back to chiropractic ce seminars neurology: hints … hints of a...exam process: read all...

Back To Chiropractic CE Seminars

Neurology: Hints of a Stroke ~ 6 Hours

Welcome to Back To Chiropractic Online CE exams:

This course counts toward your California Board of Chiropractic Examiners CE. (also accepted in other states, check our website or with your Chiropractic State Board)

The California Board requires that you complete all of your CE hours BEFORE

the end of your Birthday month. We recommend that you send your chiropractic

license renewal form and fee in early to avoid any issues.

COPYRIGHT WARNING

The copyright law of the United States (Title 17, United States Code) governs the making of photocopies or other

reproductions of copyrighted material. Under certain conditions specified in the law, libraries and archives are authorized

to furnish a photocopy or other reproduction. One of these specified conditions is that the photocopy or reproduction is not

to be "used for any purpose other than private study, scholarship, or research." If a user makes a request for, or later uses,

a photocopy or reproduction for purposes in excess of "fair use," that user may be liable for copyright infringement. This

site reserves the right to refuse to accept a copying order if, in its judgment, fulfillment of the order would involve violation

of the copyright law.

Exam Process: Read all instructions before starting!

1. You must register/pay first. If you haven't, please return to: backtochiropractic.net

2. Open a new window or a new internet tab & drag it so it's side-by-side next to this page.

3. On the new window or new tab you just opened, go to: backtochiropractic.net website.

4. Go directly to the Online section. DON'T register again.

5. Click on the Exam for the course you want to take. No passwords needed.

6. Follow the Exam instructions.

7. Upon passing exam (70%), you’ll be able to immediately download your certificate,

and it’ll also be emailed to you. If you don’t pass, you must repeat the exam.

Please retain the certificate for 5 years. DON’T send it to the state board.

If you get audited and lose your records, I’ll have a copy.

I’m always a phone call away... 707.972.0047 or email: [email protected]

Marcus Strutz, DC


33000 North Highway 1

Ft Bragg CA 95437

http://backtochiropractic.net/

http://backtochiropractic.net/

mailto:[email protected]

MANAGEMENT OF THE DIZZY

PATIENT: HINTS TO A STROKE

By:Larry E. Masula, D.C., DACNB, FAVRB, FAFICCDipolmate American Chiropractic Neurology Board,

Fellow American Vestibular Rehabilitation Board, Fellow Academy of Forensic and Industrial Chiropractic Consultants

[email protected]

Larry E. Masula, D.C. 7/1/2019 3

Larry E. Masula, DC, DACNB, FAVRB, FAFICC

Carrick Institute for Advanced Neurological Studies: Frederick C.Carrick, PhD, Cambridge University.

Diplomate American Chiropractic Neurology Board

Fellow American Vestibular Rehabilitation Board

Fellow Academy of Forensic and Industrial Chiropractic Consultatns

Evaluation and Management of Dizziness and Balance Disorders, NeilT. Shepard , PhD, director of the Dizziness and Balance DisordersProgram at the Mayo Clinic, Rochester, Minnesota, and professor ofaudiology in the Mayo Clinical School of Medicine. Joel A. Goebel,M.D., FACS. Director, Dizziness and Balance Center WashingtonUniversity School of Medicine, St. Louis, MO

American Institute of Continuing Medical Education, Certified in 101Vestibular Rehabilitation, 201 Ocular Motor Testing, 202 Gaze,Headshake and Positional Testing. Richard E. GANS, PH.D.,EXECUTIVE DIRECTOR AMERICAN INSTITUTE OF BALANCE

7/1/2019Larry E. Masula, D.C, DACNB.FAVRB, FAFICC 4

Objectives

▪ Introduction and general overview of theclinical anatomy and physiology of thevestibular system and posterior fossa(cavity.)

▪ Clinical syndromes associated with theVestibular System: Vascular (posteriorfossa stroke assessment), infectious,neoplastic, neurological, degenerative,and cerebellar conditions will bediscussed with emphasis on diagnosticsand chiropractic management.

Larry E. Masula, D.C. DACNB, FAVRB, FAFICC 7/1/2019 5

Recommended Reading▪ Clinical Neurophysiology of the Vestibular System, Edition 2,

Robert W. Baloh, Vicente Honrubia. Chapters 1-3

▪ Principles of Neural Science, 4th Edition, Eric R. Kandel, James H. Schwartz, Thomas M. Jessel, McGraw-Hill. Chapter 42: The Cerebellum

▪ Technique of the Neurological Examination, 4th Edition, DeMeyer, W. McGraw-Hill. Chapter 8: Examination of Cerebellar Dysfunction

▪ Neurological Differential Diagnosis, 2nd Edition, John Patten, Springer 1996. Chapter 12: The Extrapyramidal System and the Cerebellum

▪ The Neurology of Eye Movements, 3rd edition, Leigh & Zee

▪ The Brain That Changes Itself, Norman Doidge, M.D.

▪ Vestibular Rehabilitation, 4th Edition, Susan J. Herdman, Richard A. Clendaniel

Larry E. Masula, D.C. DACNB, FAVRB, FAFICC 7/1/2019 6

MOST OF ALL

THANK YOU !!!

Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 7/1/2019 7

Phineas GageNeurosciences Most Famous Patient1823-1860


IRISIS 1889

Larry E. Masula, D.C, DACNB, FAVRB, FAFICC 9

Almond Blossoms 1890

7/1/2019Larry E. Masula, D.C, DACNB, FAVRB, FAFICC

10

At Eternity’s Gate 1890


11

The Church at Auvers 1890


12

Prisoners Exercising 1890


13

7/1/2019Larry E. Masula, D.C.,DACNB, FAVRB, FAFICC 14

Can You Find a Common Theme

Among These 5 Paintings

Can You Find a Common Theme

Among These 5 Paintings▪ 1. Yes, they have been painted by the same

artist

▪ 2. Yes, they are all roughly painted within one year

▪ 3. Yes, the artist may well have had a disturbance of spatial orientation (vertigo). Why? Much of the paintings are leaning to the left.

▪ 4. If so, on which side is the artist’s problem?

▪ 5. What are the possible causes?

7/1/2019Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 15


Answer: The left vestibular system was most

likely affected and may have failed.

Explanation: Due to the length of time, based

on the painting dates, (over a year) it was no

longer an acute problem. We will discuss the

various problems which affect our sense of

spatial awareness. We will also discuss why

in this case; the left vestibular apparatus was

no longer being inhibited by the right and why

the left vestibular system appeared overly

active.

7/1/2019Larry E. Masula, D.C.DACNB, FAVRB, FAFICC 17

Who is the

Artist?

On the Verge of Insanity

Vincent cut off his left ear on December 23,1888 after being upset with a fellow painter. Itwas the first of several serious breakdowns thatplagued him until his tragic suicide a year and ahalf later. We don’t know precisely what hisillness was, but it had a huge impact on his life.


7/1/2019Larry E. Masula, D.C, DACNB, FAVRB, FAFICC. 20

January 28, 1889

Van Gogh’s - Letter to his brother Theo from

Arles, France

“I well knew that one could break one’s arms and legs

before, and that then afterwards that could get better

but I didn’t know that one could break one’s brain and

that afterwards that got better too.”

Why Study Dizziness, Vertigo and Stroke?


Because

▪ Patient Care and Safety are Preeminent

▪ Develop Improved Diagnostic Skills

▪ There is a Great Need for Skilled Practioners

▪ (9.47%) 31 million Americans experience Lower

back pain at any given time.

www.acatoday.org/backpain

▪ (21.1%) 69 million US adults aged 40 years and

older had vestibular dysfunction. Disorders of

Balance and Vestibular Function in US Adults. Data From the

National Health and Nutrition Examination Survey, 2001-2004



WHAT IS DIZZINESS AND

VERTIGO?

Vertigo and Dizziness are considered:

▪ Either an unpleasant Disturbance of

Spatial Orientation

▪ The Illusory perception of body

movement (spinning, wobbling, or tilting)

and/or of the surroundings

Larry E. Masula, D.C, DACNB, FAVRB, FAFICC7/1/2019 24

Centers for Disease Control and Prevention

▪ Falls Are Serious and Costly

▪ One out of five falls causes a serious injury such as broken bones or a head injury.1,2

▪ Each year, 2.5 million older people are treated in emergencydepartments (visits) for fall injuries.3

▪ Over 700,000 patients a year (1/3) are hospitalized because of a fall injury, most often because of a head injury or hip fracture.3

▪ Each year at least 250,000 older people are hospitalized for hip fractures.5 More than 95% of hip fractures are caused by falling,6 usually by falling sideways.7

▪ Falls are the most common cause of traumatic brain injuries (TBI).8

▪ Adjusted for inflation, the direct medical costs for fall injuries are $34 billion annually.9Hospital costs account for two-thirds of the total.

Larry E. Masula, D.CDACNB, FAVRB, FAFICC. 06/15/2019 25

The Burden Dizziness and Vertigo Impose

on the Community

▪ Neuhauser HK, Radtke A, von Brevern M, Lezius F, Feldmann

M, Lempert T.

▪ “Research on the personal and health care burden of

ill health usually focuses on specific diseases rather

than symptoms. The diagnosis-based approach may

underestimate the burden of common symptoms

such as dizziness and vertigo, which rank among the

most frequent complaints in primary care but remain

unexplained in 40-80% of cases.”

7/1/2019Larry E. Masula, D.C. DACNB, FAVRB, FAFICC 26

Stroke Statistics

▪ Stroke kills about 140,000 Americans each year—that’s 1 out of every 20deaths.1

▪ Someone in the United States has a stroke every 40 seconds. Every 4minutes, someone dies of stroke.2

▪ Every year, more than 795,000 people in the United States have a stroke.About 610,000 of these are first or new strokes.2

▪ About 185,000 strokes—nearly 1 of 4—are in people who have had a previousstroke.2

▪ About 87% of all strokes are ischemic strokes, in which blood flow to the brainis blocked.2

▪ Stroke costs the United States an estimated $34 billion each year.2 This totalincludes the cost of health care services, medicines to treat stroke, and misseddays of work.

▪ Stroke is a leading cause of serious long-term disability.2 Stroke reducesmobility in more than half of stroke survivors age 65 and over

▪ 1. Vital Signs: Recent trends in stroke death rates – United States, 2000-2015. MMWR 2017;66.

▪ 2. Benjamin EJ, Blaha MJ, Chiuve SE, et al. on behalf of the American Heart Association StatisticsCommittee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2017 update:a report from the American Heart Association. Circulation. 2017;135:e229-e445.


https://www.cdc.gov/stroke/types_of_stroke.htm

Ischemic Posterior Circulation Stroke:

Posterior circulation strokes (Posterior Fossa)

represent approximately 20% of all ischemic

strokes.

In contrast to the anterior circulation, several

differences in presenting symptoms, clinical

evaluation, diagnostic testing, and

management strategy exist presenting a

challenge to the treating physician.▪ Ischemic Posterior Circulation Stroke: A Review of Anatomy,

Clinical Presentations, Diagnosis, and Current Management

Amre Nouh,1 Jessica Remke,2 and Sean Ruland1,*


https://www.ncbi.nlm.nih.gov/pubmed/?term=Nouh%20A%5BAuthor%5D&cauthor=true&cauthor_uid=24778625

https://www.ncbi.nlm.nih.gov/pubmed/?term=Remke%20J%5BAuthor%5D&cauthor=true&cauthor_uid=24778625

https://www.ncbi.nlm.nih.gov/pubmed/?term=Ruland%20S%5BAuthor%5D&cauthor=true&cauthor_uid=24778625

Anatomy of Tympanic Cavity


Important Structures include: Int. Auditory meatus, Cochlea, SCC’s, Cn7, Cn 8, Eustachian

tube anteriorly, Mastoid air cells post. The middle ear functions as an amplifier. Within the

EAC - sound energy is compressed/oscillates, transfers sound energy to the Oval window.

Frequency from the TM to the Oval window (force) increases. Mechanism one - TM is 17x

larger than oval window. Mechanism two - Ossicles transfer one unit of energy by factor of

1.3. Therefore, 17 x 1.3 = sound amplified ~ 22x Pathologically, Ossicular sclerosis =dampened sound.

Anatomy of Tympanic Cavity - Cochlea

“unraveled”

7/1/2019Larry E. Masula, D.C. 30

The bony canal housing the cochlear duct is filled with? Perilymph whose

major cation is Na+. Upper part = Scala vestibuli. Lower part = Scala

tympani terminating at the Round window.

Anatomy of Tympanic Cavity - Cochlea

anatomy


The Cochlear duct is filled with? Endolymph rich in K+.

Helicotrema-(not shown) is where the 2 Scala meet. The Organ

of Corti and hair cells lie within the C. duct.

7/1/2019Larry E. Masula, D.C., DACNB, FAVRB,FAFICC 32

ANATOMY

Let’s Dive into the Anatomy

Middle Ear - Dimensions


Dimensions of middle ear

a) 1/3 of the middle ear is above TM -“Epitympanic Recess”

b) Tympanic cavity proper (waist)

c) The Head of the Malleolus and Incus lie in the Epitympanic Recess

d) H = 15mm, AP = 15mm, Width-ETR = 6mmW, TC = 2mmW, Inf. Floor

= 4mmW


The roof is small, and the floor is long. Tympanic Membrane is 9-10 mm thick and titledat 55° downward and forward toward the floor, which together predispose foreign objects

to lodge at bottom. Clinical Note: Ear Lavage is best directed toward the roof for foreign

body removal. The Lateral Wall is made up o 2 parts. A membranous part and a bony

part (Epitympanic Recess). The TM consists of 3 layers. External-skin – derived from

ectoderm. Internal – mucosa of middle ear – derived from endoderm. Middle – fibrous

layer is from Mesoderm.


Examination: Pars flaccida – perforable, Handle of malleus and Umbro, Pars

tensa – stiffer because it sits in a bony sulcus. Cone of Light is downward and

forward because of the 55° angle to the floor

,

,

Lateral Wall – (Tympanic Wall)

7/1/2019Larry E. Masula, D.C., DACNB, FAVRB 36

Nerve Supply to Tympanic Membrane

Auriculotemporal nerve-branch of mandibular div. of Cn5 which exits Foramen Ovale and suppliespars tensa and the EAC . It also innervates the teeth which is the reason why teeth pain may causereferred otalgia. CN. VII, X innervate the pars flaccida. Clinical Note: when stimulated or wax irritatesthe TM, the patient can develop reflex bradycardia, cardiac arrest or a cough. CN. IX innervates(medial) inner TM surface, parts of the external ear and the posterior 2/3 of the tongue supplying

touch, pain, and temperature.

