1) BPPV has a classic presentation of brief, severe vertigo triggered by changes in head position that is confirmed with the Dix-Hallpike test showing nystagmus.
2) Treatment involves canalith repositioning maneuvers like the Epley maneuver to move loose particles out of the semicircular canals.
3) Differential diagnosis includes other vestibular disorders, central causes, and non-vestibular issues; an oculomotor exam can help differentiate central from peripheral causes.
This document discusses tests used to assess vestibular function, including nystagmus, caloric testing, fistula testing, optokinetic testing, and galvanic testing. It also covers peripheral vestibular disorders like BPPV and vestibular neuronitis, as well as central causes of nystagmus. Diagnosis and treatment of BPPV is discussed, including Epley's maneuver and surgical options.
BPPV is characterized by vertigo brought on by certain head positions. It is caused by debris known as otoconia becoming dislodged inside the inner ear's semicircular canals. There are two types - canalithiasis where debris floats freely, and cupulolithiasis where debris adheres to sensitive cupula tissue. The Epley maneuver is a common treatment which aims to reposition the debris back into the utricle by moving the head through various positions. BPPV is diagnosed using the Dix-Hallpike test where nystagmus is observed in the critical head positions.
This document discusses testing of vestibular function. It begins by providing statistics on dizziness complaints. The rest of the document describes various office examinations and tests that can be used to evaluate vestibular function, including cranial nerve exams, positional tests like Dix-Hallpike and Fukuda stepping, and oculomotor function tests like head thrust and head shake nystagmus. It then reviews quantitative vestibular testing methods like electronystagmography (ENG), which can test individual labyrinths, and rotational chair testing, which is considered the gold standard for identifying bilateral vestibular lesions.
The document discusses various clinical and laboratory methods used to assess the vestibular system. Clinical methods include tests of spontaneous nystagmus, the fistula test, Romberg test, gait, past-pointing and falling, and the Hallpike maneuver. Laboratory methods include the caloric test, electronystagmography, optokinetic test, rotation test, and posturography. The document then provides detailed descriptions of procedures and indications for spontaneous nystagmus, the fistula test, Romberg test, past-pointing and falling test, and the Hallpike maneuver. Characteristics of peripheral and central nystagmus are also compared.
Vertigo is a common symptom that affects approximately 30% of people at some point in their life. There are many potential causes of vertigo, including benign paroxysmal positional vertigo (BPPV), vestibular neuritis, Meniere's disease, and less commonly central nervous system disorders. A thorough history, physical exam including tests of ocular motor function and positional maneuvers, and occasionally neuroimaging can help identify the underlying cause in most patients. The most common peripheral vestibular disorders like BPPV and vestibular neuritis are usually self-limited and the main treatment is symptomatic.
1. The Eustachian tube connects the middle ear cavity to the nasopharynx and equalizes pressure on either side of the eardrum. It has bony, cartilaginous, and muscular components.
2. The Eustachian tube opens during swallowing, yawning, and sneezing due to the contraction of muscles like the tensor veli palatini. This allows ventilation and drainage of the middle ear.
3. Disorders of the Eustachian tube include blockage, which can cause otitis media, as well as barotrauma from pressure changes like scuba diving. Evaluation involves tests like Valsalva maneuver and tympanometry
This document discusses tests used to assess vestibular function, including nystagmus, caloric testing, fistula testing, optokinetic testing, and galvanic testing. It also covers peripheral vestibular disorders like BPPV and vestibular neuronitis, as well as central causes of nystagmus. Diagnosis and treatment of BPPV is discussed, including Epley's maneuver and surgical options.
BPPV is characterized by vertigo brought on by certain head positions. It is caused by debris known as otoconia becoming dislodged inside the inner ear's semicircular canals. There are two types - canalithiasis where debris floats freely, and cupulolithiasis where debris adheres to sensitive cupula tissue. The Epley maneuver is a common treatment which aims to reposition the debris back into the utricle by moving the head through various positions. BPPV is diagnosed using the Dix-Hallpike test where nystagmus is observed in the critical head positions.
This document discusses testing of vestibular function. It begins by providing statistics on dizziness complaints. The rest of the document describes various office examinations and tests that can be used to evaluate vestibular function, including cranial nerve exams, positional tests like Dix-Hallpike and Fukuda stepping, and oculomotor function tests like head thrust and head shake nystagmus. It then reviews quantitative vestibular testing methods like electronystagmography (ENG), which can test individual labyrinths, and rotational chair testing, which is considered the gold standard for identifying bilateral vestibular lesions.
The document discusses various clinical and laboratory methods used to assess the vestibular system. Clinical methods include tests of spontaneous nystagmus, the fistula test, Romberg test, gait, past-pointing and falling, and the Hallpike maneuver. Laboratory methods include the caloric test, electronystagmography, optokinetic test, rotation test, and posturography. The document then provides detailed descriptions of procedures and indications for spontaneous nystagmus, the fistula test, Romberg test, past-pointing and falling test, and the Hallpike maneuver. Characteristics of peripheral and central nystagmus are also compared.
Vertigo is a common symptom that affects approximately 30% of people at some point in their life. There are many potential causes of vertigo, including benign paroxysmal positional vertigo (BPPV), vestibular neuritis, Meniere's disease, and less commonly central nervous system disorders. A thorough history, physical exam including tests of ocular motor function and positional maneuvers, and occasionally neuroimaging can help identify the underlying cause in most patients. The most common peripheral vestibular disorders like BPPV and vestibular neuritis are usually self-limited and the main treatment is symptomatic.
1. The Eustachian tube connects the middle ear cavity to the nasopharynx and equalizes pressure on either side of the eardrum. It has bony, cartilaginous, and muscular components.
2. The Eustachian tube opens during swallowing, yawning, and sneezing due to the contraction of muscles like the tensor veli palatini. This allows ventilation and drainage of the middle ear.
3. Disorders of the Eustachian tube include blockage, which can cause otitis media, as well as barotrauma from pressure changes like scuba diving. Evaluation involves tests like Valsalva maneuver and tympanometry
This document provides information about dizziness and balance disorders. It defines key terms like dizziness, vertigo, and oscilopsia. It then lists and describes common causes of dizziness including vestibular disorders, central disorders, medical disorders, drugs, and psychological factors. Specific vestibular disorders discussed include benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuronitis. Examination techniques are outlined including tests of nystagmus, vestibulospinal function, and the semicircular canals. Investigations and management approaches are also summarized, including pharmacotherapy, physical therapy, repositioning procedures, and surgery.
This document discusses dizziness and vertigo from an otoneurological perspective. It begins by outlining key questions to ask patients regarding the nature and characteristics of their dizziness. It then describes potential otologic and neurological symptoms. Specific balance and vestibular tests are discussed, including nystagmus patterns, bedside tests like head thrust and positional maneuvers for BPPV. Common causes of vertigo like BPPV, vestibular neuritis, Meniere's disease, migraines, and strokes are explained. Appropriate use of anti-vertigo medications is emphasized.
This document defines and describes stridor, which is a noisy breathing sound caused by turbulent airflow through a narrowed airway. It discusses the different types of stridor based on timing in the respiratory cycle. It also explores how and why stridor occurs based on airway dynamics and increased resistance from narrowing. The document outlines how to evaluate stridor through history, examination, and various investigations. Finally, it covers the medical and surgical management of stridor, focusing on oxygen therapy, humidification, intubation, and other approaches depending on the underlying cause of stridor.
Here are the answers to the quiz questions:
1. Nystagmus is away from the lesion side in peripheral vertigo.
2. Fitzgerald-Hallpike Test
3. Canalith repositioning maneuvers like Epley maneuver or Semont maneuver.
4. Vestibular neuronitis
5. Aminoglycoside antibiotics, quinine, aspirin, etc. can be vestibulotoxic.
Vestibular neuritis is inflammation of the inner ear and vestibular nerve that causes severe dizziness, vertigo, and balance issues. It is mainly caused by viral infections like herpes, influenza, or autoimmune diseases. Symptoms include severe dizziness, vertigo, nausea, balance issues, and sometimes hearing loss or vision problems. Treatment options include chiropractic treatments, acupuncture, and medications like Antivert. The condition varies in duration but can last from 3 weeks to several months.
Mechanism of balance & vestibular function test Dr Utkal MishraDr Utkal Mishra
This powerpoint elaborates the mechanism of balance & anatomy of vestibular apparutus. It also depicts the anatomy & physiology of haircells in detail. I also explained the vestibular function tests used for diagnosis of various vestibular disorders.
Vestibular function tests are essential tests in otorhinolaryngology examination, especially examination of ear.
This presentation explains about all the important vestibular function tests.
The document discusses diseases of the external nose and vestibule. It describes the anatomy of the external nose and lists conditions such as cellulitis, nasal deformities including saddle nose and hump deformity, and various tumors that can affect the external nose including congenital tumors like dermoids, benign tumors such as rhinophyma, and malignant tumors such as basal cell carcinoma and squamous cell carcinoma. Treatment options are provided for many of the conditions.
The cranial nerves control sensory and motor functions of the head and neck. There are 12 pairs of cranial nerves numbered I to XII. The document provides details of the origin, function and clinical evaluation methods for each cranial nerve including tests of sensory function, eye movements, facial expression, hearing and tongue movement.
The document defines vertigo and discusses its causes and treatment. It begins by defining vertigo as a hallucination of self- or environmental movement due to a disturbance in the vestibular system. It then discusses the anatomy and physiology of the inner ear and vestibular system. Several potential causes of vertigo are outlined, including problems in the peripheral vestibular system, central nervous system, visual system, and medications. Tests used in evaluation and potential treatments like medications, surgery, and physical maneuvers like the Epley maneuver are summarized. Benign paroxysmal positional vertigo (BPPV) and Meniere's disease are highlighted as specific vestibular causes.
