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Objective

Evaluate histories, clinical signs, and laboratory data of 69 horses homozygous by DNA testing for hyperkalemic periodic paralysis (HPP).

Design

Cohort study.

Sample Population

69 of 189 horses testing homozygous for HPP between October 1992 and November 1994.

Procedure

Questionnaires addressing signalment, training regimes, medical history, and current status of affected horses were sent to owners, trainers, or attending veterinarians. Data from completed questionnaires were tabulated and evaluated, using descriptive statistics.

Results

Sixty-nine (37%) of 189 questionnaires were completed and returned. Clinical episodes of muscle weakness or paralysis varied in severity and frequency from mild muscle fasciculations to recumbency and death. Sixty-three of 68 HPP-affected horses were reported to have had stridor associated with exercise, excitement, stress, or episodes of muscle paralysis. Common endoscopic findings in affected horses included pharyngeal collapse, pharyngeal edema, laryngopalatal dislocation, and laryngeal paralysis. Twelve of 27 horses receiving acetazolamide had decreases in stridor while receiving medication.

Clinical Implications

Most horses testing homozygous for HPP had clinical signs associated with pharyngeal and laryngeal dysfunction. Hyperkalemic periodic paralysis should be included on a differential list for horses examined for signs of laryngeal or pharyngeal dysfunction or stridor. Treatment with acetazolamide may help to control respiratory tract signs associated with this disease. (J Am Vet Med Assoc 1996;209:798–803)

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Intracranial pressure (icp) and cerebral perfusion pressure (cpp) were determined in 8 clinically normal neonatal foals. After the foals oriented themselves and nursed the mares, they were sedated as necessary, and local anesthesia was provided for making the skin incisions. Using a technique similar to that used in human beings, an indwelling subdural catheter was placed to measure icp. Carotid artery catheterization was used to measure arterial blood pressure. Cerebral perfusion pressure was calculated as the difference between mean arterial blood pressure and icp.

Intracranial pressure and cpp readings were taken twice during each 24-hour period, starting at 6 hours of age and continuing through 72 hours of age. Mean (± sd) icp were 5.83 ± 1.82, 8.81 ± 2.06, and 9.55 ± 1.55 mm of Hg (range, 2 to 15 mm of Hg), and mean cpp were 80.19 ± 10.34, 75.30 ± 10.86, and 76.80 ± 12.59 mm of Hg (range, 50 to 109 mm of Hg) for each of the first three 24-hour periods after birth, respectively. All 8 foals had physical and neurologic examinations, csf analysis, and computerized axial tomography evaluations. The foals manifested normal behavior during the interval of measurements, and adverse effects of the procedure were not detected during the monitoring period. Establishment of normal values for icp and cpp are important to clinicians who have the opportunity to apply this technique for monitoring and evaluating neonatal foals with signs of cns dysfunction.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To develop a method for surgical placement of a commercial microsensor intracranial pressure (ICP) transducer and to characterize normal ICP and cerebral perfusion pressures (CPP) in conscious adult horses.

Animals—6 healthy castrated male adult horses (1 Holsteiner, 1 Quarter Horse, and 4 Thoroughbreds).

Procedure—Anesthesia was induced and maintained by use of isoflurane as the sole agent. Catheters were inserted percutaneously into the jugular vein and carotid artery. A microsensor ICP transducer was inserted in the subarachnoid space by means of right parietal craniotomy. The burr hole was then sealed with bone wax, the surgical incision was sutured, and the transducer was secured in place. Measurements were collected 1 hour after horses were able to stand during recovery from anesthesia.

Results—Mean ± SD values for ICP and CPP were 2 ± 4 and 102 ± 26 mm Hg, respectively.

Conclusion and Clinical Relevance—This report describes a relatively facile technique for obtaining direct and accurate ICP measurements for adult horses. The ICP values obtained in this study are within reference ranges established for other species and provide a point of reference for the diagnosis of abnormal ICP in adult horses. (Am J Vet Res 2002;63:1252–1256)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To measure the effects of isoflurane end-tidal concentration and mode of ventilation (spontaneous vs controlled) on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in horses.

Animals—6 adult horses of various breeds.

Procedure—Anesthesia was induced and maintained with isoflurane in O2 in 6 healthy, unmedicated, adult horses. Using a subarachnoid strain gauge transducer, ICP was measured. Blood gas tensions and carotid artery pressures also were measured. Four isoflurane doses were studied, corresponding to the following multiples of the minimum alveolar concentration (MAC): 1.0 MAC, 1.2 MAC, 1.4 MAC, and 1.6 MAC. Data were collected during controlled ventilation and spontaneous ventilation at each dose.

Results—Increasing isoflurane end-tidal concentration induced significant dose-dependent decreases in mean arterial pressure (MAP) and CPP but no change in ICP. Hypercapnic spontaneous ventilation caused significant increases in MAP and ICP, compared with normocapnic controlled ventilation; no change in CPP was observed.

Conclusion and Clinical Relevance—Hypercapnia likely increases cerebral blood flow (CBF) by maintaining CPP in the face of presumed cerebral vasodilation in healthy anesthetized horses. The effect of isoflurane dose on CBF, however, remains unresolved because it depends on the opposinginfluences of a decrease in CCP and cerebral vasodilation. (Am J Vet Res 2003;64:21–25)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To assess pharmacokinetics, efficacy, and tolerability of oral levetiracetam administered as an adjunct to phenobarbital treatment in cats with poorly controlled suspected idiopathic epilepsy.

Design—Open-label, noncomparative clinical trial.

Animals—12 cats suspected to have idiopathic epilepsy that was poorly controlled with phenobarbital or that had unacceptable adverse effects when treated with phenobarbital.

Procedures—Cats were treated with levetiracetam (20 mg/kg [9.1 mg/lb], PO, q 8 h). After a minimum of 1 week of treatment, serum levetiracetam concentrations were measured before and 2, 4, and 6 hours after drug administration, and maximum and minimum serum concentrations and elimination half-life were calculated. Seizure frequencies before and after initiation of levetiracetam treatment were compared, and adverse effects were recorded.

Results—Median maximum serum levetiracetam concentration was 25.5 μg/mL, median minimum serum levetiracetam concentration was 8.3 μg/mL, and median elimination half-life was 2.9 hours. Median seizure frequency prior to treatment with levetiracetam (2.1 seizures/mo) was significantly higher than median seizure frequency after initiation of levetiracetam treatment (0.42 seizures/mo), and 7 of 10 cats were classified as having responded to levetiracetam treatment (ie, reduction in seizure frequency of ≥ 50%). Two cats had transient lethargy and inappetence.

Conclusions and Clinical Relevance—Results suggested that levetiracetam is well tolerated in cats and may be useful as an adjunct to phenobarbital treatment in cats with idiopathic epilepsy.

Full access
in Journal of the American Veterinary Medical Association