Neuromuscular Disorders in the Cat: Clinical Approach to Weakness

Volk, Holger A.; Shihab, Nadia; Matiasek, Kaspar

doi:10.1016/j.jfms.2011.09.005

Cited by 21 publications

(40 citation statements)

References 46 publications

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“…8 The combination of pelvic limb lower motor neuron signs with absent femoral pulses and cold extremities is pathognomonic for ATE. 8,9 Lower motor neuron signs may be present in forelimbs with a brachial thrombus, where pulselessness may be more difficult to recognise. Foot pads are frequently pale or cyanosed in the affected limb, which is a particularly useful finding in forelimbs.…”

Section: Clinical Presentationmentioning

confidence: 99%

Arterial Thromboembolism

Fuentes

2012

Journal of Feline Medicine and Surgery

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Practical relevance: Feline arterial thromboembolism (ATE) is a common but devastating complication of myocardial disease, often necessitating euthanasia. A combination of endothelial dysfunction and blood stasis in the left atrium leads to local platelet activation and thrombus formation. Embolisation of the thrombus results in severe ischaemia of the affected vascular bed. With the classic 'saddle thrombus' presentation of thrombus in the terminal aorta, the diagnosis can usually be made by physical examination. The prognosis is poor for cats with multiple limbs affected by severe ischaemia, but much better where only one limb is affected or motor function is present. Patient group: Cats with left atrial enlargement secondary to cardiomyopathy are typically predisposed, although cats with hyperthyroidism, pulmonary neoplasia and supravalvular mitral stenosis may also be at risk. Management: Analgesia is the main priority, and severe pain should be managed with methadone or a fentanyl constant rate infusion. Congestive heart failure (CHF) requires treatment with furosemide, but tachypnoea due to pain can mimic signs of CHF. Thrombolytic therapy is not recommended, but antithrombotic treatment should be started as soon as possible. Aspirin and clopidogrel are well tolerated. Evidence base: Several observational studies of ATE have been reported. No randomised, blinded, controlled studies have been reported in cats at risk, for either treatment or prevention of ATE, although such a study comparing aspirin and clopidogrel in cats is currently under way.

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Section: Clinical Presentationmentioning

confidence: 99%

Arterial Thromboembolism

Fuentes

2012

Journal of Feline Medicine and Surgery

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“…Among these are axonal polyneuropathy of Snowshoe cats, Birman cat distal polyneuropathy, glycogenosis type IV in Norwegian Forest cats, alpha‐mannosidosis in Persian cats, Niemann‐Pick disease type C, hyperchylomicronemia (Siamese, Persian, Himalayan, short‐ and longhair domestic cats), hyperoxaluria, hypertrophic neuropathy, and recurrent polyneuropathy in Bengal cats . Inherited or congenital neuropathies usually have an early onset of clinical manifestations within weeks to a few months of age . Acquired neuropathies can occur at any age secondary to exposure to pathogens, toxicants, ischemic events, nutritional deficiencies, endocrinopathies, trauma, neoplasia, immune‐mediated disease, or might be of undetermined cause …”

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confidence: 99%

“…Most polyneuropathies in cats have been reported to involve both sensory and motor components . However, in‐depth electrophysiologic studies for the evaluation of both components are often lacking .…”

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confidence: 99%

“…R eports of motor polyneuropathies in young cats are few, with most limited to inherited or congenital conditions in specific breeds. 1 Among these are axonal polyneuropathy of Snowshoe cats, 2 Birman cat distal polyneuropathy, 3 glycogenosis type IV in Norwegian Forest cats, 4 alpha-mannosidosis in Persian cats, 5 Niemann-Pick disease type C, 6 hyperchylomicronemia (Siamese, Persian, Himalayan, short-and longhair domestic cats), 7,8 hyperoxaluria, 9 hypertrophic neuropathy, 10 and recurrent polyneuropathy in Bengal cats. 11,12 Inherited or congenital neuropathies usually have an early onset of clinical manifestations within weeks to a few months of age.…”

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confidence: 99%

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Electrophysiologic Confirmation of Heterogenous Motor Polyneuropathy in Young Cats

