A seizure is an electrical event that is defined by the International League Against Epilepsy as a transient occurrence of signs caused by abnormal excessive or synchronous neuronal activity in the brain.1 The signs of the abnormal electrical activity can include altered mentation only, subtle twitching, generalized convulsions, or coma.2 For patients with subtle or nonconvulsive signs, diagnosis of a seizure requires EEG confirmation. For human patients, the International League Against Epilepsy has recently proposed classifying status epilepticus on the basis of type, where CSE is a tonic-clonic seizure lasting > 5 minutes and NCSE is a nonconvulsive seizure lasting > 10 to 15 minutes.1
Electrographic seizures are well described in human medicine, with nonconvulsive seizures reported in 9% to 21% of critically ill patients.3–5 In a case series6 of 164 human patients that were evaluated for electrical seizure activity after control of CSE, 79 (48%) had persistent ES and 23 (14%) were in ESE. The investigators of that study6 noted that detection of nonconvulsive seizures required use of EEG, and the in-hospital mortality rate was 32% (25/79) for patients with ES and 52% (12/23) for patients with ESE, compared with only 13% (8/62) for patients without an ictal pattern.
The use of EEG is common in human medicine but remains rare in veterinary medicine, and reports describing ES or ESE in the veterinary literature are generally lacking. The purpose of the study reported here was to define the prevalence of ES and ESE in dogs and cats that underwent an EEG because of suspected seizure activity and to characterize the clinical characteristics, risk factors, and in-hospital mortality rates for dogs and cats with ES or ESE.
Materials and Methods
Case selection criteria
The medical record database of the Bush Veterinary Neurology Service was searched to identify dogs and cats that had an EEG performed between May 2009 and April 2015. The EEGs were performed to identify electrical seizure activity and differentiate suspected seizure activity from movement, metabolic, or behavior disorders.7,8 Only patients with a complete medical record were eligible for study inclusion.
Medical records review
For each patient eligible for study inclusion, information extracted from the medical record included signalment, pertinent history (obtained from owner, referring veterinarian, or prior medical record), physical and neurologic examination findings, diagnostic test (EEG, MRI, and CSF analysis) results, diagnosis, and patient status (alive or dead) at hospital discharge. Pertinent history was defined as information regarding previous episodes of convulsive seizures, cluster seizures (≥ 2 seizures within 24 hours), or CSE; antiepileptic treatment; and time since last witnessed convulsive seizure. All final diagnoses were made on the basis of MRI findings with or without CSF analysis and histologic results by the attending neurologist. For analysis purposes, diagnoses were categorized on the basis of etiology, and the etiologic categories included open (no MRI or CSF analysis performed), reactive, structural, and unknown (eg, suspected cryptogenic or idiopathic epilepsy). Consistent with the International Veterinary Epilepsy Task Force consensus report,9 reactive seizures were defined as seizures associated with a transient change, and structural seizures were defined as seizures caused by intracranial pathology. Structural diagnoses were further categorized as meningoencephalitis of unknown etiology, neoplasia, infarct, or malformation.
EEG
All EEG recordings were obtained for diagnostic purposes with the consent of the patient's owner. For each patient, EEGa,b was performed by use of 6 to 10 EEG needle electrodes (length, 12 mm; diameter, 0.32 mm [28 gauge]) that were positioned SC as previously described.10,11 The EEG recordings were reviewed in a modified double-banana montage with F (frontal), C (central), T (temporal), and O (occipital) placement on each side plus an ECG tracing along with a ground; electrode impedance was < 10 kohm (Figure 1). Some patients also had an electromyographic lead. To facilitate EEG electrode placement and control muscle artifact, patients were sedated with dexmedetomidine (2 to 10 μg/kg [0.9 to 4.5 μg/lb]); occasionally, some patients also received an opioid (fentanyl) to achieve the desired sedation. Dexmedetomidine has minimal effect on ictal activity, and it and related sedatives have been used in conjunction with EEG in humans,12,13 cats,10,14 horses,15 and sea lions.16 The EEG was recorded until patient movement impeded interpretation (mean EEG duration, 35 minutes [range, 10 to 442 minutes]).
