Neuromuscular disorders (NMDs) in cats represent a broad and complex spectrum of diseases that affect the motor unit, encompassing the peripheral nerves, neuromuscular junctions and skeletal muscles. Although relatively less common in feline patients compared to dogs, these disorders can have significant impacts on quality of life, and in some cases, may be progressive or even life-limiting. The presenting clinical signs can often be vague and non-specific, ranging from episodic or persistent weakness, exercise intolerance, tremors, and generalised or focal muscle atrophy, to more subtle manifestations such as altered vocalisation or reluctance to jump. These clinical features can easily be mistaken for orthopaedic or central neurological conditions, which adds to the diagnostic challenge.
Given the overlapping signs and sometimes insidious onset, a logical and systematic diagnostic approach is essential to differentiate neuromuscular disease from other causes of weakness and mobility issues. This should include a detailed history, comprehensive neurological examination and targeted diagnostic testing such as haematology, biochemistry, electrodiagnostic studies and advanced imaging, along with consideration of muscle and nerve biopsy in select cases.
This article will review the classification of feline neuromuscular disorders and their pathophysiology, clinical presentation and key diagnostic strategies, before exploring treatment options and prognosis. A firm understanding of the underlying mechanisms and disease subtypes is vital to optimise outcomes and provide evidence-based care to affected feline patients.
By the end of this article, readers should be able to:
- Understand the classification and underlying pathophysiology of NMDs in cats
- Identify common clinical signs and differentiate between disorders of the lower motor neurons, neuromuscular junctions and muscles
- Apply a systematic diagnostic approach incorporating clinical, laboratory, electrodiagnostic and imaging data
- Explore treatment options and appreciate the prognostic implications of specific NMDs
- Integrate evidence-based practice and critical thinking when managing feline NMD cases
Anatomy and physiology of the feline neuromuscular system
Understanding the feline neuromuscular system is fundamental in diagnosing NMDs. The motor unit comprises the lower motor neuron (LMN), its axon, the neuromuscular junction and the muscle fibres it innervates. Disruption at any point along this pathway can result in clinical signs of neuromuscular dysfunction. LMNs originate in the spinal cord and brainstem, transmitting impulses via peripheral nerves to skeletal muscles. The neuromuscular junction facilitates signal transmission through the release of acetylcholine, which binds to receptors on muscle fibres, initiating contraction.
Clinical presentation of feline neuromuscular disorders
Cats with NMDs may present with a wide range of clinical signs, reflecting the specific location and severity of the underlying pathology
Cats with NMDs may present with a wide range of clinical signs, reflecting the specific location and severity of the underlying pathology. These signs can be subtle or episodic and are often mistakenly attributed to other systemic illnesses, making early diagnosis particularly challenging in feline patients.
- Generalised or focal weakness is among the most commonly reported signs. Owners may describe their cat as being reluctant to jump, less active than usual or exhibiting poor stamina during routine activities. Weakness may be symmetrical or asymmetrical and can vary in intensity from mild to profound. In severe cases, cats may appear crouched, drag limbs or be unable to stand or walk
- Muscle atrophy may become apparent over time, particularly in chronic or progressive conditions. This is most often noticed in the pelvic or thoracic limbs but can also affect the axial musculature. Palpable muscle wasting should prompt further investigation, especially when paired with weakness or postural abnormalities
- Hyporeflexia or areflexia, observed during neurological examination, points toward LMN dysfunction. Diminished or absent segmental spinal reflexes, such as the patellar or withdrawal reflexes, are hallmark indicators of LMN involvement and can help localise the lesion to the peripheral nerve, neuromuscular junction or muscle
- Cranial nerve deficits may be evident depending on the extent of neuromuscular involvement. These can manifest as facial asymmetry, facial paralysis, dysphagia, voice change or decreased palpebral reflex. Dysphonia or a change in vocalisation may also be noted and are important signs not to overlook
- Exercise-induced weakness is highly suggestive of a neuromuscular junctionopathy, such as myasthenia gravis (MG). Affected cats may appear normal at rest but quickly become fatigued with even minimal exertion. Owners may report episodic collapse, neck ventroflexion or transient inability to stand, which typically resolves with rest. This pattern of fatigability is a classic feature and can help distinguish junctionopathies from myopathies or neuropathies
Other possible signs can include tremors, muscle fasciculations and abnormal postural reactions, although these are less commonly observed. Megaoesophagus, though rare in cats, can occur in some cases of MG, often leading to regurgitation and secondary aspiration pneumonia.
