This document provides an overview of vertigo, including its definition, causes, symptoms, diagnosis, and treatment. Some key points:
- Vertigo is an illusion of movement and is caused by problems in the inner ear or brain. It is distinguished from dizziness and imbalance.
- Common causes include benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuritis.
- Diagnosis involves taking a history, examining for nystagmus and other neurological signs, and tests like Dix-Hallpike and caloric testing.
- Peripheral vertigo tends to be more severe with associated symptoms, while central vertigo is often less severe without
This document provides an overview of the approach to evaluating and diagnosing dizzy patients. It discusses taking a thorough history including details of episodes, performing a neurological and otological exam, and assessing eye movements, vestibular-ocular reflexes, and gait. Common causes of dizziness include peripheral issues like BPPV, Ménière's disease, and vestibular neuritis, as well as central causes like stroke and MS. Treatments for specific conditions like BPPV involve repositioning maneuvers to move canaliths like the Epley maneuver.
Approach to a vertiginous patient - clinical Dr Safika Zaman
This document discusses the anatomy and physiology of the vestibular system and its role in spatial orientation and balance. It describes the components of the vestibular system including the semicircular canals, otolith organs, vestibular nerve and nuclei. It outlines the vestibulo-ocular reflex and how different head motions activate each semicircular canal. The document also discusses the examination of patients with dizziness or vertigo, including tests for nystagmus, positional nystagmus and dynamic visual acuity. Common peripheral and central causes of vertigo like BPPV, vestibular neuritis and Meniere's disease are also mentioned.
This document provides an overview of the anatomy, physiology, and clinical examination of the vestibular system. It describes the anatomy of the inner ear structures involved in balance and spatial orientation. A number of clinical tests are outlined to evaluate vestibular function, including spontaneous nystagmus, gaze-evoked nystagmus, head impulse test, dynamic visual acuity, and caloric testing. Investigation methods like electronystagmography, videonystagmography, and vestibular evoked myogenic potential are also summarized. The goal of the clinical examination and investigations is to localize the cause of dizziness or vertigo to either the peripheral or central vestibular system.
This document provides an overview of nystagmus, including its definition, terminology, types, causes, and characteristics. Nystagmus is defined as a repetitive, to-and-fro movement of the eyes. It is classified as congenital or acquired, and includes types such as infantile nystagmus, spasmus nutans, end point nystagmus, vestibular nystagmus, optokinetic nystagmus, downbeat nystagmus, and nystagmus associated with strabismus. The document discusses the mechanisms, features, and treatments of different forms of nystagmus.
1) Destruction of one labyrinth causes acute symptoms like vertigo and nausea due to asymmetry in vestibular activity, but vestibular compensation leads to resolution of symptoms for most over time.
2) Simultaneous destruction of both labyrinths does not cause vertigo as there is no asymmetry, but causes chronic vestibular insufficiency with problems walking in the dark, seeing clearly with head movement, and orientation.
3) Vestibular neuritis is commonly caused by viral infection of the vestibular nerve, causing acute vertigo, nausea, and imbalance aggravated by head movement along with catch-up saccades on head impulse testing.
This document provides an overview of peripheral vestibular disorders (PVDs). It defines PVDs as pathologies of the inner ear vestibular structures and vestibular nerve that diminish sensory information about head movement. The peripheral vestibular system is described, including the semi-circular canals, otolith organs, and vestibular nerve. Clinical classifications, etiologies, pathophysiology, diagnosis, and treatment approaches for various PVDs are discussed at a high level. Diagnostic tests include electronystagmography and imaging, while treatment may involve vestibular suppressants, rehabilitation exercises, or ablative procedures depending on the specific disorder.
This document provides an overview of vestibular function tests. It discusses the six semicircular canal planes and their roles in detecting head rotation and translation. It describes eye movements like saccades, smooth pursuit, and vestibulo-ocular reflex that stabilize vision. Common vestibular tests are discussed like head thrust, head shaking, and dynamic visual acuity. Features of nystagmus seen with peripheral and central lesions are summarized. A history should inquire about triggers, associated symptoms, and risk factors to localize the cause of dizziness.
Vertigo is a sensation of rotational or linear movement that is not actually occurring. It is caused by disturbances in the vestibular system of the inner ear. Benign paroxysmal positional vertigo (BPPV) and labyrinthitis are two common causes of peripheral vertigo. BPPV involves detached calcium crystals in the inner ear that cause vertigo with certain head movements and is treated with repositioning maneuvers. Labyrinthitis is an inner ear infection that causes both vertigo and hearing loss. It is usually viral in origin and causes sudden onset vertigo, nausea, and unilateral hearing loss.
This document provides an overview of the approach to evaluating and diagnosing dizzy patients. It discusses taking a thorough history including details of episodes, performing a neurological and otological exam, and assessing eye movements, vestibular-ocular reflexes, and gait. Common causes of dizziness include peripheral issues like BPPV, Ménière's disease, and vestibular neuritis, as well as central causes like stroke and MS. Treatments for specific conditions like BPPV involve repositioning maneuvers to move canaliths like the Epley maneuver.
Approach to a vertiginous patient - clinical Dr Safika Zaman
This document discusses the anatomy and physiology of the vestibular system and its role in spatial orientation and balance. It describes the components of the vestibular system including the semicircular canals, otolith organs, vestibular nerve and nuclei. It outlines the vestibulo-ocular reflex and how different head motions activate each semicircular canal. The document also discusses the examination of patients with dizziness or vertigo, including tests for nystagmus, positional nystagmus and dynamic visual acuity. Common peripheral and central causes of vertigo like BPPV, vestibular neuritis and Meniere's disease are also mentioned.
