Lesion Localization Flashcards by Courtney Smith

Localization Syndromes

Localizing a neurological lesion is critically important

Consider appropriate differential diagnoses, select appropriate diagnostic tests

A simple method is the creation of “localization syndrome” or distinct areas of the nervous system

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Localization syndromes (sites)

myopathies

neuropathic

Spinal Cord: lumbosacral, thoracolumbar, Cervicothoracic, Cervical

Pontomedullary

Midbrain

Cerebral

Cerebellar

Hypothalamic

Vestibular

Multifocal

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Myopathic Syndro

Generalized weakness

exercise intolerance

Stif, stilted gait

Muscle atrophy or hypertrophy

Muscle pain

Limited join movement late in the disease

Reflexes are preserved

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Diagnostic Approach to myopathies

CBC, Chemistry, UA, T4,

Clinical characteristics and reported disease

Disease specific testing

EMG

Muscle Biopsy

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Myopathies

Immune Mediated Polymyositis

Immune-mediated, inflammatory

Middle-aged, large breed dogs

weakness worse with excercise

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Myopathies

Immune-mediated Polymositis

CK value

Usually elevated

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Myopathies

Immune-mediated Polymositis

Diagnosis

EMG

Biopsy

ANA

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Myopathies

Immune-mediated Polymyositis

Treatment

Immunosuppression

Prednisone

Azathioprine, cyclosporine

Leflunomide, Mycophenolate

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Immune-mediate Polymyositis

General Practive Guidelines

This is not a common disease, but when these dogs are presented the vague nature of the exercise intolerance can be misleading

Common differential: Myasthenia Gravis

Will not respond to pyridostigmine, will respond rapidly to pred

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Myopathies

Maticatory Myositis

The most common myopathy of dogs

Immune-mediated myositis

Large Breed Dogs

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Myopathies

Masticatory Myositis

Early

Hypertrophy, pain of masticaotry muscles

Pain on opening mouth

Ocular signs

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Myopathies

Masticatory Myositis

Late

Atrophy of muscles

Fibrosis

Inability to open mouth (trismus)

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Myopathies

Masitcatory Myositis

Diagnosis

CBC, Chemistry, UA: Normal

EMG: Myopathic potentials

Histopathology: Rarely done anymore

Serum anti-2M antibodies*

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Myopathies

Masticatory Myositis

Differentials (early/painful)

retrobulbar Abscess

TMJ disease

Otitis Externa / media

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Myopathies

Masticatory Myositis

Therapy

Prednisone: 2mg/kg/day for 4-6 weeks, gradual reduction - may be sufficient therapy for many of them

Cyclosporine, Leflunomide, Azathioprine, Mycophenolate: Used when side effects of prednisone are intolerable or corticosteroid use is contraindicated, Used when patients relapse on reduction of pred. Commit to minimum of 12 month use

Supportive

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Myopathies

Exercise-Induced Collapse

Common in Labrador Retrievers: Mutation in DNM1 gene, Defect in nerve communication during exercise, Autosomal Recessive

Clinical Signs: Onset 5 months - 3 years; fit, muscular, excitable; Weakness and collapse after 5-20 minutes of strenous exercise; high rectal temp (>107)

Myopathies

Exercise-Induced Collapse

Diangosis

Genetic testing at U of Minnesota

Myopathies

Exercise-Induced Collapse

Therapy

Avoidance of trigger activity

Steriod Myopathy

Cushing’s disease, iatrogenic

Also Pu/PD, pendulous andomen, alopecia

Generalized muscle atrophy

Steroid Myopathy

Diagnosis

Increased CK, Increased SAP:EMG

Steroid Myopathy

Treatment

Discontinue steroid, treat cushings

Hypothyroid Myopathy

Other signs present: Alopecia, weight gain, inactivity

Hypercholesterolemia, mild anemia

Myxedema

Muscle Atrophy

Hypothyroid Myopathy

Diagnsosis

Measure Total T4

Hypothyroid Myopathy

Treatment

Supplement hormone replacement

Myopathic Disorders

Musclular Dystrophy Labrador Myopathy Distal Myopathy or Rottweilers Canine Stress Syndrome Myotonia congenita Fibrotic Myopathy Nemaline Myopathy Inclusion Myopathy Episodic Muscle Hypertonicity Lipid storage, Glycogen storage Ischemic Myopathy

Feline Hypokalemic Polymyopathy Clinical Signs

Ventroflexion of the neck Muscle weakness

Feline Hypekalemic Polymyopathy Differential Diagnosis

Thiamine deficiency Feline Idiopathic polymyositis Usually have chronic renal failure Primary hyperaldosteronism is important cause

Myasthenia Gravis

N-M Junction disease Congenital: absence of ACh receptors Acquired: Antibodies against the receptor; idiopathic, secondary to thymoma Generalized weakness Normal spinal reflexes Focal MG: megaesophagus, pharyngeal dysfunction

Myasthenia Gravis Diagnosis

Detect ACh receptor antibodies Tensilon Test Nerve Stimulation

Myasthenia Gravis Therapy Pyridostigmine Bromide

Oral anticholinesterase Start low dose, gradually increase Does not improve esophageal motility

Myasthenia Gravis Therapy Immunosuppression

Corticosteroids: generally not recommended as they may worsen weakness or aggravate pneumonia Limited to pyridostigmine-resistant MG Azathioprine, Cyclosporine, Mycophenolate, Leflunomide: Limited evidence for the efficacy of any of these drugs to convert the patient to a negative status and cost/side effects may be significant Spontaneous resolution of disease may happen with no therapy given