Electroencephalography (EEG) is a non-invasive examination method for the assessment of functional central nervous system (CNS) disturbances. In human medicine it has a special importance as a diagnostic tool for epilepsy. Although many studies were done on the use of EEG for diagnostics of canine central nervous system disorders, the technique is still not applied routinely. The purpose of this paper was to review the use of the electroencephalography in canine neurological disorders of central nervous system diagnosis and assess the future perspectives of this technique in veterinary medicine.

OBJECTIVE To compare intraosseous pentobarbital treatment (IPT) and thoracic compression (TC) on time to circulatory arrest and an isoelectric electroencephalogram (EEG) in anesthetized passerine birds. ANIMALS 30 wild-caught adult birds (17 house sparrows [Passer domesticus] and 13 European starlings [Sturnus vulgaris]). PROCEDURES Birds were assigned to receive IPT or TC (n = 6/species/group). Birds were anesthetized, and carotid arterial pulses were monitored by Doppler methodology. Five subdermal braided-wire electrodes were used for EEG. Anesthetic depth was adjusted until a continuous EEG pattern was maintained, then euthanasia was performed. Times from initiation of euthanasia to cessation of carotid pulse and irreversible isoelectric EEG (indicators of death) were measured. Data (medians and first to third quartiles) were summarized and compared between groups within species. Necropsies were performed for all birds included in experiments and for another 6 birds euthanized under anesthesia by TC (4 sparrows and 1 starling) or IPT (1 sparrow). RESULTS Median time to isoelectric EEG did not differ significantly between treatment groups for sparrows (19.0 and 6.0 seconds for TC and IPT, respectively) or starlings (88.5 and 77.5 seconds for TC and IPT, respectively). Median times to cessation of pulse were significantly shorter for TC than for IPT in sparrows (0.0 vs 18.5 seconds) and starlings (9.5 vs 151.0 seconds). On necropsy, most (14/17) birds that underwent TC had grossly visible coelomic, pericardial, or perihepatic hemorrhage. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that TC might be an efficient euthanasia method for small birds. Digital pressure directly over the heart during TC obstructed venous return, causing rapid circulatory arrest, with rupture of the atria or vena cava in several birds. The authors propose that cardiac compression is a more accurate description than TC for this procedure.

Quantitative electroencephalography (QEEG) was assessed in 5 dogs anesthetized with 1.6% end-tidal concentration of isoflurane and after subsequent administration of the benzodiazepine midazolam (0.2 mg/kg of body weight, IV). Ventilation was controlled to maintain normocapnia. Effect of the benzodiazepine antagonist, flumazenil (0.04 mg/kg, IV), on QEEG in midazolam-isoflurane-anesthetized dogs was determined. Heart rate, arterial blood pressure, esophageal temperature, arterial pH and blood gas tensions, end-tidal CO2 concentration, and end-tidal isoflurane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG data. Quantitative EEG data were stored on an optical disk for later analysis. Values for absolute power of EEG were determined for delta, theta, alpha, and beta-frequencies. Cardiovascular variables remained stable throughout the study. Midazolam administration was associated with decreased absolute power in all frequencies of EEG at all electrode sites. Administration of flumazenil antagonized midazolam-induced decreased absolute power of EEG in all frequencies at all electrode sites. We conclude that QEEG provides a noninvasive, objective measure of midazolam- and flumazenil-induced changes in cortical activity during isoflurane anesthesia.