Electroencephalographic recording provided in a modified double-banana montage (impedance, < 7 kohm for all leads; sensitivity, 5 μV/mm; high frequency, 50 Hz; low frequency, 1 Hz; and paper speed, 30 mm/s) for a 6-year-old spayed female Shih Tzu. The lead I ECG tracing is also provided. Notice the persistent left-sided spikes (shaded areas) throughout this 20-minute recording, which was consistent with ESE. The patient had periods of depressed mentation with facial twitching (worse on the right side than on the left side; Supplementary Video S1, available at avmajournals.avma.org/doi/suppl/10.2460/javma.254.8.967). C3 = Left central electrode. C4 = Right central electrode. F1 = Left frontal electrode. F2 = Right frontal electrode. O1 = Left occipital electrode. O2 = Right occipital electrode. T3 = Left temporal electrode. T4 = Right temporal electrode. Inset—Transverse T2 MRI image obtained at the level of the parietal lobe for this dog. Notice the hyperintensity in the left parietal lobe. L = Left. R = Right. The final diagnosis for this dog was meningoencephalitis of unknown etiology.
Citation: Journal of the American Veterinary Medical Association 254, 8; 10.2460/javma.254.8.967
Electroencephalographic recording provided in a modified double-banana montage (impedance, < 7 kohm for all leads; sensitivity, 5 μV/mm; high frequency, 50 Hz; low frequency, 1 Hz; and paper speed, 30 mm/s) for a 6-year-old spayed female Shih Tzu. The lead I ECG tracing is also provided. Notice the persistent left-sided spikes (shaded areas) throughout this 20-minute recording, which was consistent with ESE. The patient had periods of depressed mentation with facial twitching (worse on the right side than on the left side; Supplementary Video S1, available at avmajournals.avma.org/doi/suppl/10.2460/javma.254.8.967). C3 = Left central electrode. C4 = Right central electrode. F1 = Left frontal electrode. F2 = Right frontal electrode. O1 = Left occipital electrode. O2 = Right occipital electrode. T3 = Left temporal electrode. T4 = Right temporal electrode. Inset—Transverse T2 MRI image obtained at the level of the parietal lobe for this dog. Notice the hyperintensity in the left parietal lobe. L = Left. R = Right. The final diagnosis for this dog was meningoencephalitis of unknown etiology.
Citation: Journal of the American Veterinary Medical Association 254, 8; 10.2460/javma.254.8.967
Electroencephalographic recording provided in a modified double-banana montage (impedance, < 7 kohm for all leads; sensitivity, 5 μV/mm; high frequency, 50 Hz; low frequency, 1 Hz; and paper speed, 30 mm/s) for a 6-year-old spayed female Shih Tzu. The lead I ECG tracing is also provided. Notice the persistent left-sided spikes (shaded areas) throughout this 20-minute recording, which was consistent with ESE. The patient had periods of depressed mentation with facial twitching (worse on the right side than on the left side; Supplementary Video S1, available at avmajournals.avma.org/doi/suppl/10.2460/javma.254.8.967). C3 = Left central electrode. C4 = Right central electrode. F1 = Left frontal electrode. F2 = Right frontal electrode. O1 = Left occipital electrode. O2 = Right occipital electrode. T3 = Left temporal electrode. T4 = Right temporal electrode. Inset—Transverse T2 MRI image obtained at the level of the parietal lobe for this dog. Notice the hyperintensity in the left parietal lobe. L = Left. R = Right. The final diagnosis for this dog was meningoencephalitis of unknown etiology.
