A place principle for vertigo - MM3 Admin · A place principle for vertigo Richard R. Gacek*...

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Auris Nasus Larynx 35 (2008) 1–10

A place principle for vertigo

Richard R. Gacek *

Department of Otolaryngology, Head and Neck Surgery, University of Massachusetts Medical School,

Worcester, MA 01655, USA

Received 16 March 2007; accepted 13 April 2007

Available online 24 October 2007

Abstract

Objective: To provide a road map of the vestibular labyrinth and its innervation leading to a place principle for different forms of vertigo.

Method: The literature describing the anatomy and physiology of the vestibular system was reviewed.

Results: Different forms of vertigo may be determined by the type of sense organ, type of ganglion cell and location in the vestibular nerve.

Conclusion: Partial lesions (viral) of the vestibular ganglion are manifested as various forms of vertigo.

# 2007 Elsevier Ireland Ltd. All rights reserved.

Keywords: Vertigo; Vestibular nerve; Pathology

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2. Sense organ. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

3. Ganglion cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

4. Hair cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

5. Hair cell polarization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

6. Efferent vestibular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

7. A place principle for vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

8. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

1. Introduction

Sensory systems must be highly organized to function

effectively. The special senses are especially well developed.

This organization exists at the periphery and is duplicated

with ascent of the system centrally. The auditory system

provides an excellent example of a place principle for

hearing. The reception of frequencies in orderly fashion

from low at the apex of the cochlea to high at the base is

determined by the physical characteristics of the cochlear

partition. Components in the cochlear duct (basilar

* Tel.: +1 508 856 4162; fax: +1 508 856 6703.

E-mail address: [email protected].

0385-8146/$ – see front matter # 2007 Elsevier Ireland Ltd. All rights reserved

doi:10.1016/j.anl.2007.04.002

membrane, spiral ligament, support cells in the organ of

Corti) determine the place for maximal displacement of this

partition by a given traveling wave induced by an auditory

stimulus. This orderly transmission of frequencies is

preserved over the primary auditory neuron, and multiple

central neurons to the cortex for proper integration of

auditory messages. Vision and olfaction have a similar

precise organization to their neural systems.

Sufficient morphologic, physiologic and clinical evi-

dence has accumulated in the past few decades to indicate an

organization in the vestibular system that may account for

different forms of vertigo depending on the location of

pathology in the vestibular nerve. The evidence supporting

such a ‘‘place principle for vertigo’’ will be reviewed in this

.

mailto:[email protected]

http://dx.doi.org/10.1016/j.anl.2007.04.002

R.R. Gacek / Auris Nasus Larynx 35 (2008) 1–102

Fig. 1. Section through the vestibular ganglion and nerve from a patient

with vestibular neuronitis. Arrows point to the numerous bundles of

degenerated axons resulting from degenerated groups of ganglion cells.

Fig. 2. Light microscope photomicrograph of the utricular macula demon-

strates the otoconial blanket (arrow head) resting on the neurosensory

epithelium (arrow). N: utricular nerve.

report. Such a principle might aid our clinical approach to

the evaluation and treatment of vertigo in patients, with

recurrent vertigo. The recurrent vestibulopathies are now

known to be caused by discrete vestibular ganglion cell

lesions, likely viral induced. A significant body of

histopathologic evidence has demonstrated that viral lesions

are limited to discrete clusters of degenerating neurons in the

vestibular ganglion in vestibular neuronitis, Meniere’s

disease and benign paroxysmal positional vertigo (Fig. 1)

[1–3]. This pattern of ganglion cell loss is typical of a viral

neuropathy (4) caused by re-activation of a latent

neurotropic virus (e.g. Zoster) [4]. Because the description

of dizziness by patients may vary (i.e. vertigo, unsteadiness,

positional vertigo), attempts have been made to classify

vestibular disorders according to the nature of the imbalance

symptom. An example of such a knowledge based system is

that of Mira et al. [5]. This system used vertigo and dizziness

to divide a long list of clinical pathologies encountered by

the otologist or neurologist.

The organization of the peripheral vestibular system is

determined largely by two anatomical features. These are:

(1) type of sense organ. (2) Type of ganglion cell.