The central arterial pharmacokinetics of alfentanil, a short-acting opioid agonist, were studied in rabbits, sheep, and dogs after short-duration infusion of the drug. Alfentanil was infused until a set end point (high-amplitude, slow-wave activity on the EEG) was reached. This required a larger alfentanil dose and a higher alfentanil arterial concentration in sheep, compared with rabbits and dogs. The plasma concentration-time data for each animal were fitted, using nonlinear regression, and in all animals, were best described by use of a triexponential function. In this study, differences in the disposition kinetics of alfentanil among the 3 species were found for only distribution clearance and initial distribution half-life. In dogs, compared with rabbits and sheep, the first distribution half-life was longer, probably because of pronounced drug-induced bradycardia (mean +/- SD, 48 +/- 21 beats/min). Distribution clearance was faster in sheep, compared with dogs, also probably because of better blood flow in sheep. Elimination half-life was similar in all species (rabbits, 62.4 +/- 11.3 minutes; sheep, 65.1 +/- 27.1 minutes; dogs, 58.3 +/- 10.3 minutes). This rapid half-life resulted from a small steady-state volume of distribution (rabbits, 908.3 +/- 269.0 ml/kg; sheep, 720.0 +/- 306.7 ml/kg; dogs, 597.7 +/- 290.2 ml/kg) and rapid systemic clearance (rabbits, 19.4 +/- 5.3 ml/min/kg; sheep, 13.3 +/- 3.0 ml/min/kg; dogs, 18.7 +/- 7.5 ml/min/kg). On the basis of these pharmacokinetic variables, alfentanil should have short duration of action in rabbits, sheep, and dogs. This may be beneficial in veterinary practice where rapid recovery would be expected after bolus administration for short procedures or after infusion for longer procedures.

Scalp electrode impedance measurements recorded by wired and wireless electroencephalography (EEG) machines in 7 healthy dogs were compared. Eight recordings resulted in 80 impedance readings from subdermal wire electrodes (locations F7/F8, F3/F4, T3/T4, C3/C4, Fz, and Cz). Impedance values were measured first from the wired and then the wireless EEG machine. Wireless impedance measurements were higher than the wired EEG machine in 79/80 readings (P ≤ 0.05), being on average 2.83 kΩ [P ≤ 0.05, 95% confidence interval (CI): 2.51 to 3.14, SD = 1.42] higher. Impedances from the wired machine ranged between < 0.5 and 9 kΩ (mean = 3.09, median = 2.00, SD = 2.15), whereas impedances from the wireless machine ranged between 2.69 and 6.07 kΩ (mean = 5.92, median = 5.05, SD = 2.59). Despite these differences in impedance measurements, both machines measured similar impedance patterns. The wireless EEG machine's impedance measurements, therefore, should be acceptable for veterinary clinical settings.

Objective- To evaluate physical methods for inducing death during the slaughter of American alligators (Alligator mississippiensis). Animals- 24 captive hatched-and-reared American alligators. Procedures- Baseline electroencephalograms (EEGs) were obtained for awake and anesthetized alligators. Corneal reflex, spontaneous blinking, and EEGs were evaluated after severance of the spinal cord, severance of the spinal cord followed by pithing of the brain, application of a penetrating captive bolt, or application of a nonpenetrating captive bolt (6 alligators/group). Results- Overall, alligators subjected to spinal cord severance alone differed from those subjected to the other techniques. Spinal cord severance alone resulted in postprocedure EEG power values greater than those in anesthetized alligators, whereas the postprocedure EEG power values were isoelectric for the other 3 techniques. Corneal reflex and spontaneous blinking were absent in all alligators immediately after application of a penetrating or nonpenetrating captive bolt. One of 6 alligators had a corneal reflex up to 1 minute after pithing, but all others within that group had immediate cessation of reflexes after pithing. Mean time to loss of spontaneous blinking and corneal reflex for alligators subjected to spinal cord severance alone was 18 minutes (range, 2 to 37 minutes) and 54 minutes (range, 34 to 99 minutes), respectively. Conclusions and Clinical Relevance- Spinal cord severance followed by pithing of the brain and application of a penetrating or nonpenetrating captive bolt appeared to be humane and effective techniques for inducing death in American alligators, whereas spinal cord severance alone was not found to be an appropriate method.

