Polyneuropathy in dogs and cats

Last updated July 12, 2019

Polyneuropathy in dogs and cats is a collection of peripheral nerve disorders that often are breed-related in these animals. Polyneuropathy indicates that multiple nerves are involved, unlike mononeuropathy. Polyneuropathy usually involves motor nerve dysfunction, also known as lower motor neuron disease. Symptoms include decreased or absent reflexes and muscle tone, weakness, or paralysis. It often occurs in the rear legs and is bilateral. Most are chronic problems with a slow onset of symptoms, but some occur suddenly.

The peripheral nervous system (PNS) is one of two components that make up the nervous system of bilateral animals, with the other part being the central nervous system (CNS). The PNS consists of the nerves and ganglia outside the brain and spinal cord. The main function of the PNS is to connect the CNS to the limbs and organs, essentially serving as a relay between the brain and spinal cord and the rest of the body. Unlike the CNS, the PNS is not protected by the vertebral column and skull, or by the blood–brain barrier, which leaves it exposed to toxins and mechanical injuries.

Polyneuropathy is damage or disease affecting peripheral nerves in roughly the same areas on both sides of the body, featuring weakness, numbness, and burning pain. It usually begins in the hands and feet and may progress to the arms and legs and sometimes to other parts of the body where it may affect the autonomic nervous system. It may be acute or chronic. A number of different disorders may cause polyneuropathy, including diabetes and some types of Guillain–Barré syndrome.

A motor nerve is a nerve located in the central nervous system (CNS), usually the spinal cord, that sends motor signals from the CNS to the muscles of the body. This is different from the motor neuron, which includes a cell body and branching of dendrites, while the nerve is made up of a bundle of axons. Motor nerves act as efferent nerves which carry information out from the CNS, as opposed to afferent nerves, which send signals from sensory receptors in the periphery to the CNS. There are also nerves that serve as both sensory and motor nerves called mixed nerves.

