VESTIBULAR DYSFUNCTION:
All veterinary species suffer from various forms of vestibular disease. Many of which
require only recognition, while others represent significant diagnostic challenges.
Although
there are a number of diseases which can affect the vestibular system, generally we can break
them down anatomically into peripheral and central disorders.
With certain exceptions,
peripheral diseases bear a better prognosis in most species than central vestibular disease.
Partially due to this concern, vestibular diseases represent a large number of neurologic referrals.
Often, it is only reassurance that the problem will pass that is necessary. Recognition of when to
intervene is as important as when not too.
The cardinal signs of unilateral vestibular disease are head tilt, nystagmus (spontaneous
abnormal eye movements), circling (toward the lesion in “tight” circles), and incoordination.
This is because the vestibular system is an important part of the CNS balance control system.
In
order for animals to know how they are oriented in space, three neural systems must be
functioning. The vestibular system, through the stimulus-response of the hair cells in the
semicircular canals, reacts to angular acceleration and deceleration. The visual system allows
the animal to focus on the horizontal and vertical, orienting in space. Finally, gravity is detected
by pressure receptors in the skin, orienting the animal on up and down. While the vestibular
system is a very important, it requires at least 2 of these orienting systems to function for the
animal to negotiate within its environment. This can be important with vestibular disease, since,
in acute disease, the nystagmus prevents the eyes from focusing on the horizon, effectively
eliminating spacial orientation.
The anatomic structures involved in the vestibular system include the hair cells in the
saccule and utricle (containing the semicircular canals), the vestibular portion of CN VIII, the
vestibular nuclei in the brainstem and the flocculonodular lobe of the cerebellum. The vestibular
nuclei send fibers forward in the medial longitudinal fasciculus (MLF) which coordinates ocular
movements, projects fibers to the spinal cord as the vestibulospinal tract and descending MLF,
projects fibers to the cerebellum, and sends fibers to various structures in the brainstem including
the emetic center. Involvement of any of the portions of the vestibular system will result in signs
of disfunction. Most lesions result in loss of function and, hence, are ablative in nature. The
signs develop due to the imbalance existing between the normal and abnormal sides.
The nystagmus seen in vestibular disease can be helpful in localizing the disease
process. While horizontal and rotatory nystagmus can be seen with disease anywhere within the
vestibular system, vertical and positional nystagmus are almost exclusively seen with central
vestibular diseases. Moreover, horizontal nystagmus from peripheral vestibular disease
oscillates with the fast-phase away from the direction of the head tilt. With central vestibular
disease (particularly of the cerebellum), however, the fast-phase is toward the lesion. So
although horizontal and rotatory nystagmus are not specific for peripheral disease, they are
compatible with it. Vertical and positional nystagmus suggest the lesion is within the CNS and
indicate the need for a thorough neurologic work-up.
Vestibular diseases can be classified into three major disease processes: idiopathic
vestibular disease, inner ear disease, or central vestibular disease. The former 2 represent
common forms of peripheral vestibular disease which need to be separated from each other and
from central vestibular disease.
Idiopathic Vestibular Disease:
All cranial nerves have the potential to develop specific syndromes which are clinically
classified as idiopathic disorders. This is probably due to the fact that each cranial nerve
represents a unique developmental anatomy from their respective brachial arches. This also
gives them an unique antigenic signal allowing very specific immune attack upon them.
Idiopathic vestibular disease represents one of this cranial nerve syndromes.
Clinically, idiopathic vestibular disease presents as an acute onset of vestibular signs with
severe imbalance, due to its sudden onset and the severe nystagmus which is associated with the
onset of the disorder. Since the eyes are unable to fix on the horizon and the vestibular
mechanism is defective, there is severe vertigo. This often results in the rolling and rolling
described by the owners. This can be mistaken for a seizure, which it is not. During the early
phases of idiopathic vestibular disease, the patient often experiences nausea to the point of frequent vomiting and inappetence. The head tilt will be toward the side of dysfunction and the
nystagmus will be horizontal or rotatory with the fast-phase away from the head tilt. If
supported, there are no other neurologic deficits and proprioception is normal.
