Vestibular Disorders and
the Cavalier King Charles Spaniel
- What It Is
- --idiopathic vestibular disease
- --benign paroxysmal positional vertigo
- --inner ear infections/inflammation
- --primary secretory otitis media
- --cerebellar infarcts (strokes)
- --inflammatory brain disease
- --nasopharyngeal polyps
- --intracranial neoplasia
- What You Can Do
- Research News
- Related Links
- Veterinary Resources
The vestibular system is a sensory system that enables the dog to coordinate and maintain its balance and stablize its eyes during movement of its head. The system is located in the vestibulum in the inner ear. It sends signals to the neural structures that control eye movements and to the muscles that keep the dog stable and upright. The system compensates the position of the dog's body for gravity and movement.
The components of the vestibular system are divided into peripheral (relating to the inner ear) and central components (relating to the brain stem). Therefore, vestibular disorders are distinguished between peripheral vestibular syndrome and central vestibular syndrome.
The main peripheral component of the vestibular system is a set of interconnected canals called “the labyrinth” (see drawing below). They contain sensory hair cells which convert physical motion, such as head movements, into neural impulses.
Vestibular syndrome (or dysfunction) is one of a few disorders which may be "idiopathic" (meaning that its cause is not known), or it may be the result of some other disease. Therefore, it is important to try to determine if there is an underlying disease causing the symptoms which constitute vestibular syndrome. Apart from idiopathic vestibular disease, the most common disorders causing vestibular symptoms in cavalier King Charles spaniels are: otitis media and/or otitis interna (or labyrinthitis), primary secretory otitis media (PSOM), cerebrovascular disease (cerebellar infarcts), and inflammatory brain disease (granulomatous meningoencephalomyelitis). Other causes include: nasopharyngeal polyps, intracranial neoplasia, and ototoxicity.
For those causes of vestibular syndrome other than the idiopathic variety, the diagnosis and treatment involve identifying and treating the particular disease causing the symptoms.
Idiopathic vestibular disease is the most common version of
peripheral vestibular disease in older dogs. It therefore also is
referred to as “old dog” or “geriatric” vestibular or even “Idopathic
Geriatric Vestibulitis”. The onset usually is
sudden, and symptoms typically include:
• A staggering or rolling gait (ataxia)
• Nystagmus (uncontrolled movements of the eyes, usually from side to side, or in a circular pattern)
• Strabismus (inability of the eyes to aim at the same point in space)
• Head tilt
• Falling down
Usually there is no facial nerve twitching or Horner's syndrome involved.
There is no effective medication to cure this idiopathic version. Nevertheless, improvement of symptoms usually occurs within days or a few weeks, with the nystagmus usually resolving earliest. Most dogs will make a full recovery although some may continue to have a slight head tilt.
While many veterinarians insist that idiopathic vestibular disease is, indeed, "idiopathic" -- meaning that it is a condition that appears to arise spontaneously or for which the cause is unknown -- it is very likely that many cases of idiopathic vestibular disease are, in fact, cases of benign paroxysmal positional vertigo (BPPV). BPPV occurs when microsized stones or granules -- actually calcium carbonate crystals called otoconia (right) -- become dislodged from the utricle, which is one of the inner ear sensory organs. (See the location of the utricle in the diagram above.)
These stones are embedded in a viscous fluid membrane which flows back and forth to stimulate a patch of sensory hair cells -- called the macula utricle -- to detect motion and orientation. The hair cells are weighted by the granules and membrane to provide a degree of inertia to enable the utricle to detect linear accelerations and head-tilts. When the head is tilted, gravity pulls on the gelatinous membrane, causing the hair cells to bend.
However, occasionally, one or more of these calcium granules become dislodged from the utricle and flow into one of the semicircular canals which sense the rotation of the head. Once in a canal, they may still move when the head changes position, but their movement can cause a false sense that the head and body are spinning around.
The diagnosis of BPPV is made by the characteristic symptoms and also by observing the nystagmus – the uncontrolled movements of the eyes, usually from side to side, or in a circular pattern. Then the veterinarian will conduct maneuvering tests such as the Dix - Hallpike maneuver and the side-lying maneuver, which involve protocols of postioning and then re-positioning the patient until the signs of nystagmus disappear.
As with idiopathic vestibular disease, BPPV also may resolve itself within a few days without any treatment. It is for this reason that idiopathic vestibular disease actually may be BPPV.