Nerve Supply to Tympanic Membrane

▪ Clinical Gem: The glossopharyngeal nervesupplies the posterior 2/3 of the tongue andtonsillar region. I recently had a patient, Jim,who presented with vertigo, minimal ear andpharyngeal pain. He had developed tonsillarcancer. Cancer of either structure can refersymptoms via the glossopharyngeal nerve tothe middle ear.


7/1/2019, Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 38

These few nerve fibers within the middle ear are

important in the differential of Stroke vs. Vestibular

Pathology. Why is important? Because later on, we

will learn that the Facial nerve has a Geniculate

Ganglion. It can contain a latent Herpes Zoster

virus. Sometimes this virus can be activated. It

enters the 7th fiber that travels through the middle

ear to the skin of the tympanic membrane. In this

case the patient will develop severe ear pain and/or

hemi-facial paralysis like Bells Palsy or Stroke.

During otoscopy there may be hemorrhagic blisters

on the anterior 2/3 of the tongue, the TM or within

the middle ear. “Ramsey Hunt Syndrome”

Varicella Zoster (Herpes)– can affect CN.7 and create Hemi-facial paralysis

and Tympanic hemorrhagic blisters

(Ramsey Hunt Syndrome)


Medial Wall aka (Labyrinthine Wall)


Medial Wall (labyrinthine wall)▪ Most prominent feature is a circular

inward bulge = Promontory, (Base of

Cochlea), Tympanic Plexus of nerves.

▪ Oval Window into cochlea is posterior

and superior and below is the Round

Window (secondary tympanic

membrane)

▪ Foot Plate of Stapes attaches to Oval

Window. Movement of Stapes: Annular

lig. holds stapes to Oval window.

Posterior part of annular lig, is shorter

and thicker causing the stapes to tap

the oval window like a door hinge and

not a piston.

▪ Hook in the superior anterior wall – NOT

SHOWN (processes cochleiformis) for

the tendon of tensor tympani which

bends the tendon to move it laterally to

attach to the handle of malleus. During

contraction it pulls the malleolus and the

TM medially creating tension to dampen

sound.


Medial Wall (Labyrinthine Wall)

▪ One of the most important structures isa longitudinal bulge (bony “Facial” canal)along the superior aspect of the Medialwall.

▪ It originates from the Facial Nucleus inthe Pons and moves anteriorly andmedially to enter the internal acousticmeatus. It exits and travels across thetop of the Vestibule terminating in theGeniculate Ganglion which sits behindthe superior anterior surface of themedial wall. Its first branch is theGreater Petrosal nerve before it entersthrough the boney (facial) canal in thepetrous part of the temporal bone whereit extends backwards to the posteriorwall and within the posterior wall thefacial canal and nerve turn downward.

▪ It is not exposed within the middle earcavity.

▪ The superior bulge is created by theHorizontal Semicircular canal


Internal Acoustic Meatus for Facial Nerve

and Vestibular Nerves


Acoustic neuromas are usually located in the angle between the cerebellum and the

pons, in the back of the skull (the posterior fossa) applying pressure in and around

the internal acoustic meatus. Common symptoms are one-sided hearing loss,

tinnitus, dizziness and facial paralysis

Why is this Important in Stroke Differential ?

▪ If there is pathology within the middle ear following chronicOtitis Media.

▪ 1. Cholesteatoma, forms a sack of stratified squamousepithelium. It is not cholesterol and it is not a tumor. It isdestructive by secreting products: Collagenases-eats boneand cartilage and pars flaccida creating offensive discharge,also chemicals which stimulate Osteoclasts-eats bone.Damage occurs to the Oval Window and stapes – Tinnitusor Conductive Hearing Loss develops. Facial canal damageoccurs resulting in hemi-facial palsy. Horizontal canaldamage causes vertigo.

▪ 2. Otosclerosis-abnormal bone formation takes over theannular ligament which attaches the stapes to the ovalwindow reducing stapes movement = Conductive HearingLoss.

▪ Does this look like a stroke?


Posterior Wall (Mastoid Wall) ▪ Special window in superior medial

aspect of posterior wall- “Aditus toantrum” - opening into the mastoidantrum.

▪ Facial Canal descends within theposterior wall.

▪ The bony “Pyramidal Eminence” - ishollow and contains the stapediusmuscle with an exiting tendon whichattaches to the neck of the stapes.Importance: dampen stapes movementand sound. Innervated by a branch ofthe Facial nerve.

▪ The Chorda Tympani nerve (CN.7) andthe Posterior tympanic artery (notshown) also enter the posterior wall.The chorda tympani traverses throughthe middle ear to exit through theanterior wall.

▪ Not Shown- the short process of theIncus attaches to the posterior wall atthe Fossa Incudis.


Posterior Wall (Mastoid Wall)

▪ The Facial nerve descends andwill eventually emerge throughthe styloid mastoid foramengiving off the posterior auricularbranch which supplies thestylohyoid and posterior belly ofthe digastric muscles, theoccipital region and auricularmuscles. Its terminal branchesmove forward in the face to thetemporal, zygomatic, buccal,marginal mandibular andcervical muscles.

7/1/2019, Larry E. Masula, D.C, DACNB, FAVRB, FAFICC. 46

Anterior Wall (Carotid Wall)2 Special Structures

▪ 1. Upper canal is a bony canal.

Houses the Tensor Tympani muscle

which takes 3 origins from the bony

canal, w/ the superior cartilage of the

eustachian tube, and from the

undersurface of the greater wing of

sphenoid (skull). It then enters the

canal and then converts to a tendon

which turns and moves laterally and

attaches to the handle of malleus.

Upon contraction it pulls the handle of

the malleus inward to pull the TM and

the ossicular chain tense. Purpose:

contracts to dampen loud sounds.

Innervation: mandibular division

(motor) of CN5.

▪ 2. Eustachian Tube (petrotympanic

tube) connects the tympanic cavity w/

lateral wall of pharynx.


Anterior Wall (Carotid Wall)

▪ Which artery sits anteriorly? Int. Carotid. Covered by a sympathetic plexus from the superior cervical ganglion. Sympathetic fibers enter the middle ear as superior and inferior fibers.


Anterior Wall (Carotid Wall) Summary

▪ How many features in the Anterior Wall?

1. Canal for Tensor Tympani

2. Opening of Eustachian Tube

3. Lesser Petrosal Nerve

4. Sympathetic Fibers

5. Chorda Tympani Nerve


Anterior Wall (Carotid Wall)

▪ Jugular Fossa sits directly beneaththe floor of middle ear. Contains theinternal jugular vein, CN’s 9, 10, 11.

▪ CN.9 gives off a branch which entersthe floor (not shown) bringingparasympathetic and sensory fibers tothe tympanic plexus collectivelysupplying all walls of the middle earincluding the eustachian tube andmastoid.

▪ A branch from the tympanic plexus(lesser petrosal nerve) exits theanterior wall and ascends through theforamen Ovale and descends backdownward.

▪ Chorda Tympani nerve CN.7,traverses the middle ear and exits theanterior wall via Petrotympanic fissureand through which the anteriortympanic artery enters to supply themiddle ear.


Chorda Tympani - Middle Ear


Chorda Tympani – Branch of Facial N.

What is the relationship of theChord Tympani with contentsof the middle ear?

It passes completely throughthe middle ear between theneck of the Malleus and theIncus and is covered withmucosa. It supplies theanterior 2/3 of the tongue withtaste receptors. Infections,strokes, and middle-earoperations may be damagingcausing dysgeusia (distortedtaste).


Eustachian tube

▪ Clinically Important:

Initial 1/3 is bony and last 2/3 isfibrocartilage. Angles 30º downward and35º anteromedially to open in thenasopharynx.

Remember the T. Tympani muscle? Itoriginates from the base of the skull andthe roof the bony eustachian tube before itenters the anterior wall.

Attached to the end of the tube are theSalpingopharyngeus, Tensor Veli Palitinimuscles, and the Levator Palatini muscles(CN.10)

Function: to elevate the soft palate andopen the end of the tube to equalizepressure within the middle ear.

Reason why PICA strokes, can generateswallowing impairment or having food getstuck in the throat.

7/1/2019Larry E. Masula , D.C., DACNB, FAVRB, FAFICC 53

Inferior Wall (Jugular Wall)

▪ The floor is made by the petrous part of the temporal bone with one important cuniculus.

▪ Sympathetic fibers which start from the Inferior Salvitorynucleus travel with other fibers of the 9th

nerve to enter the floor of the middle ear cavity and extend to the Promontory


Roof

▪ The roof is called the Tegmentum Tympani. The roof is very thin. Clinically it is important because middle ear infections may extend upward especially in children due to an overlying Petrous -Squamous suture which may not be ossified producing a subdural abscess, meningitis and a temporal lobe abscess or infection.


Clinical Review

▪ If the horizontal SCC is affected it will result in Vertigo.

▪ If the facial canal is damaged it will result in facial palsy.If it is damaged proximal to the nerve to the stapedius,it results in paralysis of the stapedius giving rise tohyperacusis.

▪ Middle ear infections may extend posteriorly creatinglife-threatening mastoiditis. If the infection exits theroof (Tegmentum Tympani) it can produce anextradural abscess, meningitis, or a Temporal lobeabscess.

▪ If it extends backward through the Mastoid, it candamage the Sigmoid Sinus resulting inthrombophlebitis, and further backward enter thecerebellum or brainstem.


CSF Leak from Middle Ear

▪ Fracture of the middle cranial fossa, typicallydamages the roof of the middle ear(Tegmentum Tympani which is a thin bone).This may also disrupt the ossicular chain,rupture the tympanic membrane and maydamage the roof of the external acousticmeatus. Blood and CSF leak into the middleear cavity and through the ruptured TM.

▪ This is called “Otorrhea”


Contents of Middle Ear summary

▪ Air

▪ Ossicles (Malleus, Incus, Stapes) all attached via synovial joints

▪ Muscles (Stapedius, Tensor Tympani Tendon)

▪ Nerves

▪ Vessels (Anterior tympanic artery, Posterior tympanic artery)

▪ All structures lined by mucosa



Understanding Vestibular

Neurophysiology

Understanding Neurons – the Big

Picture

▪ Stimulation of receptors results in activationof the 1st order afferent (sensory) neuron

▪ Activation of the 2nd order afferent neurons isdependent on the FOF of its pre-synapticneuronal pool (1st order neurons).

▪ Activation of the thalamus and all corticalstructures is dependent upon the FOF of ALLpre-synaptic neuronal pools of thesomatosensory system).


Central Integrative State (Health) of a Neuron and

Cellular Immediate Early Gene Response –

Constant influx of membrane potential differences are due to:

1. Spatial Summation (multimodal) on the receptor

2. Temporal Summation (high frequency unimodal) on the receptor

3. pH

4. Glucose

5. Oxygen tissue saturation

6. Temperature changes

7. Summation of all presynaptic (+) and (-) input which includes all cortical and segmental integration

8. In summary: stability or fragility of a neuron is based on the FOF of its presynaptic pools or receptor potentials


What Drives Nerve Stimulation and The Gene

Response/Replication?

Receptor Activators 5 Messenger System

▪ Activation from factors on

previous slide

▪ BDNF

▪ Neuroendocrine Hormones

▪ Neurotransmitters

▪ Good Cytokines

▪ Non-inflamed environment

▪ 1st Messenger System –

Receptor

▪ 2nd Messenger System –

Carrier Protein (calmodulin)

▪ 3rd Messenger System –

Protein Kinase

▪ 4th Messenger System –

Phosphoprotein activates the

nucleus

▪ 5th Nuclear Transcribed

Protein



When the mitochondria is damaged it all slows downWhen there is inflammation or infection it all slows downWhen you have caspase activation it all slows downIf you have head trauma it all slows downA decrease in activation and it all slows down

1. The nucleus gets activated and makes raw proteins.

2. Golgi Apparatus changes it into polysomes.

3. It is further modified in the endoplasmic reticulum and placed in a secretory

granule. Transported to a synaptic vesicle.

4. Excess neurotransmitter substance is brought back into the cell via a retrograde

vesicle.

5. Broken down after its been used by Lysosomes and where it can be re-used,

recycled and re-manufactured. The Post synaptic response is a thankyou!

What Do We Do?

“Alterations in the neuron occur at the synapse,strengthening and increasing, or weakening anddecreasing, the number of connections between theneurons.” (Michael Merzenich, considered the world’s leading researcher onbrain plasticity)

Our rehabilitative purpose is therefore to:

1. Strengthen and enhance synaptic activity

2. Improve motor function

3. Improve brain activity via cortical

re-organization


What drives this?


Cellular Survival

FuelGlucose

O2

Activation


When Neurons are Sick

▪ Na/K pumps maintain normal negativity, 3:2 ratio

▪ If there is no ATP = cannot maintain pumps &

metabolic machinery

▪ Firing Threshold Creeps upward → attempt to stay

alive

▪ Not enough fuel to maintain action

▪ Transneural Degeneration results– Hallmark is quick to fire &

quick to fatigue. The neuron becomes unstable with the nucleus becoming

eccentric, microtubular breakdown, and the neuron is trying to die

▪ Pt. waxes and wanes – good periods and low

periods


Inflammation Drives Cell DeathInflammation/trauma activate MGC’s asdo macrophages that enter from theperiphery. Macrophage “posers”develop. Bad cytokines trigger NMDAreceptors at different rates causing theCIEG to shift causing one cell to dosomething different=bad orchestra

Pro-inflammatory cytokines damagethe oligodendrocytes and otherastrocytes, opens up the blood brainbarrier triggering a TH-1 and TH-17response causing massiveinflammation, the bi-lipid membrane isdamaged, tubules breakdown, whichfurther primes the Glial system. Begintagging tissue with a TH-2 responseleading to plasma cells dumping tons ofantibodies → cellular autoimmunityand/or sustained dysfunction →TNDdomino effect


Glial cells, sometimes called neuroglia or

simply glia are non-neuronal cells that maintain homeostasis. Hold neurons in place, supply O2 and nutrition to neurons, insulate one neuron from another, destroy pathogens and remove dead neurons

Cellular Survival is Altered by:

▪ FOF of all presynaptic input (Activation)

▪ Identify and manage Dysglycemia,

Hypoglycemia, Metabolic Syndrome, Insulin

resistance. (Fuel - glucose)

▪ Identify and manage anemia (Fuel – O2)

▪ Adequate protein and fat intake

▪ Inflammatory conditions

▪ Infections

▪ Autoimmunity


`

CBC w/

Diff.

