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Background Previous study of the diagnostic validity of electroencephalography (EEG) to detect abnormalities in equine cerebral cortical function relied on the administration of various drugs for sedation, induction, and maintenance of general anesthesia but used identical criteria to interpret recordings. Objectives To determine the effects of 2 inhalation anesthetics on the EEG of healthy horses. Animals Six healthy horses. Methods Prospective study. After the sole administration of one of either isoflurane or halothane at 1.2, 1.4, and 1.6 times the minimum alveolar concentration, EEG was recorded during controlled ventilation, spontaneous ventilation, and nerve stimulation. Results Burst suppression was observed with isoflurane, along with EEG events that resembled epileptiform discharges. Halothane results were variable between horses, with epileptiform-like discharges and bursts of theta, alpha, and beta recorded intermittently. One horse died and 2 were euthanized as the result of anesthesia-related complications. Conclusions and Clinical Importance The results of this study indicate that the effects of halothane and isoflurane on EEG activity in the normal horse can be quite variable, even when used in the absence of other drugs. It is recommended that equine EEG be performed without the use of these inhalation anesthetics and that general anesthesia be induced and maintained by other contemporary means.

Background Brainstem auditory evoked response has been an underused diagnostic modality in horses as evidenced by few reports on the subject. Hypothesis/Objectives To describe BAER findings, common clinical signs, and causes of hearing loss in adult horses. Animals Study group, 76 horses; control group, 8 horses. Methods Retrospective. BAER records from the Clinical Neurophysiology Laboratory were reviewed from the years of 1982 to 2013. Peak latencies, amplitudes, and interpeak intervals were measured when visible. Horses were grouped under disease categories. Descriptive statistics and a posthoc Bonferroni test were performed. Results Fifty-seven of 76 horses had BAER deficits. There was no breed or sex predisposition, with the exception of American Paint horses diagnosed with congenital sensorineural deafness. Eighty-six percent (n = 49/57) of the horses were younger than 16 years of age. The most common causes of BAER abnormalities were temporohyoid osteoarthropathy (THO, n = 20/20; abnormalities/total), congenital sensorineural deafness in Paint horses (17/17), multifocal brain disease (13/16), and otitis media/interna (4/4). Auditory loss was bilateral and unilateral in 74% (n = 42/57) and 26% (n = 15/57) of the horses, respectively. The most common causes of bilateral auditory loss were sensorineural deafness, THO, and multifocal brain disease whereas THO and otitis were the most common causes of unilateral deficits. Conclusions and Clinical Importance Auditory deficits should be investigated in horses with altered behavior, THO, multifocal brain disease, otitis, and in horses with certain coat and eye color patterns. BAER testing is an objective and noninvasive diagnostic modality to assess auditory function in horses.

Author(s): Williams, DC; Brosnan, RJ; Fletcher, DJ; Aleman, M; Holliday, TA; Tharp, B; Kass, PH; LeCouteur, RA; Steffey, EP | Abstract: BackgroundThe effects of anesthesia on the equine electroencephalogram (EEG) after administration of various drugs for sedation, induction, and maintenance are known, but not that the effect of inhaled anesthetics alone for EEG recording.ObjectiveTo determine the effects of isoflurane and halothane, administered as single agents at multiple levels, on the EEG and quantitative EEG (qEEG) of normal horses.AnimalsSix healthy horses.MethodsProspective study. Digital EEG with video and quantitative EEG (qEEG) were recorded after the administration of one of the 2 anesthetics, isoflurane or halothane, at 3 alveolar doses (1.2, 1.4 and 1.6 MAC). Segments of EEG during controlled ventilation (CV), spontaneous ventilation (SV), and with peroneal nerve stimulation (ST) at each MAC multiple for each anesthetic were selected, analyzed, and compared. Multiple non-EEG measurements were also recorded.ResultsSpecific raw EEG findings were indicative of changes in the depth of anesthesia. However, there was considerable variability in EEG between horses at identical MAC multiples/conditions and within individual horses over segments of a given epoch. Statistical significance for qEEG variables differed between anesthetics with bispectral index (BIS) CV MAC and 95% spectral edge frequency (SEF95) SV MAC differences in isoflurane only and median frequency (MED) differences in SV MAC with halothane only.Conclusions and clinical importanceUnprocessed EEG features (background and transients) appear to be beneficial for monitoring the depth of a particular anesthetic, but offer little advantage over the use of changes in mean arterial pressure for this purpose.