Fig. 3. Photomicrograph of crista ampullaris and its cupula. Note that the

cupula is attached to the ampullary roof.

2. Sense organ

Of the two types of vestibular sense organs, the otolith

organs are probably the most important in a gravity dependent

environment. They are the oldest phylogenetically with the

canal system making a presence as more mobility (swimming,

walking, running) was acquired. Since the otolith organs

feature a covering membrane containing high specific gravity

(2.71) calcium carbonate particles (otoconia) resting on the

ciliary bundles of the hair cells in the sensory epithelium, they

are in a constant state of stimulation (Fig. 2). The canal

system, on the other hand, is activated by transitory increases

in angular acceleration or deceleration of the fluid (endo-

lymph) within the membranous canal. Such inertial changes

deform the cupular partition of the ampullary enlargement in

the canal resulting in deflection of the ciliary bundles of hair

cells in the sensory epithelium (Fig. 3) [6].

R.R. Gacek / Auris Nasus Larynx 35 (2008) 1–10 3

Fig. 4. (A) Section through a human temporal bone where the utricular

macula is divided by a cleft (arrow) where there is an absence of neuro-

epithelium (B).

Fig. 5. Drawing summarizing the organization of vestibular ganglion and

its peripheral and central axons (cat). The dark portion of the vestibular

nerve signifies the location of type I ganglion cells that supply type I hair

cells in the superior and lateral canal cristae. Cochlear and vestibular

efferent axons are located at the interface of canal and otolith axons.

SCA: superior canal ampulla; HCA: lateral canal ampulla; PCA: posterior

canal ampulla; UTR: utricle; SACC: saccule; Utric N: utricular nerve; PCN:

posterior canal nerve; OCB: efferent bundle (cochlear and vestibular).

The otolith organs are arranged horizontally (utricular

macula) and vertically (saccular macula) to record position

and position change in these two planes. There is some

anatomical evidence which suggests each macula actually

represents the merging of two smaller maculae with

oppositely polarized hair cells (Fig. 4). The interface of

this merging is located at the striola line. The vestibular

nerve and ganglion supplying afferent innervation to the

vestibular sense organs has an arbitrary division into

superior and inferior. The superior division supplies the

utricular macula, the cristae of the lateral and superior

semicircular canals and a small portion of the saccular

macula macula while the inferior division innervates the

saccule and posterior canal crista (Fig. 5).

The bipolar vestibular ganglion cells which supply

afferent input from the otolith organs are located ventrally in

the central portion of the ganglion (Fig. 5), while the canal

ganglion cells are located at the rostral and caudal ends [7].

As the axons from these ganglion cells form the vestibular

nerve trunk, those from the canals converge together in the

rostral half of the nerve trunk and the otolith axons in the

caudal half. This differential location of otolith and canal

neural input is necessary because of their different

connections with second order neurons in the vestibular

nuclei. The canal projections bifurcate on entering the

brainstem with the ascending branch terminating in the

superior vestibular nucleus (SVN) and the descending

branch ending in the medial vestibular nucleus (MVN)

(rostral part) (Fig. 6). These two nuclei project bilaterally

into the medial longitudinal fasciculus (MLF). The SVN

projects in the ipsilateral MLF to the IV and III nerve nuclei

while the MVN sends a comparable projection in the

contralateral MLF to terminate in the IV and III nuclei in a

reciprocal fashion [8]. These pathways serve the vestibule-

ocular reflex (VOR) for vertical and oblique extraocular

movements necessary for nystagmus. The MVN also

projects bilaterally to the VI nerve nucleus and to the

ipsilateral medial rectus subnucleus in III n. over a tract

called the ascending tract of Deiters. These projections are

responsible for the horizontal VOR. Some projections from


Fig. 6. Diagram of the central projections of afferents from the semicircular

canals. MLF: medial longitudinal fasciculus; VS: vestibulo-spinal; VN:

commissural; VO: vestibulo-ocular; INC: interstitial nucleus of Cajal; III:

oculomotor nucleus; VI: abducens nucleus; IV: Trochlear nucleus.

Fig. 7. Central projections of afferents from the utricular macula. LVST:

lateral vestibulospinal tract; MVST: medial vestibulospinal tract; III: ocu-

lomotor nucleus; VI: abducens nucleus.

the medial and descending vestibular (DVN) nuclei travel

down the MLF to the muscles of the neck region where they

are responsible for vestibulo-collic reflexes [8,9].

