A retrospective study of the medical records of 33 horses was performed to determine the clinical and diagnostic abnormalities associated with temporohyoid osteoarthropathy. Data collected from medical records included signalment, presenting complaints, history, physical examination findings, laboratory data, results of diagnostic imaging studies, and treatments. Follow-up information was obtained from a review of case records; by telephone conversation with the owner, veterinarian, or trainer; or by both methods. Of 33 horses with temporohyoid osteoarthropathy, 29 presented with facial nerve (cranial nerve VII) deficits and 23 presented with vestibulocochlear nerve (cranial nerve VIII) deficits. Guttural pouch endoscopy was more reliable than radiography for diagnosis. Of horses with unilateral clinical signs, 22.6% actually had bilateral disease. Magnetic resonance imaging and computed tomography identified the lesions in all horses in which these tests were performed. Of 30 horses for which follow-up information was obtained, 20 (67%) were alive. Eight horses were euthanized and 1 died because of problems associated with temporohyoid osteoarthropathy. Nineteen of 20 surviving horses (95%) were considered by the owner or trainer to be suitable for athletic use. Twelve surviving horses (60%) had residual facial nerve deficits; 11 horses (55%) had residual vestibulocochlear nerve deficits. Horses with temporohyoid osteoarthropathy have a fair prognosis for return to some type of athletic function, but there is risk of acute death. The majority of horses would be expected to have some residual cranial nerve dysfunction, and it could take a year or longer for maximal improvement to occur.

Continuous IV infusion of butorphanol for 24 hours maintained plasma butorphanol concentrations within a range associated with analgesia. Adverse behavioral and gastrointestinal tract effects were minimized during infusion, compared with a single injection of butorphanol. Continuous infusion of butorphanol may be a useful treatment to induce analgesia in horses.

A retrospective study of the medical records of 33 horses was performed to determine the clinical and diagnostic abnormalities associated with temporohyoid osteoarthropathy. Data collected from medical records included signalment, presenting complaints, history, physical examination findings, laboratory data, results of diagnostic imaging studies, and treatments. Follow-up information was obtained from a review of case records; by telephone conversation with the owner, veterinarian, or trainer; or by both methods. Of 33 horses with temporohyoid osteoarthropathy, 29 presented with facial nerve (cranial nerve VII) deficits and 23 presented with vestibulocochlear nerve (cranial nerve VIII) deficits. Guttural pouch endoscopy was more reliable than radiography for diagnosis. Of horses with unilateral clinical signs, 22.6% actually had bilateral disease. Magnetic resonance imaging and computed tomography identified the lesions in all horses in which these tests were performed. Of 30 horses for which follow-up information was obtained, 20 (67%) were alive. Eight horses were euthanized and 1 died because of problems associated with temporohyoid osteoarthropathy. Nineteen of 20 surviving horses (95%) were considered by the owner or trainer to be suitable for athletic use. Twelve surviving horses (60%) had residual facial nerve deficits; 11 horses (55%) had residual vestibulocochlear nerve deficits. Horses with temporohyoid osteoarthropathy have a fair prognosis for return to some type of athletic function, but there is risk of acute death. The majority of horses would be expected to have some residual cranial nerve dysfunction, and it could take a year or longer for maximal improvement to occur.

