Polyneuropathy in dogs and cats

Last updated December 24, 2024

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.

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]
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]

Related Research Articles

Peripheral neuropathy, often shortened to neuropathy, refers to damage or disease affecting the nerves. Damage to nerves may impair sensation, movement, gland function, and/or organ function depending on which nerve fibers are affected. Neuropathies affecting motor, sensory, or autonomic nerve fibers result in different symptoms. More than one type of fiber may be affected simultaneously. Peripheral neuropathy may be acute or chronic, and may be reversible or permanent.

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.

Tick paralysis is a type of paralysis caused by specific types of attached ticks. Unlike tick-borne diseases caused by infectious organisms, 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.

<span class="mw-page-title-main">Alcoholic polyneuropathy</span> Medical condition

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 aspiration 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.

<span class="mw-page-title-main">Giant axonal neuropathy</span> Medical condition

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. A distinguishing feature is its association with kinky, or curly, hair; in such cases it has been called Giant axonal neuropathy with curly hair.

Neuritis, from the Greek νεῦρον), is inflammation of a nerve or the general inflammation of the peripheral nervous system. Inflammation, and frequently concomitant demyelination, cause impaired transmission of neural signals and leads to aberrant nerve function. Neuritis is often conflated with neuropathy, a broad term describing any disease process which affects the peripheral nervous system. However, neuropathies may be due to either inflammatory or non-inflammatory causes, and the term encompasses any form of damage, degeneration, or dysfunction, while neuritis refers specifically to the inflammatory process.

Lymphoma (lymphosarcoma) 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.

Scottie 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.

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by canine distemper virus as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from canine herpesvirus, canine adenovirus, and canine parvovirus in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis, but failed to find any.

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.

Guillain–Barré syndrome is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. Typically, both sides of the body are involved, and the initial symptoms are changes in sensation or pain often in the back along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body. The symptoms may develop over hours to a few weeks. During the acute phase, the disorder can be life-threatening, with about 15% of people developing weakness of the breathing muscles requiring mechanical ventilation. Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure.

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.

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.

<span class="mw-page-title-main">Hereditary neuropathy with liability to pressure palsy</span> Medical condition

Hereditary neuropathy with liability to pressure palsy (HNPP) is a peripheral neuropathy, a condition that affects the nerves. Pressure on the nerves can cause tingling sensations, numbness, pain, weakness, muscle atrophy and even paralysis of the affected area. In normal individuals, these symptoms disappear quickly, but in sufferers of HNPP even a short period of pressure can cause the symptoms to occur. Palsies can last from minutes or days to weeks or even months.

Anti-MAG peripheral neuropathy is a specific type of peripheral neuropathy in which the person's own immune system attacks cells that are specific in maintaining a healthy nervous system. As these cells are destroyed by antibodies, the nerve cells in the surrounding region begin to lose function and create many problems in both sensory and motor function. Specifically, antibodies against myelin-associated glycoprotein (MAG) damage Schwann cells. While the disorder occurs in only 10% of those afflicted with peripheral neuropathy, people afflicted have symptoms such as muscle weakness, sensory problems, and other motor deficits usually starting in the form of a tremor of the hands or trouble walking. There are, however, multiple treatments that range from simple exercises in order to build strength to targeted drug treatments that have been shown to improve function in people with this type of peripheral neuropathy.

<span class="mw-page-title-main">Sensory neuronopathy</span> Sensory neuropathy caused by damage of nerve cells in the dorsal root ganglion

Sensory neuronopathy is a type of peripheral neuropathy that results primarily in sensory symptoms due to destruction of nerve cell bodies in the dorsal root ganglion. The causes of nerve damage are grouped into categories including those due to paraneoplastic causes, immune mediated, infectious, inherited or degenerative causes and those due to toxin exposure. In idiopathic sensory neuronopathy no cause is identified. Idiopathic causes account for about 50% of cases. Sensory neuronopathy differs from the more common length dependent axonal polyneuropathies in that the symptoms do not progress in a distal to proximal pattern, rather symptoms develop in a multifocal, asymmetric, and non-length dependent manner. Ataxia is a prominent symptom early in the disease course. The trigeminal nerve ganglion is also commonly affected leading to facial numbness. Motor nerves are usually not affected however some cases do have mild motor involvement in the form of weakness. Symptoms tend to develop sub-acutely, over weeks, in acquired sensory neuronopathy and more slowly in inherited or primary degenerative cases. In cases of paraneoplastic or infectious sensory neuropathy, treatment is directed at the underlying cancer or infectious cause respectively. Immunomodulatory and anti-inflammatory therapies are also commonly used however their effectiveness is limited.

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. Archived from the original on 8 April 2005. 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. Archived from the original on 10 September 2006. 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. Archived from the original on 23 February 2007. Retrieved 10 February 2007.
1 2 "Diseases of the Peripheral Nerve and Neuromuscular Junction: Degenerative Diseases". The Merck Veterinary Manual. 2006. Archived from the original on 4 May 2007. Retrieved 10 February 2007.
↑ "Diseases of the Peripheral Nerve and Neuromuscular Junction: Metabolic Disorders". The Merck Veterinary Manual. 2006. Archived from the original on 4 May 2007. 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. Archived from the original on 2 June 2007. Retrieved 11 February 2007.
1 2 "A case study of handling Coonhound Paralysis". 2007. Archived from the original on 16 June 2006. Retrieved 18 February 2007.
↑ "Diseases of the Peripheral Nerve and Neuromuscular Junction: Inflammatory Disorders". The Merck Veterinary Manual. 2006. Archived from the original on 26 September 2007. 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. Archived (PDF) from the original on 21 March 2012. Retrieved 9 March 2011.{{cite web}}: CS1 maint: location (link)
↑ 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. Archived from the original on 23 April 2007. 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. Archived from the original on 8 April 2005. 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. Archived from the original on 10 September 2006. 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. Archived from the original on 23 February 2007. Retrieved 10 February 2007.

[smdeg-7] 1 2 "Diseases of the Peripheral Nerve and Neuromuscular Junction: Degenerative Diseases". The Merck Veterinary Manual. 2006. Archived from the original on 4 May 2007. Retrieved 10 February 2007.

[8] "Diseases of the Peripheral Nerve and Neuromuscular Junction: Metabolic Disorders". The Merck Veterinary Manual. 2006. Archived from the original on 4 May 2007. 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. Archived from the original on 2 June 2007. Retrieved 11 February 2007.

[Goya_2006-12] 1 2 "A case study of handling Coonhound Paralysis". 2007. Archived from the original on 16 June 2006. Retrieved 18 February 2007.

[13] "Diseases of the Peripheral Nerve and Neuromuscular Junction: Inflammatory Disorders". The Merck Veterinary Manual. 2006. Archived from the original on 26 September 2007. 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. Archived (PDF) from the original on 21 March 2012. Retrieved 9 March 2011.{{cite web}}: CS1 maint: location (link)

[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. Archived from the original on 23 April 2007. 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.

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