Inflammatory Disorders of the Peripheral Nerves and Neuromuscular Junction in Animals

Acquired myasthenia gravis in dogs and cats is characterized by neuromuscular conduction failure resulting from a decrease in the number of acetylcholine receptors at the neuromuscular junction. It is caused by the development of circulating antibodies directed against the acetylcholine receptors at the neuromuscular junction.

Acquired myasthenia gravis is fairly common in mature dogs, especially German Shepherd Dogs, Golden Retrievers, and Labrador Retrievers; it is uncommon in cats.

In dogs and cats, as is the case for other species, acquired myasthenia gravis can occur as a paraneoplastic syndrome associated with a thymoma.

Three clinical forms of acquired myasthenia gravis exist in animals: generalized, focal, and fulminant.

Generalized myasthenia gravis is the most common form and is characterized by exercise-induced stiffness, tremors, and weakness that resolve with rest. However, weakness is not always associated with exercise. Megaesophagus is common in the generalized form and is indicated by dysphagia and regurgitation.

Focal myasthenia gravis is characterized by facial, pharyngeal, or esophageal weakness without generalized weakness.

Fulminant myasthenia gravis is the least common form and is characterized by acute, flaccid paralysis and megaesophagus; it progresses rapidly to respiratory paralysis and is often fatal.

Generalized weakness associated with myasthenia gravis often improves within 30 minutes after administration of neostigmine (0.02–0.05 mg/kg; IV, IM, or SC; once) (1), and this improvement can be considered a diagnostic indicator. Cholinergic adverse effects possible with neostigmine administration include salivation, urination, vomiting, diarrhea, increased bronchial secretions, and bradycardia; therefore, some clinicians pretreat patients (especially cats, which tend to be more susceptible to these effects) with an anticholinergic drug.

Definitive diagnosis of acquired myasthenia gravis is based on detection of acetylcholine receptor antibodies (AChRAbs) in serum. However, false-negative results on AChRAb testing can occur, especially early in the disease course or in patients previously treated with immunosuppressive medication.

Treatment of acquired myasthenia gravis consists of administering anticholinesterase drugs, such as pyridostigmine (1–3 mg/kg, PO, every 8–12 hours) or, if oral administration is not possible, neostigmine (0.04 mg/kg, SC or IM, up to every 6 hours) (1, 2). Immunosuppressive dosages of corticosteroids (eg, prednisone for dogs or prednisolone for cats) and other immunomodulating drugs are recommended for patients that do not respond to anticholinesterase treatment. Treatment is discontinued if the AChRAb titer returns to the reference range.

Associated megaesophagus is managed with upright feeding (a device such as a Bailey chair can be used to maintain animals in an upright position) and, in some cases, gastrostomy tube placement for feeding and hydration. Aspiration pneumonia is a frequent complication of megaesophagus and leads to death or euthanasia in approximately 50% of affected dogs (3).

In general, the prognosis for patients with acquired myasthenia gravis but without pneumonia is generally good, and some dogs undergo spontaneous remission, which is evident by detection of a decrease in antibody titer, usually within several months after initial diagnosis (4, 5, 6).

Feline patients with acquired myasthenia gravis are more likely to respond to immunosuppressive medication than to anticholinesterase drugs, and they are less likely to develop megaesophagus.

The prognosis for patients with acquired myasthenia gravis is better than for patients with congenital myasthenia gravis or congenital megaesophagus (7).

Acute idiopathic polyradiculoneuritis in dogs and cats primarily affects the ventral nerve roots and peripheral nerves. It is common in dogs and rare in cats.

Clinical signs often develop 7–14 days after a raccoon bite or scratch (for this reason, this condition is sometimes called Coonhound paralysis). An immune-mediated reaction to an antigen present in raccoon saliva is the suspected cause.

A similar syndrome has been reported sporadically in dogs after administration of vaccines (8, 9); however, a causal relationship with vaccination has not been definitively established. In one retrospective case-control study, vaccination was not found to be associated with development of acute canine polyradiculoneuritis (10). 

Raw chicken consumption is a risk factor in dogs, most likely because of an immune response to Campylobacter spp in contaminated raw chicken (11).

The initial clinical sign of acute idiopathic polyradiculoneuritis is a short-strided gait affecting the pelvic limbs that progresses within 1–2 days to flaccid tetraparesis or tetraplegia and, in some cases, to facial and laryngeal weakness. Occasionally, the thoracic limbs are initially affected. Death from respiratory paralysis can occur in severe cases.

Spinal cord reflexes are weak to absent, and severe muscle atrophy is evident within 10–14 days. Pain perception is intact, and some dogs might appear hyperesthetic, showing clinical signs of discomfort on palpation of the trunk or limbs. Mentation and appetite are not affected. Urination, defecation, and tail movement usually remain normal.