This document provides an overview of the anatomy, physiology, and clinical examination of the vestibular system. It describes the anatomy of the inner ear structures involved in balance and spatial orientation. A number of clinical tests are outlined to evaluate vestibular function, including spontaneous nystagmus, gaze-evoked nystagmus, head impulse test, dynamic visual acuity, and caloric testing. Investigation methods like electronystagmography, videonystagmography, and vestibular evoked myogenic potential are also summarized. The goal of the clinical examination and investigations is to localize the cause of dizziness or vertigo to either the peripheral or central vestibular system.
This document provides an overview of nystagmus, including its definition, terminology, types, causes, and characteristics. Nystagmus is defined as a repetitive, to-and-fro movement of the eyes. It is classified as congenital or acquired, and includes types such as infantile nystagmus, spasmus nutans, end point nystagmus, vestibular nystagmus, optokinetic nystagmus, downbeat nystagmus, and nystagmus associated with strabismus. The document discusses the mechanisms, features, and treatments of different forms of nystagmus.
1) Destruction of one labyrinth causes acute symptoms like vertigo and nausea due to asymmetry in vestibular activity, but vestibular compensation leads to resolution of symptoms for most over time.
2) Simultaneous destruction of both labyrinths does not cause vertigo as there is no asymmetry, but causes chronic vestibular insufficiency with problems walking in the dark, seeing clearly with head movement, and orientation.
3) Vestibular neuritis is commonly caused by viral infection of the vestibular nerve, causing acute vertigo, nausea, and imbalance aggravated by head movement along with catch-up saccades on head impulse testing.
This document provides an overview of peripheral vestibular disorders (PVDs). It defines PVDs as pathologies of the inner ear vestibular structures and vestibular nerve that diminish sensory information about head movement. The peripheral vestibular system is described, including the semi-circular canals, otolith organs, and vestibular nerve. Clinical classifications, etiologies, pathophysiology, diagnosis, and treatment approaches for various PVDs are discussed at a high level. Diagnostic tests include electronystagmography and imaging, while treatment may involve vestibular suppressants, rehabilitation exercises, or ablative procedures depending on the specific disorder.
This document provides an overview of vestibular function tests. It discusses the six semicircular canal planes and their roles in detecting head rotation and translation. It describes eye movements like saccades, smooth pursuit, and vestibulo-ocular reflex that stabilize vision. Common vestibular tests are discussed like head thrust, head shaking, and dynamic visual acuity. Features of nystagmus seen with peripheral and central lesions are summarized. A history should inquire about triggers, associated symptoms, and risk factors to localize the cause of dizziness.
Vertigo is a sensation of rotational or linear movement that is not actually occurring. It is caused by disturbances in the vestibular system of the inner ear. Benign paroxysmal positional vertigo (BPPV) and labyrinthitis are two common causes of peripheral vertigo. BPPV involves detached calcium crystals in the inner ear that cause vertigo with certain head movements and is treated with repositioning maneuvers. Labyrinthitis is an inner ear infection that causes both vertigo and hearing loss. It is usually viral in origin and causes sudden onset vertigo, nausea, and unilateral hearing loss.
This document discusses nystagmus and spontaneous eye movement disorders. It defines nystagmus as involuntary, rhythmic fixation instabilities and describes different types including jerk nystagmus, pendular nystagmus, and saccadic intrusions. It covers the background and control mechanisms of steady gaze fixation. Various characteristics of nystagmus like amplitude, frequency, and waveforms are defined. Different classifications of nystagmus like physiological, early onset, and acquired are outlined along with examples in each category. Specific types like congenital nystagmus, latent nystagmus, gaze-evoked nystagmus, and downbeat nystagmus are described.
This document discusses the evaluation and management of patients presenting with vertigo. It begins with definitions of types of dizziness including vertigo, lightheadedness, presyncope, disequilibrium, and oscillopsia. It then covers the causes of vertigo which can be peripheral involving the vestibular end organs or central involving the brainstem or cerebellum. The document outlines the history, examination including vestibular function tests like caloric testing and rotational chair, and interpretation of results for diagnosing the cause and site of lesion for vertigo.
1. Dizziness and vertigo are common yet imprecise symptoms that can have many underlying causes and need to be differentiated.
2. Vertigo is a type of dizziness characterized by a perception of motion or spinning, which can be caused by problems in the inner ear or central nervous system.
3. Benign paroxysmal positional vertigo (BPPV) is an extremely common cause of vertigo brought on by changes in head position, characterized by short-lived, intense episodes of vertigo with horizontal nystagmus.
In-service project for clinical affiliation with Hingham PT, Inc. (Januay 2014-April 2014)
Review of vestibular system, common diagnosis and how to examine, evaluate and treat.
I also reviewed and supplied the clinic with the Four Step Square Test and Dynamic Gait Index in order to allow them to implement these outcome assessments into their clinic for individuals with balance/vestibular deficits
Vestibular assessment from the physiotherapy perspective SCGH ED CME
This document discusses vestibular assessment from a physiotherapy perspective. It begins with anatomy of the extraocular eye muscles and semicircular canals. Vestibular dysfunction can cause vertigo and imbalance, and the cause may be central or peripheral. A subjective history focuses on symptoms, tempo, and circumstances. Objective assessment includes eye movement testing, cerebellar tests, Rhomberg testing, and gait observation. Specific tests like Dix-Hallpike and roll tests evaluate the semicircular canals. Differential diagnoses and treatments like canalith repositioning maneuvers are also reviewed.
Vertigo and Nystagmus - Clinical approach part-2.pptxYasser Alzainy
This document provides an overview of vertigo and nystagmus. It begins by classifying nystagmus and discussing types of non-neuropathic and neuropathic nystagmus. Central and peripheral causes of dizziness are then reviewed. For central causes, various cerebrovascular, demyelinating, and structural disorders are discussed. For peripheral causes, vestibular neuritis, benign paroxysmal positional vertigo, and Meniere's disease are described in terms of their presenting symptoms, diagnostic maneuvers, and typical clinical courses.