-- inner ear infections and inflammation (otitis media and otitis interna)
Otitis media and otitis interna are the medical terms used by veterinarians to describe an inner – or middle – ear infection (media) or inflammation (interna). They are the most common causes of peripheral vestibular disease in dogs.
Single-sided facial paralysis is the most common sign of a middle ear disorder. A myringotomy (incision of the ear drum) to obtain a sample of the infection material in the ear usually is necessary to determine the appropriate antibiotic to prescribe. Treatment with antibiotics for up to six weeks. If antibiotics are discontinued too soon, the symptoms and infection will recur and can be more difficult to treat. Corticosteroids are usually not required.
Primary secretory otitis media (PSOM) -- also known as "glue ear" or "middle ear effusion" or "otitis media with effusion" (OME) -- has been reported almost exclusively in cavaliers. It consists of a highly viscous mucus plug which fills the dog's middle ear and may cause the tympanic membrane to bulge. The mucus has also been referred to as "hyperintense material". It may result in symptoms of peripheral vestibular syndrome. PSOM is covered extensively as a separate topic here.
Cavaliers appear predisposed to develop cerebellar infarcts, or strokes. The affected dog may be behaving normally one minute, and then in an instant, become unsteady, un-coordinated, nauseous, walk uncontrollably in small circles, or even faint and fall over. The dog may tilt its head, have facial paralysis, lose its vision or control of its bowels, or change its temperament. Some symptoms may progress over the first twelve hours, presumably due to brain swelling, while others may disappear quickly. Most symptoms should begin to lessen within a day or two. All of these symptoms are consistent with central vestibular disorder.
In an August 2015 abstract, UK neurologists report finding cerebellar infarctions in 24 dogs, including 9 cavaliers, displaying ataxia (staggering or rolling gait), hypermetria (voluntary muscular movements tend to overreach their intended goals), head tilt, nystagmus (uncontrolled movements of the eyes), reduced postural reactions (e.g., replacing a foot after being lifted), and decreased menace response (eye blinking in response to an on-coming object). They concluded that cerebellar ischemic strokes should be considered an important differential diagnosis in dogs with acute vestibular signs.
Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) caused by the infiltration of normal, unaffected tissues by immune system cells, called mononuclear cells. It has been successfully treated with cyclophosphamide, an anti-cancer chemotherapy drug, and prednisone.
Nasopharyngeal polyps are non-neoplastic masses, originating from the mucous lining of the nasopharynx, the tympanic bulla, or the Eustachian tube. Dogs with these polyps often display peripheral vestibular syndrome.
Intracranial neoplasia is a brain tumor which can cause vestibular signs of either the peripheral or central variety.
Ototoxicity is poisoning which affects the ears, resulting from the reaction to drugs or chemicals which damage the inner ear or the vestibular nerve. Drugs known to cause ototoxicity include metronidazole, neomycin and streptomycin.
noted above, the typical symptoms of idiopathic vestibular syndrome
• A staggering or rolling gait (ataxia)
• Nystagmus (uncontrolled movements of the eyes, usually from side to side, or in a circular pattern)
• Strabismus (inability of the eyes to aim at the same point in space)
• Head tilt (see photo at right)
• Falling down
These are standard signs of peripheral vestibular disorders. Central vestibular disorders may also include nystagmus with the eyes moving vertically and facial nerve twitching.
Horner's syndrome is not a usual symptom of the idiopathic variety, but it is a typical sign of other peripheral versions of vestibular syndrome. Classic signs of Horner's syndrome are limited to one side of the fact and include: small pupil size (miosis), protrusion of the third eyelid, drooping of the upper eyelid (ptosis), a sunken appearance to the eye (enophthalmos), and dilation of blood vessels on affected side of the face, which may make the area feel warmer.
Diagnosis of idiopathic vestibular disorder usually involves a process of elimination of other possible causes of the symptoms. A complete neurological examination would be appropriate, along with an otoscopic examination, x-rays of the tympanic bullae, computed tomography (CT) or magnetic resonance imaging (MRI), thyroid function testing, and a brainstem auditory evoked response (BAER) test.
For those causes of vestibular syndrome other than the idiopathic variety, the diagnosis involves identifying the particular disease causing the symptoms. If benign paroxysmal positional vertigo (BPPV) is suspected, maneuvering tests such as the Dix - Hallpike maneuver and the side-lying maneuver, which involve protocols of postioning and then re-positioning the patient, should be performed.