The bifurcating axons from the otolith organs terminate in

the caudal vestibular nuclei—that is the lateral (LVN), medial

and descending nuclei (Fig. 7). The ascending branches from

utricular neurons terminate in the ventral portion of the LVN

and in the rostral MVN [7]. The descending branches connect

with cells in the caudal MVN and DVN. The LVN is

responsible for vestibulospinal tract activation of trunkal and

limb muscle reflexes [9,10]. The MVN and DVN descend in

the MLF for cervical muscle reflexes. However, the utricle

also has connections with the VI and III nuclei for horizontal

eye movements (compensatory).

Input from the saccule is similar but much smaller.

Saccular neurons project to portions of the MVN and DVN for

neck muscle activation via the MLF. Projections to the

oculomotor nucleus over the group Y nucleus permit a VOR

response from the saccule involving the superior and inferior

rectus muscles as well as the oblique eye muscles (Fig. 8) [11].

In summary, the semicircular canal sense organs

primarily project to the nuclei for VOR activation

(nystagmus) while the otolith organs are responsible for

activity in anti-gravity muscles of the neck, trunk and limbs

(ataxia). However, compensatory eye muscle activation also

occurs from stimulation of the otolith organ pathway.

3. Ganglion cells

Since the inner ear and its sense organs with their nerve

supply, develops from the same anlagen, it is not surprising

that two types of ganglion cells, as described in the spiral

ganglion of the cochlea, also exist in the vestibular nerve.

The two types of ganglion cells in these two types of sense

organs have similar features in morphology, physiology and

pathologic behavior.

Type I ganglion cells have large caliber myelinated

appendages (dendrites) which innervate type I hair cells with

1:1 or almost 1:1 ratio (Fig. 9). They possess an irregular

spontaneous discharge pattern and degenerate following

ablation of the sense organ (Fig. 10) [12–14]. In the cochlea

they provide 90% of the innervation of the organ of Corti

where they supply inner hair cells (IHC) [15]. Type I

ganglion cells are sequestered from the type II cells in the

vestibular ganglion forming the ampullary nerves but have a

dispersed pattern in the nerves to otolith organs [7]. This

distribution reflects their periphery termination on type I

HC. The dendrites of type I ganglion cells travel in the center

of ampullary nerves because they terminate on the type I hair


Fig. 8. Central projections from the saccular macula. IFC: infracerebellar

nucleus; Y: group Y nucleus; LVST: lateral vestibulospinal tract; MVST:

medial vestibulospinal tract; MLF: medial longitudinal fasciculus; III:

oculomotor nucleus.

cells which are concentrated at the crest of the crista

ampullaris [16,17]. These hair cells are positioned to be most

sensitive to cupular displacement.

The central projection of type I ganglion cells is to

vestibulo-ocular neurons in the SVN and MVN via axo-

somatic synapses (Fig. 11) [18]. Thus the type I hair cell –

type I ganglion cell – vestibulo-ocular neuron in the

vestibular nuclei (SVN, MVN) is responsible for the VOR

responses associated with stimulation or degeneration of the

cristae ampullaris. In the otolith system these type I ganglion

cells project to large multipolar neurons of the vestibulosp-

inal tracts as well as to vestibulo-ocular neurons in the

caudal vestibular nuclei.

Type II ganglion cells have small caliber myelinated

dendrites which, innervate type II hair cells in a diffuse

manner [16,17] (i.e. many HC supplied by a single fiber)

(Fig. 9), and demonstrate a regular spontaneous discharge

pattern [12,13,19]. They do not degenerate after end organ

ablation (Fig. 10) [18]. The type II hair cells located along

the slopes of the crista ampullaris are not in a position to

optimally respond to cupular displacement but may have a

supporting role in end organ sensitivity by virtue of their rich

efferent innervation.