The diagnosis of idiopathic vestibular disease is tentatively made by the presence of
acute clinical signs in the absence of other physical findings. The minimum data base include
physical examination, otoscopic examination and neurologic examination. The lack of findings
(other than the peripheral vestibular signs) supports the diagnosis. The signs of idiopathic
vestibular disease are regressive, meaning that they disappear without treatment over time. As
such, the fact that the disease is self-limiting is how the final diagnosis is achieved. The
nystagmus will usually improve or disappear all together within 3-5 days of the onset. The
patient will, then, improve in their imbalance and be more able to function normally. This
improvement will continue until minimal deficits will remain. It is possible that there will be a
residual head tilt. If the head tilt persists beyond 6 months following the onset of signs, it is
likely to permanent.
There is no treatment which will hasten the recovery from idiopathic vestibular disease.
Corticosteroids probably do not offer an effective treatment. On the other hand, since idiopathic
vestibular disease may represent an immune disease, anti-oxidant steroids (such as Solu Medral)
may decrease severe symptoms. During the early phases, anti-vertigo drugs might make the
patient more comfortable. Generally, I use diphenhydramine at 2-4 mg/kg every 8 hours as
needed. Diphenhydramine is a centrally active anticholinergic, antihistamine which helps reduce
vertigo and nausea. Assuming that the regressive course becomes evident, then I monitor the
patient periodically for the signs of continued improvement.
Antidotal evidence suggests that idiopathic vestibular disease may represent toxicity to
eating certain strains of lizards. Owners often notice the cat with a lizard in its mouth just prior
to the onset of clinical signs. However, experimental feeding of the suggested lizard species to
cats does not lead to the disease. It is still possible that laboratory conditions do not mimic field
conditions. On the other hand, idiopathic vestibular disease occurs in many animals and in
animal species where exposure to lizards plays not role in the condition. It is most likely that
idiopathic vestibular disease is an immune-related condition affecting the unique antigens
presented by the vestibular nerve. It can recur and is often more severe on recurrence.
Idiopathic vestibular disease represents an acute invasion of wind (heat)
into the inner ear. This may be secondary to an external pathogen or secondary to internal winds
from the liver. Nystagmus is a wind signs affecting the eyes which are under the control of the
liver. The liver is directly associated with the external ear via its husband-pair, the gall bladder
whose meridian passes the ears several times. The triple heater is also associated with the ear in
that its meridian wraps around the ear. The kidney is also important for the neural functions
(vestibular and hearing) of the ears and is associated with the ear through its husband-pair, the
bladder whose meridian runs just above the ears. In addition, the heart is associated with the ears
through its husband-pair, the small intestines, whose meridian ends in front of the ears. Ear
problems can result in shen disturbance either by disruption of liver blood or by insult of the
heart directly through the small intestine channel.
When wind invades the ear, there are local changes leading to imbalance and abnormal
eye movements. This leads to shen disturbance and disrupts qi flow. The disruption of qi flow
leads to perversion of stomach qi (probably from over-control of the liver on the stomach)
leading to nausea and vomiting. Due to the acute nature, signs are very dramatic, but
acupuncture can also be very helpful.
Treatment Principle: Clear wind and heat and calm the shen.
Acupuncture Therapy: Clear wind and heat (GB-20, LI-4, LI-11, GV-14). Calm the
shen (PC-6, HT-7, GV-17, GV-20, GV-21). Local points (TH-18, TH-18, TH-21, SI-19, GB-2,
er jian, an shen). Channel points (TH-4, SI-3, BL-66, GB-41, GB-43, LIV-3). Also add
constitutional points and points for specific deficiencies or excesses seen.
Herbal Therapy: Since this is an acute, regressive disease, no herbal support is
likely to be as helpful as acupuncture. Once the signs have begun to clear, any underlying excess
or deficiency can be treated appropriately.
Inner Ear Disease:
Many different problems result in inner ear disease; however, the clinical signs caused by
these diseases are similar, indicating the location of the disease rather than the specific cause.
These signs are those of peripheral vestibular dysfunction, including head tilt, nystagmus,
circling and imbalance.
On the other hand, since the diseases which cause inner ear disease are
usually slower in evolution, these signs are generally less severe than with idiopathic vestibular
disease. In addition to the vestibular signs, there are also varying degrees of facial nerve
dysfunction and often Horner’s syndrome.
Anatomically, the facial nerve and the sympathetic
fibers heading to the eye pass near the inner ear in the osseous petrous temporal bone. Damage
of these neural structure, in addition to the damage of the vestibular nerve is a hallmark for inner
ear disease. It is possible to affect both the facial and vestibular nerves together in the
calivarium, but it is rare to see Horner’s syndrome from central nervous system disease.