Background Reports of the use of brainstem auditory evoked response (BAER) as a diagnostic modality in foals have been limited. Hypothesis/Objectives To describe BAER findings and associated causes of hearing loss in foals. Animals Study group 18 foals (15 neonatal, 3 nonneonatal), control group (5 neonatal foals). Methods Retrospective. BAER records from the Clinical Neurophysiology Laboratory were reviewed from the years of 1982 to 2013. Peak latencies, amplitudes, and interpeak intervals were measured when visible. Clinical data were extracted from the medical records. Foals were grouped under disease categories. Descriptive statistics were performed. Results Ten neonatal foals had complete absence of BAER bilaterally and 5 had findings within reference range. Abnormalities were associated with common neonatal disorders such as sepsis, neonatal encephalopathy, neonatal isoerythrolysis, and prematurity. BAER loss also was observed in foals with specific coat color patterns such as completely or mostly white with blue irides or lavender with pale yellow irides. An American Miniature foal with marked facial deformation also lacked BAER bilaterally. One nonneonatal foal with an intracranial abscess had no detectable BAER peaks bilaterally, and 2 older foals, 1 with presumed equine protozoal myeloencephalitis and the other with progressive scoliosis and ataxia, had BAER within normal limits. Conclusions and Clinical Importance In neonatal foals, BAER deficits commonly are complete and bilateral, and associated with common neonatal disorders and certain coat and eye color patterns. Sepsis, hypoxia, bilirubin toxicity, and prematurity should be investigated as potential causes of auditory loss in neonatal foals.

Sensitive analytical methods indicate the presence of hundreds of chemical contaminants in our environment. However, concentration of these pollutants is usually at the low parts per million or parts per billion level. At such low levels, toxicants induce long-term (chronic) rather than short-term (acute) toxicities. Experiments are designed to evaluate chronic toxicity using early bioindicators. Recently, fish have been used as experimental animals because some species show early (weeks as opposed to years in other research animals), sensitive responses. Thus, medaka (Oryzias latipes), following exposure to diethylnitrosamine (DEN), exhibited liver tumors in several weeks; more interestingly its DNA was modified (to a 'DNA-adduct') after only 24-48 hours exposure. Such adducts show promise as early bioindicators because they are formed within hours of exposure. The formation of DNA-adducts were monitored in medaka and rainbow trout (Salmo gairdneri) exposed to DEN by aqueous or intra-peritoneal routes. Using HPLC-Fluorimetry, O (6)-ethylguanine (O (6)-EtGua) was detected and monitored in acid thermal hydrolysates of DNA isolates. (Detection limit for O (6)-EtGua was as low as 3 ng, 1.7×10(-11) moles). Fourier transform cyclotron resonance mass spectrometry with IR laser desorption/ionization was used advantageously to establish the structure of nucleotides, bases and nucleosides directly, without further cumbersome derivatizations. Other aspects of DNA-adducts are discussed.

Background Idiopathic headshaking (HSK) in horses is a distressing disorder in which the etiology and pathophysiology are unknown. Hypothesis Differences in sensory function of the trigeminal nerve exist between healthy and affected horses. Animals Six healthy mature geldings and 6 mature geldings with idiopathic HSK. Methods Prospective study. Sensory nerve action and somatosensory evoked potentials studies were performed. The stimulus site comprised the gingival mucosa dorsal to the maxillary canine. A pair of recording electrodes was placed along the sensory pathway of the trigeminal complex at the infraorbital nerve (R1), maxillary nerve (R2), spinal tract of trigeminal (R3), and somatosensory cortex (R4). Sensory nerve action potential latency (ms), amplitude (μV), duration (ms), area under the curve (μVms), and conduction velocity (m/s) were calculated. Results Threshold for activation of the infraorbital branch of the trigeminal nerve was significantly different between 5 affected (≤5 mA) and 6 control horses (≥10 mA). After initiation of an action potential, there were no differences in all parameters measured and no differences between left and right sides. A horse with seasonal HSK tested during a time of no clinical manifestations showed a threshold for activation similar to control horses. Conclusions and Clinical Importance This study confirms involvement of the trigeminal nerve hyperexcitability in the pathophysiology of disease. Further, results might support a functional rather than a structural alteration in the sensory pathway of the trigeminal complex that can be seasonal. The horse could serve as a natural animal model for humans with idiopathic trigeminal neuralgia.

