Background: Although repetitive transcranial magnetic stimulation (rTMS) has been assessed in epileptic humans, clinical trials in epileptic dogs can provide additional insight. Objectives: Evaluate the potential antiepileptic effect of rTMS in dogs. Animals: Twelve client-owned dogs with drug-resistant idiopathic epilepsy (IE). Methods: Single-blinded randomized sham-controlled clinical trial (dogs allocated to active or sham rTMS) (I) and open-labeled uncontrolled clinical trial (dogs received active rTMS after sham rTMS) (II). Monthly seizure frequency (MSF), monthly seizure day frequency (MSDF), and number of cluster seizures (CS) were evaluated for a 3-month pre-TMS and post-rTMS period and safety was assessed. The lasting effect period of rTMS was assessed in each dog treated by active stimulation using the MSF ratio (proportion of post-TMS to pre-rTMS MSF) and treatment was considered effective if the ratio was <1. Results: No adverse effects were reported. In trial I, MSF and MSDF decreased significantly (P = .04) in the active group (n = 7). In the sham group (n = 5), no significant changes were found (P = .84 and .29, respectively). Cluster seizures did not change significantly in either group. No significant differences were detected between the groups. In trial II, previously sham-treated dogs (n = 5) received active rTMS and significant decreases in MSF and MSDF were noted (P = .03 and .008, respectively). The overall effect of rTMS lasted for 4 months; thereafter, the MSF ratio was >1. Conclusions and Clinical Importance: Repetitive transcranial magnetic stimulation may be a safe adjunctive treatment option for dogs with drug-resistant IE, but largescale studies are needed to establish firm conclusions.

Currently, a histological diagnosis of highly vascularized canine (c) thyroid carcinoma (TC) is primarily obtained following excisional biopsy (EB) through thyroidectomy. Non‐EBs are contraindicated in unresectable invasive cTCs due to their highly vascularized nature, which subsequently, lack histological diagnosis. We hypothesised ultrasound‐guided core needle biopsy (UGCNB) to be a safe biopsy technique to obtain an accurate histological diagnosis in unresectable TCs. Nine client‐owned dogs with suspected naturally occurring TC, presented for surgical excision, were included. First, a UGCNB was taken from the cervical tumour, followed by EB. Haemorrhage following UGCNB was evaluated preoperatively and once the tumour was surgically exposed by visual inspection and ultrasonography. Histological analysis, including cell organisation, tumour capsular and vascular invasion, and immunohistochemistry were performed and compared between both biopsy specimens (i.e., UGCNB and EB) of the same dog. Pre‐ and peroperative visual inspection revealed minor, localised haemorrhage, subsequent to the UGCNB, in 7/9 dogs. Histology of the EBs confirmed TC in 8/9 dogs and was inconclusive in 1/9 dogs. Histology of the UGCNBs revealed neoplastic thyroid tissue in 7/9 UGCNBs and was inconclusive in 1/9 UGCNBs. The remaining UGCNB contained no mass related tissue and was, therefore, excluded. Histological parameters (i.e., cell organisation, tumour capsular and vascular invasion) were not concordant between 6/8 included UGCNBs and their respective EB. Immunolabelling for thyroglobulin and calcitonin was concordant between all eight included UGCNBs and their respective EB. The remaining evaluated immunohistochemical markers (i.e., cyclooxygenase‐2 [COX‐2], P‐glycoprotein and vascular endothelial growth factor [VEGF]) were concordant between the included UGCNBs and the EBs in 6/8 dogs. To conclude, UGCNBs can be safely obtained in suspected cTCs and enable a reliable diagnosis of the thyroid origin, thyroid cell origin and potential therapeutic markers such as COX‐2, P‐glycoprotein and VEGF. Subsequently, UGCNB enables clinicians to establish an individually tailored treatment plan in dogs with unresectable TC.

AMENVATTINGObesitas is een belangrijk probleem in de diergeneeskunde. Aangezien obesitas niet enkel een opstapeling van vet is maar ook belangrijke cardiovasculaire en respiratoire implicaties heeft, kan dit het verloop van de anesthesie sterk beïnvloeden bij de betrokken patiënten. Bovendien kan obesitas een onderliggende oorzaak hebben of leiden tot gerelateerde aandoeningen die op hun beurt de anesthesie compliceren. Tot slot leidt obesitas ook tot veranderingen in de farmacokinetiek en -dynamiek, van onder andere anesthetica. Deze veranderingen vereisen dosisaanpassingen, afhankelijk van het anestheticum. In de diergeneeskunde is de beschikbare informatie hierover echter zeer beperkt en wordt ze daarom grotendeels verkregen door extrapolatie uit de humane geneeskunde. In dit artikel wordt een overzicht gegeven van de pathofysiologische en farmacologische veranderingen bij obese dieren waarmee rekening gehouden moet worden tijdens de anesthesie. ABSTRACTObesity is a major issue in veterinary medicine. It is not only an accumulation of fat, but obesity also has important cardiovascular and respiratory implications. Therefore, it can strongly influence the anesthesia in obese patients. In addition, obesity can have an underlying cause or may lead to related conditions, which can complicate the anesthesia. Finally, obesity leads to changes in the pharmacodynamics and kinetics of certain drugs, such as anesthetics. These changes require dose adjustments depending on the anesthetic. Unfortunately, the available information is very limited in veterinary medicine and is mainly obtained by extrapolation from human medicine. In this article, an overview is provided of the pathophysiological and pharmacological changes in obese animals, which are important during anesthesia.

An eight-year-old British Shorthair (case 1), an eleven-year-old British Shorthair (case 2) and a six-year-old European Shorthair cat (case 3) showed signs of chronic T3–L3 myelopathy. Computed tomography of the thoracolumbar and lumbosacral region was performed in all three cases and magnetic resonance imaging was only performed in case 2. Cross sectional imaging revealed an enlargement of the articular process joints from T2 to T5 in case 1, from T11 to T13 in case 2 and from T10 to T13 in case 3 causing spinal cord compression. Based on the severity of the spinal cord compression, surgical decompression by hemilaminectomy was performed in case 1. In cases 2 and 3, conservative treatment was instituted, although this condition could have been an incidental finding in these two cases. To the authors’ knowledge, this is the first report describing the neurological signs, imaging findings and short-term outcome in cats with multiple thoracolumbar articular process hypertrophy.

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