Most common types of polyneuropathy

Birman cat distal polyneuropathy is an inherited disorder caused by decreased numbers of myelinated axons in the central and peripheral nervous systems.^[1] Astrogliosis (an increase in the number of astrocytes) is also noted. The lesions are most commonly found in the lateral pyramidal tract of the lumbar spinal cord, the fasciculi gracili of the dorsal column of the cervical spinal cord, and the cerebellar vermian white matter.^[2] Symptoms start at the age of 8 to 10 weeks, and include frequent falling and walking on the hock.^[3] The prognosis is poor. The disease is suspected to have a recessive mode of inheritance.^[4]
Botulism is very rare in dogs and usually follows feeding on carrion.^[5] Symptoms include weakness, difficulty eating, acute facial nerve paralysis, and megaesophagus. Compared to other species, dogs and cats are relatively resistant to botulism.^[6]
Dancing Doberman disease primarily affects the gastrocnemius muscle in Dobermans. It usually starts between the ages of 6 and 7 months.^[3] One rear leg will flex while standing. Over the next few months, it will begin to affect the other rear leg. Eventually, the dog is alternatively flexing and extending each rear leg in a dancing motion. Dancing Doberman disease progresses over a few years to rear leg weakness and muscle atrophy. No treatment is known, but most dogs retain the ability to walk and it is painless.^[7]
Diabetes neuropathy is more common in cats than dogs. It is caused in part by prolonged hyperglycemia (high blood sugar) and results in dysfunction of one or both tibial nerves and a plantigrade stance (down on the hocks). It may resolve with treatment of the diabetes.^[8] The pathology of this condition in cats has been shown to be very similar to diabetic neuropathy in humans.^[9]
Distal symmetric polyneuropathy symptoms include atrophy of the distal leg muscles and the muscles of the head, and rear limb weakness. No treatment is known and the prognosis is poor. This is most commonly seen in Chesapeake Bay Retrievers, St. Bernards, Great Danes, Newfoundlands, Collies, and Labrador Retrievers.^[3]
Dysautonomia is primarily seen in cats. Symptoms include vomiting, depression, anorexia, weight loss, dilated pupils, third eyelid protrusion, sneezing, slow heart rate, and megaesophagus. The prognosis is poor and supportive treatment is necessary. Recovery in cats may take up to one year.^[10]
Giant axonal neuropathy is a rare disease in the German Shepherd dog. It usually becomes evident between the ages of 14 and 16 months.^[1] Symptoms include rear limb weakness, decreased reflexes, muscle atrophy, megaesophagus, and loss of bark. No treatment is known and it has a poor prognosis.
Hyperchylomicronemia or hyperlipoproteinemia is a type of inherited hyperlipidemia in cats. Polyneuropathy is caused by stretching or compression of nerves near bone by xanthomas, which are lipid deposits. It can cause Horner's syndrome, facial nerve paralysis, and femoral nerve, tibial nerve, radial nerve, trigeminal nerve, or recurrent laryngeal nerve paralysis.^[3]
Hypertrophic neuropathy is also known as canine inherited demyelinative neuropathy (CIDN) and is inherited in the Tibetan Mastiff. Symptoms usually start between the ages of 7 and 10 weeks,^[3] and include weakness, decreased reflexes, and loss of bark. Sensory function remains, but a poor gait or an inability to walk may present. With no treatment available, the prognosis is guarded. The trait is inherited as an autosomal recessive.^[11]
Hypoglycemia -induced polyneuropathy is especially seen in conjunction with insulinoma.
Myasthenia gravis
Polyradiculoneuritis is inflammation of the nerve roots. The most common type is Coonhound paralysis. This is similar to Guillain–Barré syndrome in humans. Coonhound paralysis seems to be secondary to a raccoon bite, probably due to some factor in the saliva. However, it can also occur without any interaction with a raccoon. It can happen in any breed of dog. When associated with a raccoon bite, the symptoms start 7 to 11 days after the bite,^[3] and include rear leg weakness progressing rapidly to paresis, and decreased reflexes. When not associated with a raccoon bite, the same symptoms occur, with the paresis taking about 3–4 days to reach its maximum effect. Severe cases have a loss of bark, trouble breathing, and an inability to lift the head. Typically, the duration of the paralysis is 2 to 3 months,^[3] but can last up to 6 months. Treatment is proper nursing care, and the prognosis is good in mild cases.^[12] In bad cases,^[12] the dog does not completely recover the initial muscular capability but still is able to live for years. In very bad cases, breathing can be impaired, and unless the dog is placed on a ventilator, suffocation will occur. Polyradiculoneuritis has also been seen 1-2o weeks after vaccination in dogs and cats.^[13] It can also be caused by toxoplasmosis.
Rottweiler distal sensorimotor polyneuropathy is characterized by distal muscle denervation, but the cause is unknown.^[7] It affects young adult Rottweilers. The symptoms include weakness of all four legs and decreased reflexes. The disease is gradually progressive. Treatment is possible with corticosteroids, but the prognosis is poor.
Sensory neuropathies are inherited conditions in dogs and cause an inability to feel pain and a loss of proprioception. Self-mutilation is often seen. No treatment has been found, and the prognosis is poor in severe cases. Several breeds are affected:
- Boxer symptoms usually occur around two months of age as a slowly progressive disease.^[3]
- Dachshund (longhaired) disease usually occurs between 8 and 12 weeks of age,^[3] and causes urinary incontinence, loss of pain sensation all over the body, and penis mutilation. It is probably inherited as an autosomal recessive trait.^[11]
- English Pointer illness usually occurs between the ages of 3 and 8 months^[3] and most commonly involves licking and biting at the paws. No treatment is known and a poor prognosis is given. It is inherited as an autosomal recessive trait.^[11]
The Boxer is a medium-sized, short-haired breed of dog, developed in Germany. The coat is smooth and tight-fitting; colors are fawn brindled or white, with or without white markings. Boxers are brachycephalic, have a square muzzle, mandibular prognathism, very strong jaws, and a powerful bite ideal for hanging on to large prey. The Boxer was bred from the Old English Bulldog and the now extinct Bullenbeisser which became extinct by crossbreeding rather than by a decadence of the breed. The purpose of the crossbreeding was the wish to eliminate the excessive white color of the breed, and the necessity of producing thousands of dogs for one of the most popular breeds in the world. The Boxer is part of the Molosser group. This group is a category of solidly built, large dog breeds that all descend from the same common ancestor, the large shepherd dog known as a Molossus. The Boxer is a member of the Working Group.
The dachshund, also known as the sausage dog or wiener dog is a short-legged, long-bodied, hound-type dog breed. They may be smooth-haired, wire-haired, or long-haired.
The Pointer, often called the English Pointer, is a medium to large-sized breed of dog, developed in England as a gun dog. It is one of several pointing breeds.
Spinal muscular atrophy occurs in cats and dogs, and is caused by the death of nerve cells in the spinal cord. This progressive disease has no known treatment and a poor prognosis. Affected dog breeds include the Swedish Lapland Dog, Brittany Spaniel, English Pointer, German Shepherd dog, Rottweiler, and Cairn Terrier.^[3] Maine Coons are one of the affected cat breeds.^[14]
Tick paralysis is an acute, ascending motor paralysis that occurs in dogs and cats.^[15] The cause is a neurotoxin in the saliva of certain species of adult ticks. Dermacentor species predominate as a cause in North America, while Ixodes species mainly cause the disease in Australia.^[1] The onset of symptoms is 5 to 9 days after tick attachment,^[16] and include incoordination progressing to paralysis, changed voice, and difficulty eating. Death can occur secondary to paralysis of the respiratory muscles, but in North America, a good prognosis results once the ticks are removed. Recovery is usually in 1 to 3 days.^[1] In Australia, however, it is a more severe disease with cranial nerve effects, and death can occur in 1 to 2 days.^[3]
Toxic neuropathies are most commonly caused by vincristine, thallium, and lead. In cats, the symptoms include paresis, hyporeflexia, and muscle tremors.^[17]