Background The administration of certain sedatives has been shown to promote sleep in humans. Related agents induce sleep-like behavior when administered to horses. Interpretation of electroencephalograms (EEGs) obtained from sedated horses should take into account background activity, presence of sleep-related EEG events, and the animal's behavior. Hypothesis Sedatives induce states of vigilance that are indistinguishable on EEGs from those that occur naturally. Animals Six healthy horses. Methods Digital EEG with video was recorded after administration of 1 of 4 sedatives (acepromazine, butorphanol, xylazine, or detomidine). Serum drug concentrations were measured. Recordings were reviewed, states were identified, and representative EEG samples were analysed. These data were compared with data previously obtained during a study of natural sleep. Results Butorphanol was associated with brief episodes resembling slow wave sleep in 1 horse. Acepromazine led to SWS in 3 horses, including 1 that also exhibited rapid eye movement sleep. Periods of SWS were observed in all horses afer xylazine or detomidine administration. Normal sleep-related EEG events and heart block, occurred in association with SWS regardless of which sedative was used. Spectral data varied primarily by state, but some differences were observed between sedative and natural data. Conclusions and Clinical Importance Qualitatively, EEG findings appeared identical whether sedation-induced or naturally occurring. The startle response and heart block associated with some sedatives may be related to sleep. Alpha2 agonists can be used to obtain high quality EEGs in horses, but acepromazine does not promote a relaxed state in all animals.

In a survey of 900 Dalmatian dogs, brainstem auditory-evoked responses (BAER) and clinical observations were used to determine the incidence and sex distribution of bilateral and unilateral BAER abnormalities and their association with heterochromia iridis (HI). To assess the efficacy of BAER testing in guiding breeding programs, data from 749 dogs (subgroup A), considered to be a sample of the population at large, were compared with data from a subgroup (subgroup B; n = 151) in which selection of breeding stock had been based on BAER testing from the beginning of the 4-year survey. Brainstem auditory-evoked responses were elicited by applying click stimuli unilaterally, while applying a white noise masking sound to the contralateral ear. Under these conditions, BAER were either normal, unilaterally absent, or bilaterally absent. Dogs with bilaterally absent BAER were clinically deaf; dogs with unilaterally absent BAER were not clinically deaf but appeared dependent on their BAER-normal ears for their auditory-cued behavior. Dogs with unilaterally absent BAER often were misidentified as normal by uninformed observers. Among the 900 dogs, 648 (72.0%) were normal, 189 (21.0%) had unilateral absence of BAER, and 63 (7.0%) had bilateral absence of BAER or were clinically deaf and assumed to have bilaterally absent BAER (n = 4). Total incidence in the population sampled was assumed to be higher, because some bilaterally affected dogs that would have been members of subgroup A undoubtedly did not come to our attention. Among females, 24.0% were unilaterally abnormal and 8.2% were bilaterally abnormal whereas, among males, 17.8% were unilaterally abnormal and 5.7% were bilaterally abnormal.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: Facial and vestibulocochlear nerve dysfunction occurs commonly in horses with temporohyoid osteoarthropathy (THO); however, auditory dysfunction has not been thoroughly assessed. Objective: To determine if auditory abnormalities occur in horses with THO. Animals: Eleven diseased and 8 control horses. Methods: This is a prospective study in which brainstem auditory-evoked responses (BAER) were recorded in 11 horses diagnosed with THO through neurologic, endoscopic, radiographic, or computed tomographic examinations. BAER findings were compared with those recorded from 8 adult control horses. Results: All horses with THO were found to have BAER abnormalities that included complete unilateral BAER loss (82%, n = 9/11), partial unilateral BAER loss (18%, n = 2/11) on the most affected side, and contralateral partial BAER loss (46%, n = 5/11). Nine horses had bilateral THO based on diagnostic imaging findings; of these, 5 (56%) horses also had bilateral BAER abnormalities. The complete absence of BAER in affected horses was most consistent with peripheral sensorineural hearing loss. There was a significant association between complete BAER loss and neurologic and diagnostic abnormalities. Conclusions and Clinical Importance: Auditory abnormalities such as complete or partial BAER loss are common in horses with THO. The BAER test is an objective diagnostic tool that can aid along with other diagnostic modalities in the assessment, management, and follow-up of horses with THO. Furthermore, BAER studies may help to elucidate the pathophysiology of THO in horses.