Acute Lupus Acute

Hypochrom Idiopathic Pernicious Myelophistic Aplast. Polycythem Ulcer Thalassem. Hemolyt Myeloblastic Lymph Viral Bacterial

` Anemia Steatorrhea Anemia Anemia Anemia Vera Major Anemia Leukemia Cirrhos Hypothyro Hodgkin's Infect. Infection

Hemogblobin low low low low low High low low low low low low

Hematocrit low low low low low High low low low low low low

Reticulocyte Count E High High High High low low

Cell Morphology Microcyt. Macrocytosis Macrocyt Nucleated Poly- Microcytos Nucleate Myeloblas Varied Macrocyte Variable L.E. Neutro-

Hypoch. Hyperchrom Hyperchrom RBC's chromic Hypochrom RBC's Cells penia

Anisocyt. Anisocytosis Anisocytosis Occ. Target

PoikilocytosisPoikilocytosis

Myelocytes cells

Hypersegment Nucleated

neutrophils RBC's

White Cell Count low low low low High High High High E Variable low low High

Platelet Count low low low low low low

Serum Bilirubin E High E High High E

Serum Iron low E E E E E E E E

Blood Volume Increased low

Definitions: Anisocytosis- red blood cells are of unequal size

Poikilocytosis- are abnormally shaped red blood cells EQUIVOCAL

Polychromasia-is a disorder where there is an abnormally high number of RBC’s 7/1/2019Larry E. Masula, D.C. 70

Vestibular Neuronal Activation and

Neuronal Health

▪ Is dependent upon environmental

stimulation of receptors

▪ Therefore, a stimulus that is constant

would be most important

▪ The only real constant is GRAVITY


Anatomy and Physiology of the

Vestibular System


Vestibular Function:

an Overview

▪ Expressed simply, the role of the vestibular

sensory organs is to transduce the forces

associated with head acceleration and

gravity into a biologic signal.

▪ The control centers in the brain use this

signal to develop a subjective awareness of

head position in relation to the environment

and to produce motor reflexes for equilibrium.

Larry E. Masula, D.C., DACNB, FAVRB, FAFiCC 7/1/2019 73

Vestibular Function: Overview

continued

▪ The force associated with head acceleration

generates a signal in the labyrinth that is

proportional to head acceleration.

▪ The overall objective of the CNS is to

compute head position by performing the

equivalent of a mathematical integration of

the labyrinthine and otolithic input signals.


Larry E. Masula, D.C., DACNB, FAVRB, FAFCC 7/1/2019 75

Vestibular Nerve Physiology

▪ The vestibular system monitors the forcesassociated with Angular and Linear accelerationsof the head by means of 5 organs located withinthe labyrinthine cavity of the temporal bones oneach side of the skull.

▪ The Cristae Ampularis sensory organ of the 3semicircular canals senses angular accelerationof the head

▪ The Otolithic Organs (saccule and utricle)sensory organ the Maculae senses linearacceleration.


The Semi-Circular Canals

The semicircular canals provide sensoryinput about head velocity, which enables theVOR to generate an eye movement thatmatches the velocity of the head movement.The desired result is that the eye remainsstill in space during head motion, enablingclear vision. Neural firing in the vestibularnerve is proportional to head velocity overthe range of frequencies in which the headcommonly moves (0.5 to 7 Hz).


Cupula of the Semi-circular canals

▪ Fluid filled K+ rich Endolymph has a viscosity slightly greater than H2O

▪ The sensory epithelium of the cristae is covered by the gelatinous cupula



Cristae Ampularis - enlarged

Lateral Line System


A similar system is found in fish in which water passing over the tiny pores within the lateral line of the fish move the cupula resulting depolarization of the nerve inducing a motor output

Semicircular Canals

▪ The cupula has the same density as the endolymph

▪ Semicircular canals do not respond to gravity in static head positions

▪ The canals lie roughly in the same planes as the extraocular muscles

▪ Each canal excites a pair of muscles and inhibits a pair of muscles in its same plane. Its partner excites the muscles it inhibits, and vice-versa


Eye Muscles


Canal Related Eye Movements

E.g. If I rotate my head horizontally to the rightactivating the right horizontal canal, I activate theright medial vestibular nucleus, which activates theright oculomotor nucleus and the left abducensnucleus activating the right medial rectus and theleft lateral rectus. Right horizontal canal activationbiases conjugate eye movements to thecontralateral side, in this case to the left.


Activation of the Sensory Hair Cells

▪ Angular movement of the head causes

endolymph flow in one of the semicircular

canals and deflection of the cupula

▪ Deflection of the stereocilia toward the

kinocilium results in depolarization, or

increased firing rate

▪ Deflection of the stereocilia away from the

kinocilium results in hyperpolarization, or

decreased firing rate


Semi-Circular Canals

▪ The semicircular canals provide sensory

input about head velocity, which enables the

VOR to generate an eye movement that

matches the velocity of the head movement.

The desired result is that the eye remains still

in space during head motion, enabling clear

vision. Neural firing in the vestibular nerve is

proportional to head velocity over the rangeof frequencies in which the head commonlymoves (0.5 to 7 Hz).



The coplanar pairing of the canals is associatedwith a push-pull change in the quantity ofsemicircular canals output. When angular headmotion occurs, the endolymph of the coplanar pairof canals is displaced in opposite directions withrespect to their ampullae. This results in a neuralfiring increase in one vestibular nerve and ahyperpolarization (decrease) on the opposite side.For the lateral canals, displacement of the cupulatowards the ampulla (ampullopetal flow) isexcitatory, whereas for the vertical canals,displacement of the cupula away from the ampulla(ampullofugal flow) is excitatory.



Clinically, this push-pull mechanism is an

important point which explains why patients

with unilateral vestibular loss avoid head

motion towards the side of their lesion. More

will be said about this when we discuss how

the central nervous system compensates for

overload.


OTOLITHIC ORGANS: Utricle and Saccule


Otolithic System▪ Even with the head at rest, the calcareous material,

because of its mass, exerts a force (Fg) upon the receptor equal to the product of its mass and acceleration due to the gravitational pull of the earth (g), which at sea level is 9.80 m/sec².

▪ The Fg (force) acting upon the underlying sensory cells changes with different degrees of head tilt and can be represented by two vectors 1. Tangential (F1)

2. Normal to the surface of the receptor (Fn)

▪ They are sensitive to gravity and linear acceleration.Because of their orientation in the head, the utricle issensitive to a change in horizontal movement, and thesaccule gives information about vertical acceleration(such as when in an elevator). Remember Utricle islateral – Saccule is Sit and Stand. Exception: bothsubject to A/P acceleration


http://en.wikipedia.org/wiki/Gravity

http://en.wikipedia.org/wiki/Acceleration

http://en.wikipedia.org/wiki/Elevator


Otolith Function

Otolithic System

▪ Remnant of the lateral eyed animals

▪ Turned on by near vision

▪ Primes the legs

▪ Turned off by long axis distraction of the

cervical spine

▪ Fires into midline Cb specifically the

Nodulus


The Otolithic System

An otolith also calledstatoconium or otoconium, is astructure in the saccule or utricleof the inner ear, specifically in thevestibular labyrinth of vertebrates

Each macula consists of asensory membrane containingthe receptor cells that supports a“heavy load,” the otoliths.

The otolith is composed of calcareous material embedded in a gelatinous matrix


Vestibular Nerve Physiology

Each vestibular neuronfires tonically at aresting rate ofapproximately 90-100spikes per second.

Upon activation theseperipheral vestibularafferents have two maintargets: the vestibularnuclear complex andthe cerebellum


Vestibular Nuclei Complex

4 Major Nuclei1. Superior Vestibular Nucleus

VOR relay center

2. Medial Vestibular Nucleus VOR relay center

VSR relay center

3. Lateral Vestibular Nucleus VSR relay center (major-

ipsilateral LVST). Mainly LE stability. Mostly from Otoliths

4. Inferior Vestibular Nucleus Connected to all other nuclei

Larry E. Masula, D.C. DACNB DACNB, FAVRB, FAFICC 7/1/2019 94

Vestibular Nuclear Complex


The 4 vestibular nuclei are: Super Vestibular Nucleus, Medial Vestibular Nucleus,Lateral (Dieter’s) Vestibular Nucleus, and the Inferior (caudal) Vestibular Nucleus.

Vestibular Nucleus Function

The vestibular nucleus is a multi functional

nucleus with two very important functions.

1. it tells you where your head is relative to

gravity and where gravity is relative to your

head

2. it establishes appropriate postural

reflexes i.e., the vestibular ocular reflex

(VOR) and the vestibular spinal reflexes

(VSR).


Vestibular Nuclei and Their Projections

▪ The vestibular nuclei receiveprojections from the cortex,the cerebellum, subcorticalvisual centers, and the spinalcord. Vestibular circuitry istherefore embedded withinlarger networks involved in theintegration of vestibular,visual, and proprioceptiveinformation. This provides anongoing global control of eyeand body orientation in thedynamic context of voluntarymovement and externalperturbations.

7/1/2019Larry E. Masula, D.C, DACNB, FAVRB, FAFiCC 97

https://www.sciencedirect.com/topics/neuroscience/vestibular

Vestibular Nuclei Commissure

▪ Commissures link thevestibular nuclei from eitherside of the brainstemthrough mutually inhibitoryconnections

▪ This allows for informationto be shared across thebrainstem (push-pull)

▪ Which means that duringactive head rotation to theright, the right vestibularapparatus is excited andvia the commissure the leftside becomes inhibited


VOR

VOR gives us the ability tomove our head and maintainvisual fixation on a targetwithout developing any retinalslip or blurring of vision. TheVOR has a direct pathwayand an indirect pathway whichwe will talk about at anothertime. The main ascendingtracks are from the superiorand medial vestibular nucleito the extraocular musclestraveling through the mediallongitudinal fasciculus to driveoculomotor activity


VSR

The VSR has to do withmaintaining balance and this isjust one part of our balancesystem . the distributive spinalreflexes are really importantwhen you become destabilizedwhile walking on a sandy beach,wet slippery pavement, on ice orstanding on a foam surface.Vestibular spinal reflexes arehard wired reflexes that keep usupright against gravity byallowing us to create anappropriate motor command toavoid a fall .


The medial vestibular spinal nucleus

and tract The media festival spinal trackinterface of the ventral horn tocreate motor activation forcervical spine stabilization. it istherefore useful in therehabilitation of patients withligament laxity secondary 2traumatic cervical sprain andstrain.

I personally have had numerouspatients over the years whocome in the office followingphysical therapy or chiropractichere ,,which the patientterminated because they couldn'thandle the cervical exercises ormobilization. These samepatients have done exceptionallywell by putting them in arotational chair and rotating themwhile the head is stabilized,performing ocular motor therapy,implementing the SenMoCorhead laser target maze, utilizingtrigeminal stimulation, EMS andTENS stimulation


The medial vestibular spinal

nucleus and tract This can all be done without further

traumatizing an unstable region. Stimulation

in this manner is aligned at creating better

cortical representation of their head and

neck or better “Head/Neck Maps”

7/1/2019Larry E. Masula, D.C., DACNB,FAVRB, FAFICC 102

Lateral Vestibulospinal Nucleus

and TractThe LVST also innervates the anterior horn

to create motor activation it extends further

down the spine then does the medial

vestibular spinal tract to innovate the trunk

and legs must. It is pretty much ipsilateral

but there is some bilaterality to it but for the

most part it is strictly ipsilateral and

important for postural responses and

standing upright.


The Caudal Vestibular Nucleus and

TractThese guys innervate the dorsal columns(sensory) region of the spinal cord for thepurpose of receiving an effort copy of the motorcommands to gate all the incoming informationthat says the same thing and only allowing thatinformation which is leftover (the errors) toascend


CLASSIFICATION of

VESTIBULAR REFLEXES▪ Old thinking. Cristae is a kinetic receptor

and maculae are static receptors

▪ Both receptor organs produce motor

reflexes that cannot be totally

differentiated

▪ It is therefore appropriate to differentiate

the reflexes by categories based on their

functional role


CLASSIFICATION of

VESTIBULAR REFLEXES▪ Vestibulo-Ocular Reflex, The VOR normally acts to maintain stable vision

during head motion. This means that the eye must precisely counter-rotate to compensate for the head and keep the eye stable in space.

▪ Angular VOR, The angular VOR is primarily responsible for gazestabilization

▪ Linear VOR, The linear VOR, mediated by the otoliths, compensates fortranslation and acceleration in a linear direction (which is basically thesame thing). The linear VOR is most important in situations where neartargets are being viewed and the head is being moved at relatively highfrequencies.

▪ Vestibulospinal Reflex, The purpose of the VSR is to stabilize the body.

▪ Vestibulocollic Reflex, this is not an ocular reflex but a neck reflex. The vestibulocollic reflex (VCR) acts on the neck musculature to stabilize the head. The reflex head movement produced counters the movement sensed by the otolithic or semicircular canal organs.


Vestibular Reflexes summary

1. Maintain posture.

2. Evokes extensor musculature above T6 andbelow T6 activity to compensate forgravitational forces

3. Produces “kinetic” contractions of muscles formaintenance of equilibrium and ocular stabilityduring movement. Includes reflexes arisingfrom BOTH the canals during angularacceleration and the otoliths during linearacceleration.

4. Help maintain muscular tone: a role of bothmaculae and cristae


Reflexes: continued

Labyrinthine contribution to skeletal-muscular tone is demonstrated following unilateral labyrinthectomy studies in cats which results in:

Tone is decreased in the ipsilateral extensors

Tone is increased in the extensor muscles of the contralateral extremities due to loss of inhibition

Meaning that, a unilateral vestibular deficit (UVD)patient will present with ipsilateral extensor musclehypotonia and contralateral hypertonia of theextensors.

WOULD THIS AFFECT HOW YOU MANAGEYOUR CERVICAL SPINE PATIENTS?


Organization of Central Vestibular

Pathways

Components of the system:

Peripheral Receptors excite

Central Processors which

generate A Motor Output

▪ Peripheral Receptor 1

▪ Central Processor

▪ 2

▪ Motor Output Centers



DIFFERENTIAL DIAGNOSIS

Differential Diagnosis Should Include:

▪ A good diagnosis is not like a batting

average where you play the percentages.