The vestibular system located in the inner ear helps maintain equilibrium and spatial orientation. It contains two types of sensory organs - the maculae which detect linear acceleration and position with respect to gravity, and the semicircular canals which detect angular acceleration and rotation of the head. Hair cells within these organs bend in response to movement, triggering nerve signals to the brain. The brain integrates vestibular information with other sensory inputs to coordinate muscle responses and eye movements that keep vision stable and maintain balance and posture. Damage to the vestibular system can cause vertigo, dizziness and conditions like Meniere's disease.
Congenital malformation of external ear and it’s managementYousuf Choudhury
This document discusses congenital malformations of the external ear. It begins with applied anatomy of the normal ear and embryology of ear development. It then describes various congenital deformities that can occur, including pre-auricular tags, prominent ears, cryptotia, microtia, and congenital aural atresia. For treatment, options include observation, prosthetics, reconstruction with rib cartilage grafts, and surgical correction of atresia. Reconstruction is often done in multiple stages to form the shape of the pinna.
Vertigo is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.
The document discusses the vestibular apparatus, which is part of the inner ear and functions as a sensory organ for balance and equilibrium. It contains three semicircular canals oriented at right angles to detect rotational movement, as well as the utricle and saccule which contain the maculae and detect linear acceleration. Hair cells within the crista ampullaris of the semicircular canals and within the maculae transmit signals about movement and acceleration to the brainstem via the vestibular nerve. The vestibular nuclei integrate this sensory information and coordinate motor responses to maintain balance and posture.
1. The document outlines the presentation for a discussion on vertigo, including its prevalence, classification, anatomy, physiology, causes, diagnosis, and tests to differentiate between peripheral and central vertigo.
2. Common causes of peripheral vertigo include benign paroxysmal positional vertigo, Meniere's disease, and labyrinthitis, while causes of central vertigo include vertebrobasilar insufficiency, arteriosclerosis, and brain tumors.
3. Diagnosis of vertigo involves medical history, balance tests like Romberg and Unterberger tests, and analysis of nystagmus including direction and whether it is inhibited by visual fixation.
This document discusses various congenital anomalies of the larynx that can occur due to errors in embryogenesis. It begins with an overview of laryngeal development from the 4th to 6th week of gestation. It then describes several supraglottic anomalies such as laryngomalacia, laryngeal or saccular cysts, and lymphangiomas. Glottic anomalies discussed include laryngeal webs, atresia, and vocal cord paralysis. Subglottic anomalies like congenital subglottic stenosis and subglottic hemangiomas are also covered. The document concludes with descriptions of genetic and central nervous system anomalies that can involve the larynx, such as Cri du Chat syndrome and
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
This document discusses vertigo, which refers to a hallucinatory sensation of movement caused by a mismatch of sensory information from the vestibular, visual, and proprioceptive systems. Vertigo can be caused by lesions in the peripheral, intermediate, or central nervous system. Common causes of peripheral vertigo include BPPV, Meniere's disease, and labyrinthitis. Intermediate vertigo may be caused by vestibular neuronitis or acoustic neuroma. Central causes include stroke, MS, migraines, and brain tumors. Clinical tests like nystagmus patterns and the head thrust test can help differentiate peripheral from central vertigo. Treatment depends on the underlying cause but may include medications, exercises
What is the LPR
Esophageal anatomy
Pathophysiology
Risk factors
CLINICAL MANIFESTATIONS
Reinke’s edema
Patterns and Mechanism of LPR and GERD
DIAGNOSIS
Symptom Questionnaire:
Laryngoscopic Findings
Therapeutic Trial for LPR
Ambulatory PH Monitoring
Treatment
Lifestyle modifications
Dietary modification
PHARMACOLOGICAL
Drug therapy
Surgery
HINTS of Stroke, Bedside Eye Exam Outperforms MRI in Identifying StrokeErsifa Fatimah
1. HINTS merupakan tes bedside yang dapat membedakan stroke sentral dan penyebab vestibular perifer pada pasien dengan keluhan sindroma vestibular akut.
2. Tes ini meliputi penilaian nistagmus, tes kepala dorong, dan tes skew mata. Ketiga tes ini memiliki sensitivitas dan spesifisitas tinggi dalam mendiagnosis stroke.
3. Pemeriksaan HINTS lebih praktis dibandingkan MRI dan dapat membantu mendiagnosis awal stroke
Vertigo is a common condition characterized by a sensation of rotation or spinning. Common causes include BPPV, vestibular neuritis, Meniere's disease, and acoustic neuromas. BPPV is the most common cause and involves detached inner ear crystals that move within the semicircular canals and stimulate cupulae. Diagnosis is made using the Dix-Hallpike maneuver which provokes nystagmus. Treatment involves repositioning procedures like the Epley maneuver to move the crystals back into the vestibule. Vestibular neuritis is an inflammation of the vestibular nerve and causes violent vertigo on head movement that improves with time. Acoustic neuromas present with unilateral
This document provides information about dizziness and balance disorders. It defines key terms like dizziness, vertigo, and oscilopsia. It then lists and describes common causes of dizziness including vestibular disorders, central disorders, medical disorders, drugs, and psychological factors. Specific vestibular disorders discussed include benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuronitis. Examination techniques are outlined including tests of nystagmus, vestibulospinal function, and the semicircular canals. Investigations and management approaches are also summarized, including pharmacotherapy, physical therapy, repositioning procedures, and surgery.
This document discusses dizziness and vertigo from an otoneurological perspective. It begins by outlining key questions to ask patients regarding the nature and characteristics of their dizziness. It then describes potential otologic and neurological symptoms. Specific balance and vestibular tests are discussed, including nystagmus patterns, bedside tests like head thrust and positional maneuvers for BPPV. Common causes of vertigo like BPPV, vestibular neuritis, Meniere's disease, migraines, and strokes are explained. Appropriate use of anti-vertigo medications is emphasized.
This document defines and describes stridor, which is a noisy breathing sound caused by turbulent airflow through a narrowed airway. It discusses the different types of stridor based on timing in the respiratory cycle. It also explores how and why stridor occurs based on airway dynamics and increased resistance from narrowing. The document outlines how to evaluate stridor through history, examination, and various investigations. Finally, it covers the medical and surgical management of stridor, focusing on oxygen therapy, humidification, intubation, and other approaches depending on the underlying cause of stridor.
Here are the answers to the quiz questions:
1. Nystagmus is away from the lesion side in peripheral vertigo.
2. Fitzgerald-Hallpike Test
3. Canalith repositioning maneuvers like Epley maneuver or Semont maneuver.
4. Vestibular neuronitis
5. Aminoglycoside antibiotics, quinine, aspirin, etc. can be vestibulotoxic.
Vestibular neuritis is inflammation of the inner ear and vestibular nerve that causes severe dizziness, vertigo, and balance issues. It is mainly caused by viral infections like herpes, influenza, or autoimmune diseases. Symptoms include severe dizziness, vertigo, nausea, balance issues, and sometimes hearing loss or vision problems. Treatment options include chiropractic treatments, acupuncture, and medications like Antivert. The condition varies in duration but can last from 3 weeks to several months.
Mechanism of balance & vestibular function test Dr Utkal MishraDr Utkal Mishra
This powerpoint elaborates the mechanism of balance & anatomy of vestibular apparutus. It also depicts the anatomy & physiology of haircells in detail. I also explained the vestibular function tests used for diagnosis of various vestibular disorders.
Vestibular function tests are essential tests in otorhinolaryngology examination, especially examination of ear.
This presentation explains about all the important vestibular function tests.
The document discusses diseases of the external nose and vestibule. It describes the anatomy of the external nose and lists conditions such as cellulitis, nasal deformities including saddle nose and hump deformity, and various tumors that can affect the external nose including congenital tumors like dermoids, benign tumors such as rhinophyma, and malignant tumors such as basal cell carcinoma and squamous cell carcinoma. Treatment options are provided for many of the conditions.
The cranial nerves control sensory and motor functions of the head and neck. There are 12 pairs of cranial nerves numbered I to XII. The document provides details of the origin, function and clinical evaluation methods for each cranial nerve including tests of sensory function, eye movements, facial expression, hearing and tongue movement.
The document defines vertigo and discusses its causes and treatment. It begins by defining vertigo as a hallucination of self- or environmental movement due to a disturbance in the vestibular system. It then discusses the anatomy and physiology of the inner ear and vestibular system. Several potential causes of vertigo are outlined, including problems in the peripheral vestibular system, central nervous system, visual system, and medications. Tests used in evaluation and potential treatments like medications, surgery, and physical maneuvers like the Epley maneuver are summarized. Benign paroxysmal positional vertigo (BPPV) and Meniere's disease are highlighted as specific vestibular causes.
The vestibular system located in the inner ear helps maintain equilibrium and spatial orientation. It contains two types of sensory organs - the maculae which detect linear acceleration and position with respect to gravity, and the semicircular canals which detect angular acceleration and rotation of the head. Hair cells within these organs bend in response to movement, triggering nerve signals to the brain. The brain integrates vestibular information with other sensory inputs to coordinate muscle responses and eye movements that keep vision stable and maintain balance and posture. Damage to the vestibular system can cause vertigo, dizziness and conditions like Meniere's disease.