Idiopathic vestibular syndrome is known often to begin resolving itself within three days without any treatment. However, the dog needs to be closely monitored during this period. Therefore, patience is required of the dog's owner, because the symptoms of this disorder can be very disturbing. Veterinarians may prescribe cerenia (maropitant citrate) tablets, a motion-sickness medication, and/or a benzodiazepine drug called diazepam (Valium). Most dogs will make a full recovery although some may continue to have a slight head tilt.
If benign paroxysmal positional vertigo (BPPV) is suspected, physical maneuvering methods, such as canine versions of the positioning protocols such as the Semont Liberatory Maneuver and the Horizontal Canal Repositioning Maneuver, may be attempted. An example of such treatment is, first, to lie the dog on its side which seems to have the most nystagmus symptoms and watch the dog's eyes until the involuntary movements stop. Then wait about 30 seconds, holding the dog in that same position. Then turn the dog over so that it is lying on its other side. If and when any nystagmus symptoms end, hold the dog in that position for another 30 seconds. If the dog no longer has any symptoms, it would indicate that the maneuver successfully dislodged the loose granules from the canal and enabled them to flow back into the utricle.
In some cases, neuromuscular electrical stimulation (NMES) has reportedly helped to resolve the symptoms.
For those causes of vestibular syndrome other than the idiopathic variety, the treatment involves treating the particular disease causing the symptoms.
January 2016: French researchers include two cavaliers in study of facial and vestibular neuropathy of unknown origin. In a January 2016 article, the same team of French researchers who reported in July 2015 that cavalier King Charles spaniels were "highly represented in study of idiopathic labial and facial canine vestibular neuropathy", reported on 16 dogs, including 2 cavaliers, with facial and vestibular neuropathy of unknown origin (FVNUO). They stated that all of the dogs had onset of the FVNUO in less than 24 hours, and that their thyroid function was within normal limits. None of the 16 dogs received any treatment except artificial tears. Vestibular signs resolved and a return to normal facial movement occurred in one of the CKCSs. The other cavalier developed hemifacial contracture. They concluded that "FVNUO shares similarities with idiopathic facial paralysis. The prognosis for return of normal facial and vestibular function is guarded and there may be relapse after recovery."
January 2016: US Neurologist Rossmeisl finds PSOM, CM/SM, brachycephalic airway obstruction syndrome and laryngeal paralysis in a cavalier. In a January 2016 article, Virginia Tech veterinary neurologist John Rossmeisl reports on a 13-year-old, male castrated cavalier King Charles spaniel which had symptoms of vestibular disease -- a left head tilt and circling to the left, which progressed to left lateral recumbency, positional strabismus (OS), and rotary nystagmus (OU) -- and also the absence of postural reactions in all limbs, exaggerated spinal reﬂexes in all limbs, and respiratory distress. He performed an MRI and otoscopic examination and performed a myringotomy. (See specimen of mucus at right.) He found no evidence of inﬂammation or infection. He diagnosed: (a) primary secretory otitis media (PSOM), causing the peripheral vestibular signs; (b) CM/SM, causing the central nervous system symptoms; (c) brachycephalic airway obstruction syndrome (BAOS) and laryngeal paralysis, causing the dog’s inability to walk and required tracheal intubation and supplemental oxygen. The owner chose euthanasia rather than surgery to relieve the BAOS.
August 2015: Cerebellar infarction symptoms in cavaliers resemble acute vestibular signs. In an August 2015 abstract, UK neurologists (B. Thomsen, L. Garosi, G. Skerritt, C. Rusbridge, T. Sparrow, M. Berendt, H. Gredal) report finding cerebellar infarctions in 24 dogs, including 9 cavalier King Charles spaniels, displaying ataxia (staggering or rolling gait), hypermetria (voluntary muscular movements tend to overreach their intended goals), head tilt, nystagmus (uncontrolled movements of the eyes), reduced postural reactions (e.g., replacing a foot after being lifted), and decreased menace response (eye blinking in response to an on-coming object). They concluded that cerebellar ischemic strokes should be considered an important differential diagnosis in dogs with acute vestibular signs.
