Disease in Dogs

Vestibular Disease in Dogs

Syndrome Vestibular consists of a set of signs include:
-Roll or fall to one side
-Loss of ability to extensor muscles ipsilateral to the lesion.

The function of the vestibular system is to harmonize the movements of the head from the body, altering the position of the eyes, trunk and limbs, helping to maintain balance. Signs of vestibular dysfunction are well understood by knowing the functional anatomy of the vestibular system. This system works as a true reflex arc. Thus this reflection is constituted as follows:

-Receptor (inner ear)
-Afferent pathway or vestibulocochlear nerve (VIII pair)
-Central core or vestibular nucleus (located in the brainstem)
-Via efferent tract (anterior and posterior half)
-Effectors (muscles and extensor muscles of the eyeball)

Vestibular Disease

Receptors are located in ear labyrinthine internal structure called membranous utricle, saccule and the 3 semicircular canals, these are located within the temporal petrous bone of the skull and has within it a fluid called endolymph. These receptors are stimulated by movements of the endolymph. The utricle and saccule movements are stimulated in linear acceleration and deceleration of the head and the 3 semicircular canals to angular movements of acceleration and deceleration. Stimulation above, follows a strict and very fine control assumed by ciliated epithelial cells located in these labyrinthine structures. The cilia of the utricle and saccule are arranged in various directions towards the endolymph. These also are embedded in a gelatinous structure called the macula. The macula has calcium carbonate crystals or otoliths that will eventually induce the action potential to be touched by cilia. Free axons of the vestibular nerve are located between the cilia and thus respond to different stimulation patterns with respect to the movement endolínfico cilium.

The cilia of the semicircular canals are not available equally. These are embedded in a parallel position with respect to each other. These are called stereocilia. Exist, as opposed to the utricle and saccule longer called a polar cilium called cinocilio. Stimulation patterns induce opposite movements of the stereocilia toward the cinocilio. Similarly, a conduction block of information would occur when the stereocilia away from the cinocilio.In this way, it achieves a beautiful harmony between anatomical structures and the nervous system which leads to define and encode in a very precise movement of the head with respect to the body.

Afferent pathway or route by which information travels in recipients achieved, constitutes the vestibular nerve (8 th pair). Sensory endings are, as mentioned above, intertwined around structures containing labyrinthine receptors. Detects changes in stimulation and transmitted to the central nervous system or central core.The center corresponds to the Nucleus Vestibular Integrator, located in the wall of the fourth ventricle. This ends many vestibular nerve fibers and other fibers pass through the vestibular nucleus and enter the cerebellum by synapses with the fine control area of the vestibular system, the core flocculonodular cerebellum

Vestibular Disease


When the vestibular system is defective in uni-or bilateral, are the signs of vestibular syndrome. This refers vital that if the lesion is bilateral, only get a pendulum motion of the head without the characteristic signs of the syndrome mentioned above. In a normal animal, during movement of the head, eyes diverted to the opposite side of the direction you turn your head and then quickly return to that address. This occurs several times while the head is rotated, causing physiological vestibular nystagmus with a slow to fast component. Turning the head to the right, the corresponding semicircular canal on the right side is stimulated, and left semicircular canal is inhibited. The impulses travel from the receivers via the vestibular nerve to the vestibular nucleus and then go up the median longitudinal fasciculus ascending. The oculomotor nucleus (3 rd pair) ipsilateral stimulated, which contracts the medial rectus muscle of the right eye, bypassing the left eyeball. Simultaneously, the core of the abducted (6 th pair) also stimulated contralateral, which contracts the contralateral rectus muscle of the eye, diverting the left eyeball. This will produce the slow component of nystagmus. Then the eyeballs return rapidly to the right by central compensatory mechanisms (Fig. 4).Product of different diseases affecting the vestibular system, the affected side is less active and produced normal nystagmus, has a fast component (compensation) to the opposite side of the lesion, and the slow component is toward the side of the lesion.

Some axons of the vestibular nuclei project to the reticular formation and the nucleus emetic. The imbalance or vestibular stimulation produce excessive vomiting and other signs of sickness. Symptoms of disease to other neuroanatomical structures located in the vicinity of the vestibular system, are a boon to the location of the lesion within the nervous system. The facial nerve fibers (7 th pair) and the sympathetic innervation of the eye passes through the middle ear, Int. Lesions middle ear alone will not produce vestibular signs.If the middle ear and inner ear are affected simultaneously by infection, trauma or neoplasm, cause one or more of the signs of vestibular syndrome and additionally, facial paralysis and Horner syndrome (miosis, ptosis, prolapsed third eyelid). Many other anatomical structures are located in the brainstem in the region vestibular nucleus. The condition of the cerebellar peduncle produces:

-Ipsilateral dysmetria characterized by hypermetria or “stop step”
-Unconscious proprioception disorders (ataxia)
-Intentional tremor of the head
-Lack of response to the threat

CLASSIFICATION OF vestibulopathies

Vestibular disease is categorized as anterior if peripheral structures involved are hearing and vestibular nerve (8 th pair) and if they affect the central vestibular nuclei in the brainstem. The disease occurs primarily peripheral bacterial otitis commit to the inner ear, tympanic bulla trauma and nerve tumors or bone structure.The main causes of disease are neoplasms, inflammatory processes (distemper, granulomatous meningoencephalitis) or bleeding in the trunk involving the vestibular nucleus.


Physical Examination:

On examination of the external auditory canal on both sides, the tympanic membrane must be intact. Palpate the pharynx and examine it for any signs of inflammation, which can climb the auditory tube into the middle ear and inner ear affect continuity. Carefully palpate the area of the bulla bone to look for inflammation or pain.Reacuérdese in some trauma patients with TBI may compromise the integrity of the noise.