Background: The influence of sleep on the equine electroencephalogram (EEG) has not been well documented. Hypothesis: The objectives were to develop a noninvasive method of electrode placement for recording the EEG in horses and to establish normal EEG parameters for the various states of vigilance. Findings are compared with previously published reports on equine sleep based on electrocorticography (ECoG). Animals: Five neurologically normal horses. Methods: Overnight EEGs were recorded digitally in association with simultaneous videotaping of the horses' behavior. Data were analyzed by visual inspection, states of vigilance were identified, and representative segments were quantitatively processed. Transient EEG events were examined. Results: Slow wave sleep (SWS) was significantly different (P < .05) in frequency and power from drowsiness and rapid eye movement (REM) sleep. Second-degree heart block was associated with SWS as were transient events commonly recognized in EEGs of humans. Drowsiness and REM sleep were similar. In both, background activity was low-amplitude β activity admixed with prominent activity of approximately 4 Hz. Standing REM sleep was associated with numerous partial collapses in 1 horse. Conclusions and Clinical Importance: Normative data for several states were described and probable benign variants identified. This information will serve as control data for sedative and anesthetic studies in this species. The sleep patterns observed during this study are those of horses removed from their usual surroundings, and thus may represent those encountered in a clinical environment.

Background:Epilepsy is relatively uncommon in horses compared with other species and limited information is available. Hypothesis:The objectives of the study were to describe the age of onset, clinical signs, clinicopathologic data, electroencephalographic findings, treatment, and outcome, including long-term prognosis in Arabian foals with idiopathic epilepsy. Animals:Twenty-two foals were included in the study. Materials and Methods: Medical records from 1985 to 2005 were reviewed. Results:The age of onset of affected foals ranged from 2 days to 6 months. Seizures were characterized by generalized tonic and clonic motor activity, staring, and loss of consciousness. The most common postictal signs were transient blindness and abnormal mental status. The interictal neurologic examination was otherwise normal. Clinicopathologic data and imaging diagnostics were normal except in 4 foals that developed complications. Electroencephalography revealed epileptiform activity in 9 of 13 foals. Foals were treated with benzodiazepines for the short-term; whereas phenobarbital was used over the long-term. Potassium bromide was added in 3 foals in which seizures were multiple, frequent, and difficult to control. The long-term prognosis was favorable with cessation of seizures by 1 year of age. The most common complication was head trauma. The most common concurrent disease was pneumonia. Conclusions and Clinical Importance: Juvenile idiopathic epilepsy of Egyptian Arabian foals has an early clinical onset but appears to be self-limiting. Information obtained from this study strongly suggests a heritable condition that merits further investigation.

Eleven horses (3 mares, 7 stallions, 1 gelding) with clinical and biochemical evidence of hyperkalemic periodic paralysis were studied. Each horse had history of episodic weakness, muscular tremors, or collapse, which lasted for periods of a few minutes to hours. Diagnosis was based on hyperkalemia in association with a spontaneous episode of paralysis or by precipitation of an episode by oral administration of potassium chloride. Clinical and biochemical events were documented during spontaneous and induced episodes of muscular weakness. During episodes, electrocardiographic findings were consistent with hyperkalemia. Electromyography performed between episodes revealed fibrillation potentials and positive sharp waves, complex repetitive discharges, and myotonic discharges. Histologic changes in muscle biopsy specimens varied from no overt changes in some horses to vacuolation in type-2B fibers with mild degenerative changes in other horses. Electron microscopy of myofibers revealed dilatations of the sarcoplasmic reticulum. Analysis of blood samples taken serially during induced attacks in 5 horses revealed marked hyperkalemia (5.5 to 9.0 mEq/L), with normal acid-base status, hemoconcentration, and modest changes in muscle-derived enzymes. Close correlation (r2 = 0.882) between total plasma protein and plasma potassium concentrations was observed and indicated a shift of fluid out of the extracellular fluid compartment. Treatment of either spontaneous or induced episodes by IV administration of calcium, glucose, or bicarbonate resulted in rapid recovery. Dietary management or daily administration of acetazolamide effectively controlled episodes. An affected mare was bred to an affected stallion, and 3 affected offspring were produced by embryo transfer. Blood samples from another extended family of affected horses were analyzed for identification of a genetic marker.(ABSTRACT TRUNCATED AT 250 WORDS)

In the acquired form of myasthenia gravis in dogs, there are circulating antibodies to acetylcholine receptors (AChRs) and a reduction in the number of AChRs in the postsynaptic membrane. In this study, immune complexes were localized at the neuromuscular junctions in biopsy samples from 10 myasthenic dogs by immunocytochemical means employing conjugates of staphylococcal protein A and horseradish peroxidase. Immune complexes were observed in approximately 70% of the neuromuscular junctions studied in both type 1 and type 2 myofibers. Thus, acquired canine myasthenia gravis appears to involve immune-mediated mechanisms that destroy AChRs in a manner similar to myasthenia gravis in humans. Protein A was also observed to bind principally to elastic fibers in small arteries and arterioles of some myasthenic and control dogs; however, the significance of that localization is unknown.