July 2015: French researchers find cavaliers highly represented in study of idiopathic labial and facial canine vestibular neuropathy. In an April 2015 article, a team of French researchers (Aurélien Jeandel (right), J. Thibaud, F. Delisle, Stephane Blot) found 21 dogs with cases of idiopathic labial and facial canine vestibular neuropathy over the past ten years. The inclusion criteria were: (1) Dog with clinical signs consistent with vestibular syndrome and facial paralysis; (2) No argument suggesting a central nervous system; (3) Normal MRI of the brain parenchyma and absence of middle or inner ear infection. Of the 21 dogs found, there were 4 American Staffordshire Terriers, 3 cavalier King Charles spaniels, and 3 Boxers. Sixteen were male and 5 were female. The median age of presentation was 6.6 years. In all cases, the onset of the symptoms were acute. The vestibular syndrome symptoms most frequently encountered were torticollis (21/21) and nystagmus (16/21).
Vestibular Diseases of Cats and Dogs. Richard A. LeCouteur. 2002 WSAVA Congress. August 2002.
Neurological diseases of the Cavalier King Charles spaniel. Rusbridge, C. J. Small Animal Practice. June 2005;46(6): 265-272. "Vestibular syndrome is one of the most common neurological presentations. Clinical signs may include some or all of the following: head tilt, ataxia, circling, rolling, tendency to lean to side of head tilt, and deviation of eye ventrally (ipsilateral to head tilt) when the head is elevated above the horizontal plane. For prognostic purposes, it is vital to distinguish between peripheral and central disease."
Proposed Treatment for Vestibular Dysfunction in Dogs. Margaret Kraeling. CHAP Newsletter. December 2007; 6–9.
Vestibular Disease in Dogs and Cats. Simon Platt. 2008 WSAVA Congress. August 2008.
Optic neuritis in a Cavalier King Charles Spaniel. M. K. Zarfoss. Cornell Univ. September 2008. Senior seminar paper. Quote: "Betsy, a 4.5 year-old female spayed Cavalier King Charles Spaniel, was presented to the Cornell University Hospital for Animals for evaluation of acute blindness, inappetance, and lethargy. Ophthalmic examination revealed keratoconjunctivitis sicca in both eyes (OU), absent menace OU, decreased pupillary light responses OU, posterior vitreal haze OU, and optic disk enlargement OU. A diagnosis of optic neuropathy was pursued because of bilaterally enlarged optic disks in the absence of other localizing clinical signs or ophthalmic abnormalities sufficient to cause blindness. The presumptive diagnosis of optic neuritis due to granulomatous meningoencephalomyelitis (GME) was based upon: peripapillary retinal vasculitis on fluorescein angiography, severe lymphocytic inflammation within the cerebrospinal fluid (CSF), negative infectious disease serum and CSF titers, and favorable response to immuno-suppression. Granulomatous meningoencephalomyelitis is an inflammatory disease of the central nervous system (CNS) of undetermined etiology and poor prognosis. Successful treated of this dog's GME consisted of conventional treatment using oral prednisone and non-conventional treatment using an additional immunosuppressive agent, cytosine arabinoside."
Vestibular Disease: Anatomy, Physiology, and Clinical Signs. Mark Lowrie. VetLearn Compendium. July 2012;34(7). Quote: "The vestibular system is responsible for keeping an animal oriented with respect to gravity. It is a sensory system that maintains the position of the eyes, body, and limbs in reference to the position of the head. Proper interpretation of neurologic deficits and precise neuroanatomic localization are essential to diagnose and prognosticate the underlying disorder. Neurologic examination can confirm whether the vestibular dysfunction is of peripheral or central nervous system origin. Idiopathic vestibular syndrome is the most common cause of peripheral vestibular disease in dogs and, despite its dramatic clinical presentation, can improve without intervention. Central vestibular diseases generally have a poorer prognosis. ... Granulomatous meningoencephalomyelitis (GME) is a severe inflammatory disease of the central nervous system (CNS), characterised by large perivascular accumulations of mononuclear cells in the parenchyma and meninges of the brain and spinal cord (Braund and others 1978). The aetiology is unknown. It is most common in middle-aged dogs, although it can occur from age six months to 10 years (Braund 1985). Female dogs are slightly more commonly affected than male dogs (Braund 1985). Clinical signs reflect the area of brain or spinal cord affected. The most common signs are spinal pain, depression, seizures, vestibular signs, paresis and postural deficits. Disseminated and focal forms are recognised and focal forms may present with just involvement of the optic nerves manifesting as sudden onset blindness (Braund 1985). Diagnosis is suggested by appropriate MRI and CSF changes and by ruling out infectious causes of encephalitis (Fig 4), but can only be confirmed by postmortem examination."
