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yorkiegirl2 · 09-06-2006, 06:11 AM

This is from IVIS and is some good info and should be a sticky post.
n: Braund's Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment, Vite C.H. (Ed.)
International Veterinary Information Service, Ithaca NY (www.ivis.org), 2003; A3224.0203

Neurotoxic Disorders (Last Updated: 6-Feb-2003)
K. G. Braund

Veterinary Neurological Consulting Services, Dadeville, Alabama, USA.

Introduction
Neurotoxicity in dogs and cats may result from myriad agents, including metals, pesticides, solvents and other chemicals, and bacterial, animal, and plant-derived toxins, as well as therapeutic agents [1]. Drug-induced toxicity may be caused by overdosage, undesirable side effects, or accidental exposure, usually ingestion. In one study [2], the most commonly reported toxins were: lindane-based insecticides (HCB, hexachlorocyclohexane, Isotox, Lintox); pyrethrin and pyrethroid insecticides (permethrin, fenvalerate/DEET); chlorpyrifos, strychnine, lead, metaldehyde (in metaldehyde-based molluscicides), and caffeine (e.g., ingestion of caffeine-based stimulants or chocolate which contains caffeine and theobromine). In general, signs of neurotoxicity may include excitation, depression, tremors, clonic-tonic seizures, hyperactivity, ataxia, circling, salivation, hyperthermia, and coma. Treatment involves decontamination where indicated (e.g., bathing/shampooing), inducing emesis (e.g. apomorphine), correction of any fluid and electrolyte imbalances, repeated administration of activated charcoal with a saline cathartic (sodium sulfate is more efficient than magnesium sulfate) or performing gastric lavage to decrease the amount the animal absorbs, and providing demulscents (milk, kaolin-pectin) for any gastrointestinal irritation [3].
Neurotoxic agents have been arbitrarily grouped as follows:

Metals
Lead
Mercury
Automotive products
Ethylene glycol
Solvents/cleansing agents
Alcohols
Chlorhexidine
Hexachlorophene
Rodenticides
Anticoagulant Rodenticides
Bromethalin
Strychnine
Thallium
Insecticides, Molluscicides, Repellents
Amitraz
Chlorinated Hydrocarbons
Metaldehyde
Organophosphates/Carbamates
Pyrethrins and Pyrethroids
Herbicides
(2-methyl-4-chloro) Phenoxyacetic Acid
Plants
Cyanogenic
Cycad Palms
Bacterial
Botulism
Tetanus Animal
Tick Paralysis
Toad Toxicity
Therapeutic agents/drugs
Aminoglycosides
Barbiturates
Caffeine and other Methylxanthines
Bromide
Closantel
Griseofulvin
Ivermectin
Levamisole
Methionine
Metoclopramide
Metronidazole
Pemoline
Toluene/Dichlorophen
Tricyclic Antidepressants
Vincristine
Zolpidem
5-Fluorouracil
5-Hydroxytryptophan

Alcohols
Widespread utilization of short-chain alcohols in solvents and alcoholic beverages provides small animals with numerous opportunities for exposure [4]. Toxicosis most commonly occurs following ingestion but may also arise from inhalation and/or dermal absorption. The actions of short-chain alcohols are believed to result from nonspecific interactions with biomembranes altering the function of membrane-bound proteins, including the GABA-A receptor. Onset of signs typically occurs within an hour of exposure and may last for 24 hours. Clinical signs include behavioral changes such as excitability, vocalizing, and incontinence, ataxia, drowsiness, unconsciousness, loss of reflexes, respiratory compromise, respiratory and cardiac arrest, and death. Therefore, general measures for resuscitation should be followed in the initial treatment of severe alcohol toxicosis, including endotracheal intubation, mechanical ventilation, correction of acid base imbalance with bicarbonate (metabolism of alcohols alters the redox state in the liver, leading to hypoglycemia and lactic acidosis in some cases). Activated charcoal (2 g/kg PO) should be given within 3 hours of an alcohol ingestion and skin should be decontaminated.