The Birman, also called the "Sacred Cat of Burma", is a domestic cat breed. The Birman is a long-haired, colour-pointed cat distinguished by a silky coat, deep blue eyes, and contrasting white "gloves" or "socks" on each paw.

An axon, or nerve fiber, is a long, slender projection of a nerve cell, or neuron, in vertebrates, that typically conducts electrical impulses known as action potentials away from the nerve cell body. The function of the axon is to transmit information to different neurons, muscles, and glands. In certain sensory neurons, such as those for touch and warmth, the axons are called afferent nerve fibers and the electrical impulse travels along these from the periphery to the cell body, and from the cell body to the spinal cord along another branch of the same axon. Axon dysfunction has caused many inherited and acquired neurological disorders which can affect both the peripheral and central neurons. Nerve fibers are classed into three types – group A nerve fibers, group B nerve fibers, and group C nerve fibers. Groups A and B are myelinated, and group C are unmyelinated. These groups include both sensory fibers and motor fibers. Another classification groups only the sensory fibers as Type I, Type II, Type III, and Type IV.

Astrogliosis is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from CNS trauma, infection, ischemia, stroke, autoimmune responses, and neurodegenerative disease. In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function, and synaptic remodeling. Astrogliosis changes the molecular expression and morphology of astrocytes, causing scar formation and, in severe cases, inhibition of axon regeneration.

Related Research Articles

Spinal muscular atrophies (SMAs) are a genetically and clinically heterogeneous group of rare debilitating disorders characterised by the degeneration of lower motor neurons and subsequent atrophy (wasting) of various muscle groups in the body. While some SMAs lead to early infant death, other diseases of this group permit normal adult life with only mild weakness.

Peripheral neuropathy, often shortened to neuropathy, is a general term describing disease affecting the peripheral nerves, meaning nerves beyond the brain and spinal cord. Damage to peripheral nerves may impair sensation, movement, gland or organ function depending on which nerves are affected; in other words, neuropathy affecting motor, sensory, or autonomic nerves result in different symptoms. More than one type of nerve may be affected simultaneously. Peripheral neuropathy may be acute or chronic, and may be reversible or permanent.