Because the lateral canal sense organ is a recent

phylogenetic development, making an appearance in

amphibians (frog), the type I and II ganglion cell populations

are separated in the superior division ganglion [7,20]. The

type I ganglion cells are concentrated at the most rostral end

of the ganglion while type II cells occupy the caudal region

of the superior division ganglion (Fig. 5). The dendrites of

type II ganglion cells envelop those of type I ganglion cells

as the ampullary nerves are formed. This separate location of

type I and II ganglion cells in the superior vestibular division

has been confirmed in the monkey and human vestibular

nerve [20] and provides an opportunity for a differential

functional response from injury to either of these two types

of neurons.

4. Hair cells

The two types of hair cells (HC) in the vestibular organs

are somewhat similar to the inner (HC) and outer hair (OHC)

cells in the organ of corti. The type I HC in the vestibular

organs (i.e. crista) are innervated by type I vestibular

ganglion cells with the same irregular spontaneous electrical

activity as the type I spiral ganglion cells which innervate the

IHC in the organ of corti [15,16]. In both systems they are

responsible for the major afferent input to the brain for

balance and hearing.

The type II vestibular hair cells may play an enhancing

role in the sensitivity of balance organs similar to the role

that OHC impose on the IHC and auditory sensitivity. The

contractile properties of OHC allow a change in the cochlear

amplifier effect in the organ of corti [21]. This contractile

function of the OHC is under efferent neural control and

serves to enhance the sensitivity of auditory neurons (type I).

5. Hair cell polarization

In addition to the different functionalities of two types of

HC (with their innervation) in the vestibular system, an

important feature of vestibular hair cells is their alignment

within an individual sense organ and the relationship of this

orientation to that of other sense organs in the labyrinth

[16,17]. This is referred to as the ‘‘polarization of hair cells’’

in the labyrinth.

In contrast to cochlear hair cells vestibular HC have a

ciliary bundle comprised of 70–100+ stereocilia and one

longer Kinocilium [16,17]. This Kinocilium is located at the

end of the ciliary bundle where the longest sterocilia are

located. The significance of this arrangement is that when

the cilia are deflected toward the kinocilium there is

depolarization of the HC and an increase in the afferent

neural unit activity while deflection away from the

kinocilium results in hyper-polarization and a decrease in

neural activity [16]. This has great functional significance

and accounts for the different responses obtained by testing

individual canals by warm and cool caloric stimulation.

An equally important consideration, however, is the

relationship of this polarity of HC between the five sense

organs of the labyrinth. Any movement of the body and head


Fig. 9. Diagram of the innervation to the two types of vestibular hair cells.

produces activation or deactivation in all sense organs of

both labyrinths. Figs. 12 and 13 summarize this polarity of

HC in the sense organs or parts of sense organs (maculae)

[16,17]. It is obvious that the polarization of HC in coplanar

canals is opposite to each other. In this way, a given rotation

produces excitation in one canal and decreased neural input

from the opposite coplanar canal, greatly enhancing the

differential response delivered to the brainstem for a VOR

response. This difference in the input is also enhanced by

commissural inhibition of the contralateral canal by activity

generated by the activated canal.

The relationship between the canals and otolith organs is

important but under recognized. Experiments conducted in

both zero gravity and one gravity environments have

demonstrated a modulation of canal responses by stimula-

tion of the otolith organs [22–24]. Fluur and Siegborn have

shown this in the cat [25]. They demonstrated that selective

denervation of an otolith (the utricle) produced a horizontal

nystagmus if the innervation to the lateral canal crista was

intact. However, if the lateral canal sense organ was

denervated before selective denervation of the utricle, no

nystagmus was observed. A similar relationship between the

saccule and the posterior canal was observed. These

observations indicate that there is an inhibitory effect on

canal responsiveness by the otolith of the same vestibular

nerve division.

Normally a change in head position produces a force that

causes excitation of the otolith and its corresponding canal.

However, if the otolith function is deficient, its correspond-

ing canal will respond in an excitatory mode [22]. This could

be reflected in a position provoked vertigo and nystagmus. It

has been suggested that this otolith–canal relationship is

based on a velocity storage mechanism in the central

nervous system probably the vestibular nuclei [26]. The

polarization of HC in the otolith and corresponding canal

sense organs play a role in this relationship. As seen in

Figs. 12 and 13 the maculae are each divided into halves by

the striola line with each half containing oppositely

polarized HC. Each half has HC that are aligned with a

crista ampullaris. These would be activated by the same

vector during movement of the head.