Aminoglycosides
Aminoglycoside antibiotics can adversely affect auditory and vestibular mechanisms, especially after prolonged administration of large amounts of the drugs [5]. These drugs concentrate in perilymph and endolymph, thus exposing the cochlear hair cells to high concentrations of the antibiotic agents. While all aminoglycoside antibiotics can damage auditory and vestibular receptors, streptomycin and gentomycin have their greatest effects on the vestibular system, whereas, neomycin, kanamycin, tobramycin, and amikacin sulfate produce more damage to the auditory peripheral receptors [6]. The toxic effects of these drugs are heightened if the tympanic membrane is perforated. However, in one experimental study, gentamicin sulfate did not induce detectable alteration of cochlear or vestibular function in dogs with intact tympanic membranes or after experimental bilateral myringotomy [7]. In other experimental studies, ototoxicity of aminoglycosides may be enhanced by loop diuretics [8], while the severity of ototoxic side-effects can be influenced by nutritional factors [9].

Amitraz
Amitraz, an alpha-adrenergic agonist and a weak monoamine oxidase inhibitor, may induce sedation, depression, ataxia, and muscle weakness in dogs following excessive exposure, such as application to the skin for Demodex control and ingestion of tick collars [10]. Other signs may include hypertension, mydriasis, hypothermia, bradycardia, hyperglycemia, hypoperistalsis, vasoconstriction, vomiting, and diarrhea [11-13]. I have also seen brief, generalized seizures in our own Welsh Corgi following treatment for demodicosis. Nerve conduction studies are normal [13]. Treatment with yohimbine at 0.1 mg/kg IV normally reverses the signs. It has been reported that signs can be reversed by low doses of atipamezole (50 mg/kg, IM), a potent alpha 2-antagonist, within 10 minutes after injection [12].

Anticoagulant Rodenticides
A variety of anticoagulant rodenticies are available with one of the best known being warfarin. These agents interfere with vitamin K1 hydroquinone recycling in the liver leading to impaired synthesis of functional forms of clotting factors II, VII, IX, and X, and development of coagulopathies/bleeding [220]. Intrathecal or intrameningeal hemorrhage may lead to ataxia, stiffness, or seizures. Diagnosis may be made using common coagulation tests (bleeding time, blood clotting time, activated clotting time, prothrombin time, and activated partial thromboplastin time). The PIVKA test may also be useful in identifying a vitamin K1-responsive coagulopathy. Treatment may involve use of fresh frozen plasma (at 9 mL/kg) or whole blood (at 20 mL/kg) followed by oral vitamin K1 at a rate of 2.5 mg/kg sid for 2 to 4 weeks.

