Web-Vet TM Neurology Specialists
Intoxications - Brain
Neurological Manifestations of Grape or Raisin Toxicosis
Grape, raisin or currant ingestion is well known to be toxic to dogs causing acute kidney injury with resultant severe uraemia, systemic hypertension, electrolyte and metabolic derangements. Less well known are the neurological manifestations which in this study are shown to be an important feature and even may dominate the early clinical picture before the signs of uraemia emerge. Neurological signs can be of variable severity and present in about 3/4 of cases. They are mainly localised to the forebrain and cerebellum as well as sometimes including vestibular signs. They are not associated with structural changes and their reversibility suggest a functional brain alteration although the pathophysiology still remains poorly understood but believed to be related to tartaric acid. Treatment is supportive.
This case series describes fatal bromethalin intoxication in 3 cats and 2 dogs with equivocal or no CNS white matter spongiform change, illustrating that the lesions described in animal models can be absent in clinical cases of bromethalin intoxication. Cases with history and clinical signs compatible with bromethalin intoxication warrant tissue analysis for the metabolite desmethylbromethalin even when CNS lesions are not evident.
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Macrocyclic lactones (ML), used as endoparasiticides and ectoparasiticides in many species, generally have a wide safety margin in mammals attributable to the blood–brain–barrier, specifically the efflux transporter P-glycoprotein. P-glycoprotein, the ABCB1 (formerly MDR1) gene product, is expressed on mammalian brain capillaries where it effluxes substrate drugs, including ML.
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The feline MDR1 mutation (ABCB11930_1931delTC) has been associated with neurological toxicosis after topical application of eprinomectin products labeled for feline use. This paper documents 14 cats with neurological signs highly consistent with eprinomectin toxicosis. Eight cats were homozygous for ABCB11930_1931del TC (3 died; 5 recovered).
​Results indicate that topical eprinomectin products, should be avoided in cats homozygous for ABCB11930_1931delTC.
Case Report: MRI, Clinical, and Pathological Correlates of Bromethalin Toxicosis in Three Dogs
This study describes the MRI, clinical and pathological findings in 3 dogs with bromehtalin toxicosis. As with many toxicoses, bilaterally symmetrical lesions are features of the MR imaging. Of interest with this toxicosis is the localisation of these lesions being consistent with a diffuse leukoencephalopathy with restricted diffusion and prominent involvement of the corticospinal motor tracts. The discussion of this article is excellent, discussing differential diagnoses of leukoencephalopathy in dogs as well as bringing more awareness to this frequent toxicity following the phasing out of anticoagulant rodenticides.
Diazepam as a Treatment for Metronidazole Toxicosis in Dogs:A Retrospective Study of 21 Cases
Metronidazole is a nitroimidazole antibacterial and antiprotozoal compound used routinely in the treatment of giardiasis, anaerobic infections, and inflammatory bowel disease. It has high bioavailability for most tissues, including bone and the central nervous system.
Metronidazole is metabolized by the liver and has a half-life of 3–13 hours in the dog. Adverse effects of metronidazole in the dog and cat have been reported and include vomiting, hepatotoxicity, neutropenia, and neurologic signs such as seizures, head tilt, falling, paresis, ataxia, vertical nystagmus, tremors, and rigidity.
In this study, the records of 21 dogs with metronidazole toxicosis were retrospectively analyzed to determine whether diazepam improved recovery. The protocol for diazepam administration consisted of an initial IV bolus and then diazepamPO q8h for 3 days. The average dosage of both the IV and PO diazepam was 0.43 mg/kg. The average response time for the diazepam-treated dogs was 13.4 hours compared to 4.25 days for the untreated group.
