLEMS
• Tear in TM flap
– Tragal perichondrium/ fascia graft
• Subluxation/ dislocation of incus
66. Dehiscent / over hanging facial nerve
• 0.5 %
• Stapedotomy is usually possible
• FN abuts promontory inf to OW surgery should not be
completed
• Sx completed by drilling fenestra inf. Part of annular lig.
• Prosthesis must be longer
67. Bleeding
• Mucosal trauma – most common cause
• Active phase – preoperative sodium
fluoride may help
• Persistent stapedial artery – bipolar
cautery or small fenestra stapedotomy in
post segment after mobilizing the artery
68. Obliterative or solid footplate
• Incidence 7-11%
• Solid > obliterated
• Drill out 0.7mm diamond burr
• More chance of post op SNHL
• More chance of reclosure
• Post op sodium fluoride may help
69. Floating footplate
• May be avoided if control holes
are used or by using laser
fenestration
• Extraction is difficult, by
needles/hooks with hole
inferior to the oval window
• Another method is removal
after breaking into several
pieces – submerged footplate
• Fenestration before removal of
suprastructure
71. Incus problems
• Congenital anomalies – short or malformed long process
• Fixation – congenital, developmental, inflammatory
• Necrosis – due to pressure necrosis and insufficient blood
supply
• Dislocation or subluxation
– Remove incus and use malleus attachment prosthesis
72. Malleus ankylosis
• About 1% cases
• May be congenital or acquired (TS)
• Causes about 15-20 dB CHL
• Occurs in later life, Carhart notch, fixed manubrium
• Gentle tap over malleus neck may suffice
• Remove malleus head and the incus and use TORP
73. CSF Gusher
• One of the most dreaded intraoperative complication
• Incidence – 0.03%
• Most reported cases - congenital foot plate fixation
– Widened cochlear aqueduct
– Defect in fundus of IAM
74. CSF Gusher
• Management –
– Immediate head elevation
– Small fenestra stapedotomy
– Placement of large tissue graft prior to prosthesis insertion
75. Perilymph fistula
• Primary - present at the time of surgery
• Secondary – fistula occurs following initial sealing
• Occurs in 9-10% of failed surgery
• Hearing loss, tinnitus, vertigo, disequilibrium
• Several factors contribute –
– Too long prosthesis
– Gelfoam seal of oval window
• Avoid nose blowing, flying, diving, & lifting heavy objects
postoperatively
77. Reparative granuloma
• Granulation tissue formation around the prosthesis and incus
• 1-5%
• Gradual deterioration 5-15 days postoperatively
• Vertigo, tinnitus and deafness
• Otoscopy: reddish discoloration of the posterosuperior TM
• Treatment – immediate exploration and excision
78. SNHL
• 0.6-3% mostly 1st yr of surgery
• Serous labyrinthitis - high frequency hearing loss, vertigo
• Surgical trauma – excessive drilling - permanent hearing loss
• Perilymph leak
• Degeneration of cochlear component
• Reduced blood supply to cochlea
• Acoustic trauma
79. Persistence or recurrence of CHL
• Prosthesis malfunction – short prosthesis, loose wire
syndrome
• Fibrous adhesion, high membrane formation in oval window
• Incus erosion
• Missed pathology: e.g. malleus fixation, round window
otosclerosis
• Otosclerosis regrowth
80. Incus erosion
Missed pathology: e.g. malleus fixation, round
window otosclerosis , Otosclerosis regrowth
Fibrous adhesion, high membrane
formation in oval window
Prosthesis malfunction
81. Revision stapedectomy
• Delayed/immediate post op CHL
• Symptoms of PLF
• Reperative granuloma
• Less Successful results than first operation
• LA, Laser is beneficial
• 8 to 33% with worsening
• SNHL in 3 to 20%
82. Surgical treatment of bilateral otosclerosis
• Poorer ear 1st with +ve results then 2nd
• Gap – 1-180m (median 24m)
83. Cochlear implantation
• Indication – profound b/l SNHL
• In far advanced otosclerosis after failed surgery
• No improvement with hearing aids
Axial CT images of the petrous bone in patients with otosclerosis. Grade 0: normal. Grade 1: small lucent lesion at the fissula ante fenestram. Grade 2A: sclerosis and narrowing of the basal turn (also has spongiotic fenestral disease). Grade 2B: lucent lesion extending from the fissula ante fenestram to the middle turn of the cochlea. Grade 2C: patchy lucency around the lateral aspect of basal, middle, and apical turns of the cochlea, the medial aspect of the cochlea appears spared. Grade 3: severe, confluent lucency around the cochlea.