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An Urban Experience
WSVA7-0361
NAVC (HOW I TREAT...)
ACUTE ONSET NEUROMUSCULAR DISEASE IN DOGS
S. Platt1
1University of Georgia- College of Veterinary Medicine, Small Animal Medicine & Surgery, ATHENS, USA
HOW I TREAT ACUTE ONSET NEUROMUSCULAR DISEASE IN DOGS
Dr. Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Athens, GA, USA. SRPLATT@UGA.EDU
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-
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.1 Recurrences with no known stimulus have been documented in some dogs and cats.
Botulism
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
  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 7) and dysphagia may be present due to vagus nerve (CN 10) 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
 42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS
  

































































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