You might strike out. A thorough

examination is essential. You need to

know whether you are looking at:

A One level lesion

Multifocal / multiple lesions

A Central Lesion

A Peripheral Lesion


Most Frequent Vertigo Syndromes Diagnosed in a

Dedicated Neurological Dizziness Unit(N=4790) Vertigo and Dizziness by Brandt, Dietrich, and Strupp-2005

▪ BPPV 18.3%

▪ Phobic Postural Vertigo 15.9%

▪ Central Vestibular Vertigo 13.5%

▪ Vestibular Migraine 9.6%

▪ Vestibular Neuritis 7.9%

▪ Meniere’s Disease 7.8%

▪ Vestibular Paroxysmia 2.9%

▪ Perilymph Fistula 0.4%

▪ Unknown 4.2%



You must be a lot like Sherlock Holmes


Nothing Replaces a Good Bedside Neurological Examination

7/1/2019, Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 115

Frenzel Goggles are a diagnostic tool used

in ophthalmology, otolaryngology and audiovestibular medicine for the

medical evaluation of involuntary eye movement (nystagmus). They are

named after Frenzel, a German physician. The purpose of

the goggles is to disable the patient's ability to visually fixate on an

object while at the same time allowing the examiner to adequately

visualize the eye. This is done by using high-powered

(+20 diopters) magnifying glasses with an illumination system. With

such a high-powered lens, it is unlikely that the patient can adequately

focus and visually fixate on an object to suppress nystagmus.

https://en.wikipedia.org/wiki/Diagnostic_tool

https://en.wikipedia.org/wiki/Ophthalmology

https://en.wikipedia.org/wiki/Otorhinolaryngology

https://en.wikipedia.org/wiki/Nystagmus

https://en.wikipedia.org/wiki/Goggles

https://en.wikipedia.org/wiki/Diopter

https://en.wikipedia.org/wiki/Magnifying_glass


Videonystagmography (VNG) is a technology for testing inner ear

and central motor functions. It involves the use of infrared goggles to

trace eye movements during visual stimulation and positional changes.

Computerized Dynamic Posturography


Computerized Dynamic Posturography (CDP)

is well documented in the clinical and

scientific literature as an objective method of

differentiating sensory, motor, and central

adaptive functional impairments of balance.

AireX Pad®

The Airex® Balance Pad

has a smooth surface,

making it ideal for barefoot

balance testing and

training. Due to the yielding

foam, the body is constantly

challenged to maintain

balance. This pad is also

great for balance, mobility,

standing stability and

motor-skill training.


BESS Test with Airex Balance Pad

7/1/2019Larry E. Masula, D.C , DACNB, FAVRB, FAFICC. 119


While this test is

frequently used for

mTBI evaluation it is

a very useful tool for

vestibular evaluation

by means of a

Romberg test,

Tandem Romberg

and Unipedal stance.

These tests are

performed with eyes

open and then

closed both on a

compliant and then

again on a non-

compliant surface.

This form is

downloadable and

serves as a great

patient handout.

Bedside Diagnostic “Gems”

▪ V – Vascular

▪ I _ Infectious

▪ N – Neoplastic, Neurological

▪ D – Degenerative

▪ I – Inflammatory

▪ C – Connective tissue/muscle

▪ A – Autoimmune

▪ T – Trauma

▪ E – Endocrine/environmental

▪ S - Soft tissue



VASCULAR

VINDICATES

VASCULAR: Cardiovascular Disease and

Cerebrovascular Disease

▪ Everything is Considered Vascular Until Proven Otherwise Arrhythmias

Tachycardia

Bradycardia

Ischemic cardiomyopathy

Vasovagal syncope

Carotid sinus hypersensitivity

Conduction blocks w/ elongation of the PR interval

Brain ischemia

Etc.

06/21/2019Larry E. Masula, D.C. DACNB, FAVRB, FAFICC. 123

Clinical Aspects of Brainstem

DisordersCommon symptoms in the majority of

brainstem lesions include diplopia,

dysarthria, Vertigo nausea and vomiting.

These lesions are typically vascular in

nature but can be as result of other

disorders such as MS and pontine gliomas

etc ,


Clinical Case. The patient presents with the

following: What is the diagnosis?

▪ Vertigo, nausea and vomiting

▪ Ipsilateral facial pain and temperature loss

▪ Ipsilateral Horner’s▪ Ataxia and dysmetria▪ Weakness of palate,

pharynx and larynx▪ Dysphagia, hoarseness,

diminished gag reflex ▪ Contralateral pain and

temperature loss


2 Types Medullary Vascular Lesions

There are typically only 2 kinds ofmedullary ischemic attacks,dorsal lateral and then theparamedian and basil are lumpedtogether.

▪ Dorsal lateral infarctioncauses damage typicallyreferred to as a Wallenbergsyndrome. ,Typically you willhave an ipsilateral horners ,contralateral Los of pain andtemperature ,with loss of painand temperature over the faceon the same side of the lesion.You can get severe nausea,vomiting, vertigo, andnystagmus due to vestibularinfluence. There can becerebellar findings on theipsilateral side causing ataxia.Hiccups may be common doto lesion in the 9th and 10thnerves with difficultyswallowing.


Wallenberg Syndrome


Lateral Medullary Syndromeaka: Wallenberg Syndrome (posterior inferior Cb artery)

Larry E. Masula, D.C. DACNB., FAVRB, FAFICC 7/1/2019 128

Regional territories

Lateral Medullary Syndrome

“Wallenberg Syndrome”


Note the cranial nerve locations and their trajectories which become affected

Medial Medullary Syndrome (Dejerine Syndrome)Rare stroke syndrome (<1% ofvertebrobasilar strokes, Bassettiet al., 1994). Medial medullaryinfarct is associated with clinicaltriad of ipsilateral hypoglossalpalsy, contralateral hemiparesis,and contralateral lemniscalsensory loss.

The infarction (which arises inthe paramedian branches of theanterior spinal artery and/or thevertebral arteries) leads to deathof the ipsilateralmedullary pyramid,the medial leminiscus, and thehypoglossal nerve fibers thatpass through the medulla.


Medial Medullary Syndrome

Deviation of the tongue to the side of

the infarct on attempted protrusion,

caused by ipsilateral muscle

weakness. Hypoglossal nerve fibers

#8 on diagram

Limb weakness (hemiplegia

depending on severity), on the

contralateral side of the infarct.

Damage to medullary pyramids and

hence to the corticospinal fibers of

the pyramidal tract which cross over.

#5

Loss of discriminative touch,

conscious proprioception, and

vibration sense on the contralateral

side of the infarct (below the head)

Damage to medial lemniscus # 6 on

diagram7/1/2019Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 131

Clinical Case. The patient presents with the

following: What is the diagnosis?

▪ Vertigo, nausea and vomiting

▪ Ipsilateral facial pain and temperature loss

▪ Ipsilateral Horner’s

▪ Ataxia and dysmetria

▪ Ipsilateral hearing impairment


AICA (Anterior Inferior Cerebellar Artery)

The AICA syndrome

is usually

accompanied by

vertigo and unilateral

ipsilateral deafness

from labyrinthine

artery ischemia. It is

a common

brainstem stroke


AICA

▪ The anterior inferior cerebellar artery arises from the basilar artery at the level of the junction between the medulla oblongata and the pons in the brainstem. It passes backward to be distributed to the anterior part of the undersurface of the cerebellum.


http://en.wikipedia.org/wiki/Basilar_artery

http://en.wikipedia.org/wiki/Medulla_oblongata

http://en.wikipedia.org/wiki/Pons

http://en.wikipedia.org/wiki/Brainstem

Anterior Inferior Cerebellar Artery

Syndrome

Occlusion of AICA results in lateral pontinesyndrome, also known as AICA syndrome. Thesymptoms include sudden onset vertigo andvomiting, nystagmus, falling to the side of thelesion (due to damage to vestibular nuclei),ipsilateral loss of sensation of the face (due todamage to principal sensory trigeminalnucleus), ipsilateral facial paralysis (due todamage to the facial nucleus) and ipsilateralhearing loss and tinnitus (due to damage to thecochlear nuclei).


http://en.wikipedia.org/wiki/Lateral_pontine_syndrome

http://en.wikipedia.org/wiki/Nystagmus

http://en.wikipedia.org/wiki/Vestibular_nuclei

http://en.wikipedia.org/wiki/Principal_sensory_trigeminal_nucleus

http://en.wikipedia.org/wiki/Facial_nucleus

http://en.wikipedia.org/wiki/Cochlear_nuclei

Pontine Vascular Syndromes

There are numerous pontine vascular syndromes (see below) of which we will only take a few minutes and review a few in the next few slides▪ Caudal Basal Pontine Syndrome

▪ Locked-in Syndrome

▪ Medial Tegmental Pontine Syndrome

▪ Caudal Tegmental Pontine Syndrome

▪ One-and-a-Half Syndrome

▪ Rostral Basal Pontine Syndrome

▪ Dorsolateral Tegmental Pontine Syndrome

▪ Rostral Tegmental Syndrome


3 Basic Pontine Vascular Lesions based

on territory affected▪ The same thing applies

here as in the medulla. ▪ You can have

dorsal lateral paramedian and basal infarctions

A dorsal lateral lesion willgive you a probableHorner's syndrome , alongwith a loss of pain andtemperature on thecontralateral side.

If below mid-pontine level,you are likely to haveipsilateral loss of facialsensation and someipsilateral cerebellarinvolvement as well.


3 Pontine Vascular Lesions

At mid-pontine level, thelateral pontine reticularformation will be involvedcausing a loss of lateralconjugate gaze towardsthe side of the lesion.Note: if both eyes areinvolved it is usually apontine disorder and ifone eye is involved it ismost likely an individualcranial nerve.

At lower ponting levels the vestibular nuclei and Cochlear nuclei will be affected causing vestibular symptoms , nystagmus and deafness. This will frequently cause a loss of pain and temperature over the face and the opposite side of the body, Thus causing a crossed sensory loss. (see AICA syndrome)



A Pontine Paramedian infarction isidentifiable at the level of the 6thnerve nucleus and will often cause aconjugate gaze palsy which isinability to move both eyes in a singlehorizontal (most commonly) or verticaldirection

There may be damage to the 7thnerve as it sweeps around the 6:00nerve nucleus, causing contralateralfacial paralysis. If it extends farenough a clips the cortico spinal tractsthe result is contralateral arm andleg paralysis.

If the medial lemniscus is damaged,you may lose touch andproprioception on the contralateralside of the body



Basal infarctions can be verycomplex and have many aspects ofinvolvement.

Typically, there will be damage to the6th and 7th cranial nerve fasciclesand damage to the pyramidalpathways as well.

If a complete contralateralhemiplegia is present and there isipsilateral 6th nerve damage and theeye will not abduct and ipsilateral 7thnerve damage causing facialparalysis, this is called MillardGubler syndrome

If only the 6th nerve is affected with acontralateral hemiplegia, this iscalled Raymond’s syndrome

If the lesion is more lateral, then youmay have loss in conjugate gaze, aHorner’s syndrome, deafness, facialnumbness and facial palsy. this iscalled

Foville’s syndrome


Raymond’s Syndrome

▪ Corticospinal tract

involvement resulting

in contralateral

hemiplegia and 6th

nerve damage.

(Raymond’s

Syndrome)


Foville’s SyndromeInferior Medial Pontine Syndrome

Unilateral lesion in the dorsal pontinetegmentum in the caudal third of thepons

Structures affected by the infarct arethe PPRF, nuclei of cranialnerves VI and VII, corticospinal tract,

medial lemniscus, and the mediallongitudinal fasciculus.

There's involvement of the fifth toeighth cranial nerves, centralsympathetic fibers (Hornersyndrome) and horizontal gaze palsy.If the lesion is more lateral then youmay have loss of conjugate gaze aHorner’s syndrome, deafness, facialnumbness and facial palsy


https://en.wikipedia.org/wiki/PPRF

https://en.wikipedia.org/wiki/Abducens_nerve

https://en.wikipedia.org/wiki/Facial_nerve

https://en.wikipedia.org/wiki/Corticospinal_tract

https://en.wikipedia.org/wiki/Medial_lemniscus

https://en.wikipedia.org/wiki/Medial_longitudinal_fasciculus

Labyrinthine Artery - Vascular Supply

It is important at this point to also review the clinically important Labyrinthine artery.

45% from AICA

▪ 24% superior cerebellar artery

▪ 16% basilar

▪ Two divisions: anterior vestibular artery

common cochlear artery

▪ Vascular pathologies can give pulsatile tinnitus or deafness


Midbrain Vascular Lesions

3 Areas are possible. Like the medulla and

pons, these areas include:

Dorsolateral

Paramedian

Basal regions of the mesencephalon.


Nothnagel’s Syndrome

Dorsolateral Infarction.

You will see a horner'ssyndrome on the same sideand total loss on thecontralateral side of the body.You may have cerebellardeficit on the ipsilateral sidedue to damage of the superiorcerebellar peduncle . You mayhave involvement of the 3rdnerve if extensive enough. Acombination of ipsilateralcerebellar and 3rd nervefindings is called Nothnagel’sSyndrome.


Benedikt’s Syndrome

The next area that can bedamage is the paramedianarea . this will affect theocular motor nucleus andan incomplete 3rd nervelesion may occur . theremay be disruption in thedentato-rubro-thalamo-cortical pathway Thuscausing 3rd nur findings onone side and cerebellarfindings on the other.


Weber’s Syndrome

7/1/2019Larry E. Masula, D.C., DACNB, FAVRB, FAFICC, 150

Vestibular Migraine

▪ I include vestibular migraines because of its seeminglyneurovascular nature even though it is not necessarilyan ischemic lesion. It is important to know due to theclinical presentation of headaches and dizziness.

▪ Vestibular Migraine is associated with dizziness andvertigo as a common aura in migraineurs. It isestimated that about 30% of migraineurs will beaffected with this form of aura.

▪ You could get dizzy and have balance problems withouthaving a migraine at all. Other times, the vertigosymptoms happen before, during, or afterthe headache. Sometimes, you might have migrainesfor years before the vertigo symptoms begin.


https://www.webmd.com/migraines-headaches/rm-quiz-migraine-myths


Acute Vasculature

Vestibular Syndrome

Acute Vestibular Syndrome

H.I.N.T.S. to I.N.F.A.R.C.T.

“H.I.N.T.S.” Battery

1. Head Impulse Test

2. Nystagmus

3. Test of Skew

▪ STROKE FINDINGS: “I.N.F.A.R.C.T.”

▪ Impulse Normal

▪ Fast-phase Alternating

▪ Re-fixation on Alternating Cover Uncover Test

▪ Any ONE of these points to a Stroke


1. Nystagmus Testing

▪ Performed in Primary Gaze

Lateral Gaze

▪ In a normal volunteer: there is No nystagmus inprimary gaze. During lateral gaze somenystagmus may be normal. Learn to suppressthis with fixation by placing a piece of paperbetween their head and the wall and ask them tolook at the wall as if the paper was not present.Otherwise, you might see nystagmus whichwould not be there without the sheet of paper.


