Quantitative electroencephalography (qEEG) converts the raw EEG signal into reproducible numerical descriptors (spectral power, hemispheric symmetry, coherence and signal complexity) and has emerged as a candidate translational biomarker linking human and canine neurology. This integrative review examined the diagnostic, prognostic, pharmacological and translational value of qEEG, with emphasis on functional connectivity, and assessed the comparability of the dog as a natural model of human disease. Seventy-five studies were included, spanning epilepsy, acute brain injury, neurodegeneration, rehabilitation and paroxysmal disorders. In both species, epilepsy was consistently associated with altered spectral power and with reduced or reorganized coherence, and interictal abnormalities were demonstrable even in the absence of visible epileptiform discharges. Dogs reproduced the human patterns closely: phenobarbital induced the spectral redistribution predicted by human pharmaco-EEG data, canine cognitive dysfunction reproduced the slowing and the sleep-architecture changes described in Alzheimer’s disease, and a single machine-learning pipeline classified human and canine recordings with comparable accuracy. Conversely, acute brain injury remains virtually unexplored in the dog, and no canine normative database comparable to the human ones is yet available. The evidence was limited by heterogeneous acquisition protocols, small samples and scarce longitudinal veterinary data. qEEG, and coherence in particular, appears to be a promising cross-species biomarker of network dysfunction and supports the dog as a translational platform, although standardized validation remains necessary.

Serum phenobarbital (PB) monitoring is recommended after treatment initiation and periodically thereafter, but real-world data on monitoring practice are scarce, particularly where imepitoin is not marketed and PB is a controlled substance. All in-house PB determinations performed on a point-of-care analyser reporting PB with a hepatic panel at a Romanian university referral hospital between January 2022 and August 2026 were retrieved and linked to the hospital register. A total of 143 canine runs from 66 dogs were obtained; 10 (7.0%) were suppressed by severe lipaemia. At the first valid determination, 47 of 65 dogs with a valid result (72.3%; 95% CI 60.4–81.7) were within the 15–35 µg/mL target range and 16 (24.6%; 95% CI 15.8–36.3) were below it. The median dose, given as fractionated human 100 mg tablets, was 5.62 mg/kg/day and was not associated with concentration; dogs under 10 kg received almost twice the weight-based dose of larger dogs without reaching higher concentrations. Alkaline phosphatase was increased in 36% of runs and was not associated with concentration in mixed-effects models. At least one determination was obtained in 79% of dogs in continued care and 88% of dogs with six or more prescriptions, but only 40% (95% CI 27–56%) of newly treated dogs were determined within 90 days and none of the 17 dogs seen only once or twice after initiation was determined. Monitoring therefore follows continuity of care; scheduling the first determination at initiation and coupling sampling with prescription renewal are proposed measures whose effectiveness requires prospective evaluation.