A review of a lecture by Dr Laurent Garosi at Zoomies 2026

This lecture provides a systematic approach to identifying neuromuscular weakness in small animal patients, a condition with the potential to be misdiagnosed as spinal cord disease. Using clinical case examples, Dr. Garosi focuses on the telltale signs that differentiate neuromuscular disorders from spinal or brain lesions, outlines a practical two-step diagnostic workup, and reviews the four most common neuromuscular diseases encountered in practice. The emphasis throughout is on practical clinical skills, from proper reflex testing to interpreting laboratory results, enabling early recognition of these conditions, facilitating earlier and more effective management.

1. The Cardinal Signs: Differentiating Neuromuscular from Spinal Disease

The single most important clinical skill in this area is recognising that neuromuscular weakness presents differently from spinal cord disease. The key differentiators are:

• Decreased extensor tone on all four limbs: Test by observing the patient standing and lifting the contralateral limb; with neuromuscular disease, the limb sinks as the animal cannot maintain extension against gravity
• Decreased flexor withdrawal on all four limbs: Test by fully flexing the limb and then pulling it towards you; reduced resistance indicates abnormality
• Muscle wastage: Often rapid and pronounced in polyneuropathies and myopathies
• Palmigrade or plantigrade stance: Flat-footed posture due to reduced extensor tone
• Intermittent or exercise-induced weakness: Particularly characteristic of junctionopathies and some myopathies
• Cranial nerve signs: Decreased palpebral reflex, reduced gag reflex, diminished jaw tone, or altered bark/meow may be present in some neuromuscular disorders
• Ventroflexion of the neck: Decreased extensor tone of cervical muscles, more common in cats

Crucially, spinal cord disease will not cause cranial nerve signs and rarely causes exercise-induced weakness. The paw positioning (proprioceptive) response may remain normal in early neuromuscular disease, unlike spinal lesions.

2. The WEST Test: A Practical Solution for Feline Exercise Testing

Cats present a unique challenge because owners do not walk them, and exercise-induced weakness is difficult to elicit in the consultation room. The Wheelbarrow Exercise Stress Test (WEST) provides a practical solution:

• Hold the cat with its hindlimbs elevated, forcing it to walk on its forelimbs in a handstand position
• Continue for approximately one minute or until the cat shows signs of fatigue
• Observe for development of weakness, head drooping, or reduced hopping responses
• Re-test flexor withdrawal and extensor tone immediately after exercise

This simple test can reveal weakness that is not apparent at rest and is particularly valuable for cats with suspected myasthenia gravis or other intermittent neuromuscular conditions. If exercise testing is not possible, asking owners to video the dog during walks can provide similar diagnostic information.

3. The Two-Step Diagnostic Approach

When neuromuscular weakness is suspected clinically, a systematic two-step workup is essential. The most common mistake is proceeding directly to muscle and nerve biopsy without first excluding systemic causes.

Step One: Rule Out Systemic Causes of Weakness
The analogy of an iceberg is useful here: the visible neuromuscular signs are only the tip, while systemic disease forms the larger submerged portion. Investigations should include:

• Blood work: Full biochemistry (electrolytes, glucose, creatinine kinase), haematology (anaemia), and specific tests for endocrine disease
• Urinalysis: To assess for diabetes and kidney dysfunction
• Thoracic radiographs: To identify neoplasia (thymoma), megaesophagus, or aspiration pneumonia
• Serology: Toxoplasma and Neospora in dogs; Toxoplasma in cats
• Anti-acetylcholine receptor antibody testing: For myasthenia gravis
• Tensilon (edrophonium) or neostigmine test: A therapeutic trial to screen for myasthenia

Step Two: Primary Muscle and Nerve Disease
If Step One draws a blank, proceed to:

• Muscle biopsy: Cranial tibial muscle is preferred
• Nerve biopsy: Fascicular biopsy of the tibial nerve (no more than half the width, 0.8-1 cm length)
• Samples should be sent to specialised laboratories for immunohistochemistry
• Electromyography (EMG) and nerve conduction studies: Useful adjuncts when clinical signs are subtle

The biopsy results must be interpreted in the context of Step One findings. Inflammatory changes require correlation with serology to distinguish infectious from immune-mediated aetiology. Degenerative changes may indicate endocrine disease and should be correlated with endocrine testing.