Nystagmus

▪ https://youtu.be/1q-VTKPweuk?t=105

▪ Patient with vestibular neuritis. Note: here it is again, when he looks to the left see that the nystagmus increases. It is left beating and there is a rotatory component towards the left and it increases when he looks to the left and you can see the torsional component.

▪ When he looks to the right it lessens but the fast component is still towards the left.

▪ Unidirectional nystagmus, does not change direction and in this exam it is reassuring.


https://youtu.be/1q-VTKPweuk?t=105

Nystagmus


Compare to this lady who when she looks to

the right, she has small horizontal nystagmus

with the fast component to the right. Then,

when she moves more central and to the left,

you can see that the nystagmus beats towards

the left. So, she has direction beating

nystagmus or bidirectional nystagmus which is

worrisome.

Note: nystagmus is named for the direction of the fast phase



2. Test of Skew

(Vertical)

▪ Cover / Uncover test


Examiner takes their hand and covers the eyeand then quickly covers the other eye toobserve if there is any vertical movement of theeye when it is uncovered.



Test of Skew


▪ Observe that when the hand is taken away from the right eye, the eye will go medially and upward and when the examiners hand is taken away from the left eye it goes medially and downward.

▪ This abnormal skew deviation is worrisome



Test of Skew


▪ Observe that when the hand is taken

away from the right eye, the eye will go

medially and upward and when the

examiners hand is taken away from the

left eye it goes medially and downward.

▪ This abnormal skew deviation is

worrisome




This test is abnormal if you have vestibularneuritis or a peripheral vestibulopathy. Theeyes cannot remain focused on a target. If youhave a peripheral nerve problem, you probablydon’t have a brain problem.

What we are looking for is a Central VestibularSyndrome. In this case there will be nodysmetric eye movements and the test is thenconsidered negative. In this case an Abnormalfinding is a GOOD finding.




Hold onto the patients skull

Patient fixates on examiners nose (or camera)

Move head back (maybe 20 degrees), Slowly to the right,then BRISKLY to midline. What you are looking for arecatch-up Saccades of the eyes

In this video her eyes remain fixed on the camera =NORMAL or Abnormal?

7/1/2019, Larry E. Masula, D.C., DACNB, FAVRB, FAFIICC 163




Abnormal

Notice that this man presents with nystagmus

when he looks to the left and when his head is

turned to the right. Do you see that there is a

larger movement of the eyes from the right

back to the mid line? That is an abnormal HIT

which is reassuring which shows that he has a

peripheral nerve problem and probably does

not have a brain problem.





▪ This lady has a rock-solid head impulse

test. She is WORRISOME because she

has acute vertigo and nystagmus and we

cannot find a nerve problem.

▪ She probably has a BRAIN problem.



7/1/2019Larry E. Masula, D.C.DACNB 172

06/Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 173

INFECTIOUS

VINDICATES

Infectious Disorders

Otitis ExternaPathophysiology

1. Typically begins with otitis

externa in elderly diabetics.

2. Infection spreads to

surrounding tissues and

adjacent temporo-occipital

bones, almost always

secondary P. aerugiosa.

3. Commonly affects the facial

nerve in the fallopian canal or

at the stylomastoid foramen

and can spread across the dura

to produce purulent meningitis.


INFECTIOUS DISORDERS:

Malignant Otitis Externa▪ Diagnosis – CT scan of the temporal bone

may reveal:

1. External canal mass

2. Clouding of the mastoid air cells

3. Sequestra of the bony canal

4. Erosion at the base of the skull

5. Soft tissue masses within the parapharynx and

nasopharynx



Otitis Media▪ Pathophysiology

The middle ear is involved with most viral URI’s. The nasal,paranasal, and pharyngeal mucositis spreads to involve theEustachian tube and middle ear mucosa, since the mucosa ofthe pharyngeal end of the Eustachian tube is continuous withmucociliary system of the middle ear. If the eustachian tubebecomes inflamed it swells and closes. If the tube is closed /blocked, then the middle ear and mastoid system becomedisconnected with the air in the nasopharynx and atmosphericsystem. This results in the air within the middle ear and mastoidbeing absorbed by the mucosa and a negative pressuredevelops. The negative pressure causes the TM to becomesucked inward and secondly the microcirculation within thetympanic cavity is encouraged to release fluid and mucusresulting in an inability for the TM to generate sound energycausing conductive deafness. Secondary bacterial infectionmay develop leading to otitis media.


INFECTIOUS DISORDERS:▪ Otitis Media (Inflammation of the middle ear)

Is a common cause of conductive hearing loss,

particularly in children. 2 Forms

A- Suppurative Otitis (infected)

B- Serous Otitis (non-infected)

Larry E. Masula, D.C.,DACNB, FAVRB, FAFICC 7/1/2019 177


Otitis Media▪ Diagnosis

Most common organisms:

Streptococcus Pneumonia

Hemophilus Influenza

Translucency of TM is lost. The TM may be

retracted and the middle ear- atelectic. Impaired

mobility may be observed during pneumatic

otoscopy.



Otitis Media▪ More common in children. 80% of children

ages 1-6 will have at least 1 bout. <10% beyond

age 8. Why?

▪ In children the ET is very narrow so minor

swelling causes obstruction

▪ The ET is also more horizontal and shorter

allowing for infection to go backward easier

▪ Symptoms include unilateral otalgia, fever, and

conductive hearing loss

Larry E. Masula, D.C., DACNB, FAVRB,FAFICC 7/1/2019 179

Cell Scope


A great tool for showing patients a view of their Tympanic Membrane


Chronic Otomastoiditis▪ Pathophysiology

From an untreated / unresponsive acuteOtomastoiditis. Characterized by thickenedmucosa with obliteration of the mastoid air celllumen, perivascular fibrosis, and osteitis. Polypoidgranulomas may fill the mastoid antrum, the middleear, and extrude through a tympanic perforation.Cholesteatoma (keratinized squamous epithelium)can invade the middle ear destroying the ossiclesand labyrinth and pneumatized temporal bone cells.Producing conductive hearing loss and vertigo.



Cholesteatoma



Mastoiditis


Intracranial Extension of Ear Infections

Background-from either acute otitis media or mastoiditisand bone destruction. Febrile patient w/ continued ear pain,mastoid pain, headache despite antibiotic treatment.

▪ Route of Spread may spread backward-

▪ 1. Direct extension

2. Hematogenous

3. Thrombophlebitis

Resulting in:

Meningitis

Epidural Abscess

Sigmoid Sinus Thrombophlebitis

Brain Abscess



Viral Vestibular Neuritis▪ Pathophysiology-part of a systemic viral illness, i.e.

measles, mumps and mono, HERPES SIMPLEX II

A unilateral vestibular deficit (UVD), arising from a viral causein most patients, results in either sudden deafness or acuteprolonged vertigo with nystagmus rapidly beating (fastphase) toward the side of the lesion. This also results in aYaw rotation toward the side of the lesion and a Roll tilt in thesame direction. Acute symptoms usually abate within 3-5days but the patient may be left with the equivalent of avestibular neuropathy.

▪ Diagnosis-

1. Caloric responses are decreased and/or absent on the side of the lesion. Ultra-high hearing loss. ENG abnormalities

2. Must be differentiated from other forms of labyrinthitis


INFECTIOUS DISORDERS

Labyrinthitis▪ A viral or bacterial infection of the fluid within the

inner ear.

▪ Within one-week sufferers are usually able to situp and after two weeks will begin to compensatefor the dizziness/vertigo. Acute episodesusually end after one to two months. Althoughpermanent vestibular damage may remain insome cases, most people recover fully fromviral labyrinthitis.

▪ Labyrinthitis will classically affect hearing as wellas balance which are also symptoms of an AICAstroke


Differential Diagnosis of Acute Peripheral Vestibulopathy

History Examination Laboratory

Viral Neurolabyrinthitis

Developing over hours, resolving over days, prior flu-like illness

Normal except for signs of acute unilateral vestibular loss

ENG: caloric hypo excitabilityAudio: may show ultrahigh frequency loss

Bacterial Labyrinthitis Abrupt onset, hearing loss, prior ear infections

Signs of otitis mediaor meningitis

ENG: absent caloric Audio: sensorineural loss. CSF: Pleocytosis

Labyrinthine Ischemia Abrupt onset w/ neurologic symptoms, prior vascular disease

Signs of brainstem or cerebellar infarction

ENG: absent caloric Audio: sensorineural lossImaging: Brain infarction

Perilymph Fistula Abrupt onset w/ head trauma, barotrauma, or sudden strain lifting, coughing, sneezing

Positive fistula test, may be chronic otitis w/ TM perforation

ENG: caloric hypo excitabilityAudio: usually sensorineural lossImaging: CT may show erosion from cholesteatoma


AUTOIMMUNE DISEASE:

Meniere’s Disease aka “Endolymphatic Hydrops”


Cross Section of the Cochlea

▪ Endolymph is the fluid

contained in

the membranous

labyrinth of the inner

ear. It is also

called Scarpa's fluid,

after Antonio Scarpa.

(Endolymph is located

in the scala media - the

light gray region at the

middle of the diagram.)


https://en.wikipedia.org/wiki/Membranous_labyrinth

https://en.wikipedia.org/wiki/Inner_ear

https://en.wikipedia.org/wiki/Antonio_Scarpa

https://en.wikipedia.org/wiki/Scala_media

Endolymphatic Hydrops(Meniere’s Syndrome)

▪ Pathophysiology

1. An increase in the volume ofendolymph distending theendolymphatic system

2. The labyrinth dilates until thesaccular wall makes contactwith the stapes footplate andthe cochlear Scala

3. Hearing loss and vertigo arecaused by ruptures in themembranes separatingendolymph from perilymphcausing a sudden increase inpotassium which inhibitslabyrinth receptors


Meniere’s cont.

Bacterial and viral. Majority unknown

1. Family history 50% of cases

2. Considered to be rare based on AMA

epidemiological studies, perhaps as low as 1%

of vertiginous patients

... Meniere's disease is an inner ear disease that

typically affects one ear. This disease can cause a

fullness, pressure or pain in the ear, severe cases

of dizziness or vertigo, hearing loss and a ringing

or roaring noise, also known as tinnitus.


Perilymph Fistula’s

▪ A perilymph fistula (PLF) mayalso cause vertigo, It is anabnormal connection (a tearor defect) in one or both of thesmall, thin membranes (theoval window or the roundwindow) that separate the air-filled middle ear and the fluidfilled perilymphatic space ofthe inner ear. This smallopening allows perilymph(fluid) to leak into the middleear. - See more at:http://vestibular.org/perilymphfistula#sthash.bcdq3m49.dpuf


http://vestibular.org/perilymph

Perilymph Fistula’s

▪ Leaks through the round and oval windows canoccur following; sever nose blowing, strenuousexercise, barotrauma, and surgical trauma

▪ The symptoms of perilymph fistula mayinclude dizziness, vertigo, imbalance, nausea,and vomiting. Usually however, patients reportan unsteadiness which increases with activitiesthat elevate CSF pressure and which is relievedby rest. Some people experience ringing orfullness in the ears, and many notice a hearingloss. Most people with fistula’s find that they getworse with changes in altitude (fast elevators,airplanes, and travel over mountain passes.


Perilymph Fistula Test

▪ The development of nystagmus inresponse to the application of pressureon the external auditory canalconstitutes a positive result for theperilymph fistula test and suggests thepresence of a fistula between the air-filled middle ear and the fluid-filled innerear.

▪ Hosuk Chu, M.D., and Won-Ho Chung, M.D. N EnglJ Med 2012; 366:e8 January 26, 2012 DOI:10.1056/NEJMicm1010568


http://www.nejm.org/toc/nejm/366/4/


NEOPLASTIC -

NEUROLOGICAL

VINDICATE

NEOPLASM: Cerebellopontine Angle

Tumors▪ Lesions in the area of

cerebellopontine angle causesigns and symptomssecondary to compression ofnearby cranial nerves,including CN V, VII, VIII.

▪ I.E., involvement of CN Vfrom a cerebellopontine masslesion often results in loss ofthe ipsilateral corneal reflex.

▪ Patients with larger tumorscan develop Brunsnystagmus due tocompression of thecerebellar flocculi.


NEOPLASM: CPA Tumors

Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 7/1/2019, 198


Br J Neurosurg. 2008 Jun;22(3):441-3. doi:

10.1080/02688690801911614.

Cerebellopontine angle epidermoid tumor

presenting with bilateral gaze nystagmus.

Han IB1, Huh R, Chung SS, Kim OJ.

Abstract

Vestibular symptoms have been rarely described in

cerebellopontine angle epidermoid tumors. We report a case of

CPA epidermoid tumor presenting with subacute onset of

vestibular symptoms such as vertigo, gait ataxia, and nystagmus

masquerading as acute vestibular neuritis or central vertigo. The

vestibular symptoms disappeared after excision of the tumor.PMID: 18568737 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/18568737


Cerebellopontine angle epidermoid tumor


Clin Exp Otorhinolaryngol. 2012 Dec; 5(4): 234–236.

Published online 2011 Sep 15. doi: 10.3342/ceo.2012.5.4.234

PMCID: PMC3506776

A Posterior Petrous Meningioma with Recurrent

VertigoSeong Jun Choi, MD,1 Jong Bin Lee, MD,1 Joon-Ho Bae, MD,1 Jung-Hee Yoon, MD,1 Ho-Jin

Lee, MD,1 Chan-Ho Kim, MD,1 Keehyun Park, MD,2 and Yun-Hoon Choung, MD2

Abstract

Meningioma's account for around 15% of all primary brain tumors

with some 10% of meningioma's arising in the posterior fossa. In

rare cases, a meningioma can form around the endolymphatic

sac. When formed in the posterior fossa, meningioma tumors can

produce vague, non-specific vertiginous symptoms. Research

has observed that a subset of these lesions could produce

symptoms indistinguishable from those of Meniere's disease.

