Abstract
An 11-year-old neutered male Asian small-clawed otter fell down the stairs while sleeping, after which it developed left-sided paralysis. Initial treatment involved once daily administration of prednisolone at 0.5 mg/kg. Despite slight clinical sign improvements by day 10, paralysis persisted. MRI (T2WI) identified a well-defined, hyper-intense lesion on the left side within the spinal cord at the C2-3 intervertebral level. Based on CT and MRI findings, fibrocartilaginous embolus (FCE) was suspected. Prednisolone was then tapered and by day 23 of illness, the otter was able to walk normally, so prednisolone administration was discontinued. No neurological symptom recurrence was observed, and the course remained favorable. One year later, a follow up MRI revealed a diminished lesion compared to initial examination.
Keywords: fibrocartilaginous embolus, MRI, spinal cord infarction
The Asian small-clawed otter (Aonyx cinereus) is a species in the subfamily Lutrinae, within the family Mustelidae [4, 6]. This otter inhabits Southeast Asia and is listed as “VULNERABLE” on the International Union for Conservation of Nature Red List [6]. The Asian small-clawed otter is at risk due to habitat destruction by human activity along with diminished prey biomass due to pollution and overexploitation [6].
Literature exploring neurological disorders in otters is limited. In otters, paresis or paralysis are reported in association with lymphangiosarcoma and spinal metastasis of pheochromocytoma [13, 16], both of which have poor prognoses. Fibrocartilaginous embolus (FCE) is a condition characterized by acute spinal cord infarction [12]. Prognoses are generally good [1], with FCE reported in dogs, cats, horses, cattle, tayras, pigs, turkeys, and humans [1, 8, 10, 11, 15, 17, 18]. However, there are no reports of the disorder in otters to date. This manuscript details a case of suspected FCE in an Asian small-clawed otter.
A 12-year-old neutered male Asian small-clawed otter fell down the stairs while sleeping, after which it developed left-sided paralysis. Limbs on the right side were unaffected. The otter showed no pain but was unable to walk. Hindlimb radiographs, hematology, and serum biochemistry performed by the referring institution, Osaka Aquarium KAIYUKAN, revealed no abnormalities. Treatment initially involved daily administration of 0.5 mg/kg prednisolone (Prednisolone; Riken Vets Pharma Co., Ltd., Iruma, Japan) by the referring veterinarian. At this time, the otter was able to stand using only its hind limbs; however, left forelimb paralysis remained.
On day 10 of illness, as clinical signs were unchanged, the otter was referred to the Veterinary Medical Center of Osaka Metropolitan University for left hemiplegia evaluation by CT and MRI. Anesthesia was induced with isoflurane (Isoful; Zoetis Japan, Tokyo, Japan) via chamber induction until sedation. Then, an endotracheal tube was placed, with anesthesia maintained by isoflurane (2%) and oxygen. Under anesthesia, an intravenous cannula was inserted into the cephalic vein delivering 0.1 mg/kg midazolam (Dorumicum; Maruishi Pharmaceutical Co., Ltd., Osaka, Japan). The otter was placed in the supine position for CT and MRI evaluation. A total body CT scan was performed using an 80-slice CT scanner (Aquilion Lightning; Canon Medical Systems Corp., Ootawara, Japan) in helical scan mode. CT was performed with a pitch of 0.8, rotation time of 0.6 sec, scan thickness of 0.5 mm, 100 mAs, 120 kV, patient size-adjusted display FOV, and abdomen reconstruction filters. Images were reconstructed with a 2-mm slice thickness, abdomen filters (FC13), and bone filters (FC30). A stop ventilator induced apnea during total body scan acquisition. Cervical MRI was performed immediately after CT scan. MRI was performed using a 0.4 T system (APERTO Inspire version V5.0M; FUJIFILM, Tokyo, Japan). The MRI scanning protocol included transverse and sagittal fast-spin echo T2-weighted imaging (T2WI). Contrast administration was not performed. Transverse T2WI was performed using repetition time (TR)/echo time (TE) 2,700/120 msec; thickness 2.5 mm; interval 3.0 mm; number of signal averages (NSA) 30; FOV 140 mm; matrix 192 × 192; flip angle 90°. Sagittal T2WI was performed using the following parameters: TR/TE 3400/120 msec; thickness 2.0 mm; interval 2.5 mm; NSA 16; FOV 180 mm; matrix 320 × 224; flip angle 90°.
No bone abnormalities, such as bone fractures (Fig. 1A and 1B) or findings suggestive of hemorrhage within the spinal cord (Fig. 1C and 1D) were observed by CT examination. A well-defined hyper-intense lesion was observed on the left side within the spinal cord at the C2-3 intervertebral level on MRI (T2WI). The lesion maximum occupancy rate was approximately 35% in the transverse image (Fig. 1Eand 1F). From the CT and MRI findings, a diagnosis of FCE was suspected. After CT and MRI examination, prednisolone administration was tapered to 0.5 mg/kg every other day (EOD). On day 17 of illness, voluntary motor activity was observed in the left forelimb and hindlimb, so prednisolone was further tapered to 0.25 mg/kg EOD. The otter was able to walk normally, and prednisolone administration was discontinued on day 23. There was no neurological symptom recurrence, and the course remained favorable. One year later, a follow up MRI evaluated the lesion and assessed disease condition. Anesthesia and MRI were performed under the same protocol as the initial examination. A well-defined hyper-intense lesion was observed at the same location as the previous examination in MRI examination (T2WI). Compared to the initial examination, the lesion decreased in size, with a maximum occupancy rate of approximately 15% on the transverse image (Fig. 2A and 2B).
