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Potpourri of canine neurologic disorders: Parts I and II (Proceedings)

Article

First case: Infraspinatus muscle contracture in the dog

Infraspinatus muscle contracture in the dog

History/signalment –

1. Hunting/working breeds more commonly affected.

2. Dogs are presented for a chronic, non-painful paddling gait in the affected forelimb.

3. However, there usually is a history of an acute lameness several weeks prior to the presentation in #2. This initial episode of lameness is usually associated with a period of vigorous exercise and subsides in 3-4 days.

Clinical findings –

1. Non-painful gait abnormality consisting of:

- Lateral circumduction of the limb

- Elbow being maintained in adduction throughout stride

- A carpal flip in midpoint of stride

2. Prominent scapular spine

3. While standing, elbow is adducted, shoulder is abducted, and antebrachium is rotated outwardly so that digits are pointing laterally instead of toward the front

Diagnosis –

1. By history, characteristic gait, and atrophy of the infraspinatus muscle.

2. There are no definitive tests to prove diagnosis. Ultrasound could possibly reveal hyperechoic lesions in the infraspinatus muscles.

Treatment/prognosis –

1. Surgery – tenotomy or partial tenectomy of infraspinatus tendon.

2. Dramatic improvement seen immediately post-op in 95% of the cases.

Idiopathic tremor syndrome of adult dogs (white shaker dogs)

History/signalment –

1. Age-usually young adults (9 months – 2 years)

2. Small breeds with white haircoats (esp. Maltese, West Highland White Terriers) comprise the majority of cases.

3. Acute onset of head and generalized whole body tremors.

4. Tremors are exaggerated by handling, locomotion, and excitement. They are reduced at rest and totally stop when the dog is sleeping.

Clinical/neurologic findings –

1. Generalized, rapid whole body tremors. If severe enough, the animal may have trouble with locomotion.

2. Very alert, responsive animal and generally no other neurologic deficits are seen.

3. Strength is very good.

4. Very rarely, head tilt or seizures may occur.

Diagnosis –

1. Primarily made by history, signalment, and neurologic examination.

2. Routine hematology and biochemistry are normal.

3. Cerebrospinal fluid analysis may be normal or show a mild to moderate lymphocytic pleocytosis, and protein elevations.

Differential diagnosis of tremors in adult dogs –

1. Toxicities – metaldehyde, O-Ps, chlorinated hydrocarbons, hexachlorophene, mycotoxins (aflatoxins) are a few examples.

2. Metabolic – hypocalcemia, hypoglycemia.

3. Inflammatory – non-suppurative encephalomyelitis.

Treatment/prognosis –

1. Many animals spontaneously recover over several weeks to months, but mild tremors may persist.

2. Prednisone(should be used in most cases) – 2-3 mg/kg/day divided BID for 5 days, then decreasing to alternate day therapy for another 5 days, then a phased withdrawal over 6 more weeks: this usually results in dramatic disappearance of signs. In some cases, 3-4 months of glucocorticoid therapy may be needed but usually at a decreased dose and frequency.

Gracilis muscle contracture

History/signalment –

1. Most cases are seen in German shepherds but other large breed dogs can be affected.

2. Age 2-11 years (mean 4.7 years)

3. No sex predilection.

4. Lameness usually has an insidious onset, but can be acute in rare instances.

5. Lameness varies in duration prior to presentation by the owner and at times may be up to 7.5 months before the owner seeks veterinary care.

6. Lameness gradually progresses over several months and then plateaus.

Physical examination/gait abnormalities –

1. Gait: There is a shortened stride with rapid medial rotation of the paw, external rotation of the hock, and internal rotation of the stifle during mid to late swing phase of the stride. More pronounced at a trot.

2. Physical Exam: Muscles (gracilis, semitendinosus) are palpable as distinct, firm, taut bands extending from midline of the pelvis or ischiatic tuberosity to the caudomedial aspect of the stifle.

