Lecture 1
Differentiate weakness due to muscle disease and weakness due to neurological disease
Muscle disease - weakness Considerations
-Generally not ataxic
-Postural reflexes are normal (e.g., patellar reflex)
Critical to perform a thorough PE and neurologic exam when presented with a weak patient
-Weakness
-Siff/stilted gait
-Trembling
-Ventral neck flexion (low head carrying)
-Lameness
-Exercise intolerance
-Swelling and pain in affected muscles
-Atrophy or fibrosis, with or without pain in affected muscle
Acquired
a. Masticatory Muscle Myositis (MMM)
b. Extraocular myositis: focal, specific
c. Canine and Feline Idiopathic polymyositis
d. Dermatomyositis
e. Protozoal myositis (Toxoplasma gondi)
f. Fibrotic myopathy
Inherited
Masticatory Muscle Myositis
Etiology
History
Clinical Presentation
DDx
Diagnostic Plan
Treatment Plan
Prognosis
Etiology
-Immune mediated disorder
-IgG directed against unique myosin (2M) component of muscles of mastication (Master m., Temporal m., Pterygoid m., Digastric m.)
-Predisposition: large breeds, GS, Doberman, Retrieving breeds.
History
Clinical Presentation
-Early: pain opening the mouth, painful at palpation of masticatory mm., maybe swelling of temporals m. and master m.
-Late: marked atrophy and fibrosis of affected mm.
-Eyes sink into orbit, patient unable to open mouth full range.
DDx
Painful
1. Retrobulbar mass/abscess
2. Dental disease
3. TMJ or bulb disease
4. Neoplasia if unilateral
Non-painful
1. Trigeminal nerve disorder (bilateral disease, dropped jaw)
2. Diffuse polymiositis or polyneuropathy
3. systemic disease: Hypothyroidism, HAC, cancer cachexia.
Diagnostic Plan
-Suspected on clinical findings
-CBS: normal, possible mild anemia, neutrophilia, peripheral eosinophilia
-Chemistry: CK, AST and globulins maybe mildly increased
Circulating 2M antibodies (85-90% positive in acute cases) prior to steroid treatment
Immunohistochemistry on muscle biopsy
-EMG: fibrillations, positive waves, normal is quiet
Treatment Plan
-Glucocorticoids (PREDNISONE) 1-2mg/kg q 12 hours. Tapering dose after initial 3-4 weeks over 4-6 months
-Goal: LED, EOD, may be indefinite
-Commonly reoccurs if tampered too quickly
-Additional immunosupressant if not responsive (Azathioprine, Cyclosporine)
-Dietary management maybe necessary due to limited mouth opening function
Prognosis
-Guarded
Canine Idiopathyc Polymyositis
Etiology
-Presumed autoimmune, diffuse inflammation of skeletal mm. in dogs
-Can be PRIMARY autoimmune or SECONDARY to systemic immune-mediated disease, protozoal, or neoplasia
-Adults affected
-Predisposition: large breeds, GSD, boxers, Newfoundlands, Visuals over represented.
History
Clinical Presentation
-Mild to severe weakness
-Megaesophagus, regurgitation (signs that something else is going on)
-Dysphonia, Dysphagia (weak bark)
-Stiff-stilted gait, may be exacerbated by exercise
-Painful muscles in some dogs
-Prominent atrophy is masseter and temporalis mm.
