Vestibular Dysfunction
Vestibular Dysfunction
Vestibular Dysfunction
00
VESTIBULAR DYSFUNCTION
William B. Thomas, DVM, MS
Peripheral Component
From the Department of Small Animal Clinical Sciences, University of Tennessee, Knox-
ville, Tennessee
nerve VII and sympathetic innervation to the face. The saccule and
utricle are primarily responsible for detecting gravity and linear accelera-
tion, and the semicircular canals detect rotation. 27, 54
Central Component
There are three semicircular canals in each inner ear. The canals are
named according to their position in space (horizontal, rostral-vertical,
caudal-vertical); each canal lies approximately at a right angle to the
others, with one for each plane of the body. The canals are filled with
fluid called endolymph. At one end of each canal is an enlargement
(ampulla) containing the crista ampullaris. The crista ampullaris contains
the specialized hair cells responsible for transducing rotational move-
ment into neuronal impulses. These hair cells have cilia that project into
the endolymph in the canals. Under normal resting conditions, the hair
cells continuously emit neuronal discharges at a constant rate. 27, 50
When the head begins to rotate in any direction (angular accelera-
tion), the endolymph in the semicircular canals, because of its inertia,
tends to remain stationary, while the canals themselves rotate. The result
is a relative flow of fluid in the direction opposite to the rotation of the
head. This flow of fluid bends the hair cell cilia, changing the rate of
neuronal discharges. Flow of fluid in one direction increases, or stimu-
lates, neuronal activity, and flow in the opposite direction decreases, or
inhibits, neuronal activity. After a few seconds of head rotation, the fluid
"catches up" with the moving canals, the hair cell cilia return to their
resting position, and the neuronal impulses return to baseline activity.
The opposite happens if the head rotation is stopped. The endolymph
tends to continue to flow, while the canals themselves stop. Now, the
cilia are bent in the opposite direction, causing the exact opposite pattern
of neural discharges. After another few seconds, the endolymph stops
and the system returns to the resting state. 27
The most effective stimulus for each semicircular canal is rotation
of the head in the plane of the canal. Because each canal is oriented in a
230 THOMAS
The visual system performs optimally when images are held steady
on the retina. Even small movements of the head must be compensated
for to avoid images "slipping" on the retina. Normally, rotation of the
head induces a compensatory eye movement in the direction opposite
that of head movement. This serves to stabilize images on the retina.
The stimulus for this eye movement is vestibular information from the
semicircular canals. Signals from the vestibular neurons are relayed to
the appropriate motor nuclei of cranial nerves III, IV, and VI, which
control the extraocular muscles. This response is called the vestibula-
ocular reflex. 27' 50
For example, rotation of the head to the left causes the endolymph
in the left horizontal canal to flow in the direction causing increased
activity of the hair cells, while in the right horizontal canal, the endo-
lymph flows in the direction causing decreased activity. This results in
contraction of the right lateral rectus muscle and the left medial rectus
muscle, causing the eyes to move to the right. This is the "slow phase"
of the vestibula-ocular reflex. The presence of a slow compensatory eye
movement induced by head rotation (the so-called "doll's eye maneu-
ver") implies normal function of the vestibula-ocular pathways. 27, 50
With continued head rotation, the tension in the ocular muscles
becomes too great to allow further eye movement and the slow phase
of the vestibula-ocular reflex is interrupted by a corrective fast move-
ment in the direction of the head tum, the "fast phase" of the vestibula-
ocular reflex. The fast phase is a type of saccadic eye movement induced
by visual stimulus, usually an image in the visual periphery, and is
controlled by higher brain centers and not the vestibular system. 53 At
the end of the corrective fast movement, the slower compensatory move-
ment is resumed, with the eyes now pointing in a new direction. The
alternation of slow compensatory movements with fast jerks back to-
wards the central position is called nystagmus. It is customary to refer
to a nystagmus as occurring in the direction of the fast phase of move-
VESTIBULAR DYSFUNCTION 231
Head Tilt
the side of the lesion. For example, a right inner ear lesion causes the
right ear to be held lower than the left. Central lesions can cause a head
tilt to either side. Animals with bilateral vestibular disease usually do
not have a head tilt but typically stand crouched and low to the ground. 54
Nystagmus
Physiologic Nystagmus
In normal alert patients, rotation of the head initially induces nys-
tagmus in the plane of rotation. This is the normal vestibula-ocular
reflex and is characterized by a slow phase in the direction opposite that
of the head rotation and a fast phase in the same direction as the head
rotation. For example, rotation of the head to the left in the horizontal
plane causes a horizontal nystagmus with the fast phase to the left.