Therefore, we described the clinical features of a case of

posterior petrous meningioma with recurrent vertigo as well as

the substantial resolution of symptoms after tumor removal via

transmastoid approach.

http://dx.doi.org/10.3342/ceo.2012.5.4.234

http://www.ncbi.nlm.nih.gov/pubmed/?term=Choi%20SJ%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Lee%20JB%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Bae%20JH%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Yoon%20JH%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Lee%20HJ%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Kim%20CH%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Park%20K%5bauth%5d

http://www.ncbi.nlm.nih.gov/pubmed/?term=Choung%20YH%5bauth%5d

NEOPLASMA: Acoustic Neuroma (vestibular schwannoma)


Cerebellum: the Brain Behind

the Brain


Clinical Manifestations, (DDX)

▪ Tilting –

▪ Falling forward or backward –

▪ Exocentric Yaw axis (spinning) –

▪ Egocentric Yaw axis (spinning) -

▪ Most likely cortical

▪ Mesencephalic, medullary, Cb

▪ Peripheral Nerve i.e. BPPV or vestibular nerve loss

▪ Most likely cortical

7/1/2019Larry E. Masula, D.C., DACNB 204

Case report Rotational vertigo caused by cerebral lesions: Vertigo and areas

3av, 2v, and 7

▪ Eiichirou Urasaki, Akira Yokota

▪ Source

▪ Journal of Clinical Neuroscience > 2006 > 13 > 1 > 114-116

▪

Abstract - We describe two patients complaining of vertigo

associated with a small supra-tentorial convexity meningioma.

Symptoms disappeared after tumor removal, providing

evidence for an association between the vertigo and the

cerebral cortical lesions. Tumors were located in the central and

parietal areas, respectively, which are probably analogous to

the vestibular cortex in the areas designated 3av, 2v, and 7 in

animal studies

▪ *** Why you must check for non-vestibular cortical findings


https://www.infona.pl/contributor/[email protected]/tab/publications

https://www.infona.pl/contributor/[email protected]/tab/publications

https://www.infona.pl/resource/bwmeta1.element.elsevier-56b044e8-bf71-30ca-bf07-59d0fce0dc89/tab/jContent

https://www.infona.pl/resource/bwmeta1.element.elsevier-56b044e8-bf71-30ca-bf07-59d0fce0dc89/tab/jContent/facet?field=%5ejournalYear&value=%5e_02006

https://www.infona.pl/resource/bwmeta1.element.elsevier-56b044e8-bf71-30ca-bf07-59d0fce0dc89/tab/jContent/facet?field=%5ejournalYear%5ejournalVolume&value=%5e_02006%5e_00013

https://www.infona.pl/resource/bwmeta1.element.elsevier-56b044e8-bf71-30ca-bf07-59d0fce0dc89/tab/jContent/facet?field=%5ejournalYear%5ejournalVolume%5ejournalNumber&value=%5e_02006%5e_00013%5e_00001

Van Gogh

▪ In an acute right sided processsuch as vestibular neuritis, thenuclei are initially excited, and theeyes exhibit a slow phase ofnystagmus pushing the eyes tothe left, the fast phase ofnystagmus to the right. But, astime passes and the nerve diesthe right side, is no longer anacute problem and the Left sidethat is no longer being inhibitedthrough the commissure appearsoverly active. The fast phase ofnystagmus then switches, and theeyes beat Slow phase to the rightwith a Fast phase back to the left.

▪

▪ So, In Vincent's case on whichside is the probable lesion?

▪ The Right side. The slow phasegives an illusion that you aremoving to the right while theworld is moving left.

▪ Assuming that in his case it wasno longer an acute problem, theLeft side was no longer beinginhibited by the right vestibularnuclei and the left side appearsoverly active.

▪ The same is true in the acute stage of a vascular insult



Sir Gordon Morgan Holmes, (22 February 1876 – 29 December 1965) was a British

neurologist. He is best known for carrying out pioneering research into the

cerebellum

Gordon Holmes, M.D.

▪ 1917, Dr. Holmes talked about the symptoms ofacute cerebellar lesions due to WWI gun shotwounds and what he talked about is this,

“the brain (cortex) is fine but these people havethese presentations that are very severe andinvolve aberrancies’ in the frontal cortex. It is alsoincreasingly clear that there are extensiveconnections between the Cb and frontalassociative areas of the cerebral cortex that fallwell outside the classical sensory-motor circuit.”

▪ The Cerebellum. 2007; 6: 268-279


Cerebellum

▪ There are more cells in the Cb than the

entire remaining neuraxis

▪ What has the greatest input into the

Cerebellum?

▪ Answer:

The cerebral cortex (frontal and prefrontal

cortex). 20 million projections (cortico-ponto-

cerebellar) vs 1 million spino-cerebellar

projections


Functional Concepts

▪ A “BAD” Cb is known to be involved with:

Cognitive functions (ataxia of thought and represents erratic attempts to correct errors of thought or behavior)

Psychiatric Disturbances

Autonomic concomitants

Sensory Disturbances

Maintenance of Equilibrium

Breakdown in Coordination/Sequenced motor activity – walking, intention and terminal tremors (not at rest), eye movements w/ diminished pursuits and overshooting saccades. Intention tremors and terminal tremors.

Motor learning – motor skills

Monitor & predict

Horizontal & Vertical nystagmus w/ & w/o fixation

Scoliosis – genetic calcium channel mutation affecting midline Cb

Head tilt

Ocular deviations


Cortico-Ponto-Cerebellar circuit


Cerebellar Purkinje Cells

▪ The cerebellar purkinje system inhibits the deep nuclei output thus gating cerebellar outflow

▪ They are Extremely sensitive to: Hypoxia

Toxins

Inflammation

Alcohol

7/1/2019Larry E. Masula, D.C.,DACNB 212

The cerebellum is organized anatomically

and physiologically

▪ “ArchiCerebellum”

Floculonodular Lobe

▪ “Paleocerebellum”

Anterior Lobe

▪ “Neocerebellum”

Posterior Lobe

Larry E. Masula, D.C, DACNB, FAVRB, FAFICC. 7/1/2019 213

Floculonodular Aka (ancient)ArchiCerebellum

Aka Vestibulocerebellum ▪ Receives Input from thelabyrinthine system with noinvolvement of the deep Cbnuclei

▪ This has influence over theaxial musculature, someinfluence over VestibularOcular Reflexes andVestibular Reflexes

▪ Flocculus/paraflocculusmodulates the smoothnessof pursuits and calibratesthe rotational VOR

▪ Nodulus – calibrates VOR(from otoliths)


3 Functional Divisions(not labeled)

▪ Medial Zone (Vermis) Input from

spinocerebellar tracts carrying proprioception from the spine and extremities

Visual and Auditory pathways

Output to Fastigial Nucleus

Fastigial Nucleus Projects to vestibular nuclei

Pontine reticular formation

Motor cortex via the thalamus


Anterior Lobe Paleocerebellum (old-not ancient)

Spinocerebellum

▪ Associated with uprightstance, posture andbipedalism

▪ Limb coordination andfeedback fromextremities

▪ Controls proprioceptionrelated to posturalmuscle tone

▪ Axons extend to thedeep Cb nuclei


Posterior Lobe Neocerebellum (new)

Cerebrocerebellum

▪ Higher cognitiveintegration and planningof movement

▪ Development of theposterior lobe of the Cbmirrors development ofthe Neocortex

▪ Input from Cortico-Ponto-Cerebellar tract andprojects to deep Cbnuclei

▪ Associated w/ motorcontrol and coordinationof fine finger movements


Medial Zone (Vermis)

▪ Lesions in midline Cb (aka: Spinocerebellum)

▪ Gait instability

▪ Ataxia of trunk

▪ Titubation

▪ Breakdown in movements

▪ Saccadic dysmetria

▪ Vertiginous activity

▪ Note: findings may improve when lying down or with an increase in integrity into the system

▪ Ex: distract the patient’s neck and this fires midline Cb structures and the symptoms of the lesion reduce (ddx midline lesion versus lateral)

Larry E. Masula, D.C.,DACNB 7/1/2019 218

Intermediate Zone (aka Paravermis)

▪ Input from cortico-pontocerebellar fibers that originate in the motor cortex

▪ Fibers carry duplicate copy of information that was sent from the motor cortex to the spine producing movement

▪ Efferent Copy- allows feedback comparison of what muscles are supposed to be doing with what they are actually doing

▪ Receives afferent input from muscles of spine and distal extremities

▪ Output Via interposed nuclei (Globus and

Emboliform)

Projects to the magnocellular part of the contralateral red nucleus and contralateral motor cortex


Lateral Zone (aka

Neocerebellum)Receives input from the parietal cortex via the ponto-cerebellar mossy fiber projections

The information is specific to the location of the body in space

Integration of body position information, strength and speed

Input Contralateral cortical projections

Output Dentate projects to the cortex for cognition of movement. Aids in timing and planning and higher cognitive functions

Note: no balance, equilibrium or gait disorders


Comparing and Contrasting


Normal Cb Alcoholic Cb

Note the folia atrophy

Cerebellar Function

▪ Maintenance of Equilibrium

Balance, posture, eye movements

▪ Coordination/Sequenced motor activity

Walking gait

▪ Adjustment of Muscle Tone

▪ Motor Learning-Motor Skills

▪ Monitor & Prediction of Movement

▪ Cognitive Function-learning

Larry E. Masula, D.C., DACNB 7/1/2019 222

Cerebellar Stroke

▪ A cerebellar stroke is one of the least

common types of strokes. It occurs when

a blood vessel is blocked or bleeding,

causing complete interruption to a portion

of the cerebellum. This type

of stroke typically affects only one side or

section of the cerebellum. It's also

referred to as cerebellar

stroke syndrome.


Cerebellar Stroke Evaluation


Cerebellar Stroke


Clinical Signs:

Ipsilateral Cerebellar Disease

(Floculonodular Zone/Spinocerebellar lesions)

Abnormal Stance/Gait: a. Wide based, stumbling gait with truncal tremor, Falling/veering to side of the lesion, activities w/ increased speed/difficulty (tandem gait).

Titubation: rhythmic tremor of the body(trunk) and head. Note: must rule out BG lesion

Rotated/tilted head: not specific for side of lesion but related to eye movements


Clinical Signs: Cerebellar

DiseaseDecomposition of movement: both simple (one joint) orcompound (multiple joint) movements, i.e. Finger to nosetestERROR in Initiation and Breaking is delayed ( intention tremor and terminaltremor of the finger when approaching the nose

ERROR in Velocity and Acceleration

Dysmetria: lesion of range/trajectory (lesions of the Spinocerebellum Vermal Zone) Hypermetria or hypotonia, Gaze evoked nystagmus, saccadic dysmetria (hypermetria due to termination failure), and altered VOR (retinal slip)

Note: Cb initiates all movements…except oculomotor, which it terminates



Disease

Dysdiadochokinesia: error in the rate of movements and completion of movement (rapid alternating) vs loss of smooth movement

Dysrhythmokinesis: errors in timing out a beat. Note: Interactive metronome used for both testing and rehab.


Clinical Signs: Cerebellar Disease

Dysarthria: tremulous voice with errors in prosody and

intonation (Vermal - medial zone lesions) Interference

with articulation, respiration and phonation; slowness,

scanning (stretch syllables)

Kinetic Tremor: (Cerebrocerebelar lateral zone lesions)

greatly increases as movement nears target, when

accuracy is most essential. Worse with fatigue


Clinical Signs: Cerebellar Disease

Abnormal Tone:

Hypotonia, joint laxity and pendular reflexes

Relates to the alpha-gamma co-activation

Abnormal check and rebound

Check - arms outstretched and tap wrist. Should return quickly to initial point

Rebound is excessive excursion during the attempted return to initial point



DiseaseAbnormal Ocular Motor Function: (Flocculonodular lobe lesions)

Nystagmus: Gaze evoked

Skew Deviation: in primary position,one eye is elevated () and other isdepressed (hypotropia)

Saccadic dysmetria: usuallyhypermetria due to failure toterminate the movement secondaryto lesions in the Cerebellar Fastigium

Impaired Smooth Pursuit

Glissades (post saccadic drift)

Alteration in VOR (due to improper termination/hypermetria)


What Else?

▪ Altered A-P and lateral spinal curves

▪ JPE’s

▪ DJD

▪ Postural distortion

▪ Dizziness (breakdown of ocular stability)

▪ Nociception - impairs proprioception


Cerebellar Tests

▪ Middle – Sharpened Romberg’s, tandem gait, finger-nose-finger, saccade hypermetria, nystagmus, post rotational nystagmus, head thrust tests, smooth pursuits

▪ Lateral – piano playing, RAM w/ fingers, finer nose finger

▪ Intermediate - RAM w/ arms front, bent utilizing rapid pronation/supination, then windshield wiper motion, finger-nose-finger, heel to shin


Cb Lesions and the EyesCause extorsion of the ipsilateral eye and (hypotropia)

of the ipsilateral eye. Also esotropia w/ near target and

exotropia w/ far target


Head tilts often have Cb lesions affecting

their otolithic pathways


Normally, tilt in the (YAW) roll plane to the right normally produces a reflex counter

roll and Skew (hypertropic eye movement) towards the opposite side. If I lose my

Cb Pathways on the Rt. the right eye remains extorted and what do I do to

compensate for the extorsion? Tilt my head to (left) opposite side.

NormalOcular tiltReflex

Abnormal Head Posture w/

External Ophthalmoplegia▪ Eye Muscles Chin Rotation Tilt

▪ LR None Ipsi None

▪ MR None Contra None

▪ SR UP Ipsi Ipsi

▪ IR Down Ipsi Contra

▪ SO Down Contra Contra

▪ IO UP Contra Ipsi


Head tilt

▪ You can no longer say that a left head tilt

means a bad left Cb. There is no way to

do that any more. I know some people

instruct that from classes you may have

taken but there are too many factors

involved and that assumption is incorrect


Central Vestibular Disorders J Neurol (2007) 254:559-568

A tonic imbalance in YAW (rotation) is characterized by horizontal(torsional) nystagmus, lateralpulsion of the eyes, past-pointing,rotational and lateral body falls, and lateral deviation of the perceivedstraight-ahead. (Implicates a horizontal VOR type problem, i.e. vestibular nerve loss, Meniere’s,post vestibular neuronitis, or a Cb - fastigial n.). Turning ~ 35° in Fakuda test. DDX- CN8 entry intomedulla, MVN, SVN, NPHypo., PPRF demyelination or ischemia)

A tonic imbalance in ROLL is defined by torsional nystagmus, skewdeviation, ocular torsion, head tilt, body, and the perceived vertical.(Central...remember Van Gogh?, midbrain, paramedian thalamus or PIVC –parieto-insular- vestibularcx lesions)

Finally, a tonic imbalance in PITCH can be characterized by someforms of upbeat or downbeat nystagmus, for-aft tilts and falls, andvertical deviation of the perceived straight-ahead. (Central problemsomething in the midline dying off i.e. central flocculus, PPRF or bilat. medullary)WARNING…NOT GOOD!!!