09-06-2006, 06:11 AM	#1
yorkiegirl2 YT 2000 Club Member Join Date: Apr 2005 Location: Missouri Posts: 2,394	Important info on Neurotoxic Disorders This is from IVIS and is some good info and should be a sticky post. n: Braund's Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment, Vite C.H. (Ed.) International Veterinary Information Service, Ithaca NY (www.ivis.org), 2003; A3224.0203 Neurotoxic Disorders (Last Updated: 6-Feb-2003) K. G. Braund Veterinary Neurological Consulting Services, Dadeville, Alabama, USA. Introduction Neurotoxicity in dogs and cats may result from myriad agents, including metals, pesticides, solvents and other chemicals, and bacterial, animal, and plant-derived toxins, as well as therapeutic agents [1]. Drug-induced toxicity may be caused by overdosage, undesirable side effects, or accidental exposure, usually ingestion. In one study [2], the most commonly reported toxins were: lindane-based insecticides (HCB, hexachlorocyclohexane, Isotox, Lintox); pyrethrin and pyrethroid insecticides (permethrin, fenvalerate/DEET); chlorpyrifos, strychnine, lead, metaldehyde (in metaldehyde-based molluscicides), and caffeine (e.g., ingestion of caffeine-based stimulants or chocolate which contains caffeine and theobromine). In general, signs of neurotoxicity may include excitation, depression, tremors, clonic-tonic seizures, hyperactivity, ataxia, circling, salivation, hyperthermia, and coma. Treatment involves decontamination where indicated (e.g., bathing/shampooing), inducing emesis (e.g. apomorphine), correction of any fluid and electrolyte imbalances, repeated administration of activated charcoal with a saline cathartic (sodium sulfate is more efficient than magnesium sulfate) or performing gastric lavage to decrease the amount the animal absorbs, and providing demulscents (milk, kaolin-pectin) for any gastrointestinal irritation [3]. Neurotoxic agents have been arbitrarily grouped as follows: Metals Lead Mercury Automotive products Ethylene glycol Solvents/cleansing agents Alcohols Chlorhexidine Hexachlorophene Rodenticides Anticoagulant Rodenticides Bromethalin Strychnine Thallium Insecticides, Molluscicides, Repellents Amitraz Chlorinated Hydrocarbons Metaldehyde Organophosphates/Carbamates Pyrethrins and Pyrethroids Herbicides (2-methyl-4-chloro) Phenoxyacetic Acid Plants Cyanogenic Cycad Palms Bacterial Botulism Tetanus Animal Tick Paralysis Toad Toxicity Therapeutic agents/drugs Aminoglycosides Barbiturates Caffeine and other Methylxanthines Bromide Closantel Griseofulvin Ivermectin Levamisole Methionine Metoclopramide Metronidazole Pemoline Toluene/Dichlorophen Tricyclic Antidepressants Vincristine Zolpidem 5-Fluorouracil 5-Hydroxytryptophan Alcohols Widespread utilization of short-chain alcohols in solvents and alcoholic beverages provides small animals with numerous opportunities for exposure [4]. Toxicosis most commonly occurs following ingestion but may also arise from inhalation and/or dermal absorption. The actions of short-chain alcohols are believed to result from nonspecific interactions with biomembranes altering the function of membrane-bound proteins, including the GABA-A receptor. Onset of signs typically occurs within an hour of exposure and may last for 24 hours. Clinical signs include behavioral changes such as excitability, vocalizing, and incontinence, ataxia, drowsiness, unconsciousness, loss of reflexes, respiratory compromise, respiratory and cardiac arrest, and death. Therefore, general measures for resuscitation should be followed in the initial treatment of severe alcohol toxicosis, including endotracheal intubation, mechanical ventilation, correction of acid base imbalance with bicarbonate (metabolism of alcohols alters the redox state in the liver, leading to hypoglycemia and lactic acidosis in some cases). Activated charcoal (2 g/kg PO) should be given within 3 hours of an alcohol ingestion and skin should be decontaminated. Aminoglycosides Aminoglycoside antibiotics can adversely affect auditory and vestibular mechanisms, especially after prolonged administration of large amounts of the drugs [5]. These drugs concentrate in perilymph and endolymph, thus exposing the cochlear hair cells to high concentrations of the antibiotic agents. While all aminoglycoside antibiotics can damage auditory and vestibular receptors, streptomycin and gentomycin have their greatest effects on the vestibular system, whereas, neomycin, kanamycin, tobramycin, and amikacin sulfate produce more damage to the auditory peripheral receptors [6]. The toxic effects of these drugs are heightened if the tympanic membrane is perforated. However, in one experimental study, gentamicin sulfate did not induce detectable alteration of cochlear or vestibular function in dogs with intact tympanic membranes or after experimental bilateral myringotomy [7]. In other experimental studies, ototoxicity of aminoglycosides may be enhanced by loop diuretics [8], while the severity of ototoxic side-effects can be influenced by nutritional factors [9]. Amitraz Amitraz, an alpha-adrenergic agonist and a weak monoamine oxidase inhibitor, may induce sedation, depression, ataxia, and muscle weakness in dogs following excessive exposure, such as application to the skin for Demodex control and ingestion of tick collars [10]. Other signs may include hypertension, mydriasis, hypothermia, bradycardia, hyperglycemia, hypoperistalsis, vasoconstriction, vomiting, and diarrhea [11-13]. I have also seen brief, generalized seizures in our own Welsh Corgi following treatment for demodicosis. Nerve conduction studies are normal [13]. Treatment with yohimbine at 0.1 mg/kg IV normally reverses the signs. It has been reported that signs can be reversed by low doses of atipamezole (50 mg/kg, IM), a potent alpha 2-antagonist, within 10 minutes after injection [12]. Anticoagulant Rodenticides A variety of anticoagulant rodenticies are available with one of the best known being warfarin. These agents interfere with vitamin K1 hydroquinone recycling in the liver leading to impaired synthesis of functional forms of clotting factors II, VII, IX, and X, and development of coagulopathies/bleeding [220]. Intrathecal or intrameningeal hemorrhage may lead to ataxia, stiffness, or seizures. Diagnosis may be made using common coagulation tests (bleeding time, blood clotting time, activated clotting time, prothrombin time, and activated partial thromboplastin time). The PIVKA test may also be useful in identifying a vitamin K1-responsive coagulopathy. Treatment may involve use of fresh frozen plasma (at 9 mL/kg) or whole blood (at 20 mL/kg) followed by oral vitamin K1 at a rate of 2.5 mg/kg sid for 2 to 4 weeks.