Vestibular disease may cause an asymmetric rotation-induced nystagmus
when the head is moved in different directions. Animals with bilateral
vestibular disease lack rotation-induced nystagmus, as the stimulus for
this reflex is vestibular activation. 54
There are two other types of physiologic nystagmus. Caloric-in-
duced nystagmus induces flow of the endolymph in the semicircular
canals by creating a thermal gradient from one side of the horizontal
canal to the other. The test for physiologic nystagmus consists of irrigat-
ing the ear canal with warm (44°C) or iced (approximately 0°C) water
and observing for the induced nystagmus. Asymmetry in the response
234 THOMAS
Pathologic Nystagmus
Spontaneous Nystagmus. Spontaneous nystagmus is nystagmus
that occurs when the head is in the normal position and not moving. A
unilateral acute peripheral lesion often causes spontaneous nystagmus
with horizontal and rotational components. The fast phase is directed
away from the side of the lesion. Spontaneous nystagmus resulting from
a peripheral lesion is strongly inhibited by visual fixation. Unless the
patient is seen within the first few days of the occurrence of the lesion,
spontaneous nystagmus is often absent because of compensation. Spon-
taneous nystagmus of central origin is usually purely vertical, horizontal,
or rotational, as pathways for these vestibulo-ocular movements separate
beginning at the vestibular nuclei. 6 Vertical spontaneous nystagmus indi-
cates a central lesion. Spontaneous nystagmus is usually not a feature of
bilateral vestibular disease.
Positional Nystagmus. Positional nystagmus refers to nystagmus
that is present only when the head is placed in an unusual position, for
example, extended or upside down. Because spontaneous nystagmus
often resolves within several days, the examiner should always attempt
to induce positional nystagmus by extending the head and placing the
patient in left lateral, right lateral, and dorsal recumbency. The presence
of positional nystagmus indicates vestibular dysfunction but does not
further localize the lesion, as it can occur with central or peripheral
lesions. 6 Nystagmus that changes direction with differenthead positions
is most commonly seen with central lesions, however. Positional nystag-
mus is usually absent with bilateral lesions. .
Pendular Nystagmus. Pendular nystagmus refers to nystagmus that
does not have a fast and slow phase-the eyes move with equal speed
in either direction. Spontaneous pendular nystagmus is often caused by
a congenital abnormality in the visual pathways, most commonly in
oriental breeds of cats such as the Siamese and Himalyan. 34 It is im-
portant to recognize pendular nystagmus and realize that it is not a sign
of vestibular disease.
In summary, the presence of either spontaneous or positional jerk
nystagmus is always abnormal and usually indicates vestibular dysfunc-
tion. With peripheral vestibular disease, the nystagmus is either hori-
VESTIBULAR DYSFUNCTION 235
zontal or rotational and the fast phase is directed away from the side of
the lesion. With central vestibular disease, the nystagmus may be in any
direction (including vertical) and may change direction with changes in
the position of the head. In other words, vertical nystagmus or nystag-
mus that changes direction with different positions of the head indicates
a central lesion. Animals with bilateral vestibular disease do not have
spontaneous or positional nystagmus.
Strabismus
DIAGNOSTIC ASSESSMENT
Otitis Media-lnterna
Figure 1. CT of otitis media in a dog with ataxia and a head tilt to the right. On this
transverse image, there is increased density within the right tympanic bulla.
Nasopharyngeal Polyps
Figure 2. Nasopharyngeal polyp in a cat. A, There is a smooth, pale mass (arrow) in the
nasopharynx. B, The excised mass showing the stalk (arrow) that was attached to the
tympanic bulla. SP = soft palate; T = tongue.