Neurological Exam:

You must analyze the positions of the head and members with respect to the trunk, position of the eyeball, proprioception, and gait. Here are neurological signs that differentiate a peripheral vestibular disorder of the central one.

Mechanisms of the disorder:

-Congenital disorders and family (congenital or idiopathic vestibular disorders)
-Infections (middle ear)
-Toxicity (aminoglycoside antibiotics)
-Nutritional Disorders (thiamine deficiency)
-Trauma and vascular lesions (cranial trauma, hemorrhage or infarction)
-Neoplasms (meningioma, astrocytoma, oligodendroglioma)


You suspect this condition in purebred animals, from birth to twelve weeks of age develop symptoms of an acute peripheral vestibular system disease, head tilt, roll, ataxic and have no history of trauma, external otitis , pharyngitis, generalized disease or treatment with antibiotics. Litters of breeds German Shepherd, Doberman Pinschers, Beagles and Siamese cats have been affected. The prognosis is favorable as they can get to compensate for deficiencies between 2 and 4 months old.


The middle ear infections and inner ear are the most common cause of peripheral vestibular inflammation in neurological casuistry. It can affect dogs and cats of any age, race or sex. There predisposition in breeds hanging ears, which develop chronic external otitis, bacteria, parasites and fungi. These otitis may even perforate the eardrum and cause infection of the middle ear and inner ear. At neurological examination, presentation of the signs depend on the severity and extent of the injury. Unilateral paralysis of the facial nerve is often seen in middle ear disease or the petrous temporal bone, as Horner’s syndrome. Medical treatment is performed in animals with normal tympanic membranes and slight peripheral vestibular disorders: use of antibiotics (if possible with antibiograms) In many cases they have been effective association of cephalosporins with cotrimoxazole for 45 days. The prognosis for recovery is favorable. The surgical drainage treatment is performed in cases of clear exudate and thickening of the wall of the tympanic bulla and unresponsive to conventional medical treatment. In the feline vestibular syndrome can develop when the ensuing chronic tonsillitis and pharyngitis. In these cases the extent of inflammation is through the tube or auditory tube into the middle ear and inner ear. Multifocal CNS infections can affect the central vestibular structures: These are the classic case of neurological distemper, infectious canine hepatitis and feline infectious peritonitis.


With aminoglycoside antibiotics (streptomycin, neomycin, kanamycin, gentamicin), prolonged and high doses, can cause degeneration of the vestibular and auditory systems. Signs are produced unilateral peripheral vestibular and head tilt. Degenerative changes are usually found at the receptor level of the inner ear lobe and cerebellum flocculonodular. You have to remove the drug, whereas deafness would irreversible.


In cats that were fed only raw fish containing thiaminase or in cases where there is a severe and chronic anorexia may also develop signs of vestibular syndrome. They usually show signs of central vestibular disease, and cerebellar bilateral cerebrocortical necrosis. As treatment is administered 10 to 100 mg of thiamine IM every 24 hours for several days.


The possibilities that cause neoplastic vestibular signs correspond to sheath neoplasms (neurofibrosarcomas, neurinomas, schwannomas), and meningiomas affecting the vestibular nerve. Animals are usually adults, which are characterized by progressive start showing signs of peripheral vestibular disease.


Traumatic disorders that compromise the integrity of the tympanic bulla and / or temporal petrous give rise to the presence of vestibular signs of flare-ups. Neurological examinations and radiographic diagnosis will approach. A otorrhagia eardrum with structural compromise of the commitment will make us think about traumatic noise.


Idiopathic diseases are by far the most common cause in dogs and cats with vestibular syndrome, then logically, the inner ear. There are severe, abrupt onset of vestibular signs, which improved rapidly within 72 hours and return to normal within 1 to 2 weeks. This entity is common in senile dogs (over 8 years old) and adult cats. The prognosis is good and just wait for his recovery. These patients are treated with calcium channel blockers or specific cholinergic receptors as difenidol or antihistamines such as meclizine which decreases the sensation of vertigo and tilt to the side of the condition.


Treatment of vestibulopathies depends exclusively on the etiology. Undoubtedly those of central origin as ischemic, can be treated only signs that are uncomfortable to the patient through the use of calcium channel blockers such as flunarizine or cinnarizine. It has also been successful to prescribe specific anticholinergic drugs (difenidol) for decrease the sense of vertigo and / or dizziness in these patients. This directly affects the genesis of vomiting, which worsen the clinical situation.In those vestibulopathies peripheral exudative, as in the case of internal ear infections, applying sulfa antibiotics such as cephalosporins and quinolones given for a minimum of 45 days, are of great help. However, when observed radiographic signs of chronic disease, such as thickening of the wall of the bulla, decompressive surgery would be the best indication.

About Dr. Winnie 986 Articles
My name is Dr. Winnie. I earned a Bachelor of Science in Psychology from Duke University, a Masters of Science in Biology from St Georges University, and graduated from the University of Pretoria Veterinary School in South Africa. I have been an animal lover and owners all my life having owned a Rottweiler named Duke, a Pekingese named Athena and now a Bull Mastiff named George, also known as big G! I'm also an amateur equestrian and love working with horses. I'm a full-time Veterinarian in South Africa specializing in internal medicine for large breed dogs. I enjoy spending time with my husband, 2 kids and Big G in my free time. Author and Contribturor at SeniorTailWaggers, A Love of Rottweilers, DogsCatsPets and TheDogsBone

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