Citation: Journal of the American Veterinary Medical Association 254, 8; 10.2460/javma.254.8.967
All EEG recordings were read in real time by a board-certified veterinary neurologist (WWB) and were also read in real time or reviewed after the procedure by a board-certified human electroencephalographer who had experience evaluating EEGs of domestic animals (MMS). For the purpose of this study and consistent with reports17,18 in the human medical literature, ES was defined as ictal discharges that evolved in frequency, duration, or morphology and lasted at least 10 seconds. Patients with an ES that lasted ≥ 10 minutes were classified as having ESE.1
Statistical analysis
Primary outcomes of interest were identification of ES or ESE. In-hospital mortality rate was a secondary outcome of interest. Continuous independent variables assessed included patient age and weight. Categorical variables assessed included those associated with signalment (species, breed, sex, and neuter status), history (presence of blood antiepileptic drug concentrations, cluster seizures, GTCS, or CSE and time since last seizure [> or ≤ 8 hours]), initial neurologic examination findings (presence of menace responses, twitching, GTCS, and CSE), presence of abnormal MRI or CSF findings, presence of convulsion or twitching during EEG, and etiologic category (open, reactive, structural, or unknown). Examination of normal probability plots indicated that data for age and weight had approximately normal distributions. Therefore, results for age and weight were summarized as the mean ± SD. Contingency tables were used to summarize categorical variables.
For each primary outcome of interest, 2-sample t tests were used to evaluate the association between the outcome and each continuous variable and Fisher exact tests were used to evaluate the association between the outcome and each categorical variable. Dependent variables with values of P ≤ 0.05 on univariate analysis were then included in a multivariable logistic regression model, for which the outcome was modeled as the presence of ES or ESE. Variables were added and removed from the model in a stepwise manner until only variables with a value of P < 0.05 remained. A Fisher exact test was used to compare the in-hospital mortality rate between patients with and without ES or ESE. For all analyses, values of P < 0.05 were considered significant unless otherwise specified. All statistical analyses were performed with statistical software.c
Results
Animals
Ninety-four dogs underwent EEG during the study period; however, 5 dogs were excluded from the study because of incomplete medical records. Thus, 89 dogs were included in the study. The dogs ranged in age from 10 months to 17 years and included 38 spayed females, 5 sexually intact females, 37 castrated males, and 9 sexually intact males. There were 8 Labrador Retriever mixes, 6 Golden Retrievers, 5 Beagles, 5 Australian Shepherds, 4 Lhasa Apsos, 3 Boston Terriers, 3 Boxers, 3 pit bull–type dogs, 3 Shih Tzus, and 1 to 2 each of 41 other breeds and breed mixes.
Fifteen cats (8 spayed females and 7 castrated males) with ages ranging from 1 to 16 years were included in the study. There were 9 domestic shorthairs, 4 domestic longhairs, 1 Persian, and 1 Siamese mix.
Among the 104 patients (89 dogs and 15 cats), ancillary diagnostic testing performed in conjunction with the initial EEG included MRI for 76 (73%), CSF analysis for 69 (66%), and determination of serum antiepileptic drug concentration for 9 (9%). Seven patients underwent multiple EEGs during the same hospital stay, and 4 patients were hospitalized on ≥ 2 occasions. Serial EEGs were generally performed to evaluate the effect of treatment on ES activity or to reassess patients with a previously normal EEG because of continued concerns about seizure activity. For patients that underwent multiple EEGs, only the initial EEG recording was included in the analysis. One dog was examined twice, 3 years apart, because of a history of GTCSs, facial twitching, and a change in mentation. The initial EEG recording was consistent with a diagnosis of myoclonus; however, the EEG recording obtained 3 years later revealed continuous ES activity. That dog was suspected of having canine distemper virus–induced seizures in conjunction with myoclonus and was included in the ESE group for analysis purposes.