Hypothyroidism
Hypothyroidism can cause peripheral vestibular dysfunction in
dogs. 33 The onset of signs may be acute or chronic. Affected dogs also
may have unilateral or bilateral facial paresis, lethargy, and generalized
weakness; however, vestibular dysfunction is often the only clinical sign,
and obvious signs of hypothyroidism may be absent. Diagnosis is based
on laboratory evaluation of thyroid function and response to thyroid
supplementation. Vestibular dysfunction typically resolves within 2
months of treatment. 33
Neoplasia
Neoplasia originating in the ear canal can cause peripheral vestibu-
lar dysfunction in dogs and cats. Examples include squamous cell card-
240 THOMAS
Ototoxicity
Figure 3. Skull radiograph of squamous cell carcinoma of ear in a dog with ataxia, right
head tilt, and pain on opening the mouth. On this rostroventral-caudodorsal open-mouthed
view, there is lysis of the right tympanic bulla and petrous temporal bone. Compare to the
normal left tympanic bulla (arrows).
VESTIBULAR DYSFUNCTION 241
Rickettsial Encephalitis
Neurologic abnormalities are seen in about 40% of dogs with Rocky
Mountain spotted fever (RMSF) and 20% of dogs with ehrlichiosis. 29
Many affected dogs also have lethargy, fever, and thrombocytopenia.
Leukocytosis is more common with RMSF, and ehrlichiosis is more likely
to cause leukopenia and anemia. On CSF analysis, RMSF may cause
a neutrophilic pleocytosis and mildly elevated protein concentration,
although ehrlichiosis is more likely to cause a mononuclear pleocytosis
and markedly elevated protein concentration. Diagnosis of RMSF is
based on a rise in serum antibody concentration in acute and convales-
cent samples. A single positive IgG titer is usually sufficient to diagnose
ehrlichiosis. Treatment of either disease consists of administering doxy-
cycline (5 mg/kg orally twice daily) or chloramphenicol (50 mg/kg
orally every 8 hours) for 2 to 3 weeks. The prognosis is generally good
with prompt treatment, although neurologic deficits may progress or
persist, despite treatment.l 4
Fungal Encephalitis
Cryptococcosis is the most common fungus to involve the nervous
system of dogs and cats. Affected animals may have involvement of
other organ systems such as the eyes, nose, or skin. Results of CSF
analysis are variable, but organisms may be identified on cytology.
Detection of cryptococcal capsular antigen in serum or CSF is also
helpful in the diagnosis. The recommended treatment is fluconazole (5
mg/kg orally twice daily). Therapy should be continued for at least 6
months to prevent relapse?, s, 26,6 7
Blastomycosis occasionally involves the central nervous system. Af-
fected animals usually have evidence of involvement of other organs
such as the lungs, eyes, skin, or lymph nodes. There may be a neutro-
philic pleocytosis on CSF analysis. Definitive diagnosis is best made by
identifying organisms in extraneural tissue such as lymph nodes. Serum
antibody titers are also helpful. Treatment with itraconazole or ampho-
tericin B can be attempted, but the prognosis for blastomycosis that
involves the nervous system is poor. 3' 41
Coccidiomycosis should be considered in animals with a history of
being in the southwestern United States. Most affected dogs do not have
obvious signs of extraneural involvement. On CSF analysis, there may be
a neutrophilic or mixed (mononuclear cells and neutrophils) pleocytosis.
Serology is also helpful in the diagnosis of coccidiomycosis. Treatment
consists of long-term administration of fluconazole (5 mg/kg orally
244 THOMAS
twice daily). Many dogs with relatively mild signs recover if treated
early. The presence of severe neurologic deficits warrants a guarded
prognosis. 4' 12
Granulomatous Meningoencephalomyelitis
Granulomatous meningoencephalomyelitis is an idiopathic disease
that results in inflammation of the central nervous system and occasion-
ally the eyes. Adult dogs are affected, and small breeds (terriers and
poodles) may be predisposed. Signs consist of an acute or chronic onset
of focal or multifocal neurologic deficits or signs of meningitis. 1' 15, 51, 59, 63
A tentative diagnosis is based on CSF findings and exclusion of infec-
tious causes of meningoencephalitis, but definitive antemortem diagno-
sis is difficult. A mononuclear pleocytosis with an increased protein
concentration is the most common CSF finding, but a predominantly
neutrophilic response also can occur. 5' 59, 6°CT or MR imaging may show
one or more contrast-enhancing masses.23, 44' 61 A definitive diagnosis
usually requires histopathologic examination of nervous tissue obtained
by biopsy or necropsy.