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The pathogenesis of Venezuelan equine encephalitis virus (VEE) was examined in the mouse model using V3000, a virus derived from a molecular clone of the Trinidad donkey strain of VEE. These results were compared in parallel experiments with avirulent mutants of VEE derived by site-directed mutagenesis of the clone. Adult mice, inoculated subcutaneously in their left rear footpad with V3000, were followed in a time course study for 6 days in which 15 organs were tested for histopathological changes, for the presence of viral antigen by immunohistochemical staining, for the presence of viral nucleic acid by in situ hybridization analysis, and for content of viable virus. Virus was detected in the footpad inoculation site, but until 12 hr postinoculation (pi), the level of virus did not suggest early viral replication. By 4 hr pi, however, replication of V3000 was evident in the draining popliteal lymph node. At this early time point, no virus could be isolated from any other organ examined. At 12 hr, a significant serum viremia was observed, and virus was detected at a low level in a number of well vascularized organs, including spleen, heart, lung, liver, kidney, and adrenal gland. By 18 hr, high virus titers were present in serum and all the lymphoid organs examined, and these tissues appeared to be the major peripheral sites of V3000 replication. Virus in serum and peripheral organs was cleared by 3-4 days pi. In a second phase of the infection, V3000 invaded the central nervous system (CNS), replicated predominantly in neurons, and persisted in the brain until death by encephalitis. Pathologic findings as well as the results of immunocytochemical and in situ hybridization examination were generally coordinate with virus titration. A site-directed mutant of V3000, V3010, contained a mutation in the gene for the E2 glycoprotein at codon 76 (Glu to Lys) which rendered it avirulent after footpad inoculation. Detection of V3010 replication in the draining lymph node was sporadic and was sometimes delayed to as long as 3 days pi. Infrequent and/or delayed virus spread to other sites also was observed. Analogous experiments were performed with other mutants which were avirulent by the footpad inoculation route: V3014, a mutant differing from V3000 at three loci (E2 Lys 209, E1 Thr 272, and E2 Asn 239), as well as single-site mutants V3032 (E2 Lys 209) and V3034 (E1 Thr 272).(ABSTRACT TRUNCATED AT 400 WORDS)

A randomized, controlled, blinded clinical trial was performed to determine whether butorphanol administered by continuous rate infusion (CRI) for 24 hours after abdominal surgery would decrease pain and surgical stress responses and improve recovery in horses. Thirty-one horses undergoing exploratory celiotomy for abdominal pain were randomly assigned to receive butorphanol CRI (13 g/kg/h for 24 hours after surgery; treatment) or isotonic saline (control). All horses received flunixin meglumine (1.1 mg/kg IV q12h). There were no significant differences between treatment and control horses in preoperative or operative variables. Treatment horses had significantly lower plasma cortisol concentration compared with control horses at 2, 8, 12, 24, 36, and 48 hours after surgery. Mean weight loss while hospitalized was significantly less for treatment horses than control horses, whether expressed as total decrease in body weight (13.9 Ϯ 3.4 and 27.9 Ϯ 4.5 kg, respectively) or as a percentage decrease in body weight (2.6 Ϯ 0.7 and 6.3 Ϯ 1.1%, respectively). Treatment horses were significantly delayed in time to first passage of feces (median times of 15 and 4 hours, respectively). Treatment horses had significantly improved behavior scores during the first 24 hours after surgery, consistent with the conclusion that they experienced less pain during that time. Butorphanol CRI during the immediate postoperative period significantly decreased plasma cortisol concentrations and improved recovery characteristics in horses undergoing abdominal surgery.Key words: Behavior; Colic; Cortisol; Pain management; Stress.I n recent years, there has been a growing interest in recognition and management of pain and surgical stress responses in veterinary medicine. [1][2][3][4][5][6] However, investigation of analgesia in horses has been largely limited to pharmacokinetic studies of drugs or the effects of these drugs in experimental models of induced pain. 5,7-14 Evaluations of analgesic efficacy in equine clinical patients are minimal and primarily focus on responses to nonsteroidal anti-inflammatory agents in horses with orthopedic pain or retrospective studies of responses of horses with colic to various analgesic medications. 5,12,[14][15][16][17] These studies have been complicated by difficulties in accurately assessing and quantifying pain in a nonverbal species. [2][3][4][5][6]16,[18][19][20] Horses undergoing exploratory celiotomy for acute abdominal pain usually receive flunixin meglumine, a nonsteroidal anti-inflammatory drug (NSAID), although doses and dose intervals have varied. In human beings, NSAID medications are considered insufficient for management of pain related to abdominal surgery and a combination of opiates Pullman, WA 99164; e-mail: dsellon@vetmed.wsu.edu. Submitted August 11, 2003; Revised December 9, 2003; Accepted January 16, 2004. Copyright and nonsteroidal analgesic agents is preferred as a multimodal plan for pain management. [21][22][23] Horses that do not exhibit classic behavioral signs of abd...

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