This document defines and classifies different types of nystagmus. It describes the key characteristics of different nystagmus including congenital motor nystagmus, periodic alternating nystagmus, spasmus nutans, vestibular nystagmus, upbeat nystagmus, downbeat nystagmus, and nystagmus associated with strabismus. It also discusses the mechanisms, localization, and treatment options for nystagmus including optical devices, pharmacology, botulinum toxin injections, and surgery.
The document discusses vestibular rehabilitation and benign paroxysmal positional vertigo (BPPV). It notes that 90 million Americans experience dizziness each year, with the costs of treatment exceeding $1 billion annually. BPPV is one of the most common causes of dizziness, involving debris in the inner ear causing vertigo with certain head movements. Treatment options discussed include physical therapy, occupational therapy, and vestibular rehabilitation exercises and maneuvers like the Epley maneuver to reposition the debris.
Nystagmus: clinical implications in otorhinolaryngology.one should understand anatomy and physiology of semicircular canals and vestibuloocular reflex in order to understand pathophysiology of nystagmus
This document provides information on benign paroxysmal positional vertigo (BPPV), including what it is, what causes it, how it is diagnosed, and treatment options. BPPV is the most common cause of vertigo and involves dislodged crystals in the inner ear that cause brief periods of vertigo in certain head positions. It is diagnosed using tests like Dix-Hallpike that provoke nystagmus. Treatment includes exercises to reposition the crystals, like Epley maneuver, or rarely surgery.
This document discusses benign paroxysmal positional vertigo (BPPV). It begins with an overview of the anatomy and physiology of the vestibular system. It then defines BPPV and discusses its pathogenesis, symptoms, types, differential diagnosis, investigations and treatment modalities. The most common treatment is canalith repositioning procedures like the Epley maneuver which aims to move otoliths out of the semicircular canals.
Vestibular disorders and rehabilitationRuchika Gupta
This document discusses vestibular disorders, specifically Benign Paroxysmal Positional Vertigo (BPPV). It defines BPPV as the most common cause of vertigo, triggered by certain head positions. Physical therapists are well-suited to diagnose and treat BPPV using positional tests to identify affected semicircular canals, followed by repositioning maneuvers like the Epley maneuver to guide loose crystals back to their proper position. Proper diagnosis and treatment of BPPV by a physical therapist can resolve symptoms and address related functional impairments.
Nystagmus refers to involuntary eye oscillations. There are several types of nystagmus including physiological nystagmus seen with extreme gaze, optokinetic nystagmus induced by moving targets, and vestibular nystagmus caused by altered vestibular input. Infantile nystagmus syndrome includes idiopathic congenital nystagmus and nystagmus associated with visual pathway diseases. Acquired nystagmus can be conjugate seen with brainstem and cerebellar diseases, or disconjugate like acquired pendular nystagmus. Treatment is difficult but may include drugs, optical devices, or surgery to stabilize or move the null position.
Understanding & Managing Vertigo : Dr Vijay SardanaVijay Sardana
The document discusses vertigo, including its prevalence, causes, mechanisms, types, clinical evaluation, and treatment. Vertigo is a common symptom that can be caused by disturbances in the peripheral or central vestibular system. Treatment involves identifying the specific cause and providing symptomatic relief through vestibular suppression or rehabilitation to aid compensation. Medications like antihistamines and betahistine that affect the vestibular system can help manage vertigo symptoms.
This document provides information on dizziness and balance disorders from Dr. Zuraida Zainun, a senior lecturer in audiology. It includes definitions of dizziness, descriptions of different dizziness subtypes, factors to consider in the history and examination of patients with dizziness, details on various vestibular and balance tests, differential diagnoses, and concepts of management including vestibular rehabilitation exercises and follow up. References are also provided on topics related to dizziness and balance disorders.
This document summarizes clinical tests used to examine patients presenting with vertigo. It describes tests to evaluate nystagmus including spontaneous, gaze-evoked, and positional nystagmus. Pursuit, saccadic, and vestibulo-ocular reflex testing is outlined. Positional maneuvers like Dix-Hallpike and roll tests evaluate benign paroxysmal positional vertigo. Caloric testing assesses vestibular function by irrigating each ear with warm and cold water. Together, these examinations localize pathology and differentiate peripheral from central causes of vertigo.
1) Dizziness and vertigo are common, with vertigo defined as a perception of movement and dizziness having various meanings.
2) Vertigo can be peripheral or central in origin, with peripheral vertigo arising from problems in the inner ear and central vertigo from problems in the brain or brainstem.
3) A thorough history, physical exam including tests like Dix-Hallpike, and sometimes ancillary testing can help differentiate between peripheral causes like benign paroxysmal positional vertigo or Ménière's disease versus central causes like vertebrobasilar insufficiency.
Benign paroxysmal positional vertigo (BPPV) is the most common cause of positional vertigo. It involves abnormal sensations of movement triggered by certain head positions. Calcium particles in the inner ear can become dislodged and enter the semicircular canals, stimulating hair cells and causing vertigo. The Dix-Hallpike maneuver is used for diagnosis - a patient is positioned to provoke nystagmus if BPPV is present. Treatment involves maneuvers like the Epley maneuver to reposition the particles.
This document provides information on various causes of vertigo including peripheral and central causes. It discusses conditions like benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuritis. Diagnostic tests and treatments for different vertigo conditions are outlined, such as the Dix-Hallpike test for BPPV and Brandt-Daroff exercises or Epley maneuver for treatment. Surgical options are mentioned if conservative treatments are unsuccessful.