Vestibular Disease. Simon R. Platt. Clinicians Brief. December 2012.
Neck Stiffness & Head Tilt in a Young Spaniel. Louis N. Gotthelf. Clinician's Brief. March 2013: 23-25. Quote: "A 9-month-old female Cavalier King Charles spaniel presented for apparent neck pain when walked on a leash. History: The owner reported neck stiffness and head tilt. After the leash had been removed, the signs continued to persist for more than 24 hours. The puppy appeared bright, alert, and responded when called. Examination: Physical examination did not elicit a painful response when the head and neck were manipulated in any direction. A slight head tilt was observed when the puppy walked freely in the clinic; however, laboratory diagnostics were not performed. Evaluation may reveal a bulging eardrum, indicative of primary secretory otitis media (PSOM). PSOM of Cavalier King Charles spaniels (CKCSs) commonly occurs as head and neck pain that may be difficult to localize. With pressure in the bulla, Horner syndrome or facial nerve palsy may be evident. Vestibular disease may be present with increased bulla pressure and can manifest as nystagmus or head tilt. Breed-Specific Considerations: Careful examination can reveal an abnormal or bulging eardrum. Clinicians adept at visualizing a normal eardrum with a handheld otoscope can detect a bulging eardrum; the tip of the cone has to be small yet long enough to make the bend in the ear canal. The tip of the otoscope cone should be placed in the horizontal ear canal close enough to the eardrum to focus on the tympanic membrane. A highly magnified, well illuminated examination should be done with a video otoscope to determine eardrum status. Bottom Line: CKCS eardrums should always be evaluated. If PSOM is suspected, a high-magnification eardrum examination may require referral. PSOM can be asymptomatic in CKCSs, in which case myringotomy is not required; however, the owner should be educated to take appropriate steps if signs are displayed. The Take-Home: CKCSs often have a genetic defect of their eustachian tube that results in PSOM, which may be asymptomatic. Bulging eardrum and ear pain are typical of PSOM in CKCSs. PSOM should be differentiated from SM via eardrum evaluation and MRi (if necessary). Myringotomy can relieve PSOM signs. Antibiotics will not be helpful. Periodic treatment is required."
Proposed Treatment for Geriatric Vestibular Disease in Dogs. Margaret Kraeling. Topics in Companion Animal Medicine. March 2014;29(1):6-9. Quote: "Sudden-onset vestibular dysfunction in the canine is a commonly seen condition in veterinary practice, with some veterinarians reporting several cases each month. However, traditional veterinary medicine has little to offer these patients other than symptomatic relief for the severe nausea that accompanies the vertigo and supportive advice for the owners. Owners of affected dogs are informed that these symptoms usually resolve within a few days. As physical therapists, we often see cases of benign paroxysmal positional vertigo in our human practice clinics, and effective protocols for diagnosis and treatment of the condition have been developed for this condition. A modified testing and repositioning postural maneuver used successfully on 12 canine patients in our canine rehabilitation clinic (The Canine Fitness Centre, Calgary, Alberta, Canada) is hereby described."
Otitis externa and media -- pathogenisis and signs. Filippo de Bellis. Vet. Times. December 2014. Quote: "Otitis media: In dogs and cats, otitis media can be primary or secondary. In cats, primary otitis media occurs as a result of an infection ascending through the Eustachian tube to the middle ear. An exact mechanism for the development of otitis media has not been reported, although the bacterial isolates from the bullae of cats with middle ear disease are consistent with respiratory pathogens. It has been hypothesised that chronic viral upper respiratory infection early in life may play a role in initiating otitis media in cats. In dogs, primary otitis media can also originate from ascending nasal or respiratory infections through the auditory tube, although otitis media most often occurs as an extension of otitis externa. Additionally, it can occur as primary disease due to middle ear or auditory tube abnormalities such as with primary secretory otitis media, most often seen in cavalier King Charles spaniels. It has been speculated the primary otitis in these cases could occur secondarily to structural changes in the soft palate or nasopharyngeal apertures. Secondary otitis media in cats is reported as a consequence of ear mite infestation with subsequent rupture of the tympanic membrane or as extension of a nasopharyngeal polyp (Figure 3) originating from the middle ear mucosa and growing through the tympanic membrane. Secondary otitis media in dogs can be caused by draining through a damaged ear drum, of exudates, infectious organisms, debris and residuals of medications. Once an inflammatory process is established, a series of pathological changes take place including oedema, ulcerations, granulation tissue formation, and osteomyelitis. Clinical signs of otitis media are variable. Most commonly, dogs and cats with a perforated ear drum show large amount of liquid discharge within the ear canal, often with mucous material produced by the lining of the tympanic bulla. Additionally, due to the close proximity of the inner ear structures, patients with otitis media can also develop vestibular signs. Summarising, clinical presentation of otitis media can include: facial nerve paralysis; Horner’s syndrome; hearing abnormalities; ataxia; head tilt; ventro-lateral strabismus; nystagmus; respiratory signs; pain on palpation of the base of the ear; and reluctance to open the mouth."
