Abstract
We present a case in which a male harbor seal developed progressive neurologic signs while in rehabilitation, and underwent diagnostics including serial blood chemistries, blood gas and complete blood counts, MRI, and ultimately comprehensive histopathology following euthanasia. Imaging and histopathology findings resulted in the first known instance of idiopathic Fahr’s syndrome in a marine mammal. Fahr’s syndrome, as described in humans, is characterized by many of the same clinical signs exhibited by our patient, including motor impairment, tremors, and dysphagia.1,2 Structurally, the pathognomonic finding is bilaterally symmetric calcifications in the basal ganglia.1,3 We noted this on both the MRI images and brain histopathology. The objective of this case presentation is to provide a record of a unique clinical course and diagnosis in a harbor seal, with comparative medicine interest and opportunity for further investigation into the etiology of the lesion in this species and others.
The patient was a stranded premature pup and was initially in critical condition. He received intravenous fluids, dextrose, sodium supplementation, and antibiotics, and steadily improved. He underwent an episode of hyponatremia followed by an instance of suspected iatrogenic hypernatremia after oral sodium supplementation. Two months after admission, the pup began to exhibit tremors that were first noted in his front flippers and later progressed to include his entire body. He also spent long periods of time in abnormal positions (i.e., lying on his dorsum), had difficulty ambulating, and intermittently displayed signs of dysphagia. He was treated with courses of methocarbamol and gabapentin, which did not have an appreciable effect on his signs. MRI under general anesthesia revealed bilaterally symmetric lesions of the caudate nuclei, an anatomic location within the basal ganglia as well as the cerebellum.4 Recovery from anesthesia was prolonged, marked by a rapid decline in respiratory status 30 hours post procedure, which resulted in the decision for humane euthanasia for suspected pulmonary edema.
A complete necropsy was performed, the lungs were wet and heavy, there was an increase in peritoneal fluid, but no other gross findings. Histologic evaluation of the brain discovered bilateral mineralization in the basal ganglia with parenchymal loss and mild gliosis, which correlated with the imaging results. This finding is present in humans with Fahr’s syndrome, a progressive neurologic condition that causes movement disorder, tremor, seizure, and in some cases psychological and behavioral changes.1 In humans, there is a genetic etiology,3 although the syndrome can also be secondary to systemic disease such as hypoparathyroidism1. While basal ganglia calcification has not been described in a young pinniped, a clinical correlate may exist with the case of a young fur seal who was also found to have bilateral necrotic lesions of the basal ganglia and exhibited very similar behavioral and physiologic signs to our patient.5 It is intriguing to consider that there may exist some common factor to explain the similarity of lesions found in these two animals on opposite coasts of the United States and separated by a decade.
Acknowledgements
The authors wish to thank the management and staff of VCA South Shore Weymouth Animal Hospital for generously donating the hospital’s time, facilities, and equipment, making anesthesia and MRI possible, and allowing us to learn so much from this unique case.
*Presenting author
Literature Cited
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3. Donzuso G, Mostile G, Nicoletti A, Zappio M. 2019. Basal ganglia calcifications (fahr’s syndrome): related conditions and clinical features. Neurol Sci 40:2251–2263.
4. Lorenz M, Coates J, Kent M. 2011. Neurologic history, neuroanatomy, and neurologic examination. In: Handbook of Veterinary Neurology. St. Louis (MO): Elsevier Saunders. p. 2–36.
5. Fravel V, Van Bonn W, Dennison S, Spraker T. 2015. Bilaterally symmetric lesions of the caudate nucleus in a northern fur seal pup (Callorhinus ursinus). Vet Rec Case Rep 3:e000176.