Congenital malformation of external ear and it’s managementYousuf Choudhury
This document discusses congenital malformations of the external ear. It begins with applied anatomy of the normal ear and embryology of ear development. It then describes various congenital deformities that can occur, including pre-auricular tags, prominent ears, cryptotia, microtia, and congenital aural atresia. For treatment, options include observation, prosthetics, reconstruction with rib cartilage grafts, and surgical correction of atresia. Reconstruction is often done in multiple stages to form the shape of the pinna.
Vertigo is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.
The document discusses the vestibular apparatus, which is part of the inner ear and functions as a sensory organ for balance and equilibrium. It contains three semicircular canals oriented at right angles to detect rotational movement, as well as the utricle and saccule which contain the maculae and detect linear acceleration. Hair cells within the crista ampullaris of the semicircular canals and within the maculae transmit signals about movement and acceleration to the brainstem via the vestibular nerve. The vestibular nuclei integrate this sensory information and coordinate motor responses to maintain balance and posture.
1. The document outlines the presentation for a discussion on vertigo, including its prevalence, classification, anatomy, physiology, causes, diagnosis, and tests to differentiate between peripheral and central vertigo.
2. Common causes of peripheral vertigo include benign paroxysmal positional vertigo, Meniere's disease, and labyrinthitis, while causes of central vertigo include vertebrobasilar insufficiency, arteriosclerosis, and brain tumors.
3. Diagnosis of vertigo involves medical history, balance tests like Romberg and Unterberger tests, and analysis of nystagmus including direction and whether it is inhibited by visual fixation.
This document discusses various congenital anomalies of the larynx that can occur due to errors in embryogenesis. It begins with an overview of laryngeal development from the 4th to 6th week of gestation. It then describes several supraglottic anomalies such as laryngomalacia, laryngeal or saccular cysts, and lymphangiomas. Glottic anomalies discussed include laryngeal webs, atresia, and vocal cord paralysis. Subglottic anomalies like congenital subglottic stenosis and subglottic hemangiomas are also covered. The document concludes with descriptions of genetic and central nervous system anomalies that can involve the larynx, such as Cri du Chat syndrome and
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
This document discusses vertigo, which refers to a hallucinatory sensation of movement caused by a mismatch of sensory information from the vestibular, visual, and proprioceptive systems. Vertigo can be caused by lesions in the peripheral, intermediate, or central nervous system. Common causes of peripheral vertigo include BPPV, Meniere's disease, and labyrinthitis. Intermediate vertigo may be caused by vestibular neuronitis or acoustic neuroma. Central causes include stroke, MS, migraines, and brain tumors. Clinical tests like nystagmus patterns and the head thrust test can help differentiate peripheral from central vertigo. Treatment depends on the underlying cause but may include medications, exercises
What is the LPR
Esophageal anatomy
Pathophysiology
Risk factors
CLINICAL MANIFESTATIONS
Reinke’s edema
Patterns and Mechanism of LPR and GERD
DIAGNOSIS
Symptom Questionnaire:
Laryngoscopic Findings
Therapeutic Trial for LPR
Ambulatory PH Monitoring
Treatment
Lifestyle modifications
Dietary modification
PHARMACOLOGICAL
Drug therapy
Surgery
HINTS of Stroke, Bedside Eye Exam Outperforms MRI in Identifying StrokeErsifa Fatimah
1. HINTS merupakan tes bedside yang dapat membedakan stroke sentral dan penyebab vestibular perifer pada pasien dengan keluhan sindroma vestibular akut.
2. Tes ini meliputi penilaian nistagmus, tes kepala dorong, dan tes skew mata. Ketiga tes ini memiliki sensitivitas dan spesifisitas tinggi dalam mendiagnosis stroke.
3. Pemeriksaan HINTS lebih praktis dibandingkan MRI dan dapat membantu mendiagnosis awal stroke
Vertigo is a common condition characterized by a sensation of rotation or spinning. Common causes include BPPV, vestibular neuritis, Meniere's disease, and acoustic neuromas. BPPV is the most common cause and involves detached inner ear crystals that move within the semicircular canals and stimulate cupulae. Diagnosis is made using the Dix-Hallpike maneuver which provokes nystagmus. Treatment involves repositioning procedures like the Epley maneuver to move the crystals back into the vestibule. Vestibular neuritis is an inflammation of the vestibular nerve and causes violent vertigo on head movement that improves with time. Acoustic neuromas present with unilateral
1) Vertigo can be caused by issues in the inner ear lasting seconds to years, with the most common causes being BPPV, vestibular neuritis, and Meniere's disease.
2) A neurotological evaluation includes tests of the vestibulo-ocular, vestibulospinal, and otolith systems like head impulse testing, caloric testing, and subjective visual vertical to locate the source of imbalance.
3) BPPV is diagnosed and treated with particle repositioning maneuvers like Epley and Semont maneuvers to move calcium carbonate debris out of the semicircular canals. Other causes like cupulolithiasis may require different treatments.
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.
Concussions are a growing concern, especially in young athletes. Common symptoms include headaches, dizziness, and memory issues. While rest is usually recommended, longer periods of inactivity do not necessarily lead to faster recovery. Physical therapy can help address lingering symptoms through manual therapy, soft tissue work, vestibular rehabilitation, education, and light aerobic exercise. Further research is still needed to better understand and treat concussions.
The document discusses various causes of vertigo including peripheral causes like benign positional vertigo and Meniere's disease, as well as central causes like stroke and migraine. It outlines the diagnostic approach including taking a history of symptoms, performing a physical exam with tests like the Dix-Hallpike maneuver, and considering audiometric testing, imaging, or other workup based on findings. The goal is to distinguish between peripheral and central causes of vertigo based on characteristics of the nystagmus, hearing loss, imbalance, and other associated neurological symptoms.
This document discusses benign paroxysmal positional vertigo (BPPV), including its causes, types, diagnostic tests, and treatment maneuvers. It provides details on:
- Posterior canal BPPV is the most common type, accounting for 81-89% of cases. The Dix-Hallpike test is used for diagnosis. Treatment includes particle repositioning maneuvers like Epley's maneuver.
- Horizontal canal BPPV, which accounts for 8-17% of cases, is diagnosed using tests like the supine roll test. Treatments include maneuvers like the Lempert maneuver.
- Anterior canal BPPV is rare but can result from treatments for other forms
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 discusses vertigo from both peripheral and central causes. It defines different types of dizziness and outlines steps for examining patients experiencing vertigo. Key peripheral causes of vertigo include benign paroxysmal positional vertigo (BPPV), vestibular neuronitis, labyrinthitis, and Meniere's disease. Central causes include lesions of the brainstem, posterior fossa tumors, and multiple sclerosis. The duration and characteristics of vertigo can provide clues to determine if it is from a peripheral or central source.
El documento describe diferentes tipos de mareos y vértigo. Define mareo como un término impreciso que involucra desequilibrio e inestabilidad, mientras que vértigo implica una alucinación de movimiento rotatorio. Explica que el primer paso es categorizar el tipo de síntoma reportado por el paciente, siendo las categorías más comunes pacientes con vértigo, síntomas inespecíficos, o desequilibrio. Luego se enfoca en la evaluación y tratamiento del vértigo periférico posicional paroxístico benign
Posterior circulation ischaemic stroke and tiaRaeez Basheer
Posterior circulation strokes involve the vertebrobasilar arteries and account for about one-fifth of ischemic strokes. They are associated with a high risk of early recurrent stroke. Clinical features can include dizziness, limb weakness, dysarthria, and nausea. Investigations like MRI and MRA are important for diagnosis but may be normal for small brainstem infarcts. There is a higher risk of early recurrent stroke after posterior circulation events compared to carotid events. Secondary prevention focuses on antiplatelet drugs and controlling risk factors like blood pressure, though aggressive lowering is not recommended in some cases of vertebrobasilar stenosis due to risk of recurrent stroke.
Cervicogenic Dizziness - identification and treatmentNVMT-symposium
Cervicogenic dizziness is a controversial diagnosis caused by dysfunction in the upper cervical spine that results in imbalance or disequilibrium. It is identified through a 5-step process including characteristics of imbalance-type dizziness, neck pain or stiffness exacerbating dizziness, and physical exam findings. Sustained natural apophyseal glides are an effective manual therapy treatment, shown to decrease dizziness and pain more than mobilizations or placebo. Multi-modal treatment including balance exercises is also recommended. Long-term follow up shows treatment effects are maintained for up to 12 months.
This document discusses migrainous vertigo, an underdiagnosed condition where vertigo is a symptom of migraine. It defines diagnostic criteria for definite and probable migrainous vertigo. Key points include: vertigo is reported in around 10% of migraine patients, particularly those with classical migraine with aura; it is believed to be caused by neuronal hyperexcitability and mitochondrial dysfunction from magnesium deficiency leading to changes in brain areas controlling blood flow; and management involves lifestyle modifications and avoidance of trigger factors.
This document provides an overview of concussion management and vestibular rehabilitation exercises. It defines a concussion, describes how they occur and affect the brain. Assessment tools like VOMS and BESS are outlined to screen for vestibular and balance issues. A multi-disciplinary approach to management is recommended. The presentation then details vestibular exercises including gaze stability, habituation, static and dynamic balance training as well as cardiovascular exercise. Proper progression of an individualized home exercise program over 6-12 weeks is emphasized for recovery.
Vertigo is a type of dizziness characterized by sensations of movement, typically spinning or rotation. It can be caused by issues in the inner ear, vestibular nerve, or brainstem. Episodes are often unpredictable and accompanied by nausea, vomiting, imbalance, and anxiety. Between episodes, vertigo sufferers may experience headaches, instability, and depression. Long-term, vertigo negatively impacts quality of life.
