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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.

Image by Amos Bar-Zeev

Fatal bromethalin intoxication in 3 cats and 2 dogs with minimal or no histologic central nervous system spongiform change

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.

Brain Sketch

Application of eprinomectin-containing parasiticides at label doses causes neurological toxicosis in cats homozygous for ABCB11930_1931del TC

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.

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. 

Image by Cédric VT

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.

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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.

Medical Prescription
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