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Toxic Disorders of the Spinal Column and Cord

By William B. Thomas, DVM, MS, DACVIM (Neurology), Neurology and Neurosurgery, Department of Small Animal Clinical Sciences, University of Tennessee

Arsenic Poisoning:

Poisoning can be seen in swine due to an overdose of organoarsenicals, which are often used as feed additives to promote growth and to control swine dysentery. With 3-nitro-4-hydroxyphenylarsonic acid (“3-nitro”) poisoning, there is degeneration of the spinal cord, optic nerve, and peripheral nerves. Clinical signs consist of tremors and paraparesis. Mildly affected animals can recover after withdrawal of the offending feed. (Also see Arsenic Poisoning.)

Delayed Organophosphate Intoxication:

Intoxication can be seen after oral or topical administration of organophosphate-containing insecticides or anthelmintics, including haloxon. In addition to the acute signs, delayed paralysis can develop 1–4 wk after exposure. Suffolk sheep have an inherited predisposition to this neurotoxicity, because they have low levels of plasma arylesterase activity. Affected animals have progressive, symmetric paraparesis and occasionally become tetraplegic. Diagnosis is based on clinical signs and history of exposure. On histopathologic examination, there is Wallerian degeneration, most prominent in the spinal cord and brain stem. The prognosis for severely affected animals is poor. (Also see Organophosphates (Toxicity).)

Sorghum Poisoning:

Sorghum spp, such as Sorghum, Sudan, and Johnson grass, can cause degeneration of the spinal cord in horses and occasionally in cattle and sheep. The pathogenesis may be related to the high content of hydrocyanide in these grasses. There is ataxia and weakness of the pelvic limbs and incontinence. Urine retention often leads to cystitis and hematuria. Diagnosis is based on clinical features and a history of exposure. Signs may improve with removal of the offending feed, although persistent deficits are possible. (Also see Sorghum Poisoning.)


Tetanus (see Tetanus) is caused by toxins produced by the vegetative form of Clostridium tetani. Susceptibility varies markedly among species; dogs and cats are fairly resistant compared with horses. Clinical signs usually develop within 5–10 days of infection. These include localized or generalized muscle stiffness and extensor rigidity, dysphagia, protrusion of the third eyelid, and contracted masticatory (lockjaw) and facial (risus sardonicus) muscles. In severe cases, the animal may be recumbent with opisthotonos and reflex muscle spasms. Diagnosis is based on characteristic clinical features. Treatment consists of wound care, antibiotics to kill any remaining organisms, and tetanus antitoxin. In mild cases, prognosis is good with early treatment. In severe cases, death may occur due to respiratory paralysis.