Benign paroxysmal positional vertigo (BPPV) is a common inner ear condition characterized by brief episodes of vertigo triggered by changes in head position. It is caused by debris in the semicircular canals leading to abnormal signals in the vestibular system. BPPV involving the posterior semicircular canal accounts for about 94% of cases. Diagnosis is made through provocative positional tests like the Dix-Hallpike maneuver. Treatment involves repositioning maneuvers like Epley's maneuver to move the debris out of the affected canal. BPPV typically resolves spontaneously within weeks to months, but recurrence is possible in about 15-45% of cases within a year without treatment.
Nystagmus is an involuntary, repetitive eye movement that can be physiological or pathological. It is described by its position, frequency, null zone, direction, and waveform. Nystagmus can be congenital, resulting from genetic factors or acquired later in life due to injury or illness. The document provides details on different types of nystagmus such as congenital nystagmus, latent nystagmus, periodic alternating nystagmus, and acquired nystagmus. Causes, characteristics, and clinical presentations are discussed for various nystagmus conditions.
This document provides an overview of central vestibular disorders. It discusses how the vestibular system senses head motion and distributes signals to control eye movements, posture, and balance. Central vestibular disorders can cause pathological sensations of self-motion and conflicts between visual and vestibular inputs. Common causes include vascular issues like strokes, inflammation, tumors, inherited conditions, and migraines. Central vestigular disorders are challenging to diagnose but it is important to differentiate them from peripheral disorders due to their potential medical urgency and risk of long-term neurological effects.
El documento resume el vértigo postural paroxístico benigno (VPPB), incluyendo su definición, prevalencia, etiología, síntomas clínicos, teorías que lo explican, clasificación, diagnóstico, tratamiento y referencias. El VPPB se caracteriza por episodios breves de vértigo provocados por cambios de posición, y generalmente se debe a partículas en los canales semicirculares. Su tratamiento incluye maniobras de reposición como la de Epley para mover las partículas.
BPPV and its role in Geriatric functioning_Pleasant Acres_InserviceJere Hess
This document discusses benign paroxysmal positional vertigo (BPPV) and its impact on geriatric functioning. It provides an overview of the anatomy and functioning of the vestibular system, including the semicircular canals and otolithic organs. BPPV most commonly affects older adults and can significantly increase their risk of falls. It describes BPPV as a sudden onset of vertigo triggered by certain head positions. The document outlines tests like the Dix-Hallpike maneuver and supine roll test used to diagnose BPPV involving different semicircular canals. It also explains repositioning maneuvers like the Epley maneuver used to treat BPPV involving the posterior and anterior semicirc
This document provides an overview of vestibular physical therapy in an inpatient setting. It discusses the anatomy and physiology of the vestibular system, common vestibular disorders and their clinical presentations, tools for screening and assessment including tests for nystagmus and balance, diagnosis of benign paroxysmal positional vertigo (BPPV) and treatment techniques, and considerations for referring patients to outpatient vestibular therapy. The presentation aims to equip physical therapists with knowledge of the vestibular system and skills for working with patients experiencing dizziness and imbalance.
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.
BPPV is the most common cause of vertigo. It is caused when calcium carbonate crystals in the inner ear called otoconia become dislodged and enter the semicircular canals. This causes brief episodes of vertigo when moving the head into certain positions. BPPV most often involves the posterior semicircular canal. It is diagnosed using positional tests like the Dix-Hallpike maneuver. Treatment involves repositioning maneuvers like the Epley maneuver to move the crystals out of the affected canal, which is effective in 80% of cases. BPPV is usually benign and self-limiting but can recur in some cases.
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.
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.
This document discusses the evaluation and management of dizzy patients. It begins by defining vertigo and dizziness, and discusses the incidence of vertigo. It describes the initial approach to dizzy patients, including considering whether dizziness is vestibular or non-vestibular in origin. It outlines the history, exam, tests and imaging used in evaluation, and provides algorithms for common vestibular disorders. It also describes physical exercise regimens like the Cawthorne-Cooksey exercises and repositioning maneuvers for conditions like BPPV.
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
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.
Benign paroxysmal positioning vertigo (BPPV) is caused by stray crystals of calcium carbonate in the inner ear that cause brief attacks of vertigo when the head is moved into certain positions. It is diagnosed through provocative tests like the Dix-Hallpike maneuver that cause transient nystagmus. BPPV can be effectively treated with repositioning maneuvers like the Epley maneuver or Semont's maneuver to move the crystals from the affected semicircular canal. These treatments successfully resolve BPPV in most patients, with instructions to avoid certain head positions after treatment to prevent recurrence.
This document provides an overview of vertigo, including its definition, types, causes, clinical tests, and treatments. It discusses the differences between peripheral and central vertigo, with peripheral vertigo making up 85% of cases. Specific peripheral causes covered include benign paroxysmal positional vertigo (BPPV), vestibular neuronitis, and Meniere's disease. Clinical tests for evaluating vertigo include nystagmus tests, the Dix-Hallpike maneuver for BPPV, and caloric and rotational chair tests. Treatments range from reassurance and medication to repositioning maneuvers for BPPV and surgery in rare cases.
This case report discusses the evaluation and treatment of a 51-year-old male patient presenting with bilateral benign paroxysmal positional vertigo (BPPV) following a head injury. Examination revealed positive Hallpike-Dix maneuvers bilaterally, indicating involvement of both posterior semicircular canals. The patient underwent canalith repositioning techniques (CRTs) on each side separately, which resolved his vertigo symptoms. He was also given gaze stabilization and balance exercises, which further improved his visual and postural deficits. The case demonstrates that bilateral BPPV can be successfully treated with sequential CRTs on each affected canal.
Here are the answers to the quiz questions:
1. Nystagmus is away from the lesion side in peripheral vertigo.
2. Fitzgerald-Hallpike Test
3. Canalith repositioning maneuvers like Epley maneuver or Semont maneuver.
4. Vestibular neuronitis
5. Aminoglycoside antibiotics, loop diuretics, chemotherapeutic agents etc. can cause vestibulotoxicity leading to vertigo.
Learn more about the types, symptoms and causes of balance disorders. Diagnostic and treatment options such as vestibular rehabilitation and cognitive behavioral therapy will be discussed.
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.
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.
The document compares two international guidelines on the treatment of benign paroxysmal positional vertigo (BPPV). Both guidelines recommend the canalith repositioning maneuver as the most effective treatment for posterior semicircular canal BPPV based on high-quality evidence. For horizontal canal BPPV, the guidelines recommend variations of the roll maneuver. The conclusion is that while the guidelines agree on the Dix-Hallpike maneuver for diagnosis, only the canalith repositioning maneuver has a strong recommendation for treating vertical canal BPPV.
Balance requires input from sensory systems like vision and vestibular, processing in the cerebellum and brainstem, and motor output. Disorders can occur from problems with input, processing, or motor function. A careful history is needed to determine the exact nature and location of dizziness or vertigo. Physical exam may reveal sensory issues, eye movement abnormalities, or weakness depending on the site of lesion. Common causes of vertigo include vestibular disorders like acute vestibular failure, benign paroxysmal positional vertigo, and Meniere's disease.
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The document provides information on the pathology of equilibrium and diseases related to it. It discusses the anatomy and physiology of the vestibular system including the otolith organs and semicircular canals. It then describes specific diseases like benign paroxysmal positional vertigo (BPPV), Meniere's disease, and superior semicircular canal dehiscence. BPPV is the most common cause of vertigo and involves displacement of otoconia within the inner ear. Diagnosis is made using tests like Dix-Hallpike and treatment involves repositioning maneuvers. Superior semicircular canal dehiscence involves a hole in the bone over the canal and causes both vestibular and
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2. WHAT WE WILL LEARN
• BPPV has a classic and easy to identify presentation
• 1. episodes of severe spinning vertigo (<1 min) triggered by change in head position
relative to gravity.
• 2. Needs to be confirmed Dix-Hallpike. + if vertigo AND nystagmus <1 min, that has a
latency 5-20 before onset.
• Pt’s that don’t fit the above presentation most likely DON’T have BPPV
• For pts with acute vestibular syndrome (AVS), the oculomotor HINTS
exam is more sensitive than MRI in the 1st 48 hrs to differentiate posterior
CVA from vestibular neuritis
• Dizziness produced with seated neck rotation NOT indicative of BPPV;
likely cervicogenic. Need to consider for VBI, especially if c/o other VBI
symptoms + stroke risk factors or recent neck trauma (even minor!)
2
4. BENIGN PAROXYSMAL POSITIONAL
VERTIGO : OVERVIEW
• THE MOST COMMON FORM OF DIZZINESS
• Most common between ages 60-70 (Batuecas et al, 2013)
• Women 2x more likely (Kollen 2012)
• Lifetime prevelence 2.4% (Von Brevern et al 2007)
• 9% undiagnosed in young adult and older populations (Kerrigan 2013,
Oghalai 2000)
4
7. PATHOPHYSIOLOGY OF BPPV
• Otoconia to become dislodged from the utricle
• Cause unknown and/or degenerative in large majority of cases
• Recent trauma, symptom onset <1week. More common cause for
yougner pt’s
• Posterior canal most commonly affected. 85-95% (Parnes et al
2003)
7
9. BPPV VARIATIONS
• Horizontal Canal: 10-15% (Bhattacharyya et al 2008)
• Subjective symptoms indistinguishable from Posterior Canal BPPV
• Anterior Canal: 3% (Anagnostou et al 2015)
• Multiple canal involvement: RARE
• Bilateral: RARE
• Cupulolisthiasis: RARE
• Otoconia adhered to cupula instead of floating in canal.