Given the broad spectrum of clinical manifestations, it’s crucial to obtain a detailed history and perform a thorough physical and neurological examination. Video footage provided by owners of abnormal gait or behaviour at home can also be extremely useful in cases where signs are intermittent.
Diagnostic approach to neuromuscular disorders
A methodical approach is essential when investigating suspected NMDs in cats. The following steps are key to achieving an accurate diagnosis.
1. Comprehensive history and physical examination
A thorough history must be taken, focusing on the onset, duration and progression of clinical signs. Consider any known exposure to toxins, recent vaccinations, diet, trauma or potential infectious agents. A general physical exam can identify systemic abnormalities that may provide diagnostic clues.
2. Neurological examination
A complete neurological assessment is critical to localise the lesion. It is important to determine whether the dysfunction lies within the lower motor neurons (LMNs), the neuromuscular junction or the muscle itself. This helps guide further testing and narrows the differential diagnoses.
3. Laboratory testing
- Complete blood count (CBC) and serum biochemistry: useful for identifying underlying systemic or metabolic disorders that may contribute to or mimic neuromuscular disease
- Creatine kinase (CK): elevated levels are indicative of muscle damage and support a primary myopathy
- Acetylcholine receptor antibody titres: essential for confirming a diagnosis of acquired MG
4. Electrodiagnostic testing
- Electromyography (EMG): detects spontaneous electrical activity in muscles, such as fibrillation potentials and positive sharp waves, which are signs of denervation or myopathy
- Nerve conduction studies: evaluate the speed and integrity of nerve signal transmission, aiding in the diagnosis of peripheral neuropathies
5. Imaging
- Magnetic resonance imaging (MRI) or computed tomography (CT): useful in identifying structural or compressive lesions affecting the spinal cord, nerve roots or peripheral nerves
- Muscle and nerve biopsy: often provides a definitive diagnosis, particularly in cases of suspected myopathy or neuropathy. Samples should ideally be obtained from clinically affected, yet not end-stage, tissue
Common feline neuromuscular disorders
1. Myasthenia gravis
Myasthenia gravis is an autoimmune disorder characterised by antibodies acting against acetylcholine receptors, leading to impaired neuromuscular transmission. Clinical signs include generalised weakness and megaoesophagus. Diagnosis is confirmed via acetylcholine receptor antibody testing, and treatment involves anticholinesterase medications and immunosuppressive therapy.
2. Polymyositis
Polymyositis is an inflammatory myopathy presenting with muscle weakness, stiffness and pain. Elevated CK levels and EMG findings support the diagnosis, which is confirmed by muscle biopsy. Immunosuppressive therapy is the mainstay of treatment.
3. Peripheral neuropathies
Peripheral neuropathies can be hereditary or acquired. Clinical signs include weakness, muscle atrophy and decreased reflexes. Diagnosis involves nerve conduction studies and nerve biopsy. Management focuses on addressing the underlying cause and supportive care.
4. Congenital myopathies
Inherited muscle disorders, such as those seen in Devon Rex and Sphynx cats, present early in life with generalised weakness and muscle hypotonia. Diagnosis is confirmed through muscle biopsy and genetic testing. Management is largely supportive.
5. Hypokalaemic polymyopathy
Common in Burmese cats, hypokalaemic polymyopathy results from low potassium levels, leading to muscle weakness and ventroflexion of the neck. Serum biochemistry confirms hypokalaemia, and treatment involves potassium supplementation.
Management strategies for neuromuscular disorders
The successful management of feline NMDs hinges on accurate diagnosis and a targeted, multimodal therapeutic approach. Treatment protocols vary depending on the specific disorder, underlying aetiology and severity of clinical signs. The following strategies are commonly employed across various conditions.
Medical management
Medical management remains the cornerstone of treatment for many neuromuscular conditions.
Immunosuppressive therapy is indicated in immune-mediated disorders such as MG and polymyositis. Corticosteroids, such as prednisolone, are often first-line agents, although long-term use must be carefully balanced against potential side effects including muscle catabolism and increased risk of infection. In refractory or severe cases, adjunctive agents such as azathioprine or cyclosporine may be considered, although their use in cats is less well established.
In cases of focal or generalised MG, anticholinesterase agents such as pyridostigmine bromide are used to improve neuromuscular transmission by inhibiting acetylcholine breakdown at the neuromuscular junction. Dosage adjustments should be guided by clinical response and side-effect profile, with cholinergic crisis a potential risk in overdose situations. Regular monitoring of serum acetylcholine receptor antibody titres may be useful in assessing response to treatment and disease progression.
