Neurological diseases of old age chronic ‘old dog’ encephalitis

By | March 4, 2015

Canine distemper is most prevalent in young dogs, but chronic ‘old dog’ encephalitis is the neurological manifestation of canine distemper virus (CDV) infection that is seen in adult dogs which have survived the acute infection. Dogs developing this condition are usually over 6 years of age and have serological evidence of systemic immunity.

The neurological signs (see Table Neurological signs seen in the ‘old dog encephalitis’ form of canine distemper) may occur without previous evidence of systemic disease and are usually progressive and irreversible (). The involuntary muscle twitching (myoclonus) is typical of CDV infection.

Table Neurological signs seen in the ‘old dog encephalitis’ form of canine distemper.

  • Hyperaesthesia
  • Cervical pain
  • Seizures
  • Cerebellar and vestibular signs
  • Visual deficits
  • Behavioural changes
  • Head-pressing
  • Circling
  • Paraparesis or tetraparesis
  • Ataxia
  • Myoclonus

CSF examination for increased protein and increased lymphocyte count may be helpful in diagnosing dogs exhibiting neurological signs.

Histologically there is perivascular lymphoplasmacytic infiltration in areas of demyelination and neuronal degeneration which may progress to

sclerosing panencephalitis in more chronic cases. Canine distemper virus inclusion bodies are present in epithelial and other cells but their sigis not clear ().

Distemper can occur after stress, during concurrent illness or in immunesuppressed vaccinated dogs. Although vaccination with modified live CDV may confer long-term active immunity to some individuals, most manufacturers recommend booster vaccinations at 1-2 year intervals to ensure adequate ongoing protection.

The long-term prognosis is poor for most cases and, although some authors advocate a period of 1-2 weeks supportive therapy, euthanasia is usually the eventual outcome.


Seizures can begin at any age and if they occur at a frequency greater than once every 6 weeks, or if the animal has clusters of seizures more than once every 8 weeks, anticonvulsant therapy is indicated.

The onset of seizures in old animals should prompt a search for an extracranial cause (e.g. hepatic disease) or an intracranial structural lesion (e.g. brain tumour).

Phenobarbitone and primidone are the drugs of choice for managing seizures in dogs, and phenobarbitone and diazepam for cats.

In 20-25% of dogs seizures are reported to be refractory to treatment with phenobarbitone and 40% and 48% of cases are refractory to primidone. Similar results have been reported for cats ().

The most common cause of failure in treatment is inadequate dosage either by the clinician or due to owner non-compliance. The therapeutic range of serum concentration of phenobarbitone in the dog is 20-40 mg/ ml and for the cat 10-30 mg/ml. The recommended dose rate is 1.5-5.0 mg/kg body weight but if adequate serum concentrations are achieved but seizure control does not occur even higher doses are recommended by some authors. Intervals between doses should be less than the half-life of the drug in the body to minimise fluctuations in serum concentrations.

The serum concentration of a drug is determined not only by dose but also by its bioavailability, metabolism and elimination. In older animals the objective should be to reduce the dose to the minimum needed to maintain serum concentrations within the recognised therapeutic range.

The recommended dose of anticonvulsants varies from one author/ reference to another. During the initial treatment of refractory seizures the more rapidly the therapeutic dose is reached the greater the success so a high initial loading dose of phenobarbitone may be beneficial particularly for the most difficult seizures to control in dogs (clusters of generalized tonic-clonic seizures (GTCS)) and cats (complex focal seizures). For phea gradually increasing dose rate of up to 10-15 mg/kg body weight orally has been used for these cases.

Care is needed when using anticonvulsants in old animals – particularly if high doses are needed. The patient should be screened for evidence of impaired liver function and should be carefully monitored to ensure early detection of hepatotoxicity.

Primidone is not recommended at high dose rates for out-patients because it causes sedation. It is recommended to be given at 25 mg/kg body weight twice daily orally for both cats and dogs, though some authors advise administration at least three times daily.

Diazepam is the drug of choice for the initial control of status epilepticus in cats and dogs at a dose rate of 5-50mg given i.v. in 5-10mg doses followed by slow intravenous infusion at 2-5 mg/h in 5% glucose intrafluid. Orally diazepam is only 2-3% bioavailable but a dose of 0.5-2.0 mg/kg t.t.d. has been recommended for cats.

Potassium bromide and mephenytoin have been used successfully as adjuvants to conventional treatment but combination therapy should only be tried if drugs by themselves have proved to be unsuccessful. See Schwartz-Porsche 1992 for a review of adjunctive therapy.

In all cases a rapid reduction in dose rate or too sudden a change in treatment can result in relapse and recurrence of seizures.

Drug interactions are common between anticonvulsants and antibiotics, antacids, theophylline, cardiac drugs, steroids and antirheumatics. Phe(e.g. acepromazine), anthelminthics (e.g. piperazine and mebendazole) and metoclopramide administration may lower the seizure threshold and precipitate seizures in a stable case.