9
10. BPPV SYMPTOMS
KEY COMPLAINT = Brief (< 1 min) and severe episodic
rotatory vertigo related to change in head position relative
to gravity.
In between episodes of vertigo, feel generally ok but may
very mild other symptoms
• Imbalance (49%)
• Fear of falling (36%)
• Nausea (33%)
• Oscillopsia (31%)
• Falls (1%)
10
Von Brevern 2007
11. BPPV SYMPTOMS
If pt does not describe episodes brief,
severe, spinning vertigo during head
movement relative to gravity =
Pt does NOT have BPPV!
11
12. BPPV: SYMPTOMS
12
Present during change of head
position relative to gravity.
Vertigo subsides when head
and
Otoliths stop moving < 1 min
Common Complaints:
1. Sit -> laying down
2. Looking up or down
3. Bending over
4. Rolling over in bed
***Symptoms with cervical rotation in sitting/standing NOT common in BPPV.
Need to consider cervicogenic or VBI**
13. CLARIFICATION
QUESTIONS TO ASK
• Specifically how long does vertigo last?
• May feel nauseated/unwell for longer than 1 min, but true vertigo episode
will be <1 min
• Describe what their vertigo feels like
• If not described as spinning - not BPPV
• Movements or positional changes that trigger the vertigo?
• Do they get vertigo when staying perfectly still?
• If yes - not BPPV
• Presence of tinnitus, aural fullness and hearing loss
(suggests Meiner’s)
13
15. TESTING FOR BPPV
• Dix-Hallpike Test: Gold Standard for diagnosis of
posterior/anterior canal BPPV
• 79% sensitivity
• 75% specificity
• +LR 3.17
• -LR 0.28
• Sidelying Test: alternative
• Use when bed does not allow for of 30°extension off the edge, OR
• For pt’s that can’t tolerate Dix-Hallpike due to back pain, neck pain,
limited mobility
•
15
Halker et al 2008
18. DIX-HALLPIKE TEST
1. Rotate neck 45° toward side being tested
2. Rapidly lay pt down in 30° extension off edge of bed,
while maintaining 45° rotation
3. Maintain position at least 30-45 sec while observing for
vertigo and nystagmus
1. Slowly return to sitting (sometimes will have reversal of
nystagmus). Dizziness with return to sit not a + finding
2. Repeat on the opposite side
18
19. SIDELYING TEST ALTERNATIVE TO DIX HALLPIKE
19
1. Rotate head 45°
Away from side being
tested
2. Rapidly bring pt
into sidelying while
maintaining 45°
rotation
3. Maintain position
30-45 sec while
observing for vertigo
and nystagmus
4. Slowly return to sit
5. Repeat on
opposite side
20. SIDELYING TEST
ALTERNATIVE TO DIX-HALLPIKE
20
L sidelying = testing L posterior canal
R sidelying = testing R posterior canal
21. RIGHT POSTERIOR CANAL BPPV
21
Right Left
Upbeating, right torsional
+latency of onset, duration < 1 min
vertigo same latency and duration as nystagmus
22. INTERPRETATION OF
NYSTAGMUS
** Posterior canal BPPV = Upbeating/torsional**
• In BPPV, there will always be a vertical AND torsional
component toward the effected side
• R posterior canal BPPV -> upbeating/R torsional
• L posterior canal BPPV -> upbeating/L torsional
• In BPPV, vertigo and nystagmus will fatigue on repeated testing
22
23. DIAGNOSTIC CRITERIA FOR
POSTERIOR CANAL BPPV
Subjective: repeated episodes of vertigo with changes in head
position relative to gravity
Exam: Dix Hallpike
1. Vertigo with nystagmus (vertical AND torsional)
2. Latency period ( 5-20 sec) prior to onset of vertigo and
nystagmus
3. Vertigo and nystagmus increase then resolve in < 60 sec from
onset of nystagmus
• ALL of the above criteria must be present to definitively make
diagnosis
Bhattacharyya et al 2008
23
25. EPLEY MANEUVER
25
Treatment for L posterior canal shown
Each position should be maintained for
30 sec or longer, after nystagmus and
vertigo resolve
26. EPLEY MANEUVER
For treatment of Posterior Canal BPPV
1. Start in sitting, head turned 45⁰ toward the effected side.
2. Quickly lay pt supine in 30° extension while maintaining 45°
rotation toward effected side
3. Turn head 90º toward the unaffected ear
4. Turn pt to side lying while still in 45° rotation toward unaffected
ear (pt looking at floor)
5. Return to sitting at edge of bed while maintaining 45° rotation
toward unaffected ear and chin tucked
• Each position should be maintained for 30 sec or longer,
after nystagmus and vertigo resolve
26
27. PROGNOSIS
• VERY GOOD!
• Meta-analysis: 81% recovery, compared to 37.% in
placebo or untreated subjects (Helminski et al 2010)
• With repeated maneuvers in a single visit or repeated visits,
remission is >90% (Lynn et al 1995)
• 1 year recurrence rate 15% (Von Brevern 2007 )
• Referral to PT beneficial for repeated testing/CRM,
treatment of residual balance deficits, motion sensitivity
27
28. BPPV CASE
Subjective
• 59 y/o woman, insidious onset vertigo 2-3 wks ago
• Described as spinning vertigo. Intermittent. Lasts < 1 min
• Present when looking up, looking down and especially looking up
and to the R
• Also c/o constant woozy/drunk feeling that is worse when looking
down
• 1 fall down the stairs due to vertigo while looking down
• History of congenital bilat low freq hearing loss, bilat tinnitus
migraine HA (all unchanged since onset of vertigo)
• Occasional neck pain described as tension prior to migraine HA,
not present recently
• Denies other central neurological or VBI symptoms
28
29. BPPV CASE
• Objective
• Gait wnl, no unsteadiness, ataxia or other gait deviations
• C-spine ROM wnl, no pain or dizziness all directions
• VBI screen neg for dizziness or nystagmus (sustained seated
cervical rotation)
• Occulomotor testing neg for central or peripheral dysfunction
• Dix-Hallpike R: + robust vertigo and up beating/R torsional
nystagmus, latency 2-3 sec, lasted < 1 min
• Dix-Hallpike L: +slight vertigo and up beating/R torsional
nystagmus, latency 2-3 sec, lasted <1 min
• Horizontal Roll Test: neg bilat
29
30. BPPV CASE
Diagnosis = BPPV R posterior canalisthiasis
• Treatment: Epley Manuver for the R ear x 3 less vertigo/nystagmus ea
rep
• Post-Epley instructions. 48 hrs - Avoid sleeping on involved side. Avoid
forceful head movements, sustained non-neutral neck positions (beauty
parlor..)
Reevaluation and d/c: Visit 2
• No more vertigo since initial treatment
• Occasional “woozy” feeling when looking down, but very mild
• Dix Hallpike neg bilat
• Instructed in 1 habituation exercise and 1 VOR retraining to address any
potential mild vestibular hypofunction or motion sensitivity due to 2-3
week presence of BPPV
30
31. SELF EPLEY FOR DIZZY PATIENTS?
• If clear positive for BPPV on Dix-Hallpike = YES!!
• Epley with clinician preferred, pt’s may have difficulty
doing correctly
• If unclear based on history and Dix-Hallpike = NO!!
• Will not help with other peripheral vestibular d/o
• Potential VA occlusion, cervical nerve root irritation during
maneuver
• Referral to ENT and PT helpful for differential and treatment
31
32. 32
SELF EPLEY for Left Posterior canal
Wait 30 sec
after
symptoms
subside in ea
position
Do 3x/day
until symptom
free, before
bed may be
better
tolerated
Avoid sleeping
on effected
side
Should
resolve in <1
week
33. DIFFERENTIAL
DIAGNOSIS
BPPV is easily
differentiated from all
other forms of dizziness
33
If symptoms and Dix-Hallpike findings do not clearly match
the clinical pattern of BPPV, other diagnoses need to be
investigated!!
34. DIFFERENTIAL DIAGNOSIS
Vestibular: Most common
• BPPV – 50%.
• Meniere’s Disease - 18%.
• Vestibular Neuritis and Labyrinthitis – 14%.
Non-vestibular
• Central Pathology (tumor, posterior circulation CVA)
• Cardiac
• Psychiatric (anxiety, panic, hyperventilation syndrome)
• Cervicogenic
• Vertiginous migraine
• Medical (orthostatic hypotension, medications)
34
35. DIFFERENTIAL DIAGNOSIS
• history and detailed oculomotor testing very important to
differential central from peripheral vestibular disorders
35
36. OCULOMOTOR EXAM
Test CENTRAL PERIPHERAL
Resting Nystagmus* X
Gaze Holding
Nystagmus*
X + if direction
changing
or vertical
X + in vestibular
neuritis,
unidirectional
and horizontal
Smooth Pursuit X + if catch up
saccade
Saccades X + if over/undershoot
VOR cancellation X
Skew Deviation X
Head Thrust/Head
Impulse Test (VOR)
X
Dynamic Visual Acuity X + in vestibular
hypofunction
36
*better seen without visual fixation
37. MENIERE’S DISEASE
• Caused by fluctuating increased endolymphatic fluid in the inner ear
• Discrete episodic attacks with triad of sustained vertigo, fluctuating low
freq hearing loss and tinnitus
• Attacks commonly last 2-4 hours
• Constant vertigo at rest, but can get worse with change in head position
• Aural fullness during episodes
• Will feel off balance during attacks
• Some have drop attacks “crisis of Tumarkin”
37
39. MENIERE’S DISEASE
• Once diagnosed and attacks managed with medications,
salt and caffeine restrictions, PT can be helpful to restore
balance, reduce motion sensitivity, treatment of secondary
BPPV
• PT not helpful when having frequent attacks
39
40. ACUTE VESTIBULAR
SYNDROME
• Rapid onset of CONSTANT vertigo
• Nausea/vomiting
• Gait unsteadiness – significant
• Head motion intolerance
• Spontaneous nystagmus
• Lasts days to weeks
• Most acute vestibular syndrome pts have vestibular
neuritis, but some may be due to posterior circulation CVA
(Newman-Toker et al 2008)
40
41. ACUTE VESTIBULAR SYNDROME
• Vestibular neuritis and posterior CVA present very
similarly, both have symptoms of AVS
• Posterior CVA can be difficult to diagnose (Kattah et al, Stroke
2009, Newman-Toker et al Acad Emerg Med 2013)
• Often do not present with typical CVA symptoms
• High false negative rate (20%) with MRI in 1st 24 hrs.