Fig. 1.
Representative CT and MRI images from initial examination (A–F). CT image with bone filters of reformatted sagittal plane (A) and transverse plane at the C2–3 intervertebral level (B). CT image with abdomen filters of reformatted sagittal plane (C) and transverse plane at the C2–3 intervertebral level (D). Sagittal plane on T2WI (E) and transverse plane at the C2–3 intervertebral level (F). Although during the initial examination, no bone abnormalities were detected on the CT (A and B) and hemorrhage within the spinal cord (C and D), MRI (T2WI) revealed a well-defined, hyper-intense lesion on the left side within the spinal cord at the C2–3 intervertebral level (E and F, arrow).
Fig. 2.
Representative MRI images from follow up examination (A and B). Follow up MRI revealed a diminished lesion compared to initial examination (A and B, arrowhead).
FCE occurs when fibrocartilage enters the lumen of a spinal artery or vein, causing an ischemic or hemorrhagic infarction of the spinal cord [5]. The cartilage is histopathologically identical to the nucleus pulposus of the intervertebral disc [2]. The mechanism underlying vascular occlusion is not yet well understood [5]. This case involves a fall that occurred outside the surveillance camera’s coverage, so it is unclear whether the symptoms occurred before the fall or if they developed as a result of the fall. Therefore, spinal cord injury is included in the differential diagnosis for this case.
A definitive diagnosis of FCE is only possible through histopathological examination of the spinal cord segments [3]. However, MRI is commonly used for antemortem diagnosis of FCE [3, 9, 10]. MRI findings of FCE in dogs show a localized, relatively well-defined intramedullary lesion appearing hyperintense compared to normal spinal gray matter on T2WI, and is isointense or hypointense compared to normal spinal gray matter on T1WI [3]. In this case, a well-defined lesion with signal intensity on T2WI similar to that seen in dogs was observed.
In humans, diffusion-weighted imaging (DWI) MRI increases imaging sensitivity and specificity in the early stages of FCE [7, 14]. However, spinal DWI is challenging to evaluate due to the relatively small size of the spinal cord, low spatial resolution, and susceptibility to vascular and cerebrospinal fluid pulsation artifacts [7, 19]. As otters are smaller than humans, evaluating FCE by DWI was considered challenging.
The most common manifestation of FCE is an acute onset of non-progressive and non-painful clinical signs in dogs [1]. The prognosis for FCE is generally good, with 85% of dogs returning to ambulation within three weeks [1]. In this case, symptoms were acute onset, non-progressive, and non-painful with improvement over time. Although reports of tumors inducing paresis/paralysis are limited, these are also associated with an acute onset [13, 16]. However, lymphangiosarcoma shows progressive symptoms [16]. The reported case of plasmacytoma noted euthanasia at the time of diagnosis, so the clinical course is unknown [13]. An accidental fall was confirmed in this case, although confirming such events is not always possible. As FCE should be included in the differential diagnosis for otters with acute-onset paralysis, non-progressive clinical signs may serve as a diagnostic criterion for FCE.
This case used corticosteroids, the benefit of which in the treatment of FCE remains unclear [10]. To the best of our knowledge, no studies compared outcomes for animals with FCE treated with and without corticosteroids. In an otter with FCE, clinical symptoms showed a tendency to improve; however, it is difficult to determine whether this is due to corticosteroid treatment or natural recovery. Further investigation of corticosteroid treatment efficacy in otters with FCE is necessary.
In this case of FCE, the Asian small-clawed otter demonstrated an acute onset of non-progressive clinical signs and good prognosis. MRI findings of FCE revealed a well-defined intramedullary lesion that appeared hyperintense on T2WI. FCE merits consideration as a differential diagnosis in otters with neurological symptoms, alongside MRI as an effective diagnostic tool.
CONFLICT OF INTEREST
The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Acknowledgments
We thank the staff of the Veterinary Medical Center of Osaka Metropolitan University and Osaka Aquarium KAIYUKAN the for their assistance with the manuscript and patient care.