Diagnostic testing for acute idiopathic polyradiculoneuritis includes analysis of CSF collected from the lumbar subarachnoid space; results for affected patients show increased protein concentration and a normal cell count. Electromyographic testing reveals denervation, and nerve conduction studies show marked dispersion and prolonged latency of F-waves, indicative of slowed conduction in the ventral roots.

Histopathological findings include inflammation, demyelination, and varying degrees of axonal degeneration in the ventral nerve roots and peripheral nerves.

There is no effective treatment for acute idiopathic polyradiculoneuritis other than supportive care, which includes maintaining well-padded, clean, dry bedding and providing assistance with eating, drinking, urinating, and defecating. Corticosteroids are not helpful.

In the acute stage, respiration must be monitored, as dogs with respiratory paralysis require mechanical ventilation. Physical therapy, such as passive range-of-motion exercises and assisted standing or walking, is helpful.

Most patients begin to improve spontaneously within 3 weeks after the onset of clinical signs and completely recover in 2–6 months. Animals with severe clinical signs and marked muscle atrophy might recover incompletely. Relapses can occur, especially in hunting dogs that frequently encounter raccoons.

Chronic relapsing idiopathic polyradiculoneuritis in dogs and cats is a rare disease associated with inflammation of the nerves and nerve roots. It affects mature dogs and cats. The cause is unknown; however, immune-mediated mechanisms are suspected.

Clinical signs include exercise intolerance, ataxia, and weakness, which develop slowly over several months. Some patients have spontaneous temporary remissions. Spinal cord reflexes are decreased, and cranial nerves can be affected. In severe cases, decreased sensation is evident.

Diagnosis of chronic relapsing idiopathic polyradiculoneuritis is based on results of analysis of nerve biopsy specimens. Histopathological findings include nonsuppurative inflammation; axonal degeneration; and demyelination of nerves, nerve roots, and, in some cases, dorsal root ganglia.

Treatment with corticosteroids is helpful in some cases; however, chronic relapsing idiopathic polyradiculoneuritis tends to slowly wax and wane, gradually becoming more severe throughout months to years.

Chronic inflammatory demyelinating polyneuropathy is a common disorder in adult dogs and cats. The cause is unknown.

Onset of tetraparesis with hyporeflexia is insidious and sometimes accompanied by cranial nerve dysfunction.

Electromyographic findings are usually normal; however, nerve conduction velocities are slowed, accompanied by temporal dispersion. Histological evaluation of nerve biopsy specimens shows multifocal paranodal demyelination.

Administration of corticosteroids (eg, prednisone 1–2 mg/kg, PO, every 24 hours) usually improves clinical signs (12). Corticosteroids are tapered once clinical signs resolve; however, relapse might occur when treatment is stopped.

Polyneuritis equi, or neuritis of the cauda equina, is characterized by inflammation of the sacrocaudal nerves and, occasionally, other nerves. It affects adult horses of all breeds in Europe and North America.

The cause is unknown; however, an immunological reaction incited by a viral infection is possible. Some affected horses have been found to have circulating antibodies against myelin P2 protein, supporting a possible immune-mediated pathogenesis (13); however, these antibodies are not specific for the disease.

The most consistent clinical signs of polyneuritis equi reflect sacrocaudal nerve involvement and include the following:

• urinary and fecal incontinence

• tail paralysis

• perineal paresthesia or analgesia

• atrophy of the gluteal muscles

• mild pelvic limb ataxia

• penile paralysis in male horses

Affected horses might rub the tail. The thoracic limbs and cranial nerves can also be affected.

Diagnosis of polyneuritis equi is usually based on clinical findings. CSF analysis might show xanthochromia, increased protein content, and mononuclear pleocytosis. Sacral fracture should be excluded by rectal examination and radiographic imaging.

There is no treatment for polyneuritis equi, and the prognosis for recovery in affected horses is poor.

Histopathologically, there is granulomatous inflammation primarily affecting the extradural portions of the sacrocaudal nerves.

Protozoal polyradiculoneuritis occurs in dogs, especially puppies, and is caused by infection with Toxoplasma gondii or Neospora caninum. Transplacental infection is most common, and multiple puppies in a litter can be affected.

Affected puppies are healthy at birth but by 3–8 weeks old develop paraparesis, a "bunny-hopping" gait, and weak or absent spinal reflexes. Over a period of several weeks, the pelvic limbs develop severe extensor rigidity and muscle atrophy. Without treatment, protozoal polyradiculoneuritis can progress to the thoracic limbs, eventually leading to dysphagia and fatal respiratory paralysis.

Serum CK activity is often increased in affected dogs. Analysis of CSF usually shows an increased protein concentration and elevated leukocyte count (neutrophils, mononuclear cells, and eosinophils). Detection of antibodies against T gondii or N caninum in serum or CSF, or identification of either organism on muscle biopsy, can also facilitate the diagnosis.

Early treatment of protozoal polyradiculoneuritis provides the best level of efficacy; muscle contracture, severe denervation, or paralysis may be irreversible once established (14).