ES
Of the 104 patients, ES was diagnosed in 21 (20%; 17 dogs and 4 cats). Results of univariate analyses indicated that age and a history of cluster seizures were significantly (P < 0.05) associated with a diagnosis of ES. The mean ± SD age of patients with ES (3.9 ± 3.2 years) was significantly (P = 0.002) less than that of patients without ES (7.1 ± 4.2 years). The proportion of patients with ES among those with a history of cluster seizures (17/63 [27%]) was significantly (P = 0.045) greater than the proportion of patients with ES among those without a history of cluster seizures (4/41 [10%]).
On univariate analyses, the P values for time since last seizure (P = 0.054) and GTCS (P = 0.051) rounded to 0.05, so those 2 variables were eligible for evaluation in the multivariable logistic regression model. Variables evaluated in the multivariable logistic regression model included age, history of cluster seizures, time since last seizure, and GTCS. The final multivariable model included age and time since last seizure. The odds of ES decreased by 20% (OR, 0.8; 95% CI, 0.7 to 0.9; P = 0.003) for each 1-year increase in patient age and by 80% (OR, 0.2; 95% CI, 0.0 to 0.9; P = 0.039) when the time since last seizure was > 8 hours.
The in-hospital mortality rate for patients with ES (10/21 [48%]) was significantly (P = 0.012) greater than that for patients without ictal activity (16/83 [19%]). In fact, patients with ES were almost 4 times (OR, 3.8, 95% CI, 1.4 to 10.5) as likely to die while hospitalized as were patients without ES.
ESE
Electrographic status epilepticus was diagnosed in 12 of 104 (12%; 8 dogs and 4 cats) patients. Those 12 patients were a subset of the 21 patients with ES. All 12 patients had electrical activity consistent with ESE identified immediately after placement of the EEG leads, and that activity continued for durations ranging from 10 minutes to several hours. Results of univariate analyses indicated that age, history of cluster seizures, and presence of twitching during the initial physical examination were significantly associated with ESE. The mean ± SD age of patients with ESE (4.1 ± 3.0 years) was significantly (P = 0.018) less than that of patients without ESE (7.1 ± 4.2 years). The proportion of patients with ESE among those with a history of cluster seizures (11/57 [19%]) was significantly (P = 0.024) greater than the proportion of patients with ESE among those without a history of cluster seizures (1/38 [3%]). Likewise, the proportion of patients with ESE among those with twitching during the initial physical examination (7/29 [24%]) was significantly (P = 0.041) greater than the proportion of patients with ESE among those without twitching (5/66 [8%]).
Age, history of cluster seizures, and twitching during the initial physical examination were evaluated in the multivariable logistic regression model. The final multivariable model included only a history of cluster seizures. Patients with a history of cluster seizures were almost 9 times (OR, 8.8; 95% CI, 1.1 to 71.7; P = 0.041) as likely to have ESE as were patients without a history of cluster seizures.
The in-hospital mortality rate for patients with ESE (6/12 [50%]) was significantly (P = 0.029) greater than that for patients without ESE (16/83 [19%]). Patients with ESE were over 4 times (OR, 4.2, 95% CI, 1.2 to 14.7) as likely to die while hospitalized as were patients without ES or ESE.
Discussion
To our knowledge the present study was the first in which the clinical characteristics and outcomes were evaluated for a large population of dogs and cats with nonconvulsive ES. Although ES and ESE are well described in human medicine, the incidence or prevalence of those 2 conditions in veterinary medicine is unknown. Results of this retrospective study indicated that, among dogs and cats that underwent an EEG because of suspected seizure activity between May 2009 and April 2015, ES was detected in 17 of 89 (19%) dogs and 4 of 15 (27%) cats and ESE was detected in 8 of 89 (9%) dogs and 4 of 15 (27%) cats. Those numbers are fairly consistent with the prevalence of ES (19% to 44%)3–5 and ESE (up to 37% for critically ill patients)6,17 reported in the human medical literature.