3. Muscles may be painful.

4. Extension of stifles will be limited.

Treatment/prognosis –

1. Medical treatment with corticosteroids, NSAIDS, D-penicillamine, colchicine have been of no benefit.

2. Surgical: transection of associated tendons result in resolution of lameness in all dogs, but problem recurs in all dogs within 1.5-5 months. This is in contrast to the results seen with surgery for infraspinatus contracture. (See above)

Masticatory muscle myositis (MMM)

Clinical presentation –

1. Atrophy and/or swelling restricted to the muscles of mastication.

2. Abnormalities of jaw movement usually include trismus but in rare cases inability to close the jaw may be seen.

3. Inability to open the jaws under anesthesia is a classical finding in MMM.

4. Jaw pain

5. Exophthalmos if presented in the acute stage, enophthalmus seen with chronic form with associated marked muscle atrophy.

6. May be febrile

Differential diagnosis

1. Retrobulbar abscess

2. Extraocular muscle myositis

3. TMJ joint disease

4. Trigeminal neuritis

5. As part of systemic polymyositis

6. Glucocorticoid induced muscle atrophy

Diagnostics –

1. CK may be normal or mildly elevated.

2. Electromyography may demonstrate abnormalities restricted to masticatory muscles but is not necessary for the diagnosis.

3. Demonstration of autoantibodies against masticatory muscle type 2M fibers is diagnostic of MMM (see address for lab below). This test will be negative in cases of polymyositis or atrophy of the masticatory muscles secondary to denervation. This test cannot be used to determine prognosis for return of jaw function or muscle mass. It is for diagnosis only.

4. Evaluation of a muscle biopsy is essential for determining prognosis. Degree of inflammation, amount of fibrosis and myofiber destruction must all be evaluated.

5. Radiographic evaluation for temporomandibular joint abnormalities may be needed in some cases.

6. Probe behind last upper molar for presence of retrobulbar abscess. This is commonly confused with MMM.

Comparative Neuromuscular Lab

Basic Science Building, Room 2095

University of California, San Diego

La Jolle, CA, 92093-0709

www.medicine.ucsd.edu/vet_neuromuscular/index.html

Treatment/monitoring/prognosis –

1. It is important in the treatment of MMM that the correct dosage of corticosteroids be used for an adequate length of time. An immunosuppressive dosage of prednisone should be used until the serum CK returns to the normal range (if elevated) and/or jaw function returns to normal. The dosage should then be decreased until the lowest alternate day dosage needed to maintain the dog free of clinical signs. This alternate day therapy should be maintained for 4-6 months.

2. Azathioprine therapy may be added in cases that do not respond optimally to corticosteroids alone or where the side effects of the corticosteroids cannot be tolerated.

3. In the absence of marked fibrosis and myofiber destruction, the prognosis should be good for return of muscle mass and function.

4. Inflammation and myofiber destruction seems to be particularly severe in the Rottweiler, Doberman, and Samoyed breeds of dogs. Early diagnosis and treatment would be particularly important in these breeds to prevent irreversible myofiber damage.

5. With inadequate drug dosages and duration of therapy, clinical signs will return and may be more difficult to manage.

Fibrocartilaginous embolic ischemic myelopathy (FCE)

Signalment –

1. Non-chondrodystrophoid and giant breeds are more commonly affected.

2. Large breeds most commonly affected include the Labrador retriever, German shepherd, Golden retriever, Great Dane, and Doberman Pinscher. The small breeds represented most frequently include the Miniature Schnauzer, Sheltie, and Miniature Pinscher.

3. Age – most are between the ages of 3 and 7 years.

4. There is no sex predilection.

History –

Signs are typically acute to peracute developing over minutes to hours, with stabilization of signs in the first 24 hours. Signs will reflect the area and extent of spinal cord involvement (see below).

