Natural aging can have direct and indirect effect on behavior

Natural aging can have direct and indirect effect on behavior

Mar 01, 2002

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

A: A good working knowledge of geriatric medicine and the potential health-related changes associated with the natural aging process and diseases is essential for the practicing veterinarian to be an effective problem-solver when first presented with questions about why the older dog is acting abnormal at home. The natural aging process of dogs is associated with progressive and 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, neurologic disorders, cognitive decline and endocrinopathies occur more commonly in the aged dog. Because of this, natural aging and disease states often have a direct or indirect effect on the central nervous system and a dog's daily behavior.


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

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

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

Treatment consists of supportive therapy during the first seven to 10 days. The reason that limited therapy is needed is because most dogs are much improved within seven days, and all should be normal in three to four weeks. Corticosteroids may be used at 1 mg/kg/day of prednisone for seven to 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 to 48 hours of onset of signs. The neurologic examination shows a head tilt, falling and/or rolling toward the side of the head tilt, and horizontal to rotary nystagmus (spontaneous nystagmus and with the fast phase away from the head tilt).

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

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

One should realize that on the initial day of presentation, the incoordination and disorientation might be too severe to allow for adequate assessment of muscle strength and postural test reactions. Therefore, it may take 48 hours 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 vestibular system, the two primary differentials are otitis media/interna and head trauma with resultant fracture of the petrous temporal bone. If facial nerve paralysis and Horner's syndrome are present on the same side as the head tilt, this should be a clue that otitis media/interna co-exists. A thorough ear examination and skull/bulla radiographs may be necessary in some cases to help rule out these differentials.


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

A small number of dogs may have a residual head tilt and/or some incoordination when performing quick movements that require agility. Treatments that may be 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 unnecessary after 72-96 hours.

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

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

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


Bullae radiography could be done to assess for middle ear disease, especially in the dog that has had a history of chronic external ear disease. The Schirmer tear test should be done to assess for the need of tear supplementation. Although a cause and effect relationship between hypothyroidism and this cranial neuropathy has not been proven, thyroid function testing should be done because some dogs will be hypothyroid and should be treated. Treatment consists of tear supplements, thyroid replacement therapy if indicated and steroids for 14-21 days. There is no proof that steroid therapy impacts recovery. The good news is that most dogs can function well with facial nerve deficits and may only need long-term tear supplementation.

Masticatory muscle myositis

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

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

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

MMM treatment

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

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

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

Inflammation and myofiber destruction are particularly severe in the Samoyed, Doberman Pinscher and Rottweiler. Early diagnosis and treatment are essential.