• 25% of acute vestibular syndrome presentations in ED represent
posterior circulation infarcts
41
42. HINTS EXAM
• Head Impulse Test, Nystagmus, Test of Skew
• Use to differentiate CVA vs. vestibular neuritis in patients
with acute vestibular syndrome
• HINTS evaluation more sensitive than MRI in the first 48
hrs in pts with 1 or more stroke risk factors (Newman-Toker 2013)
42
43. HEAD IMPULSE TEST
• Test of VOR (Vestibulo-Ocular Reflex).
• Ability maintain gaze fixed while head moving
• Interpretation in pt’s with Acute Vestibular Syndrome
• No catch up saccade= CENTRAL
• (+) catch up saccade = PERIPHERAL
43
44. HEAD IMPULSE TEST
44
Top = normal, eyes stay forward. Normal in asymptomatic. CENTRAL finding if pt has
Bottom = abnormal, (+) catch up saccade. PERIPHERAL finding.
46. NYSTAGMUS
• Observe for spontaneous and gaze holding nystagmus
• Have pt maintain R and L gaze without visual fixation
• Frenzel goggles ideal. If unavailable, do not have pt fixate on tip of pen,
look at blank wall, piece of paper
• Interpretation
• CENTRAL (posterior CVA) = Direction changing. Highly
specific!!but low sensitivity when absent
• PERIPHERAL (vestibular neuritis) = Unidirectional.
Horizontal/torsional away from effected side.
46
50. HINTS EXAM
REVIEW
• Perform in patients presenting with Acute Vestibular
Syndrome
• Head Impulse
• Nystagmus (spontaneous and gaze holding)
• Test of Skew
50
51. HINTS EXAM INTERPRETATION FOR
AVS PATIENTS
• CENTRAL
• Head Impulse: NEG (no catch up saccade)
• Nystagmus* DIRECTION CHANGING
• Test of Skew +vertical saccade
• PERIPHERAL
• Head Impulse (+) catch up saccade
• Nystagmus* UNILATERAL
• Test of Skew NEG
*Nystagmus is tested spontaneous and gaze holding bilat
51
52. PROS AND CONS HINTS EXAM
• Fast, inexpensive and several early studies promising for
improved sensitivity for recognizing early posterior CVA
• Grounded in well-established anatomical and physiological
neuroscience
• Some skill required to interpret findings of oculomotor
tests, inter rater reliability not well studied
• Look forward to improving technology to better assess
Head Impulse test
52
53. HEAD IMPULSE TEST
53
Computerized HIT machine to measure the presence of catch up saccade
Can be screened clinically in absence of HIT machine
54. CERVICOGENIC
DIZZINESS
• Key symptom = dizziness provoked by neck rotation while
sitting or standing. Not gravity dependent
• Many potential causes
• Cervical Spine dysfunction
• VBI (atherosclerosis, dissection or rotational occlusion)
• If VBI symptoms +history or risk factors suggestive of VBI,
further imaging needed. Clinical VBI screen not sensitive
or specific
54
55. CERVICOGENIC DIZZINESS:
MUSCULOSKELETAL
Diagnosis of Exclusion
• Associated with neck pain
• Dizziness and Nystagmus may be present with seated neck rotation
• No other abnormal oculomotor findings
• Usually not spinning vertigo, often described as lightheaded or
imbalance. Variable duration
• Can feel mildly dizzy “all the time”, that’s worse with some head
movements
• Often can reproduce dizziness with palpation or joint mobility
assessment of upper cervical spine
55
57. WHEN TO BE CONCERNED FOR VBI
• VBI symptoms
• Dizziness
• Double vision
• Dysarthria
• Dysphagia
• Drop attacks
• Tinnitus
• Blurred vision
• Fainting
• Nausea/vomiting
57
58. WHEN TO BE CONCERNED FOR VBI
• VBI symptoms plus history
• of stroke risk factors (ischemia)
• of recent head/neck trauma (dissection)
• Symptoms clearly associated with neck rotation (VA rotational
occlusion)
• Presence of central oculomotor or abnormal CN findings
• Patient reports avoidance of end-range neck positions as
a result of fear, this may be indicative of VBI (Johnson et al
2007)
58
61. WHEN TO BE CONCERNED FOR
CERVICAL DISSECTION?
Transient neurological symptoms:
• Most Common: neck pain, HA, blurred vision, dysarthria, dizziness
• Present 1 month prior to diagnosis of cervical artery dissection.
Recent cervical spine trauma, even MINOR
• Most commonly jerky, abrupt movements into hyperextension or
sidebending
• Strenuous activities
Cardiovascular risk factors not strongly associated with
cervical artery dissection
61
Thomas et al 2015
62. COMPLICATED VESTIBULAR CASE
• 63 y/o woman
• History of I/M vertigo for 8 years.
• Woke up with constant vertigo and
n/v. Worse w/head rotation to the L
• Meclizine not helping
• PMH: DM, HTN,
• FMH: stroke both parents
• Soc: 1 cigarette/mo
•
62
63. COMPLICATED VESTIBULAR CASE
• Neuro Admit: 3/14
• “exam non focal except stocking glove pattern sensation loss and
hyporeflexia”
• Head CT, CTA and MRI, chest x-ray and 12 lead ECG all
WNL
• IP PT exam: 3/16
• +L saccade testing repeated overshoot (CENTRAL)
• Impaired coordination with L heel to shin and L foot RAM
• Gait ataxic due to dizziness issued walker
• D/c’d home with ref for Neuro f/u, ENT, and Vestibular PT
63
64. COMPLICATED VESTIBULAR CASE
• Next day pt developed L facial droop, returned to ED
• Exam in ED NEG for focal neurological deficits
• MRI of brain negative for acute infarct
• 3 days later: OP PT vestibular eval and Neuro f/u appt
• New onset of diplopia, dysphagia, tinnitus R>L, worsening
frontal HA.
64
65. COMPLICATED VESTIBULAR CASE
• PT Exam
• + VBI screen bilat (Sustained neck rotation in sitting x 10 sec) with
production of lightheadedness and HA
• CN exam: decr L facial light touch sensation (V) and decreased L
facial strength (VII) , +dizziness/imbalance (VIII)
• Oculomotor
• Head Impulse/Head Thrust: bilat catch up saccade (peripheral? Bilat
atypical)
• Nystagmus: +direction changing with gaze holding (CENTRAL )
• Test of Skew: neg
• Saccadic eye movemement: + overshoot bilat (CENTRAL )
65
66. COMPLICATED
VESTIBULAR CASE
• Neuro f/u appt found same CN findings
• Additional testing
• 3rd MRI subacute stroke L PICA territory
• Standard angiogram 50% focal stenosis L VA intracranial
segment, evidence of atherosclerotic disease
• Medical Treatment: aspirin, atorvastatin, strict blood
pressure and glucose control.
66
68. COMPLICATED VESTIBULAR CASE
• Symptoms improved with medical management
• Resumed outpatient PT
• After 7 days, pt had onset of episodic positional vertigo
• Seated head rotation no longer symptomatic
• Oculomotor exam unchanged
• Dix-Hallpike positive for classic BPPV with dizziness and L
torsional upbeating nystagmus/dizziness <30 sec
• Treated with Epley improved
• Continued PT for balance training until safe and IND for
d/c
68
69. COMPLICATED VESTIBULAR CASE:
WHAT DID WE LEARN?
• Combination of posterior CVA, later developed BPPV
• Oculomotor may have early cues of CENTRAL pathology
• Pt early report of symptoms with L head rotation
consistent with VBI.
• Both CTA and MRA unable to id VA stenosis intracranial
segment.
69
70. SUMMARY
If pt fits diagnostic criteria for BPPV, treat with Epley
maneuver. Repeat 2-3x for improved outcomes
BPPV CRITERIA: ALL MUST BE MET FOR DIAGNOSIS
Subjective: BRIEF episodes of spinning vertigo with changes in head position
relative to gravity
Exam: with Dix Hallpike
1. Vertigo with nystagmus (vertical AND torsional)
2. Latency period ( 5-20 sec) prior to onset of vertigo and nystagmus
3. Vertigo and nystagmus increase then resolve in < 60 sec from onset of
nystagmus
70
71. SUMMARY
• Pt’s that do not present with the classic presentation of BPPV, DO
NOT have BPPV!!
• For pts with acute vestibular syndrome (AVS), the oculomotor HINTS
exam is more sensitive than MRI in the 1st 48 hrs to differentiate
posterior CVA from vestibular neuritis.
• Dizziness produced with seated neck rotation NOT indicative of
BPPV; likely cervicogenic. Need to consider VBI, if c/o other VBI
symptoms + stroke risk factors or recent neck trauma (even minor!)