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
This document discusses nystagmus and spontaneous eye movement disorders. It defines nystagmus as involuntary, rhythmic fixation instabilities and describes different types including jerk nystagmus, pendular nystagmus, and saccadic intrusions. It covers the background and control mechanisms of steady gaze fixation. Various characteristics of nystagmus like amplitude, frequency, and waveforms are defined. Different classifications of nystagmus like physiological, early onset, and acquired are outlined along with examples in each category. Specific types like congenital nystagmus, latent nystagmus, gaze-evoked nystagmus, and downbeat nystagmus are described.
This document discusses the evaluation and management of patients presenting with vertigo. It begins with definitions of types of dizziness including vertigo, lightheadedness, presyncope, disequilibrium, and oscillopsia. It then covers the causes of vertigo which can be peripheral involving the vestibular end organs or central involving the brainstem or cerebellum. The document outlines the history, examination including vestibular function tests like caloric testing and rotational chair, and interpretation of results for diagnosing the cause and site of lesion for vertigo.
1. Dizziness and vertigo are common yet imprecise symptoms that can have many underlying causes and need to be differentiated.
2. Vertigo is a type of dizziness characterized by a perception of motion or spinning, which can be caused by problems in the inner ear or central nervous system.
3. Benign paroxysmal positional vertigo (BPPV) is an extremely common cause of vertigo brought on by changes in head position, characterized by short-lived, intense episodes of vertigo with horizontal nystagmus.
In-service project for clinical affiliation with Hingham PT, Inc. (Januay 2014-April 2014)
Review of vestibular system, common diagnosis and how to examine, evaluate and treat.
I also reviewed and supplied the clinic with the Four Step Square Test and Dynamic Gait Index in order to allow them to implement these outcome assessments into their clinic for individuals with balance/vestibular deficits
Vestibular assessment from the physiotherapy perspective SCGH ED CME
This document discusses vestibular assessment from a physiotherapy perspective. It begins with anatomy of the extraocular eye muscles and semicircular canals. Vestibular dysfunction can cause vertigo and imbalance, and the cause may be central or peripheral. A subjective history focuses on symptoms, tempo, and circumstances. Objective assessment includes eye movement testing, cerebellar tests, Rhomberg testing, and gait observation. Specific tests like Dix-Hallpike and roll tests evaluate the semicircular canals. Differential diagnoses and treatments like canalith repositioning maneuvers are also reviewed.
Vertigo and Nystagmus - Clinical approach part-2.pptxYasser Alzainy
This document provides an overview of vertigo and nystagmus. It begins by classifying nystagmus and discussing types of non-neuropathic and neuropathic nystagmus. Central and peripheral causes of dizziness are then reviewed. For central causes, various cerebrovascular, demyelinating, and structural disorders are discussed. For peripheral causes, vestibular neuritis, benign paroxysmal positional vertigo, and Meniere's disease are described in terms of their presenting symptoms, diagnostic maneuvers, and typical clinical courses.
This document defines and classifies different types of nystagmus. It describes the key characteristics of different nystagmus including congenital motor nystagmus, periodic alternating nystagmus, spasmus nutans, vestibular nystagmus, upbeat nystagmus, downbeat nystagmus, and nystagmus associated with strabismus. It also discusses the mechanisms, localization, and treatment options for nystagmus including optical devices, pharmacology, botulinum toxin injections, and surgery.
The document discusses vestibular rehabilitation and benign paroxysmal positional vertigo (BPPV). It notes that 90 million Americans experience dizziness each year, with the costs of treatment exceeding $1 billion annually. BPPV is one of the most common causes of dizziness, involving debris in the inner ear causing vertigo with certain head movements. Treatment options discussed include physical therapy, occupational therapy, and vestibular rehabilitation exercises and maneuvers like the Epley maneuver to reposition the debris.
Nystagmus: clinical implications in otorhinolaryngology.one should understand anatomy and physiology of semicircular canals and vestibuloocular reflex in order to understand pathophysiology of nystagmus
This document provides information on benign paroxysmal positional vertigo (BPPV), including what it is, what causes it, how it is diagnosed, and treatment options. BPPV is the most common cause of vertigo and involves dislodged crystals in the inner ear that cause brief periods of vertigo in certain head positions. It is diagnosed using tests like Dix-Hallpike that provoke nystagmus. Treatment includes exercises to reposition the crystals, like Epley maneuver, or rarely surgery.
This document discusses benign paroxysmal positional vertigo (BPPV). It begins with an overview of the anatomy and physiology of the vestibular system. It then defines BPPV and discusses its pathogenesis, symptoms, types, differential diagnosis, investigations and treatment modalities. The most common treatment is canalith repositioning procedures like the Epley maneuver which aims to move otoliths out of the semicircular canals.
Vestibular disorders and rehabilitationRuchika Gupta
This document discusses vestibular disorders, specifically Benign Paroxysmal Positional Vertigo (BPPV). It defines BPPV as the most common cause of vertigo, triggered by certain head positions. Physical therapists are well-suited to diagnose and treat BPPV using positional tests to identify affected semicircular canals, followed by repositioning maneuvers like the Epley maneuver to guide loose crystals back to their proper position. Proper diagnosis and treatment of BPPV by a physical therapist can resolve symptoms and address related functional impairments.
Nystagmus refers to involuntary eye oscillations. There are several types of nystagmus including physiological nystagmus seen with extreme gaze, optokinetic nystagmus induced by moving targets, and vestibular nystagmus caused by altered vestibular input. Infantile nystagmus syndrome includes idiopathic congenital nystagmus and nystagmus associated with visual pathway diseases. Acquired nystagmus can be conjugate seen with brainstem and cerebellar diseases, or disconjugate like acquired pendular nystagmus. Treatment is difficult but may include drugs, optical devices, or surgery to stabilize or move the null position.