Pathologic findings in mature dogs with old dog encephalitis were compared with the findings in multiple sclerosis, subacute sclerosing panencephalitis and neuromyelitis optica in man. Fluorescent antibody studies in animal and human tissues were compared. Optic neuritis in dogs with chronic distemper shows changes similar to those in the optic tract of human patients with severe demyelinating disease. The pathologic changes in multiple sclerosis, such as perivascular infiltration with lymphocytes, plasma cells and demyelination are similar to those seen in old dog encephalitis. Demyelination in old dog encephalitis is usually diffuse. The findings strongly support a possible relationship of old dog encephalitis to multiple sclerosis, subacute sclerosing panencephalitis, and neuromyelitis optica.

Clinical and pathologic features of a sporadic, necrotizing meningoencephalitis affecting adolescent and mature pug dogs are described. Many of the affected animals were closely related. Acute and chronic forms occur, with clinical signs reflecting the pathologic affinity of the disease for the cerebral hemispheres. No etiologic agent has been identified. The extensive necrosis and affinity for the cerebral hemispheres are similar to alphatype herpesvirus encephalitides of other species.

SUMMARY 1 Clinical and electroencephalographic observations of 70 epileptic dogs are reported. Sixty-nine dogs underwent generalized motor seizures. Typically, these consisted of loss of consciousness, generalized tonic-clonic convulsions, and autonomic signs (e.g. urination, salivation, or defecation). Some dogs also had partial motor seizures with rapid generalization. 2 A wide variety of behavioral signs were observed in 33 of the dogs. These signs were usually evident before or after generalized tonic-clonic convulsions or as separate episodes in dogs which also had tonic-clonic convulsions. One dog underwent only paroxysmal behavioral signs. 3 One or more abnormalities were observed in the interictal EEG's of 50 dogs. Thirty-eight had diffuse paroxysmal dysrhythmias and 24 had focal paroxysmal dysrhythmias. Eighteen dogs had diffuse persistent dysrhythmias (all were slow dysrhythmias), and one dog had a focal persistent dysrhythmia. The following types of dysrhythmias were noted: spikes, spike complexes, wave and spike complexes, sharp waves and slow waves. 4 Both chlorpromazine and photic stimulation appeared to be effective in activating EEG abnormalities. 5 Trauma and/or hydrocephalus were possible causative factors in some cases, however, no cause was apparent in 46 of the dogs. The genealogy of one family of dogs strongly suggested inheritance of epilepsy or at least a predisposition to seizures. 6 The data indicate that naturally occurring canine epilepsy is a suitable biological model of human epilepsy and, thus, warrants further study. RESUME 1 On presente les observations cliniques et electroencephalographiques de 70 chiens epileptiques, dont 69 chiens ont presente des convulsions motrices generalisees, caracterisees par une perte de connaissance, des secousses generalisees tonico-cloniques et des manifestations vegetatives (par example miction, salivation, defecation). Quelques chiens aussi ont presente des crises motrices partielles qui se sont rapidement generalisees. 2 On a observe une grande variete de manifestations du comportement chez 33 chiens. Ces manifestations etaient generalement evidentes avant ou apres les convulsions generalisees tonico-cloniques ou se presentaient comme des episodes independants chez des chiens qui avaient aussi des convulsions tonico-cloniques. Un chien a presente seulement des signes du comportement paroxystiques. 3 On a observe chez 50 chiens une ou plusieurs anomalies E.E.G. interictiques caracterisees soit par une dysrythmie diffuse paroxystique (38 chiens), soit par des dysrythmies paroxystiques focales (24 chiens), soit par une dysrythmie diffuse continue et lente (18 chiens); un chien avait une dysrythmie lente focale. On a observe les formes d'anomalies suivantes: pointes, bouffees de pointes et de pointes ondes, pointes lentes et ondes lentes. 4 La chlorpromazine et la stimulation photique semblaient activer les anomalies E.E.G. 5 Si le trauma et/ou l'hyprocephalie pouvaient etre consideres comme des facteurs etiologiques dans quelques cas, dans la majorite (46 chiens)on n'a pas decele de facteurs etiologiques. l'arbre genealogique d'une famille de chiens etait en faveur d'une heredite de l'epilepsie ou du moins de la predisposition aux crises. 6 l'epilepsie spontaneae qu'on observe chez le chien est un modele biologique comparable a l'epilepsie chez l'homme et merite des etudes ulterieures.