71
73. HELPFUL REFERENCES
• Dizzy patient overview:
• Huh YE and Kim JS. Beside Evaluation of Dizzy Patients. J Clin Neurol.
2013 Oct; 9(4): 203–213
• BPPV Clinical practice guidelines
• Bhattacharyya, Neil et al. Clinical practice guideline: Benign paroxysmal
positional vertigo. Otolaryngology–Head and Neck Surgery (2008) 139,
S47-S8
• Risk factors for cervical artery disection
• Thomas LC, Rivet DA, Attia JR, Levi C.. Risk Factors and Clinical
Presentation of Cervical Arterial Dissection: Preliminary Results of a
Prospective Case-Control Study J Orthop Sports Phys Ther. 2015 July;
45(7)
73
74. HELPFUL REFERENCES
• HINTS exam
• Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-toker DE. HINTS to
diagnose stroke in the acute vestibular syndrome: three-step bedside
oculomotor examination more sensitive than early MRI diffusion-weighted
imaging. Stroke. 2009;40(11):3504-10
• Newman-toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms
ABCD2 to screen for stroke in acute continuous vertigo and dizziness.
Acad Emerg Med. 2013;20(10):986-96
74
75. HELPFUL REFERENCES
• VIDEOS:
https://www.youtube.com/watch?v=FwUAUtm-_fM
Dr. Peter John, Emergency Medicine. A Basic Simplified Approach to
the Dizzy Patient Part 1 and 2. Discusses BPPV vs. AVS and
assessing HINTs to r/o stroke in pt’s with AVS.
• Websites:
http://www.dizziness-and-balance.com/
http://vestibular.org/
75
76. MORE REFERENCES
• Anagnostou E1, Kouzi I2, Spengos K Diagnosis and Treatment of Anterior-Canal Benign
Paroxysmal Positional Vertigo: A Systematic Review. J Clin Neurol. 2015 Jul;11(3):262-
7.
• Batuecas-Caletrio et al., “Benign paroxysmal positional vertigo in the
elderly,” Gerontology, vol. 59, no. 5, pp. 408–412, 2013
• Bhattacharyya, Neil et al. Clinical practice guideline: Benign paroxysmal positional
vertigo Otolaryngology–Head and Neck Surgery (2008) 139, S47-S8
• Campos-Herrera CR, Scaff M, Yamamoto FI, Conforto AB (December 2008).
"Spontaneous cervical artery dissection: an update on clinical and diagnostic aspects".
Arq Neuropsiquiatr 66 (4): 922–7
• Choi K et al. Stroke. 2013;44:1817-1824
• Gulli G, Marquardt L, Rothwell PM, Markus HS. Stroke risk after posterior circulation
stroke/transient ischemic attack and its relationship to site of vertebrobasilar stenosis
pooled data analysis from prospective studies. Stroke (2013)
• Go G et al. Rotational Vertebral Artery Compression : Bow Hunter's Syndrome. J
Korean Neurosurg Soc. 2013 Sep; 54(3): 243–245.
76
77. MORE REFERENCES
• Heikkila H. Cervical Vertigo. Chapter 17 in Grieve's modern manual therapy. The
vertebral column. Third edn. Ed Boyling JD, Jull GA, Twomey PLT). Churchill
Livngstone,Edinburgh, 2004
• Helminski JO, Zee DS, Janssen I, Hain TC. (2010). Effectiveness of particle
repositioning maneuvers in the treatment of benign paroxysmal positional vertigo: a
systematic review. Physical Therapy 90(5) 1-16
• Johnson EG, Houle S, Perez A, San Lucas S and Papa D. Relationship between the
Duplex Doppler Ultrasound and a Questionnaire Screening for Positional Tolerance of
the Cervical Spine in Subjects with Suspected Vascular Pathology: A Case Series Pilot
Study. J Man Manip Ther. 2007; 15:225-30
• Kerrigan M.A et al “Prevalence of benign paroxysmal positional vertigo in the young
adult population,” PM and R, vol. 5, no. 9, pp. 778–785, 2013.
• Kim YK, Schulman S (April 2009). "Cervical artery dissection: pathology, epidemiology
and management". Thromb. Res. 123 (6): 810–21
• Kollén L et al , “Benign paroxysmal positional vertigo is a common cause of dizziness
and unsteadiness in a large population of 75-year-olds,” Aging—Clinical and
Experimental Research, vol. 24, no. 4, pp. 317–323, 2012
77
78. MORE REFERENCES
• Liu H (2012) Presentation and outcome of post-traumatic benign paroxysmal positional
vertigo. Acta Oto-Laryngologica, 132: 803–806
• Loudon JK, Ruhl M, Field E. 1997. Ability to reproduce head position after whiplash
injury. Spine 22(8) 865-868.
• Magnusson et al. Cervical muscle afferents play a dominant role over vestibular
afferents during bilateral vibration of neck muscles. J Vest Res 16(2006) 127-136
• Oghalai, JS et al. Stewart, and H. A. Jenkins, “Unrecognized benign paroxysmal
positional vertigo in elderly patients,” Otolaryngology—Head and Neck Surgery, vol.
122, no. 5, pp. 630–634, 2000
• Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal
positional vertigo (BPPV). CMAJ 2003;169:681–93
• Strupp M, Planck JH, Arbusow V, Steiger HJ, Brückmann H, Brandt T. Rotational
vertebral artery occlusion syndrome with vertigo due to “labyrinthine excitation”.
Neurology. 2000;54:1376–1379.
78
79. MORE REFERENCES
• Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman-Toker DE. Does my
dizzy patient have a stroke? A systematic review of bedside diagnosis inacute
vestibular syndrome. CMAJ. 2011; 183:E571–92.
• Von Brevern M, Radtke A, Lezius F, et al. Epidemiology of benign paroxysmal
positionalvertigo: a population based study. J Neurol Neurosurg Psychiatry
2007;78:710–715
79
81. ROLL TEST FOR
HORIZONTAL CANAL
1. Begin supine in 30° flexion
2. Quickly rotate head about 90° to one side
3. Return to neutral slowly
3. Quickly rotated head about 90° to the other side
Maintain rotation 1-2 min in each position looking for
dizziness and nystagmus
81
83. ROLL TEST: HORIZONTAL CANAL
BPPV FINDINGS
• Same diagnosis criteria as Posterior Canal BPPV
• Brief episodic vertigo with change in head position relative to gravity
• Vertigo associated with nystagmus with horizontal roll test
• Latency prior to onset of vertigo/nystagmus
• Vertigo/nystagmus resolves <60 sec
• Vertigo/nystagmus commonly present in both L and R test
positions
• Effected side more symptomatic
• Nystagmus is horizontal
• Geotropic = toward the ground. (Most common)
• Ageotropic = away from the ground
83
85. HORIZONTAL CANAL BPPV:
SUPINE ROLL TEST
85
R L
R horizontal nystagmus in R rotation
L horizontal nystagmus in L rotation
= Geotropic
86. “SUBJECTIVE” BPPV
• Vertigo but no nystagmus during Dix-Hallpike
• Same latency, duration of symptoms during Dix-Hallpike
as “objective” BPPV
• All other subjective symptoms will be the same as typical
BPPV, but intensity of vertigo may be less severe
• Responds well to canalith repositioning such as Epley
Maneuver (Hubner et al 2013)
• Hypotheses
• resolving BPPV with only a small amount of ootoliths in the canal
(Alverenga et al. 2011)
• Chronic canalothiasis within the short arm of posterior canal (Büki et
al. 2011)
86
87. WHEN SYMPTOMS/FINDINGS
CONCERNING FOR VBI
• Refer to physician to consider arterial imaging
• CTA highest sensitivity (100%) vs. MRA (77%). (Systemic Review,
Gottesman 2012)
• Angiogram may be needed for intracranial VA segment
• In the rare case of suspected VA rotational occlusion (bow hunters
syndrome), angiogram in rotation most sensitive (Goo et al 2013)
87
88. BPPV VS. VBI
• BPPV will not have additional neuro symptoms, central
ocuolmotor findings or other abnormal neurological
findings
• Dix-Hallpike Testing will not fit typical BPPV pattern in VBI
• VBI symptoms during Dix-Hallpike will not resolve in <1
min, will not fatigue with repeated testing and will have
central nystagmus patterns (downbeating, pure vertical or
direction changing)
88
89. MUSCULOSKELTAL CERVICAL
DIZZINESS VS VBI
• Presence of VBI symptoms + history of stroke risk factors
or recent head/neck trauma (even minor!) = imaging is
needed!!
• If low suspicion of VBI + findings of c-spine dysfunction, a
trial of gentle manual therapy to c-spine will very likely
reduce symptoms of dizziness/nystagmus with immediate
re-test of cervical rotation
89
Dizziness produced with seated neck rotation NOT indicative of BPPV; likely cervicogenic. Need to consider VBI, if c/o other VBI symptoms + stroke risk factors or recent neck trauma (even minor!)
Term “Positional” can be misleading because it’s present when moving from one position to another. Not by static positions.
In older adults, ~50% of dizziness due to BPPV
Organs for detecting head movements = utricle, saccule and semi-circular canals
Otoconia of calcuim carbonate crystals in utrice and saccule that deflect in response to acceleration movement, causing firing of the hair cells
Ampula in the base of semi-ciruular canals will deflect in response to angluar movement of fluid in the canal
The otoconia, which is heavier than the endolymph, fall toward the cupula and bring on endolymphatic flow in an ampullopetal direction, causing stimulation of the HC
Otoconia present in the canal changes the speed of movement in the canal
Can also develop BPPV due due Virus that causes vestibular neuritis/labyrithitis and Meniere’s disease
Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). CMAJ 2003;169:681–93.