As
such, Horner’s syndrome suggests that the disease in process is in the peripheral C8-T2 nerve
roots, the vagosympathetic trunk, the inner ear or within the orbit. When Horner’s syndrome is
seen in combination with vestibular disease and facial nerve disease, the location must be in the
peripheral vestibular system in the region of the osseous petrous temporal bone.
The signs of facial nerve dysfunction include paresis or paralysis of the muscles of facial
expressions (lack of ear movement, lack of blink and lack of buccal muscle reaction on
palpation). This leads to deficiency of the vibrissa reaction, decreased to absent menace
response and diminished to absent palpebral response. In addition, the facial nerve supplies
parasympathetic innervation to the lacrimal gland of the eye. As such, peripheral facial nerve
disease can lead to diminished tear production in the eye on the affected side. This can be rather
catastrophic in inner ear disease where the facial nerve dysfunction results in the inability to
close the eye, while also decreasing tear production. As such, every dog with inner ear disease
should have a Schirmer’s tear test run on the eyes and appropriate treatment instituted if tear
production is deficient.
Horner’s syndrome varies among species. In small animals the ocular signs predominate,
including myosis, ptosis and enophthalmos. In horses, the signs of Horner’s syndrome are
expressed primarily as excessive sweating on the affected side of the face. In cattle, there is a
lack of sweating on the muzzle of the affected side.
The most common cause of inner ear disease in all species is secondary in inner ear
infection. Most of these represent bacterial extension from otitis media which can arise from
hematogenous spread from bacteremia or from spread up the eustachian tube to the middle ear.
Luckily, these infections, once recognized, can often be successfully treated. Other causes of
inner ear disease may not be treatable, including fungal infections and neoplasia.
Therefore, it is
generally best to “treat-for-the-treatable” when dealing with inner ear disease, using appropriate
antibiotic therapy.
The minimum data base for diagnosis of inner ear disease includes physical and
neurologic examination, Schirmer’s tear test, otoscopic examination (with culture of the external
ear canal, if indicated), pharyngeal examination, CBC and urinalysis. If there is evidence of
cardiac murmur, then cardiac ultrasound should be performed. Skull radiographs are then
necessary to evaluate the degree of change in the osseous structures of the inner ear.
This will be
helpful in making the diagnosis and in monitoring the response to treatment.
The treatment of bacterial inner ear infection must consider the fact that the disease
represent bone infection. As such, the antibiotic must be able to penetrate bone, develop good
tissue concentrations (including the blood-ear barrier) and, preferably, be bactericidal in action.
Many veterinarians use enrofloxacin as their antibiotic of choice. I find that enrofloxacin is
great for treating gram negative infections in the lung, but it may not reach tissue concentrations
within neural structures like the inner ear. It needs additional help to do this. Therefore, if I do
not use my treatment of choice, I will add a sulfa drug to enrofloxacin to take advantage of the
synergistic effect of sulfa drugs. My antibiotic regime of choice is cephalosporins and sulfa
drugs (sulfadimethozine) in combination. This meets the criteria for the ideal therapy for inner
ear disease. It is excellent in treating gram positive bacteria, which are the most common
organisms infecting the inner ear. Since this is a bone infection, the treatment must be continued
for 6-8 weeks, minimum. The most common cause of treatment failure is not treating long
enough.
Diagnosis and Treatment:
Inner ear disease represents a more chronic invasion of wind, heat and
damp into the ear. This is usually secondary to an external pathogen or can be secondary to
stagnation caused by chronic internal problems. However, unlike idiopathic vestibular disease
which is confined to the qi level, inner ear disease is usually deeper and involves the Ying and
xue (blood) stages. Overall, the same internal connections and meridians are involved in the
disease processes.
When wind and heat invades the ear, causing the initial signs. The heat boils the fluids
and leads to the accumulation of damp or phlegm. Alternatively, the qi and blood stagnate
leading to local heat which in turn leads to the accumulation of damp.
Treatment Principle: Quiet the wind, reduce the heat, disperse the damp, activate the blood to dissolve stagnation, and calm the shen.
Acupuncture Therapy: Clear wind and heat (GB-20, LI-4, LI-11, GV-14, ST-44). Calm
the shen (PC-6, HT-7, GV-17, GV-20, GV-21). Eliminate the damp and disperse the phlegm
(SP-9, ST-40). Activate the qi and blood (ST-36, Xin shu, SP-10, BL-17). Local points (TH-18,
TH-18, TH-21, SI-19, GB-2, er jian, an shen). Channel points (TH-4, SI-3, BL-66, GB-41, GB-
43, LIV-3). Also add constitutional points and points for specific deficiencies or excesses seen.