Signs often improve with 1 to 2 mg/kg of prednisone daily. The
dose is tapered gradually to establish the minimal effective dose. Radia-
tion therapy is successful in some patients and should be considered in
dogs refractory to corticosteroids. 47 Most patients improve with therapy,
but relapse is common, and many dogs are eventually euthanized be-
cause of neurologic disability. Some dogs do recover with therapy,
however. 47' 61
Neoplasia
Figure 5. MR imaging of a choroid plexus papilloma in a dog with ataxia, head tilt to the
left, and right hemiparesis (paradoxical vestibular syndrome). On this transverse plane, T1-
weighted image obtained after contrast administration, there is a homogeneously enhancing
mass (arrow) in the region of the right lateral aperture of the fourth ventricle (0.5 Tesla; TR
450 msec; TE 20 msec).
246 THOMAS
Metronidazole Toxicity
References
11. Burke EE, Moise NS, de Lahunta A, et al: Review of idiopathic feline vestibular
syndrome in 75 cats. JAVMA 187:941-943, 1985
12. Burtch M: Granulomatous meningitis caused by Coccidioides immitis in a dog. JAVMA
212:827-829, 1998
13. Cole LK, KwochkaKW, Kowalski JJ, et al: Microbial flora and antimicrobial susceptibil-
ity patterns of isolated pathogens from the horizontal ear canal and middle ear in
dogs with otitis media. JAVMA 212:534-538, 1998
14. Cormer KM: Rocky Mountain spotted fever. Vet Clin North Am Small Anim Pract
21:27-44, 1990
15. Cordy DR: Canine granulomatous meningoencephalomyelitis. Vet Pathol 16:325-333,
1979
16. Davis LE: Viruses and vestibular neuritis: A review of human and animal studies.
Acta Otolaryngol Suppl (Stockh) 503:70-73, 1993
17. Dow SW, LeCouteur RA, Poss ML, et a!: Central nervous system toxicosis associated
with metronidazole treatment of dogs: Five cases (1984-1987). JAVMA 195:365-368,
1989
18. Dubey JP: Neospora caninum: A look at a new Toxoplasma-like parasite of dogs and
other animals. Compend Contin Educ Pract Vet 12:653...{)63, 1990
19. Dubey JP, Greene CE, Lappin MR: Toxoplasmosis and neosporosis. In Greene CE (ed):
Infectious Diseases of Dogs and Cats. Philadelphia, WB Saunders, 1990, pp 818-834
20. Dubey JP, Carpenter JL, Topper MJ, et a!: Fatal toxoplasmosis in dogs. J Am Anim
Hosp Assoc 25:659...{)64, 1989
21. Dubey JP, Hattel AL, Lindsay DS, et a!: Neonatal Neospora caninum infection in dogs:
Isolation of the causative agent and experimental transmission. JAVMA 193:1259-
1263, 1988
22. Dubey JP, Carpenter JL, Speer JA, et al: Newly recognized fatal protozoan disease of
dogs. JAVMA 192:1269-1285, 1988
23. Dzyban LA, Tidwell AS: Imaging diagnosis-Granulomatous meningoencephalitis in
a dog. Vet Radio! Ultrasound 37:428-430, 1996
24. Fitch R, Moore M, Roen D: A warming to clinicians: Metronidazole neurotoxicity in a
dog. Prog Vet Neural 2:307-309, 1991
25. Foley JE, Lapointe J-M, Koblik P, et al: Diagnostic features of clinical neurologic feline
infectious peritonitis. J Vet Intern Med 12:415-423, 1998
26. Gerds-Grogan S, Dayreli-Hart B: Feline cryptococcosis: A retrospective evaluation. J
Am Anim Hosp Assoc 33:118-122, 1997
27. Gernandt BE: Vestibular mechanisms. In Field J (ed): Handbook of Physiology: Section