You become dizzy because now that rate that should be happening equally on both sides is mismatched. This mismatch of signals from the nerves on either side results in dizziness. Because the nerve on one side is telling you where your head is at, and how fast it’s moving, and the nerve on the other side is giving you different information. The result is dizziness!
Dizziness stops when the otoconia stop moving.
Canalithiasis: MOST COMMON
Otoconia in the semi-circular canal.
Otoconia moving in the canal produces symptoms
Symptoms resolve once otoconia stop moving
Anteior Canal: Will have Downbeating/torsional nystagmus in Dix-Hallpike, however Downbeating nystagmus without torsion is a CENTRAL finding
Bilateral rare: But can be more common after trauma (Katsarkas 1999)
Cupulolisthiasis: Will produce non fatiguing dizziness and nystagmus in the test position. Need to consider cervicogenic cause (vascular or musculoskeleta
When interviewing the pt, they will appear well. May have learned to avoid the provoking movements.
If
Start at 0:20
Dr. Teixido – Otolaryngologist from Deleware
Cannot make diagnosis based on subjective history alone
Maintain position at least 30-45 sec while observing for vertigo and nystagmus
Slowly return to sitting (sometimes will have reversal of nystagmus). Dizziness with return to sit not a + finding
Repeat on the opposite side
Named for the fast phase
Wil l someimes l have a reversal of nystagmus during return to sitting
Upbeating = Posteior Canal (85-95% of all cases)
Downbeating = Anterior Canal (RARE. Also can be a CENTRAL finding)
R torsion = R side involved
L torsion = L side involved
Vertigo and nystagmus < 1 min = CANALISTHIASIS
Vertigo and nystagmus > 1 min = CUPULOLISTHIASIS
RARE! Consider other non-BPPV causes as well
Nystagmus will have vertical AND torsional component toward the effected side. Named for the fast phase.
Special considerations are warranted in the geriatric population, because geriatric patients with BPPV usually report dizziness or imbalance and do not always describe a rotatory crisis. Batuecas-Caletrio and colleagues have argued that the Dix-Hallpike and supine roll tests should be performed in older patients with dizziness, despite the fact that they do not complain of spinning sensation with positional changes
Canalith = Otolith
Each position is maintained for about 30 seconds to allow the particles to move by gravity into a different part of the canal.
Higher recurrence in elderly (Batuecas et al 2013) and with head trauma (Liu 2012)
Gaze holding aka eccentric gaze
If pt has clear subjective symptoms of BPPV may be uneccessary to do oculomotor exam unless findings on Dix-Hallpike do not confirm.
Most will eventually have complete hearing loss in effected ear
No other neuro symptoms, usually normal oculomotor testing
Easy to differentiate from BPPV
BPPV: vertigo < 1 min, brought on by change in head position relative to gravity
BPPV = No presence of spontaneous nystagmus, gaze holding nystagmus, or other CENTRAL oculomotor findings
AVS: constant vertigo, worsened by change of head position
AVS: +spontaneous and/or gaze holding nystagmus
.
High false neg because of Physiolgoical symptoms prior to anatomical changes
Up to 35% of strokes can be missed when presenting with vertigo and dizziness
Stroke risk factors: smoking, hypertension, diabetes, hyperlipidemia, atrial fibrillation, eclampsia, hypercoagulable state, recent cervical trauma, prior stroke, or myocardial infarction
Repeat delayed MRI was obtained in patients with initially normal imaging if clinical signs suggested a central lesion or new neurologic signs appeared during the inpatient admission
Sensitivity: 96.5%, Specificity: 84.4% (Newman)
Central eye movement findings predict stroke with high accuracy (Tarnutzer et al 2011)
https://www.youtube.com/watch?v=Wh2ojfgbC3I
Can see it best at the end of video
Only 20% of patients with central lesions had direction changing. But very specific when you see it.
+spontaneous nystagmus to the L
L beating nystagmus looking L
R beating nystagmus looking R
http://www.kaltura.com/index.php/extwidget/preview/partner_id/797802/uiconf_id/27472092/entry_id/0_jw26j6hk/embed/auto?
+ vertical eye movement
https://www.youtube.com/watch?v=zgqCXef-qP
Nystagmus in gaze holding DIRECTION CHANGING = highly specific, but only present 20% in HINTS study
Head impulses assess the integrity of primary vestibular pathways from the labyrinth to the lateral pons.40
Tests for gaze-evoked nystagmus assess gaze-holding circuits in the brainstem and cerebellum.41
Tests for vertical ocular alignment primarily assess central otolithic pathways in the brainstem.
NOT that hard to learn. PT’s especially good. No data on interrater reliability of HINTS between specialists and EPs, but novice and experienced specialists interpret head impulse test result
Oostendorp [23] reported a latency period of approximately 55 seconds after assuming a cervical extension-rotation position for patients with suspected VBI
f there are other potential explanations, they need to be ruled out!!
Vertigo uncommon, but ~50% whiplash pts report dizziness and imbalance (Oostervield et al 1991, Skovoron et al 1998
Oosterveld WJ, Kortschot HW, Kingma GG, et al. Electronystagmographic findings following cervical whiplash injuries. Acta Otolaryngol 1991; 111:
201–205.
Skovron ML. Epidemiology of Whiplash. In: Szpalski M, Gunzburg R, editors. Whiplash injuries: current concepts in preventions, diagnosis, and treatment of the
cervical whiplash syndrome. Philadelphia: Lippincott-Raven; 1998. pp. 61–67.
Dominant VA compressed at C1-2 level during contralateral neck rotation
Compromises blood flow in the vertebrobasilar artery territory
Rare, most reports are case series.
Oostendorp R. Functionele Vertebrobasilaire Insufficientie [Functional Vertebrobasilar Insufficiency]. Dissertation. Nijmegen, The Netherlands: Katholieke Universiteit Nijmegen; 1988
.
Vertebral Artery or Internal Carotid involved
Firstly, the flow through the blood vessel may be disrupted due to the accumulation of blood under the vessel wall, leading to ischemia.
OR irregularities in the vessel wall and turbulence increase risk of thrombosis and embolism = MORE COMMON
catching volleyball overhead, playing Wii, rugby, racing go-cart, difficult dental extraction, overhead house painting
high impact gym exercises, running on treadmill while using arm support, sustained flexion in child birth, lifting a heavy object on 1 shoulder
Less common symptoms: balance disturbance, generalized limb weakness, non-dermatomal paresthesia, ptosis
Cardiovascular risk factors (HTN and HL), with the exception of migraine, not strongly associated with cervical artery dissection
lung surgery, appendectomy, cholecystectomy, head trauma
Mentioned turning to the L as aggrivating to many providers
HINT neg for central, but skew deviation not tested
Head Impulse/head thrust (neg)
Nystagmus: +L gaze unilat (peripheral)
Test of Skew – N/T
Dix Hallpike neg
G
No HINTS exam in ED
Doesn’t clearly fit HINTs criteria for either peripheral or central. Signs concerning for central due to pt symptoms and findings with sustained neck rotation
Spontaneous nystagmus: negative
Gaze-holding nystagmus: +for direction changing nystagmus (R>L)
Eye movement ROM: WNL
Vergence: NT
Smooth pursuit eye movements: negative
Saccadic eye movement: + on the R and L
VOR Cancellation: WNL
Head Thrusts
Horizontal: consistently + to the R, IM + to the L
Static and Dynamic Visual Acuity: WNL, 7 lines in each condition
Easing: meclizine helps control the spinning sensation
“Repeat MRI brain w/wo contrast with thin cuts through brainstem as well as base of skull.”
Oculomotor still with + overshoot with saccade and direction changing nystagmus with lateral gaze
PT: initiated habituation exercises for motion sensitivity, VOR retraining, balance training
BPPV Clinical Practice Guidelines: Bhattacharyya, Neil et al. Clinical practice guideline: Benign paroxysmal positional vertigo Otolaryngology–Head and Neck Surgery (2008) 139, S47-S8
.
Unable to isolate 1 horizontal canal during testing
Others suggest that this condition may be related to chronic canalolithiasis within the short arm of a posterior canal [145]
J Am Acad Audiol. 2013 Jul-Aug;24(7):600-6. doi: 10.3766/jaaa.24.7.8.
Treatment of objective and subjective benign paroxysmal positional vertigo.
Huebner AC1, Lytle SR, Doettl SM, Plyler PN, Thelin JT.
G. A. Alvarenga, M. A. Barbosa, and C. C. Porto, “Benign Paroxysmal Positional Vertigo without nystagmus: diagnosis and treatment,” Brazilian Journal of Otorhinolaryngology, vol. 77, no. 6, pp. 799–804, 2011
B. Büki, L. Simon, S. Garab, Y. W. Lundberg, H. Jünger, and D. Straumann, “Sitting-up vertigo and trunk retropulsion in patients with benign positional vertigo but without positional nystagmus,” Journal of Neurology, Neurosurgery and Psychiatry, vol. 82, no. 1, pp. 98–104, 2011
CT more risky due to radiation and toxicity of contrast dye – may not be suitable
VOR: rotation of the head signals inhibiatory signal to the extraocular muscles on one
https://www.youtube.com/watch?v=BNP5UiRlmiU
https://youtu.be/BNP5UiRlmiU
All 3 tests consistent with peripheral findings
1. Head Impulse: + catch up saccade
2. + Gaze holding nystagmus to R = horizontal unidirectional
3. Neg test of skew