The vestibular and facial idiopathic neuropathy in dogs: 21 cases study (Les neuropathies vestibulaires et faciales idiopathiques chez le chien : étude de 21 cas). A. Jeandel, J. Thibaud, F. Delisle, S. Blot. Revue Vétérinaire Clinique. April 2015;50(2):76-77. Quote: [Google translation] "The peripheral vestibular syndrome (PVS), secondary to impairment of the vestibular nerve or its receptors, often idiopathic or inflammatory origin (otitis interna) in dogs. In otitis media / internal, one can observe a SVP associated with facial paralysis. Yet described vestibular damage associated with facial paralysis without abnormality of the middle / inner ear during the MRI. Similarly, considered idiopathic facial paralysis are sometimes associated with vestibular symptoms. No item specifically addresses these labial and facial idiopathic neuropathy (NVFI) 0030, 0035, 0040, 0045 and 0050. The aim of our study was to retrospectively identify cases of NVFI, to describe the epidemiology, clinical presentation, paraclinical changes and the evolution of these animals in the long term. The cases of NVFI within the last ten years were reviewed. The inclusion criteria were as follows: (1) Dog with clinical signs consistent with vestibular syndrome and facial paralysis; (2) No argument suggesting a central nervous system; (3) Normal MRI of the brain parenchyma and absence of middle or inner ear infection. Twenty-one dogs have fulfilled these inclusion criteria. The most represented breeds are American Staffordshire Terriers (4), the Boxers (3), the cavalier King Charles (3). Sixteen males are identified against five females. The presence of male was significantly higher (p = 0.027). The median age of presentation was 6.6 years [0.5 to 12.5]. In all cases, the reported method of onset is acute (less than 72 h). The symptoms most frequently encountered vestibular syndrome are torticollis (21/21), nystagmus (16/21). A dog was being treated for diabetes mellitus. A Schirmer test was performed in seven dogs: one case of quantitative tear deficiency was observed. The cytological examination of CSF is normal in all dogs removed. By cons, compared to a contemporary witness population with idiopathic epilepsy, protein level was significantly increased (p <0.001): median 0.40 g / L [0.20 to 0.90]. A search of infectious agents was performed in three animals (PCR LCS) the examination was normal. Cholesterol assays, triglycerides, total T4 and TSH, performed in 10 animals are within the usual values. The clinical evolution of the vestibular and facial involvement was documented in these seventeen of these animals (followed six months). Clinical remission is random and its duration is very variable. About residual vestibular disorders, permanent torticollis is reported in three cases, intermittent in four cases. The median disease duration was 60 days [1-730]. Regarding the signs of facial involvement, the return to proper function (eyelid closure, no food waste) is reported in fourteen cases, including six cases with hemifacial spasm sequelae. The median disease duration was 53 days [7-730]. Self-resolvent recurrences are reported by owners in three animals during the telephone follow-up. A recurrence was observed during monitoring by a clinician to establish the contralateral part in two animals after remission of the first episode. An MRI control and LCS puncture confirmed contralateral recurrence in one of them. When SVP associated with facial paralysis of acute onset with a dog, so it should be integrated in the diagnostic hypotheses NVFI. The origin of this concomitant damage is probably related to nearby course of these nerves when they entered in their respective channel in the temporal bone through the internal acoustic meatus. Recovery is variable. An inflammatory origin is suspected given the protein level changes observed."