DDx
-Neoplasia.. think paraneoplastic 2 lymphoma (substances produced by tumor, anal gland carcinoma)
-Systemic Lupus Erythematosus (SLE)
-Toxoplasmosis, Neospora
Diagnosis
-Neurologic exam usually normal unless concurrent polyneuritis
-ELEVATED CK (2-100 fold) and AST
-Elevated gamma globulins
-EMG demonstrates multiple muscle groups affected
-MUSCLE BIOPSY definitive diagnosis
Diagnostic Plan
-CBC, Chemistry, UA, joint taps, protozoal testing, ANA testing, thoracic/abdominal radiographs, ultrasound, fine needle aspirate
-Arthrocentesis
-Even normal size LNs can have abnormal cells and need to be aspirated
Treatment Plan
-Based on Dx findings
-Rule out or treat underlying disease
-Autoimmune diagnosis: PO PREDNISONE 1-2mg/kg q 12 hours, tapering dose at 14 days and 28 days if responding
-May require additional immunosuppressants
-Megaesophagus: elevated feeding, small and frequent meals. Monitor for aspiration
Prognosis
-Varies
-Good if no severe megaesophagus/aspiration
Feline Idiopathic Polymyositis
Profile
-RARE
-Causes diffuse weakness in cats
Very important to rule out common acquired causes of diffuse weakness: hypokalemia and Thiamine deficiency
Clinical Presentation
-Sudden onset of diffuse muscle weakness
-Ventral Neck flexion
-Inability to jump
- +/- muscle pain
Diagnosis
-Neurological exam generally normal
CK AST elevated
70% affected with mildly hypokalemia
-Additional testing for Toxoplasma, FeLV/FIV, thoracic radiographs (Thymoma)
-Muscle biopsy
-EMG: multifocal abnormalities
Treatment Options
**Treat for other more common underlying causes **
-Correct hypokalemia (IV fluids, oral supplementation)
-Treat for thiamine deficiency (IM injections)
-Consider toxin or drug-induced (ex: antibiotics)
-Empirical treatment for toxoplasmosis (Clindamycin) if indicated
Glucocorticoids
-4-6 mg/kg/day
-Tapering over 8-12 weeks
- PO PREDNIDOLONE is preferred in feline patient due to bioavailability. Cats have decreased efficiency of conversion. Less bioavailability
Prognosis
-Spontaneous recovery occurs 1/3 of cases, but recurrence is common
Hypokalemic Myopathy
Clinical Presentation
-Metabolic disorder that affects mainly cats
-Weakness, stiff-stilted gait, exercise intolerance and muscle pain
Diagnosis
-Straightforward with compatible signs
-Potassium <4.0 mEqL
Treatment
-Potassium supplementation and correction of underlying cause
-IV fluids and add Potassium Gluconate (Tumil-K) 1/4 Tsp per 4.5 Kg BW PO BID in food
Dermatomyositis
Profile
-Uncommon inherited autoimmune disease in dogs
-Characterized by dermatitis, vasculitis and polymyositis
-Predisposition: Collies, Shelties, Australian Cattle Dogs, Border Collies
-Skin lesions appear by 3-6 mts of age and may fluctuate
-Erythema, crusts, ulcers, scales, alopecia of inner pinnae on head, face, body
Diagnosis
-High index of suspicion on clinical presentation
-Skin and muscle biopsies
-EMG: spontaneous myofiber electrical activity
Treatment Options
-Oral tetracyclines and Niacinamide orPentoxifylline
-Myositis may require further addition of glucocorticoids when involving the muscle and leading to muscle weakness
-Low stress environment
-Minimize sun exposure
Prognosis
-Variable - overall good but may flair intermittently
Fibrotic Myopathy
-Non-painful disorder
-Characterized by the formation of fibrous band within the muscle
-Likely due to repetitive muscle injury
-Excessive jumping/sprinting can lead to inflammation, hemorrhage, edema, fibrosis in the affected muscles
-Predisposition: GSD, any breed
Clinical Presentation
-Mechanical lameness in the affected limb
-Neurologically normal
-Can palpate a tight, usually non-painful band within the affected muscle
Gracilis and semitendinosis muscles quadriceps, biceps femoris, and semimembranosus (pelvic limb); suprastinatus and infraspinatus mm. (thoracic limb)
Diagnosis
-Based on characteristic lameness and palpation of fibrotic band
-Ultrasound of affected muscle
Treatment Options
-Surgical approaches are described but recurrence is high
-Management through physical conditioning, rehabilitation, pain control as needed
Prognosis
-Guarded, usually not cure
-Quality of life and function can be good in affected patients
Acquired Myopathies - Endocrine/Metabolic (common)
-Glucocorticoid excess/deficiency
-Hyper or Hypo adrenocorticism, resp.