Understanding & Managing Vertigo : Dr Vijay SardanaVijay Sardana
The document discusses vertigo, including its prevalence, causes, mechanisms, types, clinical evaluation, and treatment. Vertigo is a common symptom that can be caused by disturbances in the peripheral or central vestibular system. Treatment involves identifying the specific cause and providing symptomatic relief through vestibular suppression or rehabilitation to aid compensation. Medications like antihistamines and betahistine that affect the vestibular system can help manage vertigo symptoms.
This document provides information on dizziness and balance disorders from Dr. Zuraida Zainun, a senior lecturer in audiology. It includes definitions of dizziness, descriptions of different dizziness subtypes, factors to consider in the history and examination of patients with dizziness, details on various vestibular and balance tests, differential diagnoses, and concepts of management including vestibular rehabilitation exercises and follow up. References are also provided on topics related to dizziness and balance disorders.
This document summarizes clinical tests used to examine patients presenting with vertigo. It describes tests to evaluate nystagmus including spontaneous, gaze-evoked, and positional nystagmus. Pursuit, saccadic, and vestibulo-ocular reflex testing is outlined. Positional maneuvers like Dix-Hallpike and roll tests evaluate benign paroxysmal positional vertigo. Caloric testing assesses vestibular function by irrigating each ear with warm and cold water. Together, these examinations localize pathology and differentiate peripheral from central causes of vertigo.
1) Dizziness and vertigo are common, with vertigo defined as a perception of movement and dizziness having various meanings.
2) Vertigo can be peripheral or central in origin, with peripheral vertigo arising from problems in the inner ear and central vertigo from problems in the brain or brainstem.
3) A thorough history, physical exam including tests like Dix-Hallpike, and sometimes ancillary testing can help differentiate between peripheral causes like benign paroxysmal positional vertigo or Ménière's disease versus central causes like vertebrobasilar insufficiency.
Benign paroxysmal positional vertigo (BPPV) is the most common cause of positional vertigo. It involves abnormal sensations of movement triggered by certain head positions. Calcium particles in the inner ear can become dislodged and enter the semicircular canals, stimulating hair cells and causing vertigo. The Dix-Hallpike maneuver is used for diagnosis - a patient is positioned to provoke nystagmus if BPPV is present. Treatment involves maneuvers like the Epley maneuver to reposition the particles.
This document provides information on various causes of vertigo including peripheral and central causes. It discusses conditions like benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuritis. Diagnostic tests and treatments for different vertigo conditions are outlined, such as the Dix-Hallpike test for BPPV and Brandt-Daroff exercises or Epley maneuver for treatment. Surgical options are mentioned if conservative treatments are unsuccessful.
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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2. INTRODUCTION
5–10 % of all patients seen in general practice
Dizziness/vertigo/unsteadiness accounts for 25 % of
referrals to ENT and neurology clinics [Bronstein, 2008]
Associated symptoms include nausea, emesis, and
diaphoresis
Vertigo should be distinguished from “mimickers”, viz
imbalance (disequilibrium), light-headedness (giddiness),
presyncope
3. Latin word ‘vertere’ : ‘to turn’
Unpleasant feeling of subjective sense of movement of body
(subjective vertigo) or of surrounding environment (objective vertigo)
DEFINITION
American Academy of Otolaryngology - HNS Foundation [AAO-HNSF]-
2017 Update: “An illusory sensation of motion of either self or
surroundings in absence of true motion”
4. Positional Vertigo:
“A spinning sensation produced by changes in head position relative to
gravity”
- [AAO-HNSF]-2017 Update
BPPV:
“A disorder of the inner ear characterized by repeated episodes of
positional vertigo”
- [AAO-HNSF] - 2017 Update
5. “Dizziness” – lay term; non specific
Denote lightheadedness / giddiness / faintness
Causes include medical conditions
Can often accompany vertigo, but can appear
independently
Light headedness/ giddiness – non specific
Range from uneasy feeling/nauseating feel/imbalance
Presyncope – feeling of upcoming swoon/collapse with
darkening sight or tinnitus; without LOC.
If LOC (+) - syncope
8. Features of a Vestibular Disorder
Pathways Cardinal features
Vestibulo-ocular tracts (VOR) Nystagmus
Vestibulospinal tracts (VST) Falling to side
Vestibulocerebellar tracts (VCT) Ataxia, imbalance
Emetic pathways Nausea, vomiting
Parietotemporal cortex Vertigo
Vestibulohypothalamic tracts Autonomic features
9.
10. Vertigo implies dysfunction of vestibular system [4 events]
Postural imbalance (dystaxia)
Ocular motor movts (nystagmus)
Autonomic symptoms (Nausea/vomiting/sweating)
Perceptal alterations (vertigo)
11. HISTORY
EXAMINATION
GENERAL
HEAD AND NECK
EAR
NEURO-OTOLOGICAL
VOR TEST –DIX HALLPIKE & LATERAL SEMICIRCULAR CANAL TEST
HEAD THRUST TEST ,CALORIC TEST
CRANIAL NERVE EXAMINATION
COORDINATION &POSTURE
GAIT & SPECIAL TEST
12. HISTORY
• Key history points
• Is it vertigo?
• Duration
• What are precipitating factors?
• Accompanying symptoms
14. PERIPHERAL VS CENTRAL ORIGIN VERTIGO
Feature Peripheral Central
Severity Severe vertigo/nausea &
vomiting
Less severe
Onset Acute Subacute or slow
Duration Short duration; subsides Persists
Otological
symptoms
Common Rare
Asso neurological
symptoms
Absent Present
Change with OF Reduces No change
Abolition of OF Aggravates No change
OF : optic fixation
16. DURATION OF VERTIGO
TIME PERIPHERAL CENTRAL
Seconds BPPV VB-TIA ,aura of epilepsy
Minutes Perilymph fistula VB-TIA ,aura of migraine
Hours Meniere’s disease
Vestibular migraine
Basilar migraine
Days Vestibular neuritis
labyrinthitis
VB- stroke
Weeks , months Acoustic neuroma
Drug toxicity
Multiple sclerosis,
cerebellar degenerations
Varies SSCD
17. SINGLE VERTIGO EPISODE
Hearing Possible cause
Hearing spared Vestibular neuritis
Or viral labyrinthitis
Head injury
Hearing involved Head injury
Labyrinthine fistula
Viral infection( mumps , Ramsay hunt)
Vascular(labyrinthine stroke)
18.
