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Nigropallidal encephalomalacia or Chewing disease is a neurological condition that affects horses that have eaten certain toxic plants. Affected animals are unable to prehend food because of lip and tongue paralysis, and may appear to keep their jaws open with the tongue protruded because of reduced jaw tone. [ 1 ]
A horse may be returned to work if symptoms have ceased and is no longer on NSAIDs or other prescribed drugs related to treatment of ER, this can otherwise can hide signs of another bout of ER. If NSAIDs or other treatment drugs are needed to keep the horse comfortable, or if the horse is reluctant to continue work, the animal is not yet ready ...
Romifidine is a drug that is used in veterinary medicine as a sedative mainly in large animals such as horses, [1] although it may be used in a wide variety of species. [2] [3] It is not used in humans, but is closely related in structure to the commonly used drug clonidine. Romifidine acts as an agonist at the α 2 adrenergic receptor subtype.
This is a list of drugs and substances that are known or suspected to cause Stevens–Johnson syndrome This is a dynamic list and may never be able to satisfy particular standards for completeness. You can help by adding missing items with reliable sources .
Xylazine is a common veterinary drug used for sedation, anesthesia, muscle relaxation, and analgesia in animals such as horses, cattle, and other mammals. [2] In veterinary anesthesia, it is often used in combination with ketamine. Veterinarians also use xylazine as an emetic, especially in cats. [4] Drug interactions vary with different animals.
Side effects are not common, but the use of acepromazine in stallions should be used with caution (but is not absolutely contraindicated) due to the risk of paraphimosis and priapism. [6] Acepromazine also lowers blood pressure, and should therefore be used with caution in horses that are experiencing anemia, dehydration, shock, or colic.
Detomidine is a sedative with analgesic properties. [3] α 2-adrenergic receptor agonists produce dose-dependent sedative and analgesic effects, mediated by activation of α 2 catecholamine receptors, thus inducing a negative feedback response, reducing production of excitatory neurotransmitters.