Clinical/neurologic findings –

1. The signs seen are referable to a focal spinal cord lesion.

2. Signs may range from ataxia or mild paresis to upper or lower motor neuron paralysis with loss of pain recognition and may include paraparesis/plegia, tetraparesis/plegia, or hemiparesis/plegia.

3. FCE should be suspected when there is significant lateralization of signs or if there are unusual disparities between sensory and motor function.

4. Lateralizing infarctions in the cervical or cervicothoracic cord may result in an ipsilateral Horner's syndrome with associated ipsilateral hemiparesis.

5. It is important to assess whether deficits are due to lower or upper motor neuron damage since this affects prognosis (see below).

6. Lastly, pain is not a consistent feature of FCE and focal spinal column hyperesthesia is unusual.

Differential diagnosis –

1. Trauma – gunshot wound, fractures.

2. Acute intervertebral disc herniation. (Type I disc)

3. Discospondylitis with associated spinal cord compression.

4. Other vascular disease of the spinal cord.

5. Acute cord trauma secondary to cervical spondylopathy (Wobbler's disease)

Diagnosis –

1. History!!

2. FCE is a diagnosis made by ruling out other causes of acute myelopathy by way of the following tests:

- Survey spinal radiographs – should rule out trauma (fractures), discospondylitis and vertebral neoplasia. It has been stated that in FCE partially collapsed disc spaces may be seen in the area of the suspected lesion, but this author believes this is rare.

- CSF analysis – helps rule out the unusual infectious/inflammatory myelitis which may have an acute onset.

- Myelography – rule out other compressive cord lesions such as disc herniation, hematoma, abscess, etc.

- Potentially, magnetic resonance imaging to assist in determining compressive lesion versus a parenchymal lesion.

3. Reported changes in CSF from dogs with FCE have included hemorrhage, protein elevations with normal white cell numbers, mononuclear pleocytosis with protein elevation, and mixed mononuclear/neutrophilic pleocytosis with protein elevation. One must remember though, that in the majority of cases, the CSF analysis will be normal.

Pathology –

1. Hemorrhagic necrosis and malacia of gray and/or white matter of the spinal cord resulting from occlusion of veins and/or arteries with emboli which have the appearance of fibrocartilage.

Treatment/prognosis –

1. Excellent patient husbandry is important.

2. The only medical therapy with any rationale is to treat FCE similar to that for acute spinal cord injury from concussive trauma. These measures though, have not significantly affected recovery rate or time in animals with FCE. As with spinal cord trauma, animals presented 24 hours to several days after the onset of FCE will probably not benefit from medical therapy.

3. Prognosis:

- The absence of deep pain perception and/or presence of lower motor neuron deficits represent an extremely poor prognosis in this author's opinion.

- Dogs with upper motor lesions have a better prognosis than those with lower motor neuron lesions. Those with lateralization also appear to have a better prognosis than those with a transverse myelopathy.

- Most patients that will improve should do so or begin to within 7-21 days.

Hypomyelination/dysymyelinogenesis of the CNS

Signalment –

1. The breeds that have been reported in the literature include: Bernese mountain dog, Chow Chow, Dalmatian, Lurcher dog, Samoyed, Springer Spaniel, and Weimaraner. The author has also documented this problem in two vizslas, a Norwegian elkhound, and a litter of Catahoula puppies (unpublished observations). It has been reported in Siamese cats also.

Clinical presentation/signs –

1. All puppies present with signs soon after weaning, if not before (2 weeks to 8 weeks of age). There is no sex predilection in most breeds, but in the Springer Spaniel, only males are affected due to an X-linked recessive mode of inheritance.

Differentials to consider –

1. Cerebellar hypoplasia

2. Tremorogenic toxins

3. Glycogen storage disease

4. Hypoglycemia

5. Spongy Degeneration of CNS

Signs –

1. Wide-based stance

2. Motor difficulties (S.Spaniel, Vizslas)

3. Hypermetria

4. Head and body tremors (very rapid and course)

5. Bouncing of pelvic limbs when standing

6. "Bunny-hopping" gait

7. All of the signs dissipate when the puppy is at rest or asleep. Excitement and increased motor activity will worsen the signs.