The number of neural units supplying the otolith and canal

sense organs is important in understanding the vulnerability of

this otolith-canal interrelationship. In the mammalian ear

where numerical data are available for the innervation of

individual vestibular sense organs (guinea pig, cat, monkey),

the number of afferent neural units in the vestibular nerve

branches is approximately equal [27]. However, the otolith

innervation modulating each crista ampullaris is represented

by one half the total innervation of the macula, making the

effective otolith neural input one-half that supplying the crista

ampullaris. Quantitative assessment of the vestibular ganglion


Fig. 10. Photomicrograph of the rostral part of the superior division axons

in the cat. (A) Normal vestibular nerve demonstrates the high concentration

of large diameter axons (type I ganglion cells). (B) Six months after

labyrinthectomy the large axons have degenerated.

Fig. 11. Diagram of the central projections of types I and II hair cells and

ganglion cells in the cristae.

Fig. 12. View of the human vestibular nerve branches and sense organs

demonstrating the polarization of hair cells in the cristae and utricular

macula supplied by the superior division. F: facial nerve; V: vestibular

nerve; S: saccular macula; U: utricular macula; PC: posterior canal crista;

LC: lateral canal crista; SC: superior canal crista.

of TB from patients with BPPV have shown a greater than

50% loss of ganglion cells in both vestibular divisions [28]. A

loss of this magnitude in afferent units already a fraction of

those to the crista ampullaris is likely to cause a disruption in

the otolith-canal relationship resulting in BPPV.

This neuropathologic explanation may account for the

various categories of BPPV. Posterior canal BPPV is by far

the most common possibly because the saccular nerve is the

smallest in all species studied [27]. Thus it represents the

greatest mismatch between otolith and canal innervation and

most likely to lose its inhibitory effect on posterior canal

Fig. 13. Posterior view of the specimen in Fig 12 shows the polarization of

hair cells in the saccular macula and posterior canal crista (PC).


excitation. Lateral canal and anterior canal BPPV are less

commonly recognized because of a smaller mismatch

between otolith and canal innervation.

Fig. 15. Transverse section of the vestibular (V) and cochlear (C) nerves in

the cat shows the efferent labyrinthine pathway (arrow) in the center of the

vestibular nerve. Acetylcholinesterase preparation. F: facial nerve.

6. Efferent vestibular system

The final form of vestibular injury which may present as

dysequilibrium relates to the efferent vestibular pathway.

The vestibular efferent pathway originates bilaterally in the

MVN just lateral to the abducens nucleus [29]. Axons of

these neurons [30] merge with and travel with the efferent

cochlear pathway (olivo-cochlear pathway) in the vestibular

nerve as it exits the brainstem (Fig. 14) [31]. This common

efferent bundle is clearly demonstrated by the high aceteyl

cholinesterase activity which suggests acetycholine as its

neurotransmitter agent (Fig. 15) [32]. This efferent bundle

passes through the saccular portion of the vestibular

ganglion and, therefore, may be affected (loss of function)

by inflammatory lesions in this area (Fig. 16). Individual

efferent axons ramify as they travel in a dispersed

arrangement to the sense organs (Fig. 17). This branching

pattern permits a rich efferent termination on HC in the sense

organ neuroepithelium.

Although an inhibitory effect is associated with stimula-

tion of the vestibular efferent pathway [33–35], the function

of this neural system in balance has not been demonstrated.

However, certain established facts on efferent systems

permit speculation on the role that the efferent system may

play in balance.

Fig. 14. Diagram of the efferent vestibular pathway (solid lines); stippled area =

vestibular nucleus; DCN: dorsal ventral cochlear nuclei; VCN: ventral cochlear

superior olivary nucleus; LSO: lateral superior olivary nucleus.