Aleman

Dickinson

Williams

et al. 2014

Veterinary Internal Medicne

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BackgroundReports of motor polyneuropathies in young cats are scarce. Further, in‐depth electrophysiologic evaluation to confirm a motor polyneuropathy in young cats of various breeds other than 2 Bengal cats is lacking.Hypothesis/ObjectivesTo confirm a motor polyneuropathy in young cats of various breeds.AnimalsFive young cats with heterogenous chronic or relapsing episodes of weakness.MethodsRetrospective case series. Cats were presented for evaluation of generalized neuromuscular disease and underwent electrophysiologic examination including electromyography, nerve conduction, and repetitive nerve stimulation. Minimum database and muscle and nerve biopsy analyses were carried out. Descriptive statistics were performed.ResultsDisease onset was at 3 months to 1 year of age and in 5 breeds. The most common clinical sign (5 of 5 cats) was weakness. Additional neurologic deficits consisted of palmigrade and plantigrade posture (4/4), low carriage of the head and tail (4/4), and variable segmental reflex deficits (5/5). Motor nerve conduction studies were abnormal for the ulnar (4/4), peroneal (5/5), and tibial (2/2) nerves (increased latencies, reduced amplitudes, slow velocities). A marked decrement was observed on repetitive nerve stimulation of the peroneal nerve in 3 cats for which autoimmune myasthenia gravis was ruled out. All sensory nerve conduction studies were normal. Histologic evaluation of muscle and nerve biopsies supported heterogenous alterations consistent with motor polyneuropathy with distal nerve fiber loss.Conclusions and Clinical ImportanceHeterogenous motor polyneuropathies should be considered in young cats of any breed and sex that are presented with relapsing or progressive generalized neuromuscular disease.

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“…Regarding the presence of appropriate clinical signs, as no other case of polyneuropathy associated with toxoplasmosis in cats was previously described it may be difficult to support the fulfilling of this criterion; however, as reported above, toxoplasmosis is a recognised differential diagnosis of polyneuropathy in dogs, 10–12 and it has been previously discussed by other authors as a possible cause of similar signs in cats. 14 Despite the absence of direct parasite identification on histopathology, a causal relation between T gondii and the clinical signs in this case is suggested by the serology titres compatible with active infection at both initial presentation and relapse (significant increase of IgG in 4 weeks from clinical recurrence) and by the rapid response to clindamycin in three different occasions. Further tests to detect the presence of T gondii in the muscle samples, including PCR, could have been performed; however, a positive result would have not necessarily supported the causal relation between the parasite and the clinical signs as detectable parasitic DNA does not necessarily differentiate between chronic and acute forms of the disease.…”

Section: Discussionmentioning

confidence: 65%

Distal polyneuropathy in an adult Birman cat with toxoplasmosis

Mari

Shelton

Risio

2016

Journal of Feline Medicine and Surgery Open Reports

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Case summaryA 6-year-old female spayed Birman cat presented with a history of weight loss, stiff and short-strided gait in the pelvic limbs and reluctance to jump, progressing to non-ambulatory tetraparesis over 6 weeks. Poor body condition, dehydration and generalised muscle wastage were evident on general examination. Neurological examination revealed mildly depressed mental status, non-ambulatory flaccid tetraparesis and severely decreased proprioception and spinal reflexes in all four limbs. The neuroanatomical localisation was to the peripheral nervous system. Haematology, feline immunodeficiency virus/feline leukaemia virus serology, serum biochemistry, including creatine kinase and thyroxine, thoracic radiographs and abdominal ultrasound did not reveal significant abnormalities. Electromyography revealed fibrillation potentials and positive sharp waves in axial and appendicular muscles. Decreased motor conduction velocities and compound muscle action potential amplitudes were detected in ulnar and sciatic–tibial nerves. Residual latency was increased in the sciatic–tibial nerve. Histologically, several intramuscular nerve branches were depleted of myelinated fibres and a few showed mononuclear infiltrations. Toxoplasma gondii serology titres were compatible with active toxoplasmosis. Four days after treatment initiation with oral clindamycin the cat recovered the ability to walk. T gondii serology titres and neurological examination were normal after 11 and 16 weeks, respectively. Clindamycin was discontinued after 16 weeks. One year after presentation the cat showed mild relapse of clinical signs and seroconversion, which again resolved following treatment with clindamycin.Relevance and novel informationTo our knowledge, this is the first report of distal polyneuropathy associated with toxoplasmosis in a cat. This case suggests the inclusion of toxoplasmosis as a possible differential diagnosis for acquired polyneuropathies in cats.

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Neuromuscular Disorders in the Cat: Clinical Approach to Weakness

Abstract: Many diseases affecting the feline neuromuscular system have been well described in the veterinary literature, mostly based on retrospective case reports and series. The evidence base for the treatment of feline neuromuscular diseases remains very limited.

Cited by 21 publications

References 46 publications

Arterial Thromboembolism

Arterial Thromboembolism

Electrophysiologic Confirmation of Heterogenous Motor Polyneuropathy in Young Cats

Distal polyneuropathy in an adult Birman cat with toxoplasmosis

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