I: Neurophysiology. Washington, DC, American Physiology Society, 1959, pp 549-564
28. Glass EN, Cornetta AM, de Lahunta A, et a!: Clinical and clinicopathologic features in
11 cats with Cuterebra larvae myiasis of the central nervous system. J Vet Intern Med
12:365-368, 1998
29. Greene CE, Burgdorfer W, Cavagnolo R, eta!: Rocky Mountain spotted fever in dogs
and its differentiation from canine ehrlichiosis. JAVMA 186:465-472, 1985
30. Hass JA, Shell L, Saunders G: Neurological manifestations of toxoplasmosis: A litera-
ture review and case summary. JAm Anim Hosp Assoc 25:253-260, 1989
31. Herdman SJ: Role of vestibular adaptation in vestibular rehabilitation. Otolaryngol
Head Neck Surg 119:49-54, 1998
32. Hoskinson JJ: Imaging techniques in the diagnosis of middle ear disease. Semin Vet
Med Surg 8:10-16, 1993
33. Jaggy A, Oliver JE, Ferguson DC, et al: Neurologic manifestations of hypothyroidism:
A retrospective study of 29 dogs. J Vet Intern Med 8:318-336, 1994
34. Johnson BW: Congenitally abnormal visual pathways of Siamese cats. Com pend Contin
Educ Pract Vet 13:374-377, 1991
35. Kapatkin AS, Matthiesen DT, Noone KE, et al: Results of surgery and long-term follow-
up in 31 cats with nasopharyngeal polyps. J Am Anim Hosp Assoc 26:387-392, 1990
36. Kirpensteijn J: Aural neoplasms. Semin Vet Med Surg 8:17-23, 1993
37. Kline KL, Joseph RJ, Averill DA: Feline infectious peritonitis with neurologic involve-
ment: Clinical and pathological findings in 24 cats. J Am Anim Hosp Assoc 30:111-
118, 1994
248 THOMAS
38. Knowler C, Skerritt G: How do I treat? Canine neosporosis and toxoplasmosis. Prog
Vet Neural 5:167-169, 1994
39. Kraft SL, Gavin PR, DeHaan CE, eta!: Retrospective review of 50 intracranial tumors
evaluated by magnetic resonance imaging. JVet Intern Med 11:218-225, 1997
40. Krakowka S, Olsen R, Confer A, et a!: Serologic response to canine distemper viral
antigens in gnotobiotic dogs infected with canine distemper virus. JInfect Dis 132:384-
392, 1975
41. Legendre AM, Rohrbach BW, Toal RL, et a!: Treatment of blastomycosis with itracona-
zole in 112 dogs. JVet Intern Med 10:365-371, 1996
42. Little CJL, Lane JG: An evaluation of tympanometry, otoscopy and palpation for
assessment of the canine tympanic membrane. Vet Rec 124:5-8, 1989
43. Little CJL, Lane JG, Pearson GR: Inflammatory middle ear disease of the dog: The
pathology of otitis media. Vet Rec 128:293-296, 1991
44. Lobetti RG, Pearson J: Magnetic resonance imaging in the diagnosis of focal granulo-
matous meningoencephalitis in two dogs. Vet Radio! Ultrasound 37:424-427, 1996
45. Love NE, Kramer RW, Spodnick GJ, et a!: Radiographic and computed tomographic
evaluation of otitis media in the dog. Vet Radio! Ultrasound 36:375-379, 1995
46. Moore MP, Bagley RS, Harrington ML, eta!: Intracranial tumors. Vet Clin North Am
Small Anim Pract 26:759-777, 1996
47. Munana KR, Luttgen PJ: Prognostic factors for dogs with granulomatous menin-
goencephalomyelitis: 42 cases (1982-1996). JAVMA 212:1902-1906, 1998
48. Peppard SB: Effect of drug therapy on compensation from vestibular injury. Laryngo-
scope 96:878-898, 1986
49. Remedios AM, Fowler JD, Phar JW: A comparison of radiographic versus surgical