Objective: To evaluate the influence of various anesthetic protocols and 3 multiples of isoflurane minimum alveolar concentration (MAC) before and after supramaximal stimulation on electroencephalographic (EEG) variables in dogs. Animals: 6 healthy adult Beagles (mean ± SD body weight, 16.3 ± 1.0 kg). Procedures: All dogs underwent 3 anesthesia sessions with a minimum of 1 week separating sessions: isoflurane alone, isoflurane and a constant rate infusion of dexmedetomidine (3 μg/kg/h, IV; ID), and isoflurane and a constant rate infusion of remifentanil (18 μg/kg/h, IV; IR). The MAC of isoflurane was determined via supramaximal electrical stimulation. Quantitative variables (frequency bands and their ratios, median frequency, 95% spectral edge frequency [SEF], and an EEG index) were determined directly before and after supramaximal stimulation at 0.75, 1.0, and 1.5 times the MAC for each session of 20-second epochs. Results: Mean ± SD isoflurane MACs for isoflurane alone, ID, and IR were 1.7 ± 0.3%, 1.0 ± 0.1%, and 1.0 ± 0.1%, respectively. Prestimulation 95% SEF decreased significantly with increasing MAC during the isoflurane alone and ID sessions. Significant decreases in δ frequency band (0.5 to 3.5 Hz) presence and significant increases in β frequency band (> 12.5 Hz) presence, median frequency, and 95% SEF after stimulation were dependent on the MAC and anesthetic protocol. The EEG index had the strongest correlation with increasing MAC during the isoflurane-alone session (ρ = −0.89) and the least in the IR session (ρ = −0.15). Conclusions and Clinical Relevance: Anesthesia with isoflurane alone resulted in the greatest overall EEG depression of all protocols. Use of remifentanil depressed the EEG response to nociceptive stimulation more strongly than did dexmedetomidine. The EEG variables evaluated did not appear useful when used alone as indicators of anesthetic depth in dogs.

Objective—To characterize the electroencephalogram (EEG) in young cats. Animals—23 clinically normal cats. Procedures—Cats were sedated with medetomidine hydrochloride and butorphanol tartrate at 2, 4, 6, 8, 12, 16, 20, and 24 weeks of age, and an EEG was recorded at each time point. Recordings were visually inspected for electrical continuity, interhemispheric synchrony, amplitude and frequency of background electrical activity, and frequency of transient activity. Computer-aided analysis was used to perform frequency spectral analysis and to calculate absolute and relative power of the background activity at each age. Results—Electrical continuity was evident in cats ≥ 4 weeks old, and interhemispheric synchrony was evident in cats at all ages evaluated. Analysis of amplitude of background activity and absolute power revealed significant elevations in 6-week-old cats, compared with results for 2-, 20-, and 24-week-old cats. No association between age and relative power or frequency was identified. Transient activity, which consisted of sleep spindles and K complexes, was evident at all ages, but spike and spike-and-wave discharges were observed in cats at 2 weeks of age. Conclusions and Clinical Relevance—Medetomidine and butorphanol were administered in accordance with a sedation protocol that allowed investigators to repeatedly obtain EEG data from cats. Age was an important consideration when interpreting EEG data. These data on EEG development in clinically normal cats may be used for comparison in future studies conducted to examine EEGs in young cats with diseases that affect the cerebral cortex.

We compared the anesthetic combination of detomidine, ketamine, and halothane in control horses not undergoing apparently painful procedures with that in horses during arthroscopic surgery. The effectiveness of this regimen in suppressing neurologic response to surgery was, thus, evaluated. In this study, significant differences were not observed in electroencephalographic total amplitude, spectral edge, or beta-to-delta frequency ratio between surgically treated and nonsurgically treated (control) horses. On the basis of its attenuation of encephalographic responses, we conclude that detomidine (20 microgram/kg of body weight, IV) and ketamine (2.2 mg/kg, IV) induction of anesthesia followed by maintenance with halothane is an effective regimen for control of pain in horses during arthroscopic surgery. The insignificant frequency changes observed without any other signs of inadequate anesthesia or pain may indicate a surgical stress response. We hypothesize that brain activity monitoring may give an earlier index to initiation of surgically induced stress than do hormonal responses, because endocrine alterations are not as rapidly perceived as is the electroencephalogram. Analysis of spectral edge frequency changes could be used to evaluate anesthetic regimens to find those that cause the least stress to the CNS during surgery in horses. Differences in species responses to an anesthetic agent or the regimen's effectiveness in prevention of pain during surgery may be identified by adoption of the study model. Evaluation of cardiopulmonary variables during anesthesia, with and without surgery, did not reveal any alterations that would be relevant to CNS responses. Blood pressure, heart rate, PAO2, PACO2 and pH were stabilized by use of intermittent positive-pressure ventilation in all horses, and dobutamine was administered as needed, to avoid bias of electroencephalogram data.

Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the EEG were determined for delta, theta, alpha, and beta frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the delta band. Hypocapnia caused an increase in the absolute power of delta, theta, and alpha frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.