19. RED FLAGS IN ACUTE VERTIGO
INDICATION FOR BRAIN IMAGING
Modified from Seemungal and Bronstein
Acute Unilateral deafness
Acute (occipital headache)
Any central symptoms or signs
A negative (normal )head –impulse test
24. Nystagmus :
Greek word – “tired/sleepy”
Involuntary rhythmic oscillating & conjugate movt of eyes, due
to defect in vestibular system
Slow drift in 1 direction (vestibular/visual induced component),
then fast flicking movt in opp direction (centrally controlled
movt-cerebral compensation) : Jerk nystagmus
Paradoxically nystagmus direction termed wrt fast movt
Horizontal/rotatory/vertical
25. Physiological nystagmus
• Continuation of visual fixation. A form of OKN
Induced nystagmus
• Caloric/position tests
Spontaneous nystagmus
• Always pathological
26. Optokinetic nystagmus (OKN):
Involved in maintainance of visual fixation on moving object
in absence of head movts
Movt of image across retina results in compensatory eye
movts which keep image fixed on fovea
Slow movt (smooth pursuit) & restorative fast movt (saccade)
27. Ewald’s law
Regarding relationship b/w labyrinthine receptors & vestibular reflexes which they mediate
1st law – Head & eye movements always occur in plane of canal being stimulated & in direction of
endolymph flow
2nd law - In LSCC, ampullopetal endolymph flow causes a greater response than ampullofugal flow
3rd law - In PSCC, ampullofugal endolymph flow causes a greater response than
ampullopetal response
• Excitatory stimuli & their responses are of greater amplitude than inhibitory stimuli
• Fast component of nystagmus always opp to direction of flow of endolymph
28. ALEXANDER’S LAW
Vestibular nystagmus, if present, can be enhanced by moving the eyes in direction of fast
phase, & decreased by moving eyes to direction of slow phase
For peripheral origin nystagmus
Direction of nystagmus is dependent on the direction of fast component
A second/third degree nystagmus will enhance on gaze deviation in the direction of fast
phase
29. NYLEN’S CLASSIFICATION
Severity of nystagmus wrt fast component
According to Alexander’s law, holds ground for nystagmus of peripheral origin
1st degree – Present when pt looks in direction of fast component. Weak
nystagmus
2nd degree – Present when pt looks straight ahead (neutral gaze)
3rd degree – Present even when pt looks in direction of slow component. Most
severe
30. LSCC: maximally excited by rotation toward side of canal &
inhibited by rotation in opposite direction
Results in excitatory slow phase movt toward opp side & a resetting saccade
towards canal (Horizontal nystagmus)
SSCC: excited by rotation downward and to side, in the plane of canal
Results in vertical-torsional nystagmus, with slow phase of vertical component
upward & resetting saccade downward (Downbeat torsional nystagmus)
PSCC: excited by upward rotation & to side, in plane of canal, so that slow phase
is downward & resetting phase upward (Upbeat torsional nystagmus)
31. Feature Peripheral Central
Latency 2-20 s No latency
Duration < 1 mt > 1 mt
Direction of
nystagmus
Fixed (towards
undermost ear)
Changing
Fatigablility Fatiguable Non fatiguable
Habituation Yes No
Acc symptoms Severe None or slight
Fatiguability – Response remit spontaneously as position maintained
Habituation – Attenuation of response as position repeatedly assumed
32. Elicit nystagmus
• Pt seated comfortably in front
• Examiner keeps finger 30 cm in front of pt’s eye in central position, &
moves it sideways & upward-downward within 30 degree (never beyond
30 degree)
• Keep finger in each position for about 5 sec
• Frenzel glass
33. • Positive
1.Erosion of horizontal semi circular canal
2.Fenestration surgery
3.Post stapedectomy fistula
4.Rupture of round window membrane
• False positive
1. Congenital syphilis (Hennebert sign)
2. Menieres ds
3. SSCC dehiscence
FISTULA TEST
35. Head shaking nystagmus test
• Test of dynamic vestibular function
• Pt asked to shake head vigorously 30 times horizontally, with chin placed about 30
degree downward
• Stop head shaking abruptly – w/f nystagmus
• (N) – no or occassionally 1-2 beats
• U/L peripheral vestibular deficit – nystagmus (initial phase with slow phase towards
lesion side; then reversal )
• Cerebellar defects – vertical nystagmus (cross coupled nystagmus)
36. • Patient is asked to follow series of vertical stripes on a moving drum
(moving in alternate directions)
• Normally produces nystagmus- slow component in the direction of
moving strips, & fast component in opp direction
• Useful to detect central lesions (brainstem/cerebral hemisphere
lesions)
OPTOKINETIC TEST
38. CALORIC TEST
• Induce nystagmus by thermal stimulation of labyrinth
• Allow separate testing of each labyrinth
• Stimulates LSCC
Modified Kobrak test-
1. Pt seated with head tilted 60 deg backward (place LSCC in vertical position)
2. 5 ml of ice water instilled for 60 sec. If no response; then 10ml, 20ml, 40ml
3. (N)-nystagmus to opp side with 5 ml water
4. Response with increased quantities - hypoactive labyrinth
5. No response at 40ml – dead labyrinth
39. Fizgerald Hallpike test (bithermal caloric test)
• PRINCIPLE: thermal change induces convection currents in LSCC
(when placed vertically) and thus cupular deflection
• Patient is made to lie down with head raised 30 deg above
horizontal