Tick paralysis is the only tick-borne disease that is not caused by an infectious organism. The illness is caused by a neurotoxin produced in the tick's salivary gland. After prolonged attachment, the engorged tick transmits the toxin to its host. The incidence of tick paralysis is unknown. Patients can experience severe respiratory distress.

Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously. It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.

Laryngeal paralysis in animals is a condition in which the nerves and muscles that control the movements of one or both arytenoid cartilages of the larynx cease to function, and instead of opening during inspiration and closing during swallowing, the arytenoids remain stationary in a somewhat neutral position. Specifically, the muscle that causes abduction of the arytenoid cartilage, the cricoarytenoideus dorsalis muscle, ceases to function. This leads to inadequate ventilation during exercise and during thermoregulatory panting as well as incomplete protection of the airway during swallowing.

The health of dogs is a well studied area in veterinary medicine.

Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function.

Lymphoma (lymposarcoma) in animals is a type of cancer defined by a proliferation of malignant lymphocytes within solid organs such as the lymph nodes, bone marrow, liver and spleen. The disease also may occur in the eye, skin, and gastrointestinal tract.

Scotty Cramp is a disease in Scottish Terriers causing spasms and hyperflexion and hyperextension of the legs. It is caused by a disorder in serotonin metabolism that causes a deficiency of available serotonin. It is inherited as an autosomal recessive trait.

Chronic inflammatory demyelinating polyneuropathy is an acquired immune-mediated inflammatory disorder of the peripheral nervous system. The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy. CIDP is closely related to Guillain–Barré syndrome and it is considered the chronic counterpart of that acute disease. Its symptoms are also similar to progressive inflammatory neuropathy.

Progressive bulbar palsy (PBP) is a medical condition. It belongs to a group of disorders known as motor neuron diseases. PBP is a disease that attacks the nerves supplying the bulbar muscles. These disorders are characterized by the degeneration of motor neurons in the cerebral cortex, spinal cord, brain stem, and pyramidal tracts. This specifically involves the glossopharyngeal nerve (IX), vagus nerve (X), and hypoglossal nerve (XII).

Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi, and boxer dog, though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier, Chesapeake Bay retriever, Rhodesian ridgeback, and Cardigan Welsh corgi. Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord. One proposed cause of degenerative myelopathy is that the immune system attacks this sheath, breaking it down. This results in a loss of communication between nerves in lower body of the animal and the brain.

Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are overlapping syndromes of diffuse, symmetric, flaccid muscle weakness occurring in critically ill patients and involving all extremities and the diaphragm with relative sparing of the cranial nerves. CIP and CIM have similar symptoms and presentations and are often distinguished largely on the basis of specialized electrophysiologic testing or muscle and nerve biopsy. The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome. Corticosteroids and neuromuscular blocking agents, which are widely used in intensive care, may contribute to the development of CIP and CIM, as may elevations in blood sugar, which frequently occur in critically ill patients.

Progressive inflammatory neuropathy (PIN) is a disease that was identified in a report, released on January 31, 2008, by the Centers for Disease Control and Prevention. The first known outbreak of this neuropathy occurred in southeastern Minnesota in the United States. The disease was reported among pig slaughterhouse workers who appeared at various care facilities in the area reporting similar neurological symptoms. The disease was later identified at pork processing plants in Indiana and Nebraska as well. The condition is characterized by acute paralysis, pain, fatigue, numbness, and weakness, especially in extremities. It was initially believed that workers might have contracted the disease through inhaling aerosols from pig brains blown through a compressed-air hose and that this exposure to pig neural tissue induced an autoimmune response that might have produced their mysterious peripheral neuropathy. These suspicions were confirmed in reports and investigations conducted at the Mayo Clinic in Rochester, Minnesota.