Herbal Therapy: Inner ear disease secondary to Damp-Heat shows the tongue is
red or purple with a yellow, greasy coating. The pulse is rapid (heat), wiry (liver) and slippery
(damp). You can use Long Dan Xie Gan Tang (Snake and Dragon) or Damp-Heat formula (bi
xie sheng shi tang). The former formula clears the heat, soothes the liver, and moves the damp
from the whole body, while the latter is more specific for the skin. If only the ears are involved,
you might try Ear itching formula which also soothes the liver, clears heat and helps resolve
stagnation, but contains an ear transporter (luo shi teng).
When the excess is secondary to blood stagnation (associated with swelling, structural
disease and pain). The tongue is usually pale or purple with a white greasy coating. The pulse is
wiry (liver) and slippery (damp). Treatment principles are to expel phlegm, extinguish the wind,
open the orifice and invigorate the blood. Use Ding Xian Wan and Tao Hong Si Wu San (moves
blood).
Once the excess is cleated, then you should look for any underlying deficiencies and treat
these until resolved. You may also want to use Ear drop formula to help treat the external signs
of ear infection. In addition, you can use a standard approach to treating and maintaining ears
using a series of natural products to clean the ears and protect against pathogenic invasion. The
general purpose of this procedure is to gently clean the ears, correct their pH to help prevent
microorganisms from invading and provide an antibacterial, antifungal, anti-inflammatory agent
to clear any existing problems. In the beginning, it may be necessary to use the solutions to clean
the ears three times a day. After the problem is under control, daily or biweekly cleansing may
be sufficient even in the worst initial cases. This should be used in conjunction with an
“Integrative Program” to help improve the animals ability to heal from the inside, as well.
The initial solutions should be instilled into the ear. The ear can be manipulated to work
the solution around in the ear canal. Then, the excess can be wiped away with a cotton ball.
Usually, the animal will help by shaking the head. It is not advisable to use cotton swabs in the
ear canal, unless specifically instructed to do so by your veterinarian, who has demonstrated the
technique for you. Use the solutions in sequence, since this is how they are designed to work.
The detergent solution gets rid of wax and debris. The vinegar solution adjusts the pH of the ear
to normal. The vitaminE/garlic oil helps treat and prevent infection. It should not be used if the
eardrum is ruptured.
Detergent Solution:
• 1 drop of “free” dishwasher soap
• 8 ounces of water
Vinegar Solution:
• 1 ounce apple cider vinegar
• 3 ounces of water
VitaminE/garlic oil:
• crush one clove of garlic (use press) into
• 1 ounce of extra virgin olive oil
• let sit overnight at room temperature
• pour oil into dropper container
• add content of a 1000 IU vitamin E capsule
• use 2-3 drops in the ear canals, plus 1-2 on the pinnae
Central Vestibular Disease:
Whenever anything else is seen other than the signs above, one must consider the
likelihood that the problem is due to central vestibular disease. Additional cranial nerve deficits,
proprioceptive deficits and motor deficits indicate brainstem damage affecting the vestibular
nuclei and sensor and motor pathways which course through the vestibular region of the
brainstem. In addition, the nystagmus seen in central vestibular disease will often be vertical or
positional in nature, supporting the location of the disease process within the brainstem or
cerebellum. If there is whole body and head tremors, the lesion is likely to be within the
flocculonodular lobe of the cerebellum. While diseases which affect the peripheral vestibular
system are usually good diseases; that is, diseases which regress without treatment or which
respond to appropriate antibiotic therapy, most central vestibular diseases carry a less optimistic
prognosis.
The major causes of central vestibular disease are inflammatory/infectious diseases or
neoplasia. Organophosphate intoxication, liver disease (with metabolic brainstem degeneration)
and thiamine deficiency can occasionally result in central vestibular disease (depending upon the
species of animal), but these causes are far less than the inflammatory or neoplastic causes. In
dogs, canine distemper virus, granulomatous meningoencephalitis, toxoplasmosis,
neosporidiosis, aspergillosis, cryptococcosis, steroid-responsive meningoencephalitis, Lyme’s
disease, Rocky Mountain spotted fever and ehrlichiosis are the most common inflammatory and
infectious diseases recognized. In the cat, FeLV, FIP, and cryptococcosis are the most common
infectious diseases. Any of the primary brain tumors can occur in dogs, while only meningiomas
are common in cats. Cats who are not eating and stressed can easily develop thiamine deficiency
and this should not be overlooked in treating sick cats with vestibular signs.