In the present study, 11 dogs were in CSE when initially examined by the neurology service, and 4 (36%) and 2 (18%) were subsequently determined to have ES and ESE, respectively, on the basis of EEG recordings that were performed after the convulsive manifestations of the seizure activity were controlled. Those proportions were lower than the proportion of human patients (48%) for whom ES was subsequently diagnosed following control of CSE in 1 study.6 The discrepancy in the number of patients with CSE for which ES was subsequently detected between that study6 and the present study might have been caused by differences in the drugs used for placement of the EEG electrodes or duration of the EEG recording. In the present study, patients were sedated, and the EEG was recorded for approximately 30 minutes. If ES was not identified during that time, the patient was allowed to awaken slowly, and the EEG was discontinued when movement impaired interpretation. Among critically ill human patients with ES, only 43% are identified within the first 30 minutes after initiation of EEG,17 whereas 71% to 88% are identified during the first 24 hours after initiation of EEG.3,5,17 Thus, it is possible that the EEG recording duration used in the present study might not have been sufficient to identify ES in all affected patients. In a previous case series19 of 7 dogs and 3 cats with CSE, ES was identified by EEG in all 10 patients after convulsive signs were controlled. The fact that the prevalence of ES was substantially greater in that study,19 compared with the present study, was most likely a reflection of the more stringent inclusion criteria used for ES in the present study; ictal discharges observed on EEG had to persist for at least 10 seconds for a patient to be classified as having ES in this study. Regardless, it is important that clinicians be aware that patients with CSE can continue to have ES or ESE after convulsive signs have been controlled.
The in-hospital mortality rate was 25% (49/194) for dogs with CSE in another study,20 which is similar to the mortality rate for human patients with CSE.21 In human medicine, the mortality rate ranges from 31% to 33% for patients with nonconvulsive seizures and 51% to 57% for patients with NCSE, compared with a mortality rate of only 13% to 14% for patients without ES or ESE.4,6,22 In the present study, the in-hospital mortality rate was 48% (10/21; 8/17 dogs and 2/4 cats) for patients with ES and 50% (6/12; 4/8 dogs and 2/4 cats) for patients with ESE, whereas the in-hospital mortality rate was only 19% (16/83; 14/72 dogs and 2/11 cats) for patients without ES or ESE. Thus, patients with ES or ESE were approximately 4 times as likely to die while hospitalized as were patients without ES or ESE.
For patients with CSE, the cause of death is generally believed to be the result of multiple detrimental physiologic alterations subsequent to continuous motor activity.23 Results of studies involving animals24,25 and human patients26 indicate that NCSE can cause neuronal damage regardless of the underlying etiology. The cause of neuronal death in individuals with status epilepticus is thought to be the result of glutamate-related excitotoxicosis and movement of extracellular calcium through N-methyl-d-aspartate glutamate receptors.23 The duration of nonconvulsive ESE required to cause irreversible neuronal injury and clinically evident brain damage is unknown.1 For the patients of the present study that died while hospitalized, it was unclear whether death was a direct result of ES, some other underlying abnormality, or euthanasia owing to a poor prognosis or owner financial constraints.
One of the goals of the present study was to evaluate whether certain clinical characteristics of affected patients were risk factors for or predictive of ES or ESE. Results indicated that, for the dogs and cats of this study, none of the physical or neurologic examination findings assessed were predictive for ES, and EEG was necessary to distinguish patients with ES from those with clinical signs secondary to other CNS diseases. Likewise, in human medicine, neurologic examination findings alone are insufficient to identify the presence of ictal activity.6 Additionally, the presence of subtle twitching is not pathognomonic for ES activity as evidenced by the fact that 10% to 22% of human patients with encephalopathy may have movements that are not associated with ES.27,28
Although autonomic changes were not formally evaluated for the patients of the present study, several patients with ES were noted to have an abnormal respiratory rate or hyperthermia during hospitalization. The retrospective nature of this study prevented further investigation of those variables as potential predictors for ES or ESE, but they should be considered in future prospective studies.