Hereditary motor and sensory neuropathies (HMSN) is a name sometimes given to a group of different neuropathies which are all characterized by their impact upon both afferent and efferent neural communication. HMSN are characterised by atypical neural development and degradation of neural tissue. The two common forms of HMSN are either hypertrophic demyelinated nerves or complete atrophy of neural tissue. Hypertrophic condition causes neural stiffness and a demyelination of nerves in the peripheral nervous system, and atrophy causes the breakdown of axons and neural cell bodies. In these disorders, a patient experiences progressive muscle atrophy and sensory neuropathy of the extremities.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Nerve compression syndrome Human disease

Nerve compression syndrome or compression neuropathy, is a medical condition caused by direct pressure on a nerve. It is known colloquially as a trapped nerve, though this may also refer to nerve root compression. Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. Nerve conduction studies help to confirm the diagnosis. In some cases, surgery may help to relieve the pressure on the nerve but this does not always relieve all the symptoms. Nerve injury by a single episode of physical trauma is in one sense a compression neuropathy but is not usually included under this heading.

Peripheral mononeuropathy is a nerve related disease where a single nerve, that is used to transport messages from the brain to the peripheral body, is diseased or damaged. Peripheral neuropathy is a general term that indicates any disorder of the peripheral nervous system. The name of the disorder itself can be broken down in order to understand this better; peripheral: in regard to peripheral neuropathy, refers to outside of the brain and spinal cord; neuro: means nerve related; -pathy; means disease. Peripheral mononeuropathy is a disorder that links to Peripheral Neuropathy, as it only effects a single peripheral nerve rather than several damaged or diseased nerves throughout the body. Healthy peripheral nerves are able to “carry messages from the brain and spinal cord to muscles, organs, and other body tissues”.

References

1 2 3 4 Chrisman, Cheryl; Clemmons, Roger; Mariani, Christopher; Platt, Simon (2003). Neurology for the Small Animal Practitioner (1st ed.). Teton New Media. ISBN 1-893441-82-2.
↑ Braund, K.G. (2003). "Neuropathic Disorders". Braund's Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment. Retrieved 5 September 2006.
1 2 3 4 5 6 7 8 9 10 11 12 Ettinger, Stephen J.; Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine (4th ed.). W.B. Saunders Company. ISBN 0-7216-6795-3.
↑ LeCouteur, Richard A. (2003). "Feline Neuromuscular Disorders". Proceedings of the 28th World Congress of the World Small Animal Veterinary Association. Retrieved 5 September 2006.
↑ Elad D, Yas-Natan E, Aroch I, Shamir M, Kleinbart S, Hadash D, Chaffer M, Greenberg K, Shlosberg A (2004). "Natural Clostridium botulinum Type C Toxicosis in a Group of Cats". J Clin Microbiol. 42 (11): 5406–8. doi:10.1128/JCM.42.11.5406-5408.2004. PMC 525276 . PMID 15528757.
↑ "Botulism". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.
1 2 "Diseases of the Peripheral Nerve and Neuromuscular Junction: Degenerative Diseases". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.
↑ "Diseases of the Peripheral Nerve and Neuromuscular Junction: Metabolic Disorders". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.
↑ Mizisin, Andrew P.; Nelson, RW; Sturges, BK; Vernau, KM; Lecouteur, RA; Williams, DC; Burgers, ML; Shelton, GD (2007). "Comparable myelinated nerve pathology in feline and human diabetes mellitus". Acta Neuropathol. 113 (4): 431–42. doi:10.1007/s00401-006-0163-8. PMID 17237938.
↑ "Feline Dysautonomia". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.
1 2 3 "Peripheral Nerve and Muscle Disorders: Small Animals". The Merck Veterinary Manual. 2006. Retrieved 11 February 2007.
1 2 "A case study of handling Coonhound Paralysis". 2007. Retrieved 18 February 2007.
↑ "Diseases of the Peripheral Nerve and Neuromuscular Junction: Inflammatory Disorders". The Merck Veterinary Manual. 2006. Retrieved 11 December 2007.
↑ John C. Fyfe. "Spinal muscular atrophy in Maine Coon Cats (SMA)" (PDF). 2209 Biomedical Physical Sciences, Michigan State University, East Lansing, MI 48824: Laboratory of Comparative Medical Genetics. Retrieved 9 March 2011.
↑ Edlow, J. A.; McGillicuddy, D. C (2008). "Tick Paralysis". Infectious Disease Clinics of North America. 22 (3): 397–413. doi:10.1016/j.idc.2008.03.005. PMID 18755381.
↑ "Tick Paralysis: Introduction". The Merck Veterinary Manual. 2006. Retrieved 11 February 2007.
↑ Chandler, E. A.; et al. (2004) Feline Medicine and Therapeutics. Oxford, UK: Blackwell Pub.; Ames, Iowa: Iowa State Press, pp. 159–160, ISBN 978-1-4051-2814-8.