ONTOLOGICAL EXAMINATION

- VESTIBULAR ASSESSMENT

Tests performed in lighted room

Spontaneous nystagmus

Gaze holding nystagmus

Skew deviation

Vergence

Decreased VOR

i. Head thrust test

ii. Dynamic visual acuity

Visual tracking

i. Smooth pursuit

ii. Saccadic eye

movement

iii. VOR cancellation

Gait and balance

i. Feet together

ii. Tandem

iii. Single leg stance

7/1/2019Larry E. Masula, D.C.,DACNB, FAVRB, FAFiCC 240

Tests performed in dark

Tests performed using Frenzel lenses or IR goggles (Real Eyes®)

Spontaneous nystagmus

Gaze holding nystagmus

Decreased vestibular ocular reflex

Head thrust (head shaking nystagmus )


VOR

▪ The VOR maintains foveal fixation on a targetduring head movement.

▪ The vestibular system therefore has two mainfunctions for its coordination; detection of gravityand velocity

▪ Patient symptoms of a bad VOR are thereforetypically triggered by changes in head and orbody position/movement in specific directions atspecific speeds (frequencies)

▪ Head and Eye coordination are out of sync

▪ Both vestibulopathy and stroke may impair aVOR


VOR (vestibulo-ocular reflex)

▪ The Horizontal rotational VOR

▪ Head position 40° = 40 ° eye movement in the oppositedirection = Normal gaze position

▪ Horizontal Translational VOR - keeps the eyes stillwhen the head moves laterally utilizing a combinationof the rotational (canal) and translation (otolith) VOR’s

▪ A good Cb (flocculonodular lobe) is necessary for bothsuppression of the VOR and for slip-induced gainchange i.e. OPK and head-thrust test

▪ VOR suppression - when you don’t want it, it can besuppressed by focusing on an object i.e. motionsickness, sea-sickness and ice skating. It is effective forperipheral lesions and has no effect on central pathologies


Various VOR Tests

▪ Dynamic Visual Acuity Tests – looks at the breakdown in visual acuity with head movement in VOR. Oscillopsia-blurred vision with head movement (snellen chart vert./horiz. Static at 15’, + Dynamic test =needing to go up in font size by 2-3 lines or more)

▪ Vestibular –Optokinetic-Reflex – with use of OPK drum, tape or App. Asymmetric nystagmus indicates a weak /uncompensated side when the stimulus is moving toward the lesion

▪ Provoked Vertigo Test – hallucination of or exaggerated sense of motion - looking for right/left asymmetry i.e Dix-Hall pike, Romberg in plane of canals

▪ Head Shake Nystagmus Test – indicates uncompensated VOR w/ fast phase toward the stronger ear Ewald’s 2nd law (excitation is stronger than inhibition) Req. video goggles

7/1/2019Larry E. Masula, D.C.DACNB 244

Oculomotor Muscles


Integration of Canal Based Eye

Movements



The vestibular system shares many brain stem circuits and

functions with the neural systems for controlling the

extraocular muscles that move the eyes. The vestibular

and oculomotor systems coordinate head and eyes during

head movement

Frontal Eye Fields & Pursuits

▪ Ventral Inferior

Frontal Eye Fields =

Frontal Pursuit Area

▪ Deficits in Pursuits

implicate a

“hemisphere”, but do

not localize a lobe,

must perform other

tests to determine

lobe



Notice that the canal system utilizes the same pathways


Both pathways shown together

Vertigo & Nystagmus

▪ The vestibular system has a tonic signalwhich fires at 100spikes/sec. and changesduring head motion. i.e. a rapid right headrotation increases firing of the rightvestibular complex

▪ Anything that deranges that signal causesVertigo, a perception of head movementwhen the head is still.

▪ This may be associated with visio-vestibular conflict, nausea and vomiting


Nystagmus


In a Normal patient both sides of

the Vest. System are firing

Tonically and equally always!

Pathological Nystagmus – eg. If I lose

my right side? Slow phase nystagmus

to the right and a fast re-fixation back to

the left due to the tonic firing of the left

vestibular input to the PPRF which

monitors the eyes in the orbit and the

velocity of the saccades

VNG recording; upward deflection is to the rightand the downward deflection is to the left

VNG


This can best be assessed by infrared goggles

Pathophysiology of Nystagmus

A disorder affecting any of the 3 mechanismsthat control eye movements may result innystagmus. Both focal and diffuse disordersmay cause nystagmus. The characteristics ofthe nystagmus, as well as associated signs andsymptoms help to localize the lesion andsuggest possible etiologies.


Peripheral Causes of Nystagmus

BPPV-otoconia most often in the PC w/ down beating nystagmus

Acute Viral Labyrinthitis

Alcohol- lighter than blood so the haircells float in the endolymph and thinsblood affecting the anterior

Meniere’s Disease

Toxins – especially antibiotics such as streptomycin and gentamycin

Sequeala of Peripheral Vestibular Dysfunction

Head tilt

Cb dysfunction

Vestibular system dysfunction

Ipsi Neocortex dysfunction

Torticollis

Difficulty compensating for perturbations of head position-functional imbalance

Worse with eyes closed because a normal Cb and FL’s can use vision to suppress the nystagmus


2 Forms of Nystagmus. Peripheral

and Central

Vertigo of peripheral origin generally manifestsby horizontal, rotatory, or absent nystagmus,but horizontal nystagmus is not a specific signof peripheral vertigo.

It is the most common typeof nystagmus observed in patients withcerebellar infarction. Vertical nystagmus isalways considered specificfor central pathology.



Here we seen in the far-left diagram, equal tonic input from both vestibular

nuclei, thus no perceived movement. In the middle diagram, during right head

rotation, the right canal system and the right vestibular nuclei become excited

and motion is detected rightward. In the far-right diagram there is a left sided

vestibular deficit. The right side is no longer being inhibited and again the

perception is a rightward rotation.

Physiologic vs. Pathologic

Nystagmus

PhysiologicRotation-induced

Caloric-Induced (cows) remember fast phase names the nystagmus

Optokinetic stimulation induced

End Point- there is a point at which it usually slows and stops. The exception is a cupulolithiasis

Fixating on a target suppresses the nystagmus

PathologicSpontaneous-the nystagmus isspontaneous and is best seen indarkness w/ goggles, becausethe patient cannot fixate onobjects in the room. The slowphase points to or looks at thelesion

Central Nystagmus is not suppressed by fixating eyes on a target


The topographic diagnosis of acquired

nystagmus in brainstem disorders▪ Dieterich M, Strabismus. 2002 Jun;10(2):137-45

▪ Abstract

▪ Evidence is presented for a clinical classification of central vestibular syndromes according to the three major planes of action of the vestibulo-ocular reflex (VOR): yaw, pitch, and roll. The plane-specific vestibular syndromes are determined by ocular motor, postural, and perceptual signs. Yaw plane signs are horizontal nystagmus, horizontal past pointing, rotational and lateral body falls to the right or to the left, and horizontal deviation of perceived straight-ahead. Pitch plane signs are upbeat/downbeat nystagmus, forward/backward tilts and falls, and upward or downward deviations of the perceived horizontal. Roll plane signs are torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and perceived subjective visual vertical. The VOR syndromes defined in this way allow a precise topographic analysis of brainstem lesions according to their level and side.

▪ The lesion sites of yaw syndromes are restricted to the pontomedullary level (vestibular nucleus).

▪ A tone imbalance in pitch indicates bilateral (paramedian) lesions of the medullary or pontomesencephalic brainstem or bilateral dysfunction of the flocculus.

▪ A tone imbalance in roll indicates unilateral lesions, ipsiversive at the pontomedullary level (vestibular nuclei) and contraversive at the pontomesencephalic level (MLF and INC).

▪ A unilateral lesion (or stimulation) of the graviceptive pathways, which transduce input from vertical semicircular canals and otolith, affects function in roll, whereas bilateral lesions affect function in pitch.

▪ PMID: 12221493 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/?term=Dieterich%20M%5bAuthor%5d&cauthor=true&cauthor_uid=12221493


Saccades & Cerebellum

▪ Upward Saccades – terminated by Anterior Vermis

▪ Downward Saccades – terminated by Posterior Vermis and…Posterior Interposed Nuclei. Lesions here cause hypermetric of upward saccades, hypometria of downward saccades

▪ Ipsilateral Horizontal Saccades to a target are terminated by the cerebellar Lateral Vermis and Fastigial Nuclei

▪ Midline Cerebellar lesions for the most part cause saccadic hypermetria (overshoot the target)


Central vs. Peripheral induced

Nystagmus▪ Example – a patient presents with no

nystagmus in light during fixation, but you

see nystagmus in darkness without

fixation

▪ Central or Peripheral lesion?

▪ Answer : fixation in light indicates central

is ok therefore problem is peripheral

▪ If they cannot suppress it in the light with

fixation=central lesion


Central Vestibular Disorders

▪ J Neurol. 2007 May;254(5):559-68. Epub 2007 Apr 6.

▪ Dieterich M1.

▪ Abstract

▪ … vertigo is not a well-defined disease entity, but rather a multisensory syndrome that results when there is a pathological dysfunction of any of the stabilizing sensory systems (e.g., central vestibular disorders, peripheral vestibular diseases with asymmetric input into the vestibular nuclei). … they can be separated according to the three major planes of action of the vestibulo-ocular reflex: yaw, roll, and pitch.

▪ A tonic imbalance in YAW is characterized by horizontal nystagmus, lateralpulsion of the eyes, past-pointing, rotational and lateral body falls, and lateral deviation of the perceived straight-ahead.

▪ A tonic imbalance in ROLL is defined by torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and the perceived vertical.

▪ Finally, a tonic imbalance in PITCH can be characterized by some forms of upbeat or downbeat nystagmus, fore-aft tilts and falls, and vertical deviation of the perceived straight ahead.

▪ The thus defined syndromes allow for a precise topographic diagnosis as regards their level and side.

▪ PMID: 17417688 [PubMed - indexed for MEDLINE]



http://www.ncbi.nlm.nih.gov/pubmed/?term=Dieterich%20M%5bAuthor%5d&cauthor=true&cauthor_uid=17417688

Pitch – is a Central (CNS) problem

▪ Downbeat nystagmus

▪ Upbeat nystagmus

▪ Deviation of subjective visual horizontal upwards or downwards

▪ Falling tendency or sense of falling backwards or forwards

▪ If FNL the pursuits will not be smooth but choppy

▪ Means something in the midline (bilateral FNL, bilateral paramedian pontine, bilateral paramedian medullary) is dying off. Note: not good when bilateral structures die off!! Check for ischemic causes…imaging suggested, check autoimmune

▪ Treatment-excite midline structures, do not exceed FOF


Roll – is a Central (CNS) problem

▪ Ocular tilt reaction

▪ Skew deviation

▪ Ocular torsion

▪ Head tilt

▪ Deviation of Subjective visual field, Clockwise or

Counter Clockwise

▪ Falling tendency to one side or tilting

▪ Lesions:

Paramedian thalamus

PIVC lesions

Midbrain


YAW (rotation)– can be a Central (CNS) problem or a Peripheral

problem

▪ Horizontal nystagmus with a little bit of torsion twisting with it

▪ Horizontal past pointing

▪ Turning during the Fakuda test ~50 steps and 35 degrees

▪ Where you may have Yaw problems: Where Cn 8 enters the medulla

Medial Vestibular nucleus

Superior Vestibular nucleus

Nucleus prepositus hypoglossi

Paramedian Pontine Reticular Formation (PPRF)

MS Demyelination of vestibular nerve

Ischemic infarctions

▪ Falling tendency to one side due to loss of canal, vestibular nerve loss, Meniere’s, vestibular neuronitis or a Cb problem not processing signals from that area


Oculomotor ExaminationEye movement ROM (Cardinal Fields of Gaze)

Eye movement ROM Procedure (CFG): Holdpatient’s head with one hand. Ask the patientto follow your finger (keeping it 18-24 inchesaway from the patient’s face) to test for fullvertical and horizontal eye movements. Lookfor: • ROM • Conjugate eye movement

Note: • Vertical movements decrease slightly in older people

A small amount of “end point” nystagmus may beseen at the point of full ocular range in all directions,minimal in young people and increases with age


Tests performed in room light Spontaneous Nystagmus Procedure: Hold patient’s head with one hand. Ask patient to look straight ahead at a point several feet away. Look for: Nystagmus and note direction.

Gaze Holding Nystagmus Procedure: Hold patient’s headwith one hand. Ask patient to follow your finger (keeping it 18-24 inches away from the patient’s face) while you move yourfinger 30 degrees to the left, right, up and down. Pause in eachposition to observe nystagmus, note direction.

Skew Deviation Procedure: Hold patient’s head with onehand. Cover one eye. Switch the cover from one eye to the othereye. Look for: a vertical corrective movement of the eye as it isuncovered. Note: Effect of direction of gaze on the skew deviation• Any spontaneous tilt of the head and the effect of tilt on the skewdeviation


Gaze-Evoked Nystagmus

Gaze-evoked nystagmus is produced by the

attempted maintenance of an extreme eye

position. It is the most common form of

nystagmus. Gaze-evoked nystagmus is due to

a deficient eye position signal in the neural

integrator network which is dispersed between

the vestibulocerebellum, the medulla (region of

the nucleus prepositus hypoglossi and adjacent

medial vestibular nucleus [NPH/MVN]), and the

interstitial nucleus of Cajal (INC).


Gaze Evoked Nystagmus

Gaze Holding Nystagmus - Hold patient’s

head with one hand. Ask patient to

move their eyes to look 30 degrees to the

left, right, up and down. Pause in each

position to observe nystagmus, note

direction. Note: If patient looks beyond 20

to 30 degrees, end point nystagmus may

be observed rather than gaze holding

nystagmus


Oculomotor ExaminationVergence

Hold the patient’s forefinger in your hand about 2 feet away from the

patient’s face. Ask the patient to focus on the finger while you move it

toward the patient’s nose. Look for : Convergence of the eyes • Conjugate

eye movement • Pupillary constriction

Decreased vestibular ocular reflex (VOR) Head thrust test Seated slow

and fast-abnormal start pt. supine, progress to seated, then standing.

Inform the patient that you will be moving their head very quickly, but only

through a small range. Grasp patient’s head firmly with both hands on the

sides of the head. Tilt the head forward 30 degrees so that the horizontal

semicircular canal is level in the horizontal plane. Instruct the patient to

look at your nose. Move the patient’s head side to side slowly. Then,

suddenly move the patient’s head in one direction and stop. The head

movement should be small amplitude with the position held at the end.