For the patients of the present study, history, signalment, results of ancillary diagnostic testing, and disease etiology were also assessed as potential risk factors for ES or ESE. Results of multivariable logistic regression revealed that the odds of an ES diagnosis decreased by 20% for each 1-year increase in patient age and by 80% for patients for which the time since last convulsive seizure was > 8 hours before the EEG. Patients with ES and ESE were more likely to have a history of cluster seizures than were patients without ES or ESE. Likewise, in human medicine, patients who are young3,29 or have a history of epilepsy3,4 or convulsive seizures3,5,30 are more likely to have nonconvulsive seizures than older patients and patients without a history of epilepsy or convulsive seizures. Therefore, the index of suspicion for ES should be increased for young patients and those with a history of epilepsy or convulsive seizures, and clinicians should consider recommending EEG for such patients. Various etiologies have been associated with ES and ESE in human patients3,4,31; however, disease etiology was not significantly associated with the presence of ES or ESE for the patients of the present study. That finding may have been the result of insufficient power owing to the small study population and the fact that each etiologic category contained only a few patients.
In the present study, patients with a history of cluster seizures were almost 9 times as likely to have ESE as were patients without a history of cluster seizures. Although the association between cluster seizures and ESE needs to be investigated further, that finding suggested that aggressive prophylactic antiseizure treatment might be beneficial for patients with cluster seizures. Results of another studyd indicate that levetiracetam pulse therapy is effective for reducing cluster seizures in dogs with idiopathic epilepsy receiving maintenance therapy with phenobarbital and potassium bromide.
Seventeen (13/17 dogs and 4/4 cats) of the 21 (81%) patients with ES activity had no (n = 9 dogs and 4 cats) or only subtle (4 dogs) clinical signs of seizures and would have remained undetected without EEG. Four dogs had a convulsive seizure during the EEG. A high percentage of human patients with ES activity likewise have no or only subtle clinical signs of disease. In 1 study,17 ES activity was classified as nonconvulsive in 27 of 28 (96%) pediatric patients with acute encephalopathy who underwent EEG. In another study3 of 110 critically ill human patients who underwent continuous EEG monitoring, 101 (92%) had only nonconvulsive seizure activity detected.
In human medicine, patients with NCSE are often treated by means of barbiturate anesthesia and continuous EEG monitoring. Important treatment end points include the cessation of clinical seizures, elimination of electrographic epileptiform complexes, and establishment of a burst suppression pattern.32–34 In veterinary medicine, use of continuous EEG has been described for the diagnosis and monitoring of treatment for NCSE in a cat.10 Evaluation of continuous EEG to guide treatment of patients with ESE was not a goal of the present study; however, we did informally assess the anesthesia and EEG protocols for several patients with ESE. Six (4 dogs and 2 cats) of 12 patients with ESE received anesthetic doses of phenobarbital (30 to 108 mg/kg [13.6 to 49.1 mg/lb]) and continuous EEG monitoring with the recorded intent to eliminate clinical signs of seizure activity and epileptiform complexes and reestablish a burst suppression EEG pattern. Among those 6 patients, 4 achieved the desired end points and survived to hospital discharge. The other 6 (4 dogs and 2 cats) patients with ESE received routine doses of phenobarbital without the use of EEG to guide therapy, and only 2 (both dogs) survived to hospital discharge. In human medicine, outcomes for patients with ES and ESE are improved when continuous EEG is used to monitor treatment until predefined EEG end points are achieved, compared with that for patients that undergo treatment without continuous EEG. In a study19 of 10 dogs and cats with CSE, anesthesia was induced with phenobarbital (12 to 20 mg/kg [5.5 to 9.1 mg/lb]) and maintained with pentobarbital or propofol, and patients underwent continuous EEG until epileptiform discharges were eliminated. A burst suppression pattern was achieved in 5 of those patients, and 3 survived to hospital discharge. Further research is necessary to determine whether the administration of anesthetic doses of barbiturates or other anticonvulsants and continuous EEG until specific EEG end points are achieved will improve the outcome for veterinary patients with ES or ESE, compared with treatment without continuous EEG monitoring.