-Hypothyroidism (dogs)
-Hypokalemia (especially in cats)
-Hypocalcemia (especially postpartum)
-Thiamine deficiency (cats)
Postpartum Hypocalcemia
-Nutrition-associated
-Hypokalemic muscle weakness
-Ventral neck flexion
Treatment
-IV fluid and potassium administration
Hypocalcemia postpartum tetani AKS
Clinical signs
Intermittent tremors, painting, painful muscle twitching, disorientation, panting, Eclampsia-tremors
Tetanus
-Sustained contraction of extensor muscles
-No muscle relaxation
-Dogs»_space; cats
-Gram POSITIVE anaerobe Clostridium tetani
-Horses most susceptible, birds less susceptible
Clinical signs
-Appear 5-10 days after wound infection
Treatment
-Wound debridement
-Penicillin
-Antitoxin
-Control muscle spasm
Not a disease of the muscle
“Risus Sardonicus”
-Contracture of the facial muscles if localized “frowned look”
-Saw horse stance if generalized
Inherited Myopathies
-Muscular dystrophy
-Centronuclear myopathy (CNM) of Labrador retrievers
-Myotonia
-Inherited metabolic myopathies
CNM of Labrador Retriever
Inheritance
-Autosomal recessive
Gender
-Both
Clinical signs
-Stiff/stilted gait
-Bunny hopping
-Muscle atrophy
-Poor conformation
Tendon reflexes
-Often reduced
CK levels
-Normal to elevated
Therapy
-L-carnitine supplementation
-Avoid cold.stress/excitement
Prognosis
-Guarded
-Disease often stabilized by 1 year of age
-May have acceptable quality of life
Muscular Dystrophy of Labrador Retrievers
Inheritance
-X-linked
Gender
-Mostly Male
Clinical signs
-Stiff/stilted gait
-Dysphagia
-Tongue hypertrophy
-Ptyalism
Tendon reflexes
-Normal until end stage
CK levels
-Markedly elevated
Therapy
-None
Prognosis
-Poor due to progressive disease
Muscular Dystrophy in Cats
Profile
Clinical signs
-Appear at 5-6 mts of age
-Marked muscular hypertrophy
-Protruding tongue
-Stiff/stilted gait
-Bunny hopping
Diagnosis
-Muscle biopsy
**Markedly elevated CK >30,000 IU/ML
-Immunohistochemistry
Extraocular Myositis (FYI)
Profile
-Myositis confined to extraocular mm. in dogs
-Bulging eyes
-Predisposition: Golden Retrievers, Labradors, Large breed dogs, females
Lecture 2
Clinical Manifestations of and Diagnostic Test for Joint Disorders
General Considerations
-Animals with joint disease commonly present with a history of lameness or gait abnormality
-Lameness may involve ONE joint/limb or MULTIPLE
-Typically traumatic or developmental if ONE joint
-Typically degenerative or inflammatory if multiple joints involved
General Considerations
Inflammatory
-Suppurative cells: neutrophils
-Infectious: Borrelia burgdorferi, Staphylococcus, Ehrlichia spp., Pasteurella multicocida in cats.
-Non-infectious
Erosive: Rheumatoid-like arthritis, Erosive polyarthritis of Greyhounds
Non-erosive: IMPA, SLE, Reactive polyarthritis. Most common in dogs.
Non-Inflammatory
-Non-suppurative cells: mononuclear cells
-Developmental: UAP, FCP, OC/OCD
-Degenerative: hip dysplasia
-Neoplastic
-Traumatic processes
General Considerations
Inflammatory Joint Disease
Inflammatory Joint Disease
-Very painful joints
-Shifting leg lameness “walking on egg shells”
-Reluctance to exercise or move
-Multiple joints usually affected: as many as 25% of dogs with immune mediated polyarthritis DO NOT have obvious pain or swelling
Signs of systemic disease
-Fever, lethargy, inappetence, weakness, stiffness, exercise intolerance
General Considerations
Non-inflammatory Joint Disease
Degenerative
-Low-grade chronic discomfort
-Fluctuating/intermittent lameness
-Reluctance to exercise
-NO SYSTEMIC signs
-Multiple joints may be affected
-Signs are usually consistent from day to day
-Patient often “warms” out of lameness
PE
-Conduct physical examination to localize a region of pain or inflammation
-Animal’s posture and gait
-Manipulate and palpate the spine and muscles, bones, and joints of each limb
-Give equal consideration to systemic examination (e.g., auscultation and abdominal palpation).
PE - DDx for pain upon palpation
-Bones: trauma, panosteitis, hypertrophic osteodystrophy, osteomyelitis, bone neoplasia
-Muscles: myositis, strain/sprain injuries
-Neck: spinal cord or vertebral abnormalities such as IVDD, intracranial disease, meningitis, polyarthritis
-Spine: spinal cord or vertebral abnormalities, IVDD, diskospondylitis, intervertebral facet joint inflammation
PE - Decreased range of motion, crepitation and joint instability suggests:
-Articular damage and wear
-Osteophytes (Bone spurs, or osteophytes, are smooth, bony growths, usually near joints, develop over time in patients with arthritis or joint damage).
-Peri-articular changes
-Tendon/ligament damage
Enthesophytes, Osteophytes Reminder
Osteophytes can be defined as lateral outgrowths of bone at the margin of the articular surface of a synovial joint. An enthesophyte is a bony spur forming at a ligament or tendon insertion into bone, growing in the direction of the natural pull of the ligament or tendon involved.