Dynamic visual acuity

Patient sits the appropriate distance from theacuity chart, wearing their glasses if they needdistance correction. Patient reads to the lowestline that they can until they cannot correctlyidentify all the letters on a given line. Note theline where this occurs and the number of lettersthe patient incorrectly identifies. Standingbehind the patient, grasp the patient’s headfirmly with both hands. Tilt the head forward 30degrees so that the horizontal semicircularcanal is level in the horizontal plane.


Oculomotor Examination

While moving the patient’s head side to side at afrequency of 2Hz (2 complete side to side cycles persecond) through a ROM of 1-2 inches in each direction,(so as to not restrict the visual field which may occur inpatients who wear glasses) ask them to read the lowestline that they can until they cannot correctly identify allthe letters on a given line.

Note the line and where this occurs and or the number ofincorrect letters. A difference of less than or equal to 2 lines isnormal. A difference of greater than or equal to 3 lines isabnormal. (likely vestibular deficit). If the patient has restrictionof the cervical movement which limits your ability to perform thehead movement the test cannot be properly performed andshould be ceased.


Smooth Pursuit eye movements

Ask the patient to follow your slowly moving finger (< 20 degrees per second) horizontally, 30 degrees from the center to the left and to the right

Repeat vertically, moving 30 degrees above and below the horizontal.

Abnormal is jerky (or saccadic)Note: Eye movements may besaccadic if you are moving yourfinger too fast. Slow the speedof your finger to see if theperson can follow smoothly.

Smooth pursuit eye movementsbecome more and moresaccadic with age. Vertical eyemovement is often interruptedby a saccades in youngerindividuals.


Saccadic eye movements

Hold the patient’s head with one hand. Hold your

finger about 15 degrees to one side of your nose.

Ask the patient to look at your finger and then at

your nose several times. Perform this left, right, up

and down. Look for: The number of eye

movements it takes for the patient’s eyes to reach

the target, normal is less than 2. Abnormal is

several small movements or a big movement with

an overshoot. (Hypermetria)


VOR Cancellation

The VOR is essential for maintaining stablevision on a target when the head is moving butthe brain must also have a mechanism forsuppressing the VOR when it is necessary tomove the head and eyes in the same direction.This task is managed by thevesstibulocerebellum (Flocculonodular lobe).Failure to suppress the VOR indicates probablevestibulocerebellar contribution to thepatient's vertigo.


VOR Cancellation

Grasp patient’s head firmly with both hands onthe sides of the head. Tilt the head forward 30degrees so that the horizontal semicircularcanal is level in the horizontal plane. Instructthe patient to look at your nose. Move thepatient’s head from side to side approximately30 degrees while you move in the samedirection so that your face remains directly infront of the patient’s face. Look for: Patient’sability to maintain visual fixation and/or if thepatient makes saccadic eye movements.


BESS Test

The Balance Error ScoringSystem provides a portable,cost‐effective, and objectivemethod of assessing staticpostural stability. In theabsence of expensive,sophisticated postural stabilityassessment tools, the BESScan be used to assess theeffects of mild head injury onstatic posturalstability. Information obtainedfrom this clinical balance toolcan be used to assistclinicians in making return toplay decisions following mildhead injury.


Optokinetic Eye Movements

The optokinetic (OPK) tape is anessential part of the functionalneurologist's toolkit. It can beused to evaluate optokineticnystagmus, which provides awindow of assessment into thefunctionality of the frontal lobe,parietal lobe, cerebellum andother brain regions involved inthe generation and control ofoptokinetic eye movements. Theoptokinetic tape can also be usedto rehabilitate functional deficitswithin these brain areas, whichalso makes it a powerfultreatment modality.


OPK (Optokinetic)

▪ Tape or iPad may be used

▪ Procedure: Best seen withVNG. Running tapehorizontally results in areflexive Slow Phase eyemovement. The Parietalregion pursues and theFrontal lobes refixate orsaccade back to the center.The contralateral Cb normallystops the eyes in the midline.

▪ Isolated impairment of verticalOPK nystagmus indicatesimpaired midbrain functionthat may also be seen inProgressive SupranuclearPalsy or Niemann-Pick type C


Tests best performed using Frenzel lenses or IR

goggles

Spontaneous nystagmus denotes movement of the

eyes without a cognitive, visual or vestibular stimulus.

Most commonly spontaneous nystagmus is caused

by a vestibular imbalance

Hold patient’s head with one hand. Ask patient to look

straight ahead. Look for: Nystagmus and note

direction. And those abnormalities with tests performed

in room light


Decreased Vestibular Ocular

Reflex (VOR)

Head shaking nystagmus test. Procedure: Inform thepatient you will be moving their head from side to side.Grasp patient’s head firmly with one hand on either side ofthe head. Tilt the head forward 30 degrees so that thehorizontal semicircular canal is level in the horizontalplane. Have the patient close their eyes. Move the headside to side 20 times, asking the patient to help with themovement.

Ask patient to open their eyes quickly. Look for:Nystagmus, noting direction . 1 or 2 beats of nystagmusis not significant . If horizontal head shaking inducespersistent nystagmus the procedure should be repeatedvertically, but only moving the patient’s head 10 times.


Dix Hallpike Test for Posterior Canal

BPPVPatient seated on table and head is rotated 450

The head and trunk are quickly taken straight backso the head is over the edge of the table. Hold 30-45 seconds, observing for nystagmus and questionfor vertigo. (latency of 5-10 sec.). Patient is thenbrought up slowly to a sitting position with the headmaintained in 450 rotation. Again, observe fornystagmus and question for vertigo. Test isrepeated with head rotated 450 in oppositedirection. Look for: Up beating or down beatingNystagmus, indicative of central lesion. Note:Critical element is position of the head in space(not relative to the body).


Head roll test for Horizontal canal

BPPV

Procedure: patient is supine with thehead flexed 20 degrees. Head is turnedquickly to one side. Hold 30 seconds,observing for nystagmus and question forvertigo. Roll the head slowly back to thesupine position, hold for 30 seconds.Roll the head quickly to the other side.Observe for nystagmus/vertigo. Observenystagmus, noting direction, latency andduration. Ask the patient which side isworse.



VESTIBULAR ASSESSMENT

AND TREATMENT

Vestibular Adaptation and

Compensation Thomas P. Wellings*, Alan M. Brichtaand Rebecca Lim

School of Biomedical Sciences and Pharmacy, The University of Newcastle, and Hunter Medical

Research Institute, NSW, Australia

The balance or vestibular system is often

overlooked as a major sensory system

(Goldberg et al. 2012). Even less appreciated

is the vestibular system’s inherent plasticity

and capacity for self repair. Two phenomena

known as vestibular adaptation and vestibular

compensation are exquisite examples of

innate plasticity


Vestibular Adaptation

(compensation) Exercises

▪ Vestibular adaptation describes the

routine changes in sensitivity (gain) of

reflexive eye movements (VOR)

responsible for stabilizing images on the

retina during head movements


Vestibular Habituation Exercises

The goal of habituation exercise is to reduce the dizziness through repeated exposure to specific movements or visual stimuli that provoke patients' dizziness. These exercises are designed to mildly, or at the most moderately, provoke the patients' symptoms of dizziness.


Vestibulospinal Reflex Symptoms


7/1/2019Larry E. Masula, D.C/DACNB. 290


It is important to realize that eye movement alone or head movements alone, will

have extremely limited benefit. Introduction of head movement together with

visual acuity, (within the frequency of the VOR) , is extremely beneficial.

Management

1. Dix Hall Pike - PC

2. Epley Maneuver - PC

3. Semont Maneuver – PC

4. Lempert Maneuver – HC

5. Gufoni Maneuver – HC

6. Reverse Dix Hallpike – AC

7. Reverse Epley - AC


Benign Positional Vertigo (BPPV)

▪ Two Forms: Canalithiasis and Cupulolithiasis.

Canalithiasis (otoconia is free in the canal) and is the single mostcommon cause of vertigo lasting less than 30 seconds withposition change-typically when turning over in bed, getting in andout of bed, bending over and straightening up, and extending theneck to look up. Cupulolithiasis (otoconia stuck to the cupula)causes immediate vertigo and nystagmus and does not fatigue.

Pathophysiology-Not entirely understood although an abnormalityof the posterior canal is strongly implicated. Barany- found lesionsof the otolith organs. Dix-Hallpike-found unilateral degeneration ofthe utricular macula at necropsy. Schuknecht-found basophilicdeposits on the cupulae of the posterior canal proposing otoconiafrom degenerating utricular macula settles on the cupula of theposterior canals


Posterior Canal BPPV

Two most convincing pieces of clinical evidence supporting a posterior canal are:

▪ 1. The positional nystagmus is in the plane of the posterior canal

▪ 2. Sectioning of the ampullary nerve from the posterior canal stops BPPV

▪ Schuknecht’s cupulolithasis theory is supported byany type of damage to the inner ear (trauma,infection, ischemia, age related degeneration) whichcan lead to dislodging of the calcium carbonatecrystals from the otolith and deposition on the cupulaof the posterior semicircular canal


Posterior Canal BPPV

Diagnosis-

1. Rests on finding the characteristic fatigable paroxysmal positional nystagmus. The Nystagmus is torsional and in the plane of the affected canal.

2. Caloric hypo excitability is seen on the ipsilateral side presumably involving both the horizontal and posterior canals

3. Canals may also be tested w/o eye fixation in a Dis-Halpike position (Frenzel lenses) for better optimization

▪ Management- positional exercises. Epley or Semont. Resume upright position once the vertigo has ceased. Repeat x 3 - t.i.d.


Dix-Hallpike Test for posterior canal

BPPVExplain procedure to patientbeforehand that it mightinduce vertigo. Ensure thatthere are no neck/backproblems that would beaggravated by sudden changein posture. Stand to the sideof the patient • Pt sitting withhead turned to examiner • Ptsat so that when supine, thehead will be beyond the endof the couch • Patient lain flatin one quick, smoothmovement • Eyes must stayopen • Repeat on other side.

Positive test: – Rotatory (torsional) nystagmus (& vertigo): • Diseased ear downmost

3 important features include:

▪ Latency – delay of up to 20 seconds before onset of nystagmus

▪ Fatigueability – nystagmus fades if head held in provoking position

▪ Habituation – Repeating DH test produces less vigorous response


Interpretation of Dix Hallpike Test

Consider central problem if atypical any of the following occur:

▪ Non-rotatory

nystagmus

▪ No latency

▪ No fatiguability

▪ No habituation


Posterior Canal Rehab.

▪ Semont

▪ Epley


Epley Maneuver-posterior canal


Semont Maneuver - Right PC


Roll Test for Horizontal Canal

BPPV(Herdman, 2007)

Patient lies supine with neck flexed 20º, head isquickly rolled 90º to one side to orient thehorizontal canal. Hold for up to one minute andobserve presence & direction of nystagmus, andthen return slowly to midline; maintaining theneck flexion, the procedure is repeated to theother side. Note patient report of vertigo.


Roll Test, Interpretation

Horizontal canalithiasis –nystagmus is geotropic(toward the earth) when thehead is rolled to the rightand left, and lasts a shortduration (approximately<60 seconds)

Horizontal cupulolithiasis –nystagmus is apogeotropic(away from the earth) whenthe head is rolled right andleft, and it is persistent (>60seconds)


Horizontal Canal Rehab.

▪ Gufoni Maneuver

▪ Lempert Maneuver


Gufoni Maneuver - Horizontal Canal rehab.


Lempert Maneuver (BBQ Roll)

Horizontal Canal rehab.


Rehab. Gem

▪ Vestibular rehabilitation utilizing Otolith

stimulation (A/P and Up/down) also

provides lot of frontal lobe stimulation.

This application may also useful for ADD

kids with right frontal lobe problems.


VOR Rehabilitation Exercises

Eye exercises, X2

viewing may be used

for rehabilitation of

Smooth pursuits.

Holding a single target,

keep eyes fixed on

target. Slowly move it

side-to-side/up-

down/diagonally while

head stays still.


VOR Gaze stabilization rehab.

X1 viewing exercise, maybe used for rehabilitatinggaze holding failure. Whileseated keep eyes fixed onsingle stationary target heldin hand or placed on wallmove head side to side.Repeat while moving headup and down. This like alltests should be performedboth sitting and standing.


VOR rehab: X1 viewing

Head/eyes moving insame direction Holding asingle target, keep eyesfixed on target. Slowlymove target, head andeyes in same directionup-down/ side toside/diagonally


VOR rehab: X2 viewing

Head/eyes moving in

opposite direction

Holding a single target,

keep eyes fixed on

target. Slowly move

target up-down/side to

side/diagonally while

moving head in

opposite direction of

target


Saccades Rehabilitation

Holding two stationarytargets placed inchesapart side-to-side/up-down/diagonally, moveeyes quickly from targetto target as head staysstill.


Have a Vestibular Questionnaire Questionnaire


VRT(vestibular rehabilitation therapy)

Therapeutic Goals▪ Enhance existing vestibular capabilities

▪ Strengthen compensatory mechanisms

By improving Proprioceptive input

By increasing Visual Input

Other sensory systems


Additional Rehab. Strategies

▪ OPK▪ Cb Rehab Exercises▪ Head Laser Maze▪ NSI Unit▪ Metronome▪ Simon▪ Gaze Stability - Dots on Wall▪ Wii▪ Fit Ball▪ Wobble Board▪ Mini Trampoline


Additional Testing

▪ Berg Balance Scale

▪ Dynamic Gait Index

▪ Modified Clinical Test of Sensory Interaction in Balance (mCTSIB)


Thanks for taking Online Courses with Back To Chiropractic CE Seminars.

I hope you enjoyed the course. Please feel free to provide feedback.

Check out: Back To Chiropractic Resource Pages

Chiropracticpedia Informational website for chiropractic patients

Free Materials Over 200 files: Posters, newsletters & more

Adjusting & Office Skills Free help from DCs that care

DCs Looking For DCs Looking to hire, or for a job?

Chiropractic Neurologists

Classifieds Looking to buy or sell a Practice

Memorials Tributes to great DCs who have passed

Marcus Strutz DC


33000 North Highway 1

Ft Bragg CA 95437

707.972.0047

https://chiropracticpedia.org/

https://www.backtochiropractic.net/Free Materials.html

http://www.backtochiropractic.net/Adjusting Help and Practice Management.html

http://www.backtochiropractic.net/DCs Looking For DCs.html

https://acnb.org/DoctorLocator.aspx

http://www.backtochiropractic.net/For Sale.html

http://www.backtochiropractic.net/Memorials.html

https://www.backtochiropractic.net/

back to chiropractic ce seminars neurology: hints … hints of a...exam process: read all...

Documents