Treatment consists of antiprotozoal treatment (see Neosporosis in Dogs and Toxoplasmosis in Animals) and supportive care (eg, physical therapy, nutritional support, or fluid therapy to maintain hydration).

The prognosis for neurological recovery is poor in dogs with pelvic limb rigidity.

Sensory ganglioneuritis affects dogs of any breed; however, Siberian Huskies are at increased risk. It typically occurs in dogs aged 1–6 years old. The cause is unknown; however, loss of neurons in dorsal root ganglia with infiltration of lymphocytes and macrophages is observed at necropsy.

Dogs with sensory ganglioneuritis develop ataxia of all limbs with no paresis, as well as dysphagia, regurgitation, and difficulty prehending food. Hyperesthesia and self-mutilation occur in some cases. There is decreased proprioceptive positioning, weak to absent patellar reflexes, and decreased to absent pain perception in the limbs and face.

Diagnosis is based on clinical signs, electrodiagnostic testing that demonstrates slowed sensory nerve conduction, and biopsy of a mixed or sensory nerve that shows loss of myelinated axons and endoneural fibrosis.

There is no effective treatment for sensory ganglioneuritis; the disease typically progresses and leads to a decision of euthanasia.

Idiopathic trigeminal neuropathy (also known as "dropped jaw syndrome") is characterized by acute onset of flaccid jaw paralysis in the absence of an identifiable underlying cause. Despite the historical use of the term "trigeminal neuritis," definitive evidence of inflammation within the trigeminal nerve is limited (15, 16, 17).

Idiopathic trigeminal neuropathy is a well-recognized disorder in dogs but is poorly documented in cats (17).

Affected animals cannot close the mouth and have difficulty eating and drinking. Horner syndrome, facial paresis, and decreased facial sensation can be associated with idiopathic trigeminal neuropathy.

Histopathological findings can include bilateral nonsuppurative inflammation and demyelination in the motor branches of the trigeminal nerve (17).

Patients with idiopathic trigeminal neuropathy usually recover spontaneously within 3–4 weeks after the onset of clinical signs.

Fluid therapy and nutritional support might be necessary. Steroids have not been proven to shorten the recovery period for affected patients.

• Myasthenia gravis. Cornell Richard P. Riney Canine Health Center.

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7. Mignan T, Targett M, Lowrie M. Classification of myasthenia gravis and congenital myasthenic syndromes in dogs and cats. J Vet Intern Med. 2020;34(5):1707-1717. doi:10.1111/jvim.15855

8. Schrauwen E, Van Ham L. Postvaccinal acute polyradiculoneuritis in a young dog. Prog Vet Neurol. 1995;6(2):68-70.

9. Gehring R, Eggars B. Suspected post-vaccinal acute polyradiculoneuritis in a puppy. J S Afr Vet Assoc. 2001;72(2):96. doi:10.4102/jsava.v72i2.626

10. Laws EJ, Harcourt-Brown TR, Granger N, Rose JH. An exploratory study into factors influencing development of acute canine polyradiculoneuritis in the UK. J Small Anim Pract. 2017;58(8):437-443. doi:10.1111/jsap.12683

11. Martinez-Anton L, Marenda M, Firestone SM, et al. Investigation of the role of Campylobacter infection in suspected acute polyradiculoneuritis in dogs. J Vet Intern Med. 2018;32(1):352-360. doi:10.1111/jvim.15030

12. Braund KG, Vallat JM, Steiss JE, Panangala VS, Zimmer PL. Chronic inflammatory demyelinating polyneuropathy in dogs and cats. J Peripher Nerv Syst. 1996;1(2):149-155.

13. Aleman M, Katzman SA, Vaughan B, et al. Antemortem diagnosis of polyneuritis equi. J Vet Intern Med. 2009;23(3):665-668. doi:10.1111/j.1939-1676.2009.0285.x

14. Silva RC, Machado GP. Canine neosporosis: perspectives on pathogenesis and management. Vet Med (Auckl). 2016;7:59-70. doi:10.2147/VMRR.S76969

15. Levitin HA, Lampe R, Hecht S. Case report: meningoencephalomyelitis of unknown etiology manifesting as a bilateral cranial polyneuropathy in 3 dogs. Front Vet Sci. 2020;7:326. doi:10.3389/fvets.2020.00326

16. Musso C, Le Boedec K, Gomes E, Cauzinille L. Diagnostic values of clinical and magnetic resonance findings in presumptive trigeminal neuropathy: 49 dogs. J Am Anim Hosp Assoc. 2020;56(2):106-113. doi:10.5326/JAAHA-MS-6997

17. de Lahunta A, Glass E. Lower motor neuron: general somatic efferent, cranial nerve. In: Veterinary Neuroanatomy and Clinical Neurology. 3rd ed. Saunders; 2009:134-167.