Acute Onset Neuromuscular Disease in Dogs
World Small Animal Veterinary Association Congress Proceedings, 2017
Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Small Animal Medicine & Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA

Idiopathic Acute Polyradiculoneuritis (Coonhound Paralysis)

Acute polyradiculoneuritis produces acute flaccid quadriparesis or quadriplegia in any breed of dog or cat. In dogs, the condition was originally called "Coonhound paralysis" as it was first described in Coonhounds 7–10 days after exposure to an antigen in raccoon saliva. The inciting cause is often unknown although recent vaccination or illness can be documented in some cases. There has been some evidence to suggest the involvement of clostridial organisms in the intestine as a source of antigen. These external antigens are apparently similar to proteins comprising part of the ventral nerve roots and motor nerves, and clinical signs are caused by an immune-mediated attack of these structures with the invasion of inflammatory cells. Animals are presented with an acute, progressive, flaccid quadriparesis that often ascends from the pelvic limbs to the thoracic limbs over a 12–24-hour period. On rare occasions, the thoracic limbs are more involved than the pelvic limbs. The palpebral reflex may be depressed or absent in both eyes due to involvement of the facial nerve (CN VII) and dysphagia may be present due to vagus nerve (CN X) dysfunction. If respiratory involvement is severe, abdominal respirations, hypoventilation and hypoxia occur. Hyporeflexia or areflexia with hypotonicity is usually present in all four limbs. Some tail movement may be preserved. Sensation remains intact, and some animals have generalized hyperesthesia. Affected dogs should be closely monitored as they may worsen over a seven-day period before they stabilize and begin to slowly improve. Paresis, then paralysis of intercostal and diaphragmatic muscles can occur, so respiration should be monitored to detect hypoventilation and hypoxia. Blood gas determinations should be evaluated, if possible, to detect increased pCO2 and decreased pO2. Oxygen therapy or assisted ventilation may be necessary for a few days in some cases. Severe generalized muscle atrophy may occur making physical therapy essential. The prognosis is usually good with adequate support and most dogs recover in 4–12 weeks. Avoidance of known antigenic stimuli such as vaccinations should be considered to prevent recurrence of signs. Recurrences with no known stimulus have been documented in some dogs and cats.


Ingestion of toxin from the organism Clostridium botulinum is a rare cause of flaccid quadriparesis or quadriplegia in dogs. Cases documented in dogs have been associated with type C toxin. Natural occurring botulism has not been documented in the cat. The most common source of infection is probably through the ingestion of carrion, although clostridial infections may play a role. The toxin interferes with the release of acetylcholine from the endplates of motor neurons, resulting in failure of neuromuscular transmission. Acute, progressive quadriparesis develops over a 12–24-hour period and varies in severity depending on the amount of toxin ingested. All limb spinal reflexes are depressed or absent and muscle tone is reduced. Facial paralysis, dysphonia, dysphagia and megaesophagus from cranial nerve involvement are often seen. Constipation and urinary retention have also been documented. As the toxin only affects the motor endplates, sensation remains intact. The EMG changes are similar to tick paralysis and coral snake envenomation. The toxin can be identified in the serum, feces, vomitus or carrion by a mouse neutralization test, although this must be done early on in the disease process to be useful. Although a type C antitoxin is available, to be effective it must be administered before entry of the toxin into the nerve endings and most cases already have neurologic signs on presentation. Many affected dogs recover fully within 2–3 weeks.

Myasthenia Gravis

Myasthenia gravis commonly presents as episodic or exercise-induced weakness due to impaired transmission of acetylcholine at the neuromuscular junctions (NMJ) of skeletal muscles. Other clinical presentations of myasthenia gravis include dysphagia, laryngeal paresis, regurgitation, paraparesis and quadriparesis. Myasthenia gravis may be congenital or acquired associated with an immune-mediated or paraneoplastic process. Congenital myasthenia gravis occurs in Jack Russell terriers, smooth fox terriers, Samoyeds and various breeds of cats. Acquired myasthenia gravis may occur in some cats 2–4 months following initiation of methimazole (Tapazole) therapy for hyperthyroidism. The weakness resolves following discontinuation of the methimazole. In immune-mediated myasthenia gravis, antibodies are formed against the acetylcholine receptors (AChR) of skeletal muscles and interfere with normal muscle contraction. Affected animals will develop a progressive shortened stride with exercise, which progresses to total fatigue and inability to walk. Strength returns with a brief rest and they are again able to ambulate for short distances. The palpebral reflex will fatigue with repeated testing and sometimes facial nerve paresis is present.

Despite profound weakness, conscious proprioception and spinal reflexes are usually normal. Megaesophagus and dysphagia are common and can result in excessive salivation, regurgitation, aspiration pneumonia and death. Intravenous administration of the short-acting anticholinesterase, edrophonium chloride (Tensilon) 1–5 mg in dogs and 0.2–1 mg in cats may cause a dramatic improvement in strength during an episode of collapse. If higher doses are given, a cholinergic crisis of bradycardia, profuse salivation, dyspnea, cyanosis and limb tremors may result which can be reversed with intravenous atropine 0.05 mg/kg. Both false-positive and false-negative Tensilon tests can occur.

Other causes of weakness like polymyositis commonly improve with edrophonium chloride. A definitive diagnosis can be made with serology documenting elevated AChR antibodies in the serum. As some cases may be falsely seronegative, re-testing is important in all weak animals suspected to have myasthenia gravis.

The severity of clinical signs may not correspond with the degree of elevation of AChR antibody titers. Megaesophagus and aspiration pneumonia may be seen on thoracic radiographs. In paraneoplastic myasthenia gravis, a thymoma may be seen as a cranial mediastinal mass on thoracic radiographs. A thorough physical and radiographic examination including abdominal ultrasonography should be performed to search for neoplasia. Some dogs with myasthenia gravis have concurrent hypothyroidism and weakness will not improve until both disorders are treated. The serum total T4 or free T4 levels are usually reduced and TSH levels are usually elevated in hypothyroidism. Myasthenia gravis and polymyositis may also occur concurrently and serum CK levels may be elevated. EMG is often normal except for a decremental evoked muscle response on repetitive nerve stimulation of 5/second.

Initial therapy usually consists of the administration of oral pyridostigmine bromide (Mestinon) 0.5–3 mg/kg every 8–12 hours with food. A liquid formulation of pyridostigmine bromide is recommended so that the dose can be easily adjusted to the level needed to control the clinical signs. With high doses, weakness may occur as a result of a cholinergic crisis and therefore a low dose of pyridostigmine is initially given, then slowly increased until weakness is resolved. Oral famotidine (Pepcid AC) 5 mg/kg/day may reduce the nausea and gastrointestinal irritation from the pyridostigmine bromide. Resolution of clinical signs can be seen in many dogs on a spontaneous basis.

Exercise-Induced Collapse of Labrador Retrievers

Young Labrador retrievers between 7 months and 2 years of age may present with weakness and collapse during exercise. The weakness begins in the pelvic limbs but can progress to total collapse followed by a period of confusion. The body temperature is often severely elevated (up to 107°F) and a severe alkalosis is present on blood gas analysis immediately following exercise. Most mildly affected dogs return to normal within 20 minutes. All remaining clinicopathological and electrodiagnostic tests and histological examination of muscle biopsies are normal.


Speaker Information
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Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
University of Georgia
Athens, GA, USA

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