4. Creatine Kinase: Interpretation and Pitfalls

Creatine kinase (CK) is a muscle enzyme that rises when muscle membranes are damaged, but its interpretation requires care:

When CK is elevated:

• Very high levels (thousands to tens of thousands) suggest myositis or myonecrosis
• Polymyositis typically causes markedly elevated CK
• Muscle trauma, seizures, or exhausting exercise can cause transient elevation that normalises within days
• In cats, anorexia or chronic debilitating disease (e.g. chronic kidney disease, cachexia) can elevate CK into the thousands, mimicking primary muscle disease
• Myopathy due to hypokalaemia in cats produces high CK due to myonecrosis

When CK is normal:

• Does not rule out muscle disease, as many myopathies do not cause membrane damage
• Junctionopathies (myasthenia) and neuropathies typically have normal CK
• Some myopathies may show normal CK if biopsy is performed during a quiescent phase

Clinical pearl: If CK is mildly elevated and clinical signs are intermittent, repeat testing in one to two weeks. Increasing levels indicate ongoing muscle membrane damage requiring further investigation.

5. The Four Most Common Neuromuscular Diseases

Acute Idiopathic Polyradiculoneuritis (Coonhound Paralysis)

• Rapid onset over 24-72 hours, often starting in one hindlimb then generalising
• Progressive weakness up to 10 days from onset
• No megaesophagus (distinguishes from myasthenia)
• Sensation may be reduced or hyperaesthetic
• CSF shows elevated protein with normal cell count
• Prognosis: most recover spontaneously over 3-4 weeks (up to 6 months)
• Treatment: supportive care only; steroids are not beneficial
• Campylobacter jejuni (often from raw chicken) is a recognised trigger in some cases

Acquired Myasthenia Gravis

• Autoantibodies targeting acetylcholine receptors on muscle membrane
• Classic presentation: exercise-induced weakness improving with rest
• Commonest form is generalised, affecting all four limbs (hindlimbs often worse)
• Megaesophagus occurs in approximately 80% of affected dogs (less common in cats)
• Focal forms: cranial nerve signs (decreased gag, altered voice) or megaesophagus alone
• Diagnosis: anti-acetylcholine receptor antibody titres; Tensilon/neostigmine test can provide rapid support
• Treatment in dogs: pyridostigmine bromide (Mestinon) alone initially; spontaneous remission occurs in many cases within six months
• Immunosuppression is reserved for refractory cases or those failing symptomatic treatment
• Cats: always use immunosuppression from the start; thymoma present in 25% of cases
• Prognosis: poor in dogs (40% survival to one year) due to aspiration pneumonia; better in cats

Polymyositis (Immune-Mediated Inflammatory Myopathy)

• Muscle biopsy shows inflammatory infiltrate
• Must rule out infectious (protozoal) and paraneoplastic causes
• Treatment: combination of prednisolone and azathioprine to reduce catabolic effects of high-dose steroids
• Treatment duration: minimum six months with gradual tapering

Hypokalaemic Myopathy in Cats

• Potassium < 3.5 mmol/L (more significant if < 3.0)
• Causes: chronic kidney disease, hyperthyroidism, reduced intake
• CK is often markedly elevated due to myonecrosis from low potassium
• Clinical signs: ventroflexion of neck, generalised weakness, muscle pain
• Treatment: intravenous potassium supplementation followed by oral; treat underlying cause
• Congenital form described in Birman and Burmese cats

6. Megaesophagus: A Critical Clue

The presence of megaesophagus is a pivotal differentiating feature:

• Myasthenia gravis: Megaesophagus is present in 80% of affected dogs; less common in cats due to anatomical differences in oesophageal muscle composition
• Polyradiculoneuritis: Megaesophagus is NOT a feature; if present, myasthenia is much more likely
• Aspiration pneumonia: A major complication and cause of mortality, particularly in myasthenic patients
• Management: Feeding in an elevated position (Bailey Chair) or PEG tube placement may be required for severely affected animals

7. Treatment Considerations and Prognostic Factors

Supportive care is paramount across all neuromuscular conditions:

• Recumbent patients require careful nursing, physiotherapy, and monitoring for hypoventilation
• Ventilatory failure is the most common cause of death; respiratory function must be monitored closely
• Aspiration pneumonia prevention through appropriate feeding positioning

Myasthenia gravis specific considerations:

• Pyridostigmine dosing is highly individualised; start low and titrate to effect
• Cholinergic crisis (overdosing) mimics underdosing; Tensilon test differentiates
• Serial antibody titres guide treatment duration in dogs not receiving immunosuppression
• Thymectomy may be curative in cases with thymoma

The biggest killer in neuromuscular disease is not limb weakness but respiratory complications – hypoventilation and aspiration pneumonia. Clinicians must monitor ventilation carefully and be prepared to intervene early with appropriate respiratory support.