diagnosis of otitis media. JAm Anim Hasp Assoc 27:183-188, 1999
50. Roberts TDM: Neurophysiology of Postural Mechanisms. London, Butterworths, 1978
51. Sarfaty D, Carrillo JM, Greenlee PG: Differential diagnosis of granulomatous meningo-
encephalitis, distemper, and suppurative meningoencephalitis in the dog. JAVMA
188:387-392, 1986
52. Saxon B, Magne ML: Reversible central nervous system toxicosis associated with
metronidazole therapy in three cats. Prog Vet Neural 4:25-27, 1993
53. Scagliotti RH: Comparative neuro-ophthalmology. In Gelatt KN (ed): Veterinary Oph-
thalmology, ed 3. Philadelphia, Lippincott, 1999, pp 1307-1400
54. Schunk KL: Disorders of the vestibular system. Vet Clin North Am Small Anim Pract
18:641-665, 1988
55. Schunk KL, Averill DR: Peripheral vestibular syndrome in the dog: A review of 83
cases. JAVMA 182:1354-1357, 1983
56. Shapshak P, Graves MC, Imagawa DT: Autologous and allogenic antibody responses
to canine distemper virus isolates from dogs with chronic neurological diseases. Viral
Immunol1:45-52, 1987
57. Shell LG: Canine distemper. Compend Cantin Educ Pract Vet 12:173-179, 1990
58. Sims MH: Evoked response audiometry in dogs. Prog Vet Neural 1:275-283, 1990
59. Sorjonen DC: Clinical and histopathological features of granulomatous menin-
goencephalomyelitis in dogs. JAm Anim Hasp Assoc 26:141-147, 1990
60. Sorjonen DC: Total protein, albumin quota, and electrophoretic patterns in cerebrospi-
nal fluid of dogs with central nervous system disorders. Am JVet Res 48:301-305, 1987
61. Speciale J, Van Winkle TJ, Steinberg SA, eta!: Computed tomography in the diagnosis
of focal granulomatous meningoencephalitis: Retrospective evaluation of three cases. J
Am Anim Hasp Assoc 28:327-332, 1992
62. Summers BA, Greisen HA, Appel MJG: Canine distemper encephalomyelitis: Variation
with virus strain. J Camp Pathol 94:65-75, 1984
63. Thomas JB, Eger C: Granulomatous meningoencephalomyelitis in 21 dogs. J Small
Anim Pract 30:287-293, 1989
64. Thomas WB: What is your diagnosis? (Feline infectious peritonitis virus encephalitis.)
Prog Vet Neural 6:35-37, 1995
65. Thomas WB, Sorjonen DC, Steiss JE: A retrospective evaluation of 38 cases of canine
distemper encephalomyelitis. JAm Anim Hasp Assoc 29:23-28, 1993
VESTIBULAR DYSFUNCTION 249
66. Thomas WB, Wheeler SJ, Kramer R, et al: Magnetic resonance imaging features of
primary brain tumors in dogs. Vet Radio! Ultrasound 37:20-27, 1996
67. Tiches D, Vite CH, Dayrell-Hart B, et al: A case of canine central nervous system
cryptococcosis: Management with fluconazole. J Am Anim Hosp Assoc 34:145-151,
1998
68. Tipold A: Diagnosis of inflammatory and infectious diseases of the central nervous
system in dogs: A retrospective study. J Vet Intern Med 9:304-314, 1995
69. Tipold A, Vandevelde M, Jaggy A: Neurological manifestations of canine distemper
infection. J Small Anim Pract 33:466-470, 1992
70. Turrel JM, Fike JR, LeCouteur RA, et al: Computed tomography characteristics of
primary brain tumors in 50 dogs. JAVMA 188:851-856, 1986
71. Zee DS: Perspectives on the pharmacotherapy of vertigo. Arch Otolaryngol 111:609-
612, 1985
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