The role of the efferent cochlear pathway has been shown

to be one of modifying the physical characteristics of the

sense organ to enhance sensitivity for stimulation of the

primary auditory unit. By activating the contractile potential

of the OHC to lengthen or shorten thus adjusting the reticular

lamina and the tectorial membrane to sharpen the tuning

curves for the primary auditory units (IHC and type I spiral

ganglion cells) [21]. Otoacoustic emissions (OAE) gener-

ated by this ‘‘cochlear amplifier’’ [36] have been shown to be

efferent cochlear pathway. LVN: lateral vestibular nucleus; MVN: medial

nuclei; VII: genu of facial nerve; VI: abducens nucleus; ASO: accessory


Fig. 16. This section through the same specimen as Fig. 15 shows the

efferent cochlear pathway (OC) leaves the saccular nerve while vestibular

efferents have entered the vestibular nerve branches.

inhibited by the activity of the crossed (efferent) olivo-

cochlear pathway.

Efferent vestibular activity in lower forms (fish) has been

shown to be increased before vigorous movement (swim-

ming) which would over stimulate the organ of balance

(lateral line) [37–39]. Presumably this efferent activation is

intended to reduce (prevent) self-stimulation by the animals

activity.

This a role is compatible with the numerous demonstra-

tions of inhibition of afferent neural transmission following

stimulation of the vestibular efferent system [33,34]. Such a

system may play a role in preventing auto stimulation of

vestibular sense organs during physical activity.

A suggested corollary in the vestibular system would be

for the efferent pathway to prevent auto-stimulation of sense

organs by mechanically changing the sensitivity of the sense

Fig. 17. The vestibular efferent axons (arrows) are spread throughout the

afferent fibers before reaching the sense organ epithelium.

organs by altering the covering membrane (cupula,

otoconial blanket) during vigorous physical activity. The

clinical syndrome that could result from dysfunction of the

efferent vestibular system might be motion sickness. A

particularly efficient efferent system would be a requirement

for a gymnast or figure skater.

7. A place principle for vertigo

This anatomical organization (supported by physiologi-

cal correlates) provides a basis for attributing various forms

of vertigo to pathology in discrete part of the vestibular

ganglion. There is increasing pathologic evidence that the

recurrent vestibulopathies (ventricular neuronitis, Meniere’s

disease, benign paroxysmal positional vertigo) are caused by

discrete ganglion injury (degeneration) from reactivation of

neurotropic viruses (herpes virinae family) [1–3]. The

severity and form of dysequilibrium described by such

patients will depend on the location and number of

vestibular ganglion cells injured by virus [40]. The location

of sites in the vestibular ganglion responsible for different

forms of vertigo are represented by the numbers 1–5 in

Fig. 5.

1. L
esions in the most rostral part of the vestibular ganglion
(type I GC) are responsible for episodes of rotatory

vertigo. A strong VOR disturbance (nystagmus) signals

this form of vertigo.

2. I
f the ganglion cell lesion is located immediately caudal
to this rostral pole of the superior division type II GC are

affected. Unsteadiness, especially on head movement,

will be experienced because these type II GC project to

commissural pathways.

3. D
egeneration of ganglion cells in ventral parts of both
the superior (utricle) and inferior (saccule) divisions of

the vestibular ganglion, causes loss of function in the

vestibulospinal tract to neck, trunk and limb muscles.

Frequently these are described by patients as ‘‘drop’’

attacks. Ataxia may be a lingering form of this form of

dysequilibrium.

4. T
he most common form of vertigo encountered in
practice is position induced. Short duration episodes of a

rotatory vertigo which is fatiquable have been described

since Barany [41]. Both Barany [41] and Citron and

Hallpike [42] felt this was an otolith disorder but the

nystagmus response observed in this syndrome prevented

acceptance of an otolith cause. Hallpike’s description of

utricular degeneration [42] in the TB of BPPV was not

enough to neutralize the predominant support of a canal

etiology. Although the clinical response is a rotatory form

of vertigo, the uninhibited response is caused by loss of

the inhibitory role of the otolith organs.

5. L
esions in the saccular portion of the vestibular ganglion
(inferior vestibular) may secondarily interrupt the

efferent pathways to the cochlear and vestibular sense


organs. Clinically, the loss of this control may be

perceived as tinnitus and mot’on sickness.

8. Conclusion

This review is an attempt to provide a guide to

pathologies involving portions of the peripheral vestibular

pathway. It is unusual that only a specific location of

pathology will be present in a given patient. More often, a

mixture of locations will be present. However, the goal here

is to establish a map or framework to guide the evaluation

and management of patients with recurrent vestibulopathy.

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