Neurological signs in 24 dogs with rostral cerebellar infarction. B. Thomsen, L. Garosi, G. Skerritt, C. Rusbridge, T. Sparrow, M. Berendt, H. Gredal. 27th ESVN-ECVN Symposium. J.Vet.Int.Med. August 2015; ESVN-ECVN Abstracts p.27. Quote: "Studies on canine ischemic stroke suggest an overrepresentation of cerebellar cases. Although not the leading localization in humans, a cerebellar stroke syndrome characterized by vertigo, ataxia, nystagmus, and headache is described. Purpose of the present study was to characterize neurological signs in dogs with cerebellar infarction. A retrospective multicenter study of dogs examined 2010–2014 was performed. Dogs with acute non-progressive neurological deficits and magnetic resonance imaging suggestive of cerebellar infarction were eligible for inclusion. Twenty-four dogs (16 females, 8 males) with a median age of 8 years (range 3–11 years) were included. Breeds comprised the Cavalier King Charles Spaniel (n = 9), Greyhound (n = 3), Labrador Retriever (n = 2), and ten other breeds. In all dogs, infarcts were located to the rostral cerebellum and the territory of the rostral cerebellar artery (left n = 13, right n = 10, midline n = 1). Common neurological deficits were ataxia (n = 24), hypermetria (n = 12), contralateral head tilt (n = 13), nystagmus (n = 8), reduced postural reactions (n = 8), and decreased menace response (ipsilateral n = 4, bilateral n = 2). Four dogs had additional non-cerebellar brain infarcts. Six dogs had a history suggestive of a possible transient ischemic attack. Cerebellar ischemic stroke should be considered an important differential diagnosis in dogs with acute vestibular signs. A syndrome of canine cerebellar ischemic stroke caused by infarction in the territory supplied by the rostral cerebellar artery with neurological deficits resembling its human counterpart does seem to exist."
What is your diagnosis? Middle ear material from a dog. Nicole M. Weinstein, Katie M. Boes, Elizabeth Mauldin, John Rossmeisl. Vet. Clinical Pathology. January 2016. Quote: “Case Presentation: A 13-year-old, male castrated Cavalier King Charles Spaniel (CKCS) was referred ... for suspected vestibular disease of 2 days duration. The clinical history included a left head tilt and circling to the left, which progressed to left lateral recumbency within approximately 12 hours. Upon admission, respiratory distress was also noted. Relevant physical and neurologic examination ﬁndings included moderate bilateral otic discharge, positional strabismus (OS), rotary nystagmus (OU) with a fast phase to the right, absence of postural reactions in all limbs, and exaggerated spinal reﬂexes in all limbs. The clinical examination ﬁndings supported a multifocal neurologic condition that included dysfunction of both peripheral and central vestibular systems. Magnetic resonance imaging (MRI) and an otoscopic examination were performed. MRI revealed material in both the left and right ear bullae as well as caudal occipital malformation syndrome–syringohydromyelia (COMS-SM). During the otoscopic exam, the left tympanic membrane was bulging, but intact, while the right was ruptured. Slides of material obtained during myringotomy on the left ear were submitted for cytologic evaluation. Interpretation: Primary secretory otitis media. ... No evidence of inﬂammation or infection was identiﬁed. The combination of patient breed, gross appearance, and cytologic ﬁndings was compatible with primary secretory otitis media (PSOM). While the peripheral vestibular signs were explained by PSOM, the central nervous system signs were attributed to COMS and syrinx formation. Both brachycephalic airway syndrome and laryngeal paralysis were also diagnosed and may have contributed to the patient’s inability to ambulate given persistent hypoxemia that required intubation and oxygen supplementation. Surgery to alleviate the upper airway disease was discussed, but the owner elected euthanasia. Discussion: ... Common clinical signs in dogs with PSOM include head and cervical pain, and vocalization. Some dogs also exhibit aural pruritus with or without obvious otitis externa. Neurologic signs are present less often and may include ataxia, nystagmus, head tilt, facial paralysis, or seizures. The tympanic membrane is often intact but may be bulging and appear opaque. A white to yellow mucus plug can be visualized during myringotomy or if the tympanic membrane is not intact. Recurrence following ear ﬂushing is common, but the prognosis is considered good, including in dogs with progressive disease. In approximately 50% of CKCS dogs undergoing imaging, PSOM is an incidental ﬁnding. The resolution of vestibular signs following removal of the mucus plug, even in dogs with COMS with or without syringomyelia, supports PSOM as a distinct disease entity rather than as an entirely incidental ﬁnding. The exact cause of PSOM in dogs is unknown.”
