A 13-year-old female white-crowned pionus (Pionus senilis) was examined because of seizures 22 months after it was treated for a traumatic brain injury (TBI) characterized by vision loss, hemiparesis, nystagmus, circling, and head tilt.
Bloodwork performed during the initial seizure workup revealed hypercalcemia and hypercholesterolemia, which were attributed to vitellogenesis given the bird's previous egg-laying history and recent onset of reproductive behavior. Magnetic resonance imaging of the brain revealed diffuse right pallium atrophy with multifocal hydrocephalus ex vacuo, which were believed to be the result of the previous TBI. Findings were most consistent with post-traumatic seizures (PTS).
TREATMENT AND OUTCOME
Levetiracetam (100 mg/kg [45 mg/lb], PO, q 12 h) was initiated for PTS management. A 4.7-mg deslorelin implant was injected SC to suppress reproductive behavior. The bird was reexamined for presumed status epilepticus 5 times over 22 months. Seizure episodes coincided with onset of reproductive behavior. The levetiracetam dosage was increased (150 mg/kg [68 mg/lb], PO, q 8 h), and zonisamide (20 mg/kg [9.1 mg/lb], PO, q 12 h) was added to the treatment regimen. Additional deslorelin implants were administered every 2 to 6 months to suppress reproductive behavior. The owner was trained to administer midazolam intranasally or IM as needed at home. The treatment regimen helped control but did not eliminate seizure activity. The bird was euthanized 22 months after PTS diagnosis for reasons unrelated to the TBI or PTS.
Long-term management of PTS in a pionus was achieved with levetiracetam and zonisamide administration.
Objective—To evaluate whether biochemical or genetic alterations in AMP-activated protein kinase (AMPK) play a role in the development of polysaccharide storage myopathy (PSSM) in Quarter Horses.
Animals—30 PSSM-affected and 30 unaffected (control) Quarter Horses.
Procedures—By use of an established peptide phosphotransfer assay, basal and maximal AMPK activities were measured in muscle biopsy samples obtained from 6 PSSM-affected and 6 control horses. In 24 PSSM-affected and 24 control horses, microsatellite markers identified from the chromosomal locations of all 7 AMPK subunit genes were genotyped with a fluorescent DNA fragment analyzer. Alleles of 2 of the AMPK γ subunit genes were genotyped via DNA sequencing. Allele frequencies of DNA markers in or near the AMPK subunit genes were measured in isolated genomic DNA.
Results—No differences in basal or maximal muscle AMPK enzyme activities between PSSM-affected and control horses were detected. There were also no differences in allele frequencies for microsatellite markers near any of the 7 AMPK subunit genes between the 2 groups. Furthermore, previously known and newly identified alleles of 2 equine AMPK γ subunit genes were also not associated with PSSM.
Conclusions and Clinical Relevance—These results have provided no evidence to indicate that AMPK plays a causative role in PSSM in American Quarter Horses.
Objective—To compare electroencephalography (EEG) artifact associated with use of the subdermal wire electrode (SWE), gold cup electrode (GCE), and subdermal needle electrode (SNE) over an 8-hour period in sedated and awake dogs.
Animals—6 healthy dogs.
Procedures—8 EEG channels were recorded during 20-minute video-EEG recording sessions (intermittently at 0.5, 2, 4, 6, and 8 hours) with and without chlorpromazine sedation. Nonphysiologic artifacts were identified. Duration of artifact was summed for each channel. Number of unaffected channels (NUC) was determined.
Results—NUC was significantly affected by electrode type and sedation over time; median for SWE (2.80 channels; 95% confidence interval [CI], 0.84 to 5.70 channels) was significantly different from medians for GCE (7.87 channels; 95% CI, 7.44 to 7.94 channels) and SNE (7.60 channels; 95% CI, 6.61 to 7.89 channels). After 4 hours, NUC decreased in awake dogs, regardless of electrode type. In awake dogs, duration of artifact differed significantly between SWE and GCE or SNE; medians at 8 hours were 61.55 seconds (95% CI, 21.81 to 173.65 seconds), 1.33 seconds (95% CI, 0.47 to 3.75 seconds), and 21.01 seconds (95% CI, 6.85 to 64.42 seconds), respectively.
Conclusions and Clinical Relevance—The SWE had a significant duration of artifact during recording periods > 2 hours, compared with results for the GCE and SNE, in awake dogs. The GCE, SNE, and sedation resulted in significantly more channels unaffected by artifact. For longer recordings, caution should be exercised in selecting EEG electrodes and sedation state, although differences among electrodes may not be clinically relevant.