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Natural aging can have direct and indirect effect on behavior


Q: Could you review some neurologic diseases of the older dog?

Q: Could you review some neurologic diseases of theolder dog?

A: A good working knowledge of geriatric medicine and the potentialhealth-related changes associated with the natural aging process and diseasesis essential for the practicing veterinarian to be an effective problem-solverwhen first presented with questions about why the older dog is acting abnormalat home. The natural aging process of dogs is associated with progressiveand usually irreversible changes in multiple body systems.

Older dogs are seldom afflicted with a single disease or organ dysfunction,but rather varying degrees of multiple system disease and/or dysfunction.

Cancer, degenerative conditions, immune-mediated diseases, neurologicdisorders, cognitive decline and endocrinopathies occur more commonly inthe aged dog. Because of this, natural aging and disease states often havea direct or indirect effect on the central nervous system and a dog's dailybehavior.


Idiopathic trigeminal neuritis or mandibular paralysis (ITN) can affectany dog breed and there is no sex or age predilection. The case historyis repeatable and consists of acute onset (usually within 24 hours) of adropped jaw and inability to close the mouth.

If the case history reveals a progressive jaw weakness that occurs overdays to weeks, then the dog does not have this cranial nerve syndrome. Theneurologic examination shows bilateral dysfunction of the mandibular nerve.Remember that unilateral mandibular nerve damage will not result in a droppedlower jaw.

There should be no sensory deficits to the head and face, no gait orpostural test deficits and no other cranial nerve deficits. In addition,dogs with ITN are alert, very responsive, and have no problem swallowingfood if it is placed at the base of the tongue.

Treatment consists of supportive therapy during the first seven to 10days. The reason that limited therapy is needed is because most dogs aremuch improved within seven days, and all should be normal in three to fourweeks. Corticosteroids may be used at 1 mg/kg/day of prednisone for sevento 10 days, but clinically do not appear to shorten the recovery time.

Canine peripheral vestibular syndrome

Canine peripheral vestibular syndrome is usually an idiopathic syndrome.The case history is characterized by a peracute onset (usually within hours)of head tilt, incoordination and nystagmus.

The incoordination may be severe enough that the dog is non-ambulatory.Vomiting that is secondary to vertigo may be seen during the first 24 to48 hours of onset of signs. The neurologic examination shows a head tilt,falling and/or rolling toward the side of the head tilt, and horizontalto rotary nystagmus (spontaneous nystagmus and with the fast phase awayfrom the head tilt).

The type of nystagmus does not change. There may be a generalized incoordinationand base-wide stance. No other cranial nerve deficits will be noted, andthere is no weakness or postural test deficits.

If these signs are seen, then a brainstem lesion involving the vestibularsystem is most likely. If the nystagmus type is vertical, a brainstem lesionis most likely.

One should realize that on the initial day of presentation, the incoordinationand disorientation might be too severe to allow for adequate assessmentof muscle strength and postural test reactions. Therefore, it may take 48hours before this assessment can be used to help separate central (brainstem)vestibular disease from peripheral (inner ear) vestibular disease.

Once the vestibular signs have been localized to the peripheral vestibularsystem, the two primary differentials are otitis media/interna and headtrauma with resultant fracture of the petrous temporal bone. If facial nerveparalysis and Horner's syndrome are present on the same side as the headtilt, this should be a clue that otitis media/interna co-exists. A thoroughear examination and skull/bulla radiographs may be necessary in some casesto help rule out these differentials.


Treatment is supportive since the vestibular problem will resolve inall dogs on its own. The resolution timetable is usually consistent fromcase to case and if the dog does not follow this timetable, there shouldbe concern that the initial diagnosis was wrong. The nystagmus should disappearwithin four days; the dog should be able to ambulate fairly well withinseven days, and the gait should be normal by three weeks.

A small number of dogs may have a residual head tilt and/or some incoordinationwhen performing quick movements that require agility. Treatments that maybe helpful during the first few days such as fluid therapy for euhydration,diazepam (5-15 mg three times daily) for sedation if disorientation is severe,meclizine (Antivert) (25 mg once daily) for vertigo and diphenhydramine(Dramamine) 4-8 mg/kg orally in dogs. These treatments are usually unnecessaryafter 72-96 hours.

Idiopathic facial nerve paralysis is acute in onset, but because thedeficits are not as alarming to the owner, they may not recognize the facialproblem as being acute in onset. The facial problem is seen primarily inadults, and the Cocker Spaniel is affected more often than the other breeds.

The owner complains that their dog is unable to blink; has a droopinglip and/or ear; drools from one of side mouth, and/or has excessive tearingor a dry eye. Neurologic examination shows deficits related only to 7thcranial nerve dysfunction: wide palpebral fissure, lack of menace and palpebralreflexes, drooping lip/ear, drooling on affected side, and some dogs mayhave decreased tear production.

Sensation to the face is normal. In long-standing cases when resolutionhas not occurred, facial muscle contractures may develop. The primary differentialsinclude: otitis media, neoplasia of peripheral 7th cranial nerve (uncommon),brainstem disease (one should detect other cranial nerve deficits, motordeficits and/or postural test reaction deficits exist), and 7th cranialnerve deficits associated with myasthenia gravis, coonhound paralysis orgranulomatous meningoencephalitis (GME).


Bullae radiography could be done to assess for middle ear disease, especiallyin the dog that has had a history of chronic external ear disease. The Schirmertear test should be done to assess for the need of tear supplementation.Although a cause and effect relationship between hypothyroidism and thiscranial neuropathy has not been proven, thyroid function testing shouldbe done because some dogs will be hypothyroid and should be treated. Treatmentconsists of tear supplements, thyroid replacement therapy if indicated andsteroids for 14-21 days. There is no proof that steroid therapy impactsrecovery. The good news is that most dogs can function well with facialnerve deficits and may only need long-term tear supplementation.

Masticatory muscle myositis

Masticatory muscle myositis (MMM) is a specific immune-mediated muscledisease involving only the muscles of mastication (primarily temporalisand masseter muscles). The dog is usually presented for a combination ofjaw pain, swollen painful muscles of the head and jaw, exophthalmos and/ortrismus (inability to open jaw or mouth). The jaw may be dropped open insteadof trismus and, occasionally, a dog will be febrile.

It is important to note that this muscle group is generally affectedalone. The masticatory muscles may be involved as part of a polymyositissyndrome but, in this instance, there will be no autoantibodies to the myofibers.The differential diagnosis for MMM includes a jaw fracture, temporomandibularjoint and/or bulla disease, retrobulbar abscessation, possibly tetanus,extraocular muscle myositis and as part of a polymyositis syndrome. Theremay be obvious trismus and the classical finding is the inability to openthe jaw under anesthesia.

Specific tests for MMM include muscle biopsy and demonstration of serumautoantibodies to the type 2M fibers.

MMM treatment

The treatment begins with corticosteroids (such as prednisone) at animmunosuppressive dose (2 mg/kg per day; some dogs may require 3-4 mg/kgper day). This dosage is used until clinical signs abate and jaw functionis much improved. Some form of corticosteroid therapy should be maintainedfor at least three to four months.

In dogs that do not respond optimally to corticosteroids or have significantside effects, the use of azathioprine (2 mg/kg per day, alternating dailywith prednisone) can be used to decrease the dosage of corticosteroids given.

Supportive therapy with subcutaneous fluids and gastrostomy tubes formaintenance of hydration and a positive nutritional status, respectively,may be necessary during the first few weeks.

Inflammation and myofiber destruction are particularly severe in theSamoyed, Doberman Pinscher and Rottweiler. Early diagnosis and treatmentare essential.

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