Facial and vestibular neuropathy of unknown origin in 16 dogs. A. Jeandel, J. L. Thibaud, S. Blot. J. Sm. Anim. Pract. January 2016. Quote: "Objectives: The aim of this study was to describe the signalment, clinical presentation, diagnostic findings and long-term follow-up in dogs with concomitant facial and vestibular neuropathy of unknown origin [FVNUO]. Methods: Appropriate cases were located through medical record searches. Inclusion criteria comprised dogs that had: clinical signs of facial paralysis with concomitant peripheral vestibular syndrome, thyroid function tests, no abnormalities on magnetic resonance imaging of the brain and tympanic bullae, and cerebrospinal fluid analysis. Results: Sixteen dogs met the inclusion criteria [including 2 cavalier King Charles spaniels]. Facial paralysis had acute onset (<24 hours) in all dogs, thyroid function was within normal limits. ... None of the 16 dogs received any treatment except artificial tears. Follow-up was incomplete for three dogs. In eight dogs (62%), vestibular signs resolved [including one of the cavalier King Charles spaniels]. The median time to complete PVS [peripheral vestibular syndrome] resolution was 55 days (range, 3 to 365). A return to normal facial movement was reported in five dogs (39%) [including one of the cavalier King Charles spaniels]. The median time to FP [facial paralysis] resolution was 45 days (range, 7 to 730). Complete resolution of both PVS and FP was observed in four dogs (31%) [including one of the cavalier King Charles spaniels]. The nine other dogs exhibited long-term sequelae: five dogs (38%) displayed a persistent or intermittent head tilt; two dogs (15%) did not recover facial motor function after 18 and 24 months; ipsilateral hemifacial contracture developed in six other dogs (46%) [including one of the cavalier King Charles spaniels]. The median time between the initial and last follow-up examination was 18 months (range, 6 to 42). ... Clinical Significance: Facial and vestibular neuropathy of unknown origin shares similarities with idiopathic facial paralysis. The prognosis for return of normal facial and vestibular function is guarded and there may be relapse after recovery."
Síndrome Vestibular em Animais de Companhia: estudo retrospetivo de 29 casos clínicos (Vestibular Syndrome in Small Animals: retrospective study about 29 clinical cases). Carolina Das Neves Campos Barata Gonçalves. Univ. of Lisbon. March 2016. Quote: "The vestibular system is the sensory system responsible for maintaining the animal’s balance relative to the gravitational field of the earth, and to adjust de position of the eyes, neck, trunk and limbs during the movement of the head. This system is divided in two functional components: the peripheral component, composed by the vestibulocochlear nerve (VIII) and its sensory receptors in the inner ear, and the central component, composed by the vestibular nuclei and pathways in the brainsteam and cerebellum. When one of these components is affected, the animal develops signs characterizing the vestibular syndrome. These clinical signs include loss of coordination and balance, falls, head tilt and positional strabismus, all to the side of the lesion, and pathologic nystagmus. The neurological examination allows to predict the location of the lesion and to clinically differentiate peripheral from central and paradoxical vestibular syndrome. This differentiation is important in determining the differential diagnoses, the diagnostic plan and also the prognosis and therapeutic plan. Several diseases could cause the onset of vestibular signs. The most common causes of peripheral vestibular syndrome are otitis media/interna and idiopathic vestibular syndrome, while the most common causes of central vestibular syndrome are inflammatory/ infectious diseases of the central nervous system and neoplasia. The practical component consists in a retrospective study of 29 clinical cases who presented at the clinic Referência Veterinária with signs of vestibular syndrome and were evaluated through magnetic resonance imaging. At the end of the study it was concluded that vestibular syndrome is a neurologic dysfunction who affects animals at any age, and it was confirmed that the most common etiologies described correspond to the observed at clinical practice. This study was important to understand that the use of magnetic resonance imaging is important at the evaluation of animals with central vestibular syndrome, and even with peripheral vestibular dysfunctions. There are some cases where the clinical signs used to differentiate the types of vestibular syndrome are subtle and can be attenuated by the administered drugs. Finally, it was also concluded that the neurological examination is a very reliable method to predict the location of the lesions and to differentiate between peripheral, central and paradoxical vestibular syndrome."
Vestibular Syndrome – Tilting, Rolling and Falling, Oh My! BVNS Neurotransmitter 2.0 Technically Speaking November 2016. Quote: “Vestibular Disease” is actually a misnomer. There are many diseases that can cause vestibular dysfunction, but since there are many causes (or in some cases a cause cannot be found), and there is not a consistent change in anatomy, it is incorrect to refer to it as a disease. It is referred to it as a syndrome - a collection of clinical signs often observed together; or simply “vestibular dysfunction”.