The incidence of seizures may be altered by the presence of concurrent disease – see Table Concurrent diseases which may alter the incidence of seizures in older animals. For this reason routine screening is advisable in geriatric patients with seizures.

Table Concurrent diseases which may alter the incidence of seizures in older animals.

  • Gastroenteritis
  • Hepatic disease
  • Renal disease
  • Pneumonia
  • Metabolic disorders

Peripheral polyneuropathies

Neuropathies can occur secondary to multisystemic disorders (e.g. neodiabetes mellitus) so a full clinical examination is necessary (see Table Presenting signs in peripheral neuropathy for presenting signs). In older animals it may be difficult to difpoor proprioception from severe muscle weakness.

Table Presenting signs in peripheral neuropathy.

  • Ataxia
  • Muscle atrophy
  • Hyporeflexia/hypotonia or paresis
  • Difficulty rising
  • The muscle weakness may be progressive, usually affects the hindlimbs before the
  • forelimbs and is not exercise dependent
  • Loss of bark (neuropathy of the recurrent laryngeal nerve)
  • Megaoesophagus
  • Megacolon


Central nervous system

Brain tumours can occur at any age but the incidence is very rare in aniunder 5 years of age (). They are usually focal lesions and cause neurological signs directly related to the site at which they occur.

Localisation of brain tumours can be achieved from a complete neurological examination and the use of modern imaging techniques particomputerised tomography (CT scans) and magnetic resonance imaging (MRI). Plain radiography is rarely helpful unless the tumour involves the bony parts of the cranium causing osteolysis or new bone deposition, and the use of contrast studies (positive or negative) alone is less reliable than CT or MRI. Many brain tumours produce hot spots’ that can be detected by scintigraphy and photon emission computed tomography

Meningiomas are the most common form of brain tumour in dogs and cats. In the dog these and gliomas are often locally invasive, and gliomas are particularly aggressive. Some brain tumours are accessible to surgery and, if benign and well described, may be successfully removed, e.g. meningiomas in cats, but the prognosis is guarded. Radiotherapy and chemotherapy have also been reported to lead to remission in some patients.


Spinal tumours can occur at any age but (with the exception of lymphoare most prevalent in older animals. They may cause pain or neusigns which are usually insidious in onset. Spinal tumours are uncommon in dogs but account for up to 50% of cats with spinal disease, though many of these are lymphosarcoma in young individuals.

CSF examination is sometimes helpful, but myelography is usually needed to identify the site of the lesion.

Extradural tumours are usually primary bone neoplasms and occasecondary (e.g. from a prostatic carcinoma). In cats lymphois the most common extradural tumour. Radiographic findings may include new bone deposition, bone loss or vertebral collapse. Surgery is possible for some tumours and medical treatment and/or radiotherapy for others.

Intradural neoplasms are usually either:

(1) meningiomas which in dogs occur most often in the cervical spine where they may be amenable to surgery; or

(2) nerve sheath tumours including neurofibromas and neurosarcomas which often occur in the brachial plexus and are difficult to remove surgically.

Primary intramedullary tumours are the least common. They are usually glial cell tumours or result from secondary metastatic spread.

The prognosis for patients with spinal tumours is guarded.

Peripheral nerves

Neoplasia of the brachial plexus are most prevalent in middle-aged and old animals and in dogs they are most often nerve sheath tumours, e.g. schwannomas, neuromas and neurofibromas. They are usually slow growing but are locally invasive and though they rarely spread to the lungs the prognosis is poor.

In dogs a mean age of 7.4 years has been reported for brachial plexus tumours (). Most of the dogs were medium or large breeds and they all presented initially with unilateral intractable foreleg lameness or paresis with muscle atrophy and pain. The spinatus muscles over the scapular were most often involved. Over 45% had radiological or clinical evidence of spinal cord compression or invasion and often a small mass was palpable in the axilla. Homer’s syndrome may occur in conjunction with these tumours in both dogs and cats.


Biopsy of the tumour tissue which is hard and discoloured grey or off-white is possible during exploration of the plexus ().


In dogs with spinal cord involvement dorsal laminectomy is recommended to confirm the diagnosis and assess for surgical removal by a craniolateral approach (). If the proximal border of the tumour can be identified high limb amputation with removal of local spinal nerves is the treatment of choice as local excision will usually result in severe neurolodeficits and local recurrence of the tumour.


Guarded. Local recurrence is common.


Reticulosis is an uncommonly diagnosed condition of adult dogs which causes neurological signs either suggestive of a focal lesion with unilateral signs, or with multifocal signs, including hyperaesthesia. These signs are usually slowly progressive. Severe visual deficits may also be associated with reticulosis.