Limitations of the present study included its retrospective nature and the lack of a uniform sedation protocol for the study population. For 9 patients, EEG was performed after the individual was anesthetized with isoflurane for other diagnostic procedures (MRI or CSF collection), which might have affected the EEG results. Because the number of cats that met the study inclusion criteria was small, we chose to combine cats and dogs for statistical analyses. We felt that was acceptable because the clinical signs of ES and ESE and EEG morphology are similar between the 2 species. The study population contained dogs and cats that were examined because of clinical signs consistent with seizure activity that were subsequently proven by EEG to not be seizure related and vice versa. The proportion of cats with ESE (4/15 [27%]) was numerically greater than the proportion of dogs with ESE (8/80 [10%]), but the difference between those 2 proportions was not significant (P = 0.093). A proportionately greater number of study dogs than study cats had a history of GTCS, antiepileptic drug administration, and abnormal results on CSF analysis, but none of those variables were identified as significant risk factors for ES or ESE. A larger study population might have provided us sufficient power to detect significant differences between the 2 species. Other limitations of this study were the limited duration of EEG (mean, 35 minutes) and the lack of diagnostic test (CSF analysis, MRI, and histopathologic evaluation) results for some patients. The results of this study may also have been affected by bias owing to the euthanasia of patients with ES or ESE because of a perceived poor prognosis.
Results of the present study indicated that the prevalence of ES (21/104 [20%]) and ESE (12/104 [12%]) was fairly high among dogs and cats that underwent EEG at a referral neurology service during a 6-year period. The majority (17/21 [81%]) of patients with ES had no overt clinical signs, and the seizure activity would have remained undetected had EEG not been performed. Identification of patients with ES and ESE is important because those patients are approximately 4 times as likely to die while hospitalized, compared with patients without ictal activity. Unfortunately, none of the clinical characteristics assessed were significantly associated with detection of ES or ESE. However, age was negatively associated and the presence of overt seizure activity in the 8 hours before EEG was positively associated with the risk for ES, and a history of cluster seizures was positively associated with the risk for ESE. Thus, ES or ESE should be suspected in young dogs and cats with overt signs of seizure activity and a history of cluster seizures, and those patients should undergo EEG to definitively confirm or rule out those 2 conditions. Prospective research is necessary to evaluate whether the use of anesthetic doses of barbiturates or other anticonvulsants in conjunction with continuous EEG to monitor electrical brain activity until specific EEG end points are achieved is beneficial to the outcome for patients with ES and ESE.
Acknowledgments
Patients were evaluated at 1 of 4 Bush Veterinary Neurology Service locations: Leesburg, Va; Rockville, Md; Springfield, Va; or Richmond, Va.
Supported in part by the Bush Veterinary Neurology Service Rascal Foundation, a nonprofit organization founded to support clinical research in companion animal neurology.
The authors declare that there were no conflicts of interest.
Presented in part at the American College of Veterinary Internal Medicine Forum, Indianapolis, June 2015.
ABBREVIATIONS
| CI | Confidence interval |
| CSE | Convulsive status epilepticus |
| EEG | Electroencephalography |
| ES | Electrographic seizure |
| ESE | Electrographic status epilepticus |
| GTCS | Generalized tonic-clonic seizure |
| NCSE | Nonconvulsive status epilepticus |
Footnotes
Neurofax, Nihon Kohden Corp, Tokyo, Japan.
Easy II EEG, Cadwell Industries, Kennewick, Wash.
SAS, version 9.4, SAS Institute Inc, Cary, NC.
Bentley RT, Logan M, Sangster A, et al. A pilot study of levetiracetam pulse therapy for canine cluster seizures (abstr). J Vet Intern Med 2014;28:1357.
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