• each irrigation lasting 40 sec alternatively with water at 30 deg & 44
deg C
• Gap of 5 min is given between the irrigation
• If no response – repeat with 20 deg C water for 4 mts before
labelling the labyrinth dead
40. • “COWS” – Cold water – nystagmus to opp side
Warm water – nystagmus to same side
• Observe for nystagmus till its end point
• Chart time taken from start of irrigation to end point of nystagmus on
calorigram
41. Cold air caloric test
• In TM perforations (irrigation C/I)
• Dundas Grant tube : coiled copper tube wrapped in cloth
• Air in tube cooled by pouring ethyl chloride, & then blown into ear
42. • Method of detecting & recording of nystagmus
• Used in caloric/positional/rotational/optokinetic stimulus
• Detects corneoretinal potentials by placing electrodes
around eyes
Uses-
• Permanent record
• Detect nystagmus not seen with naked eye
ELECTRONYSTAGMOGRAPHY
43. Typical pattern of nystagmus to the left. This trace
represents the eye movement amplitude in degrees
(vertical) as a function of time in seconds (horizontal)
44. • Patient seated in Barany’s revolving chair with head tilted
300 forward
• Rotated 10 turns in 20 sec
• Nystagmus (25-40s) observed on abrupt stopping of
chair
• Uses – congenital EAC stenosis/agenesis : when caloric
tests cannot be done
• Disadvantage- both labyrinths are stimulated
ROTATION TEST
45. • The only vestibular test differentiating end organ lesion from
vestibular nerve lesions
• Pt erect with feet together, eyes closed & arms outstretched
• Current of 1mA passed to one ear
• If Current is positive- person sways towards the stimulated ear
• If current is negative – person sways away from the stimulated ear
GALVANIC TEST
46. • Method to evaluate vestibular function by measuring postural
stability
• Principle- maintenance of posture depends on 3 sensory inputs –
visual, vestibular, somatosensory
POSTUROGRAPHY
49. TREATMENT OF VERTIGO
• TREATMENT OF CHOICE DEPEND ON THE CAUSE OF VERTIGO
General rehabilitation measures
• Physical exercise programs
• Rehabilitation : Correction/remedial measures
• Psychological support
• Pharmacotherapy
• Social/familial/economic rehabilitation
• Monitoring, feedback & follow-up
50. General rehabilitation measures :
• Individualized program of physical rehabilitation
• Mx of musculoskeletal disorders, retraining of gait & stance
• Correction of optic disorders
• Biofeedback : retraining in age related disequilibrium
51. Physical exercise regimens
• Systematic exercise program
Cooksey Cawthorne regimen
• Customized exercise program
Individualized program based on functional difficulties
Pts instructed to work at limit of their ability
Initial home training program – by physiotherapist
• Specific therapies
Epley/Semont/Brandt Daroff maneuvers
52. Cooksey Cawthorne regimen :
• For peripheral vestibular disorders (1940s)
• Aimed at encouraging head & eye movts that provoked dizziness
in systematic manner
• 80% pts – effectively benefitted
• Perform with eyes open & closed – promote compensation using
vestibular & propioceptive mechanisms
• Resting, sitting, standing & moving about positions
• Eye & head movts; throwing ball from 1 hand to other; walk across
room; walk up & down stairs; bending forward to pick up objects
53. Pharmacotherapy
• Vestibular sedatives/Vasodilators/Anti emetics/ Central depressants
• GABA – Inhibitory NT in vestibular system
• Avoid chronic use & in C/c symptoms : suppress central vestibular activity which is crucial for
development of compensatory mechanisms
• Use judiciously in acute symptomatic pts to enable initiation of exercise regimes. To be withdrawn
as soon as possible
• In anticipated position testing, withdraw medications at least 48 hrs prior to test
54. Commonly used agents for the management of
vertigo
Agent Dose
Antihistamines
Meclizine 25-50 mg 3 times a day
Dimenhydrinate 50 mg 1-2 times daily
Promethazine 25 mg 2-3 times daily
Benzodiazepines
Diazepam 2.5 mg 1-3 times daily
Clonazepam 0.25 mg 1-3 times daily
Anticholinergic
Scopolamine transdermal Patch
55. Agent Dose
Others
Diuretics or low sodium diet (1g/d)
Methylprednisolone 100 mg daily (1-3) days
Anti migrainous drugs
Dopamine blocker :
Prochlorperazine
5 mg TID (30 mg daily)
Vasodilators
Betahistine 4/8/16/32 mg BD/TID
Cinnarizine 25 mg 1-2 times daily
Flunnarizine 5/10 mg OD
56. Betahistine
Reduce endolymphatic pressure by improved microcirculation in stria vascularis
of cochlea or inhibit activity of vestibular nuclei
Prochlorperazine (Stemetil)
Dopamine antagonist
Block CTZ & hence vomiting center
Antihistaminics
H1 blockers – act on vomiting center
Sedation
57. Surgery : reserved for those severe cases where medical therapy fails or
debilitate person affected
Over the years, several surgical options have evolved from endolymphatic sac
surgery, labyrinthectomy to vestibular neurectomy to singular neurectomy and
now vestibular implants
58. Surgery for SSCC dehiscence
• Plugging the dehiscence via MCF approach
• Dehiscence detected by HRCT temporal bone parasagittal cut
Surgery for Perilymph fistula
• Exploratory tympanotomy
(LA with IV sedation to enable valsalva manuevre to detect leaks)
• EUM repair by sealing suspected area with fat; fascia & sealed with bone
wax
59. Surgery for Meniere’s disease
• Cochleosacculotomy (endolymphatic shunt procedure)
Connect endolymphatic sac with subarachnoid space- drain excess endolymph