REFERENCES
- 1.Bartholomew KA, Stover KE, Olby NJ, Moore SA. 2016. Clinical characteristics of canine fibrocartilaginous embolic myelopathy (FCE): a systematic review of 393 cases (1973–2013). Vet Rec 179: 650. doi: 10.1136/vr.103863 [DOI] [PubMed] [Google Scholar]
- 2.Bichsel P, Vandevelde M, Lang J. 1984. [Spinal cord infarction following fibrocartilaginous embolism in the dog and cat]. Schweiz Arch Tierheilkd 126: 387–397. [PubMed] [Google Scholar]
- 3.De Risio L, Adams V, Dennis R, McConnell F, Platt S. 2007. Magnetic resonance imaging findings and clinical associations in 52 dogs with suspected ischemic myelopathy. J Vet Intern Med 21: 1290–1298. doi: 10.1111/j.1939-1676.2007.tb01951.x [DOI] [PubMed] [Google Scholar]
- 4.Fernandez-Moran J. 2003. Mustelidae. pp. 501–516. In: Zoo and Wild Animal Medicine, 5th ed. (Fowler ME, Miller RE eds.), WB Saunders, Philadelphia. [Google Scholar]
- 5.Gandini G, Cizinauskas S, Lang J, Fatzer R, Jaggy A. 2003. Fibrocartilaginous embolism in 75 dogs: clinical findings and factors influencing the recovery rate. J Small Anim Pract 44: 76–80. doi: 10.1111/j.1748-5827.2003.tb00124.x [DOI] [PubMed] [Google Scholar]
- 6.International Union for Conservation of Nature and Natural Resources. Species Survival Commission: 2000, IUCN Red List of Threatened Species. IUCN, Cambridge. [Google Scholar]
- 7.Küker W, Weller M, Klose U, Krapf H, Dichgans J, Nägele T. 2004. Diffusion-weighted MRI of spinal cord infarction—high resolution imaging and time course of diffusion abnormality. J Neurol 251: 818–824. doi: 10.1007/s00415-004-0434-z [DOI] [PubMed] [Google Scholar]
- 8.Landolfi JA, Saunders GK, Swecker WS. 2004. Fibrocartilaginous embolic myelopathy in a calf. J Vet Diagn Invest 16: 360–362. doi: 10.1177/104063870401600421 [DOI] [PubMed] [Google Scholar]
- 9.MacKay AD, Rusbridge C, Sparkes AH, Platt SR. 2005. MRI characteristics of suspected acute spinal cord infarction in two cats, and a review of the literature. J Feline Med Surg 7: 101–107. doi: 10.1016/j.jfms.2004.08.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Mikszewski JS, Van Winkle TJ, Troxel MT. 2006. Fibrocartilaginous embolic myelopathy in five cats. J Am Anim Hosp Assoc 42: 226–233. doi: 10.5326/0420226 [DOI] [PubMed] [Google Scholar]
- 11.Renner MS, Bryant W, Kennedy GA. 1998. Fibrocartilaginous emboli in a tayra (Eira barbara): a case report. J Zoo Wildl Med 29: 470–473. [PubMed] [Google Scholar]
- 12.Risio L, Platt SR. 2010. Fibrocartilaginous embolic myelopathy in small animals. Vet Clin North Am Small Anim Pract 40: 859–869. doi: 10.1016/j.cvsm.2010.05.003 [DOI] [PubMed] [Google Scholar]
- 13.Schlanser JR, Patterson JS, Kiupel M, Hencken C, Sikarskie JG, Harrison TM. 2012. Disseminated pheochromocytoma in a North American river otter (Lontra canadensis). J Zoo Wildl Med 43: 407–411. doi: 10.1638/2011-0144.1 [DOI] [PubMed] [Google Scholar]
- 14.Shinoyama M, Takahashi T, Shimizu H, Tominaga T, Suzuki M. 2005. Spinal cord infarction demonstrated by diffusion-weighted magnetic resonance imaging. J Clin Neurosci 12: 466–468. doi: 10.1016/j.jocn.2004.01.010 [DOI] [PubMed] [Google Scholar]
- 15.Stedman NL, Brown TP, Rowland GN. 1998. Intravascular cartilaginous emboli in the spinal cord of turkeys. Avian Dis 42: 423–428. doi: 10.2307/1592498 [DOI] [PubMed] [Google Scholar]
- 16.Swenson J, Carpenter JW, Janardhan KS, Ketz-Riley C, Brinkman E. 2008. Paresis in an Asian small clawed otter (Aonyx cinereus) associated with vertebral and ischial osteolysis caused by a malignant lymphangiosarcoma. J Zoo Wildl Med 39: 236–243. doi: 10.1638/2007-0029R1.1 [DOI] [PubMed] [Google Scholar]
- 17.Taylor HW, Vandevelde M, Firth EC. 1977. Ischemic myelopathy caused by fibrocartilaginous emboli in a horse. Vet Pathol 14: 479–481. doi: 10.1177/030098587701400507 [DOI] [PubMed] [Google Scholar]
- 18.Tessaro SV, Doige CE, Rhodes CS. 1983. Posterior paralysis due to fibrocartilaginous embolism in two weaner pigs. Can J Comp Med 47: 124–126. [PMC free article] [PubMed] [Google Scholar]
- 19.Ueno H, Shimizu J, Uzuka Y, Kobayashi Y, Hirokawa H, Ueno E, Suzuki A, Yamada K. 2005. Fibrocartilaginous embolism in a chondrodystrophoid breed dog. Aust Vet J 83: 142–144. doi: 10.1111/j.1751-0813.2005.tb11620.x [DOI] [PubMed] [Google Scholar]


