Comparison of the Use of Medetomidine and Medetomidine-Butorphanol to Facilitate Electroencephalography in California Sea Lions (Zalophus californianus)
IAAAM Archive
Sophie Dennison1; Martin Haulena1; Frances Gulland1; Denise Greig1; D. Colette Williams2
1The Marine Mammal Center, Sausalito, CA, USA; 2Veterinary Medical Teaching Hospital, University of CA-Davis, Davis, CA, USA


Free-ranging California sea lions (Zalophus californianus) naturally exposed to domoic acid frequently strand with clinical signs of domoic acid toxicosis and are treated at rehabilitation centers throughout California.5 The acute effects of domoic acid toxicosis in these sea lions, including seizures and death, are well documented but the long term effects are not yet fully understood. California sea lions that survive exposure are only released once neurologically normal. This assessment has previously been based on clinical observations (neurological examination, behavioral observations, ability to forage) and magnetic resonance imaging.1

Electroencephalography (EEG) is used in a variety of species to investigate neurological disorders.3 It is currently under investigation at The Marine Mammal Center as a tool to assess neurological function in sea lions suspected of having the long-term effects of domoic acid toxicosis. It requires the use of safe and reliable chemical restraint that does not excessively potentiate or suppress cortical or sub-cortical electrical activity that may be associated with seizures.

Medetomidine, a potent but fully reversible alpha2-agonist, has been used safely in a wide variety of species and described in pinnipeds in combination with other anesthetic agents.2 Unlike benzodiazepines it is not used as an anti-epileptic, nor reported to potentiate seizure activity like the phencyclines.2,4

This study investigated the use of medetomidine alone and in combination with butorphanol to facilitate electroencephalography in 11 sea lions that had intermittent seizures or behavioral abnormalities, and two control animals with no history of neurological signs. Sea lions were sedated using 0.07 mg/kg medetomidine alone (n=6) or in combination with 0.2 mg/kg butorphanol (n=11), administered intramuscularly. Their average weight was 39.5 kg. EEG's were achieved using subcutaneously placed Grass platinum needle leads in a modified canine pattern and recorded using a Nihon Kohden EEG system. Following EEG all animals were anesthetized and maintained with 1.0-1.5% isoflurane for 20-45 minutes for radiographs and cerebrospinal fluid tap.

Both drug regimes provided rapid immobilization in mean (± SD) times of 9 (± 2) minutes for medetomidine alone and 13 (± 4) minutes for medetomidine-butorphanol. Both provided good sedation facilitating the placing of EEG leads and subsequent recording for up to 50 (range 20-50) minutes. Heart rate means (±SD) demonstrated bradycardia in both groups, with 50 (±13), 42 (± 10), and 49 (±11) bpm for the medetomidine group and 37 (±11), 39 (± 9) and 38 (± 9) bpm for the medetomidine-butorphanol group at 0, 15 and 30 minutes, respectively. Heart rates were significantly lower in the medetomidine-butorphanol group at 0 and 30 minutes (p< 0.05). Respiratory rates were calculated at 0, 15 and 30 minutes with no significant difference between groups or times giving an overall mean (±SD) of 7 (± 3) respirations per minute. The sp02, EtC02 and rectal temperature remained within levels safe for pinnipeds.2 Time to standing without stimulation after atipamezole reversal @ 0.25 mg/kg IM, was not statistically significant between groups; however, the ranges may have clinical significance. Mean time to standing (± SD) for medetomidine alone was 20 (± 10; range 6-32) minutes and medetomidine-butorphanol was 28 (± 24; range 5-71) minutes. Muscle tremors and twitching were observed with medetomidine-butorphanol and correlated with movement artifact on the EEG. The corresponding control and medetomidine alone animals did not show these changes.

To our knowledge this is the first discussion of chemical immobilization appropriate for obtaining electroencephalograms in rehabilitated Californian sea lions.


1.  Gulland FMD, et al. 2002. Domoic acid toxicity in Californian sea lions (Zalophus californianus): clinical signs, treatment and survival. Vet Rec. 150: 475-480.

2.  Haulena M, et al. chapter, Marine Mammal Anesthesia. (ed). 2001. CRC Handbook of Marine Mammal Medicine. CRC Press LLC, Florida. 655-657pp and 662-669pp.

3.  Klemm WR. 1974. Current status in trends in veterinary encephalography. JAVMA 164(5):529-532.

4.  Plumb DC. 1995. Veterinary Drug Handbook, 2nd edition. 345-346pp and 604-606pp.

5.  Scholin CA. et al. 2000. Mortality of sea lions along the central California coast linked to a toxic diatom bloom. Nature. 403:80-84.

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Sophie Dennison

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