For inherited or degenerative myopathies (eg muscular dystrophies), pharmacological interventions may be limited, and treatment is often supportive rather than curative.
Supportive and multimodal care
Supportive care plays a pivotal role in improving quality of life and minimising complications.
- Nutritional support is crucial, particularly in patients with dysphagia, muscle wasting or poor body condition. In cases of megaoesophagus secondary to MG, feeding strategies such as elevated feeding positions or gastrostomy tube placement may be required to reduce the risk of aspiration pneumonia
- Physiotherapy and rehabilitation therapy are increasingly recognised as beneficial in maintaining muscle mass, improving mobility and slowing contracture formation. Tailored exercise regimens, hydrotherapy and passive range-of-motion exercises can be implemented depending on the cat’s functional capacity and tolerance
- Airway management and monitoring for respiratory compromise are vital, particularly in conditions associated with hypoventilation or aspiration. Prompt treatment of secondary infections, particularly aspiration pneumonia, is essential and may require oxygen supplementation, antimicrobial therapy and intensive nursing care
- Environmental modification (eg non-slip flooring, raised food bowls, easily accessible litter trays) can greatly enhance comfort and autonomy in affected cats
Pain management
While not always central in neuromuscular diseases, pain management should not be overlooked, particularly in cases with concurrent musculoskeletal strain or neuropathic pain.
Monitoring and long-term follow-up
Long-term monitoring is essential to track disease progression, assess response to treatment and modify therapeutic plans.
Regular neurological re-evaluations, serum biochemistry and specific biomarkers (eg creatine kinase for myopathies, acetylcholine receptor antibody titres in MG) should be incorporated into the management plan.
Periodic electrodiagnostic studies (EMG, nerve conduction studies) may be beneficial in assessing disease trajectory or the emergence of new clinical signs.
In idiopathic or autoimmune conditions, monitoring for spontaneous remission is important. MG, for example, may spontaneously remit in some cats within 6 to 12 months, allowing for eventual tapering or discontinuation of treatment.
Client education and regular communication are key. Owners should be informed about potential complications such as aspiration pneumonia, signs of relapse or medication side effects, and the importance of adhering to the treatment plan.
Case studies
Six-month-old Devon Rex
A six-month-old male Devon Rex presented with progressive exercise intolerance and a stiff, short-strided gait. Neurological examination revealed normal reflexes but obvious muscle fatigue after minimal exertion. Serum biochemistry and CK were unremarkable. EMG revealed decreased muscle fibre recruitment with normal nerve conduction velocity. Genetic testing confirmed the presence of the COLQ variant. A diagnosis of hereditary myopathy was made.
| Discussion points: 1. What are the implications for breeding animals with known genetic variants? 2. How would you counsel the owner regarding long-term prognosis and quality of life? |
Eight-month-old domestic shorthair
An eight-month-old neutered male domestic shorthair presented with acute-onset weakness and episodic collapse. The cat exhibited ventroflexion of the neck and marked generalised weakness. Serum potassium was significantly low (2.2mmol/l); other parameters were within normal limits. The cat responded dramatically to potassium supplementation, confirming a diagnosis of hypokalaemic polymyopathy.
| Discussion points: 1. What are the common causes of hypokalaemia in cats, and how do they contribute to neuromuscular dysfunction? 2. Would you investigate for any underlying disorders in this patient? |
Prognosis
Prognosis in feline NMDs is highly variable and depends on several key factors, including the underlying condition, the extent of neuromuscular involvement, the chronicity of the disease and the cat’s overall health status
Prognosis in feline NMDs is highly variable and depends on several key factors, including the underlying condition, the extent of neuromuscular involvement, the chronicity of the disease and the cat’s overall health status. Some disorders, such as acquired myasthenia gravis, may respond well to appropriate therapy and allow for a good quality of life with ongoing management. Others, like certain congenital myopathies or inherited neuropathies, may carry a more guarded to poor prognosis, especially in cases where progression is rapid or supportive care options are limited. Early identification, accurate diagnosis and prompt initiation of treatment are vital to maximise therapeutic success and improve long-term outcomes. Regular monitoring and client education also play a crucial role in the ongoing management of these patients.
Conclusion
Neuromuscular disorders in cats, while challenging to diagnose, can often be effectively managed with a systematic approach and appropriate therapy. Continued research and awareness are essential for advancing our understanding and treatment of these complex conditions.