• Portman procedure (decompression of endolymphatic sac)
Create permanent fistula in endolymphatic sac : ensure expansion of endolymph sac during
crisis
• Sacculotomy (Fick’s operation)
Puncturing distended saccule via stapes footplate
62. 50 yr female c/o recurrent brief periods of rotatory vertigo ; often with nausea
& vomiting. They aggravated with certain head positions & also rolling over in
bed. The episodes typically came in spells, and lasted < 1 mt
O/E- TM (N), Position test (+), PTA (N), CT & MRI (N)
63. MC disorder of peripheral vestibular system
50-70 % - idiopathic
Secondary BPPV- Trauma (7-17 %)
Viral neumolabyrinthitis
Meniere’s disease
Migraine
Ischemic processes
Iatrogenic – otological surgery;
reposition manouevres
5th – 7th decade
♀ > ♂ (in young onset BPPV ♀ =♂)
BPPV
64. Posterior Canal BPPV – MC (> 90%)
Lateral canal BPPV
Superior canal BPPV (rare)
2 etiopathologies attributed
Canalolithiasis : free floating otolith debris within SCCs. Now identified as the major
mechanism of all subtypes of BPPV
Cupulolithiasis : deposits adhering to cupula (proposed by Schuknecht in 1969). More
significant role in lateral canal BPPV
65. BPPV
• Cupulolithiasis theory (Schuknecht;1969)
Degenerated end pdts of otoconia dislodged from utricular macula
Cause – trauma including iatrogenic; viral inf;vascular insufficiency
Deposit on cupula : density differential b/w perilymph & cupula
Gravity dependent deflection of cupula – continues as long as provocative
orientation was maintained – sustained nystagmus
66. • Canalithiasis theory (Hall 1979; Epley 1980)
Canaliths – loose otoconia debris dislodged from utricle
Gravitate into SCCs (MC PSCC)
hydrodynamic drag in endolymph
evidenced by presence of “densities” within SCC
67. Depiction of canalithiasis of the posterior canal and cupulolithiasis
of the lateral canal (left inner ear)
69. CANAL REPOSITIONING MANEUVER :
Epley maneuver
Semont(liberatory)maneuver
Brandt Daroff exercise
Cupulolithiasis : Little latency; slightly longer duration of
nystagmus (compared to canalithiasis)
Vertical upbeating & rotatory nystagmus towards downward ear : Position test (+)
70. • Canaliths aggregrate in PSCC near ampulla (Most dependent
location in upright position)
• Provocative head position : detached otoconia gravitate as bolus
(as canal assume vertical position)
• Ampullofugal hydrodynamic drag on endolymph (enhanced by
advantage offered by canal:ampulla cross section differential)
71. o Latency – Few sec needed prior to displacement of endolymph & cupula (to
overcome inertia & resistance of endolymph within canal,& elasticity of cupula
o Typical torsional nystagmus
Flouren’s law : axis of eyeball rotation from induced nystagmus parallels axis of
generating SCC, & direction of its slow phase conforms to direction of endolymph
(cupular) displacement
o Limited duration – canaliths stop gravitating when they reach the more horizontal
portion of canal (where drag on endolymph ceases). Elasticity returns cupula to its
neutral position, nystagmus & vertigo ceases (fatiguability)
72. o Reversal – head in upright position – canaliths gravitate back towards ampulla,
causing ampullopetal drag on endolymph.
After a period of latency cupular deflection cause torsional nystagmus in
direction but in same axis
o Habituation – response declines with repeated provocation.
Each procedure cause canalith to be more dispersed (traverse less length of
canal) – less effective endolymph displacement
76. Brandt Daroff exercise
• More of habituation rather than Rx
• 5 exercises = 1 set
• 1 set each in morning, noon & evening
• Do for 14 days
77. Supine log roll test
Purely horizontal nystagmus without a horizontal
(rotatory) component
Canalithiasis : Geotrophic nystagmus
Side with stronger response is the affected canal
Cupulolithiasis : Ageotrophic/apogeotrophic nystagmus
Side with weaker response is the affected canal
82. BPPV variant Test Direction of
nystagmus
Duration of
nystagmus
Rx of choice
PSCC
cupulolithiasis
Dix Hallpike Upbeat torsional
towards affected
side
Persistant > 1 mt
(immediate
onset)
Semont/
Brandt Daroff
PSCC
canalithiasis
Dix Hallpike Upbeat torsional
towards affected
side
5-45 s (latent ) Epley/Semont/
Brandt Daroff
LSCC
canalithiasis
Roll test Horizontal
(geotrophic)
Sec-mts Barbecue/Gufoni
LSCC
cupulolithiasis
Roll test Horizontal
(ageotrophic)
Sec-mts Convert to
geotrophic;
then as above
SSCC
canalithiasis
Dix Hallpike Downbeat
torsional towards
unaffected side
5-45 s Epley on opp
side/
Brandt Daroff
83. Malignant positional paroxysmal
vertigo (MPPV)
• Position changing nystagmus associated with PCF tumours
(MC : CPA tumours)
• Not self limiting
• Constant alteration of nystagmus characteristics on repeating
position test
• Presence of non BPPV symptoms :
persisting imbalance/tinnitus/SNHL/Facial paresthesia/Facial
paralysis
• Persistence of symptoms & signs beyond 1 month
84. Singular neurectomy –
• Selective division of br of inf vestibular nerve innervating PSCC ampulla
• Gacek’s technique : transcanal approach; drill inferior to RW
PSCC occlusion -
• Occlusion of bony lumen of dome of PSCC without disrupting lumen of
SCC
• Postaural mastoidectomy approach
• Identify dome of PSCC b/w LSCC & post fossa dural plate, drill it
& plug with small periosteal plugs
Procedures for BPPV