8. Mentation is normal

Course of disease –

Most puppies with this problem will have signs that plateau by 6 months of age and develop gradual improvement until they are normal. I have seen puppies return to normal by 3-4 months of age. Therefore, one should not be hasty in recommending euthanasia. Some breeds appear to have a more severe form, such as the Springer Spaniel and Vizsla. These two breeds have more significant motor difficulties in addition to the tremors.

Pathology –

The peripheral nerve myelin is usually normal, although peripheral hypomyelination has been reported in Golden retrievers. The lesions are confined primarily to the CNS, where hypomyelination is the predominant finding. It does not appear to be a disorder of myelin breakdown. Oligodendrogial deficiencies manifested by reduced numbers, immature development, and lack of oligodendrocyte differentiation may also be seen. There is variability among the breeds with regard to the histopathologic changes. Whether the breeds which do improve just have delayed maturation and/or differentiation of oligodendrocytes is a theory suggested by some authors.

Treatment –

There is no treatment other than supportive care and allowing the puppies to mature. Certainly, the bitch and stud should be neutered and not used for future breeding.

Steroid – Suppurative Responsive Meningitis (SSRM)

There are approximately 95 cases reported in the literature. The following information is compiled from these reports. The author believes this is a common problem and that the private practitioner will definitely see this disorder if they keep aware of it.

Clinical picture –

1. Age range: 4 mos – 7 yrs (by far most dogs are young, 7 mos – 18 mos of age).

2. Sex predilection: None

3. Breeds- Primarily large breeds, and in some reports Boxers and Bernese mountain dogs seemed to have a predisposition.

4. Clinical Signs- most dogs are presented within a few days of onset of signs, although, some dogs may have a more protracted course before presentation (up to one year in one report).

Most Common Signs

  • Fever (almost all)

  • Cervical rigidity/pain (all)

  • Stiff, stilted gait (all)

  • Anorexia

  • Lethargy

  • Reluctance to rise

Less Common Signs

  • Postural test deficits

  • Vision deficits-optic neuritis

  • Hypermetria

  • Ataxia

  • Degrees of paresis

Even though it is uncommon for these dogs to have neurologic deficits (see above), some defects may be seen, but having said that, it is very unusual for these animals to be so weak that they are non-ambulatory. They may be reluctant to move (due to pain) but if coaxed to get up there is usually minimal weakness.

Diagnosis –

1. CBC: 38/95-Mild-moderate leucocytosis, primarily neutrophilic. 12/95-left shift present.

2. CSF analysis –

- Protein- 15-940 mg/dl

-WBC ct- 4-22,000/μl

- 70-90% neutrophils

- Pandy test- positive in 29/40 tested

Treatment –

1. Minimum of 2-4 mg/kg/day of prednisone until improvement is noticed. (This usually is within 7-10 days)

2. If it is difficult to give oral medication or if one does not have formulated injectable prednisone, then one can use dexamethasone injectable. Use one-seventh of the prednisone dose if you use dexamethasone. (i.e., if your prednisone dose was a total of 70mg per day, then give 10mg of dexamethasone).

3. Once improvement is seen, a slow dose taper over 6-8 weeks is recommended. I usually cut my dose by ½ the 1st taper, and then slowly decrease to alternate day and then every 3-day dose by the end of the 8-week period.

4. Important aspect is not to taper too quickly. These dogs need to be on "some" dose for at least 8 weeks in my opinion. A few patients require "some dose" for months (see below).

Take home messages from these reports concerning treatment for SSRM

1. Have client prepared for long-term steroid therapy. 4-24 months of prednisone therapy (at some minimal dose) may be required.

2. CSF analysis is probably the best way to monitor whether prednisone should be terminated. 3. Relapses are common if you stop steroids too soon (i.e. < 4-6 weeks of therapy).

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