Abstract

Neurologic disease in stranded harbor seal pups has been reported however the cause of primary neurologic disease remains minimally described. Previous reported causes include occipital bone malformation with atlantoaxial subluxation¹ and hemicerebral anomaly², in addition to more commonly reported infectious diseases (morbillivirus, herpesvirus, influenza, protozoa)^3-7 and mercury.⁸ Clinical signs may be subtle or pronounced, and often include tremors, ataxia, paresis, hypotonia, nystagmus, blindness, disorientation, obtundation or seizures. Clinical neurologic assessment has been extrapolated from other mammalian species; however, some methodologies are not applicable to phocids due to anatomical and behavioral differences. Additionally, many stranded pups have reduced mentation due to systemic illness on admission, requiring repeated evaluation after initial stabilization to determine whether a primary neurologic abnormality exists. Between 2014–2017, magnetic resonance imaging (MRI) was performed on eight pups with persistent neurological deficits. Diagnoses included cerebellar hypoplasia (n=3); generalized cerebral atrophy (n=2); otitis media with cervical myelopathy (n=1); porencephaly (n=1), and mild ventriculomegaly (n=1). Starting in 2017, standard physical examination techniques were enhanced by the development of phocid-specific, dedicated neurological assessment protocol, which included postural, tactile, visual and behavioral tests. These phocid-specific techniques are currently being used in conjunction with standard physical examination and clinical diagnostics to better localize and define primary neurologic lesions in harbor seal pups.

Acknowledgements

This work was supported in part by the John H. Prescott Marine Mammal Rescue Assistance Grant Program. We thank the dedicated animal care volunteers and staff at The Marine Mammal Center for their excellent animal care, and the staff of AnimalScan for their assistance with the MRI.

* Presenting author

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