CSF examination may help in diagnosis though the neurological signs are usually non-specific. On histological examination the disease is charby perivascular mononuclear cell infiltration with proliferation of histiocyte and microglial cellular elements.

Three forms of the disease have been defined cytologically:

(1) granulomatous reticulosis (or granulomatous meningoencephalitis)

(2) neoplastic reticulosis and

(3) microgliomatosis.

Prednisolone at 1-2 mg/day orally has been recommended as treatfor this condition but the long-term prognosis is poor.

Spinal disease

There are several diseases that may involve the spinal canal producing clinical signs including neurological deficits and these need to be differ Radiography is important in reaching an accurate diagnosis and myelography is usually needed to identify space occupying lesions. Aniwith gait abnormalities should also have non-neurological causes eliminated including osteoarthritis (or degenerative joint disease), hip dysplasia, bilateral osteochondritis dessicans and generalised bone dise.g. renal secondary hyperparathyroidism.


Discospondylitis may occur at any age and occurs most frequently in the cervical spine or at the lumbosacral junction. It is an inflammatory process (usually secondary to bacterial infection) of the intervertebral disc space which extends into the vertebral bodies either side and encroaches on the spinal canal. The diagnosis is confirmed by radiology and it needs to be differentiated from spondylosis which is a common incidental radiofinding in older dogs.

Cervical spondylopathy usually occurs in an earlier age (up to 7 years in Dobermans).

Degenerative disc disease

Degenerative disc disease is common in young chondrodystrophic dogs and clinical signs associated with disc degeneration are unusual in geriatric patients of these breeds. In other large breed dogs the condition is more likely to be seen in middle-aged or older animals and they usually present with a gradually progressive hindleg ataxia and paresis. Anti-inflammatory drugs are the treatment oT choice, and surgery is less likely to be successful in these patients than in young animals with acute disc prolapse. Somethere is a concurrent degenerative myelopathy.

Chronic degenerative radiculomyopathy

Most central and peripheral myopathies occur in young animals, but chronic degenerative radiculomyelopathy (CDRM) is frequenfly seen in elderly male German shepherd dogs and it is occasionally seen in other breeds. There is degeneration of the lumbar dorsal columns, fasciculus gracilis, lateral corticospinal tract and around the ventromedian fissure of the white matter of the cord. Lesions also involve the dorsal spinal roots and the thoracolumbar grey matter and nucleus gracilis show asytrocytic sclerosis. These degenerative changes are typical of a ‘dying-back’ disease ().

The cause is unknown although vitamin B12 (cobalamin) deficiency has been suggested by some workers.

Diagnosis is based upon the presenting clinical signs (Table Clinical signs of CDRM) and absence of a space occupying spinal lesion on myelography. Treatment is symptomatic, for example the provision of boots to protect the dorsa of the feet and there is no treatment that can reverse the neurological deficit.

Table Clinical signs of CDRM.

  • Chronic progressive ataxia with paresis and loss of proprioception but no loss of pain sensation.
  • Excessive wearing of the dorsum of the claws (often with skin abrasions) is usually present due to the feet being dragged along the ground.
  • Flexing the hindpaw with its dorsum to the ground fails to elicit a normal placing reflex and turning the dog in a tight circle causes affected dogs to criss-cross their legs and trip themselves up.

Lumbosacral spondylopathy

There are a number of pathological changes that may occur at the lumjunction leading to signs of low back pain or hyperaesthesia with decreased ability to exercise, difficulty in rising, and sometimes faecal or urinary incontinence. The signs are usually bilateral and weak hock flexion is the main neurological deficit (). Large breed working dogs are most often affected though a similar condition has been reported in smaller toy breeds.

The aetiopathogenesis may be due to spinal stenosis, disc protrusion, spondylosis deformans or discospondylitis. Myelography, epidurography, transosseus venography or CT scan are useful for differentiating the cause and electrophysiological testing (EMG) is also helpful.

Decompressive surgical treatment (dorsal laminectomy or foris reported to provide good success, and antibiotic treatment is required for discospondylitis.

Vestibular disease

Both adult cats and dogs can present with acute onset severe vestibular signs including head tilt, circling, leaning and nystagmus In both species the condition is frequently misdiagnosed as stroke’ although post-mortem examinations of the brain in such cases have failed to detect the presence of haemorrhages or infarcts.

The aetiopathogenesis of this syndrome is unknown but it needs to be differentiated from vestibular signs associated with infection (particularly from otitis externa/interna/media, or haemotogenous spread), toxicity (particularly antibiotics such as neomycin, streptomycin and gentamicin), nutritional deficiency (e.g. thiamin deficiency in cats) or neoplasia. Vessigns associated with neoplasia are usually slowly progressive and refractory to treatment.

No specific treatment can be recommended but in both species the condition is self-limiting. Dogs are usually normal within 1-2 weeks, cats in 2-3 weeks.

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