Diagnosis of central vestibular disease involves the minimal data based for inner ear
disease, but must be expanded to include a chemistry profile, a CSF tap and analysis (including
species specific titers) and, often, advanced brain-imaging techniques, such as MRI examination.
Since CSF cytology is important in assessing central vestibular disease and advanced imaging
techniques are needed, central vestibular disease crosses “the referral line”, the point in assessing
disease which may require the interaction or interpretation of a neurologist.
The treatment and prognosis for central vestibular disease depends upon the cause. In
neoplasia, biopsy may help determine whether radioablative surgery might be useful.
Unfortunately, the brainstem is not an area amenable to conventional neurosurgery. In small
animals, bacterial infections causing central vestibular disease is uncommon. Rickettsial
infection is also rare. In cats, cryptococcosis may respond to therapy whether with remission or
control of the neurologic signs. In dogs, fungal diseases usually progress in spite vigorous
treatment. Toxoplasmosis may be controllable for a period in the dog and treatable in the cat.
Canine distemper virus infection may run its course and stop or be chronic and progressive.
FeLV and FIP infections are generally, rapidly progressive. Granulomatous
meningoencephalitis (GME) will respond temporarily to corticosteroid therapy, but ultimately
progress. Steroid-responsive meningoencephalitis can be controlled with medication for long
periods in the dog. Finally, organophosphate intoxication and thiamine deficiency may respond
to appropriate therapy.
So, while central vestibular disease has many causes, in the absence of specific disease
processes, there is limited hope for successful treatment and that hope is often based upon the
response of the animal to medical management. The medical management is largely based upon
the responsiveness of the disease process to corticosteroids. In other words, there are many
causes of central vestibular disease, but often only one treatment approach. If the client
understands this, it is possible to treat central vestibular disease without a specific diagnosis,
realizing that the response to therapy can suggest whether the disease was “good” or “bad”. The
treatment approach that I use when a specific diagnosis cannot be made (either because the
patient is too ill to undergo the diagnostic test or the client cannot afford them) is to treat with
corticosteroids (usually oral prednisolone) and antibiotics (doxycycline and sulfadimethozine).
The prednisolone will reduce inflammation while the doxycycline can help control bacterial and
rickettsial disease while the sulfadimethozine may help control protozoal infection. I take a
more pro-active approach in cats, since toxoplasmosis and cryptococcosis might be treatable.
Therefore, I prefer to always perform CSF tap and analysis in cats with central vestibular
disease, particularly when they also exhibit active chorioretinitis. I also add parenteral thiamine
therapy when treating cats.
We have made important strides in understanding the breadth of central vestibular
diseases. There are new promising approaches which may help treat more of the diseases than
we have previously been able to treat. New antifungal drugs offer hope in controlling CNS
fungal infections. More potent cytotoxic drugs may help diminish the effects of GME in the
dog. Computer-Assisted Radioablative surgery offers hope in treating brainstem tumors. On the
other hand, we have a long way to go. These new methods are expensive and not always
available to every pet owner. We are, however, investigating whether natural medicine might be
useful adjunctive therapies in many vestibular diseases. These approaches might reduce the cost
and improve the outcome and prognosis for many patients.
Diagnosis and Treatment:
Central vestibular diseases like many other problems in the central
nervous system can be highly variable as to cause including excess conditions or deficiencies.
They can be inflammatory which is most likely secondary to invasion of external pathogens at the xue level and include wind, heat and damp or wind and cold. Blood stagnation can lead to
mass formation and cause central vestibular disease. Liver and kidney yin deficiency and kidney
jing deficiency also can lead to central vestibular problems. Therefore, you should identify what
you see (tongue and pulse) and treat accordingly. It can also help to know for sure what the
Western diagnosis is, since there are TCM herbal approaches that can be used based upon these
findings. In fact, I highly encourage traditional veterinarians to seek this information before
treating, as well.
Acupuncture Therapy: Based upon findings for constitutional issues, 8 principle and
Zang-Fu indications.
Herbal Therapy: Treat what you find.
fuente: UNIVERSIDAD DE FLORIDA (USA)
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