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[Chrisman_2003-1] 1 2 3 4 Chrisman, Cheryl; Clemmons, Roger; Mariani, Christopher; Platt, Simon (2003). Neurology for the Small Animal Practitioner (1st ed.). Teton New Media. ISBN 1-893441-82-2.

[Braund-2] Braund, K.G. (2003). "Neuropathic Disorders". Braund's Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment. Retrieved 5 September 2006.

[Ettinger_1995-3] 1 2 3 4 5 6 7 8 9 10 11 12 Ettinger, Stephen J.; Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine (4th ed.). W.B. Saunders Company. ISBN 0-7216-6795-3.

[LeCouteur-4] LeCouteur, Richard A. (2003). "Feline Neuromuscular Disorders". Proceedings of the 28th World Congress of the World Small Animal Veterinary Association. Retrieved 5 September 2006.

[5] Elad D, Yas-Natan E, Aroch I, Shamir M, Kleinbart S, Hadash D, Chaffer M, Greenberg K, Shlosberg A (2004). "Natural Clostridium botulinum Type C Toxicosis in a Group of Cats". J Clin Microbiol. 42 (11): 5406–8. doi:10.1128/JCM.42.11.5406-5408.2004. PMC 525276 . PMID 15528757.

[6] "Botulism". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.

[smdeg-7] 1 2 "Diseases of the Peripheral Nerve and Neuromuscular Junction: Degenerative Diseases". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.

[8] "Diseases of the Peripheral Nerve and Neuromuscular Junction: Metabolic Disorders". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.

[9] Mizisin, Andrew P.; Nelson, RW; Sturges, BK; Vernau, KM; Lecouteur, RA; Williams, DC; Burgers, ML; Shelton, GD (2007). "Comparable myelinated nerve pathology in feline and human diabetes mellitus". Acta Neuropathol. 113 (4): 431–42. doi:10.1007/s00401-006-0163-8. PMID 17237938.

[10] "Feline Dysautonomia". The Merck Veterinary Manual. 2006. Retrieved 10 February 2007.

[small-11] 1 2 3 "Peripheral Nerve and Muscle Disorders: Small Animals". The Merck Veterinary Manual. 2006. Retrieved 11 February 2007.

[Goya_2006-12] 1 2 "A case study of handling Coonhound Paralysis". 2007. Retrieved 18 February 2007.

[13] "Diseases of the Peripheral Nerve and Neuromuscular Junction: Inflammatory Disorders". The Merck Veterinary Manual. 2006. Retrieved 11 December 2007.

[14] John C. Fyfe. "Spinal muscular atrophy in Maine Coon Cats (SMA)" (PDF). 2209 Biomedical Physical Sciences, Michigan State University, East Lansing, MI 48824: Laboratory of Comparative Medical Genetics. Retrieved 9 March 2011.

[15] Edlow, J. A.; McGillicuddy, D. C (2008). "Tick Paralysis". Infectious Disease Clinics of North America. 22 (3): 397–413. doi:10.1016/j.idc.2008.03.005. PMID 18755381.

[16] "Tick Paralysis: Introduction". The Merck Veterinary Manual. 2006. Retrieved 11 February 2007.

[17] Chandler, E. A.; et al. (2004) Feline Medicine and Therapeutics. Oxford, UK: Blackwell Pub.; Ames, Iowa: Iowa State Press, pp. 159–160, ISBN 978-1-4051-2814-8.