Concurrent ANNPE and vertebral T‐cell lymphoma in a dog: A case report

Abstract

Acute non‐compressive nucleus pulposus extrusion (ANNPE) is a recognised cause of peracute spinal cord injury in dogs, involving sudden extrusion of non‐degenerated nucleus pulposus with minimal compression. While often linked to vigorous activity, its triggers remain unclear. This case describes an 8‐year‐old neutered male poodle cross dog who developed peracute non‐ambulatory paraparesis while running to retrieve a ball. Neurological examination was consistent with a T3–L3 myelopathy. Magnetic resonance imaging (MRI) revealed disc space narrowing with intramedullary T2W hyperintensity at T13–L1 consistent with ANNPE and a T13 vertebral body lesion that was hyperintense in T1W/STIR and contrast‐enhancing, later confirmed as T‐cell lymphoma by surgical biopsy. The dog demonstrated rapid clinical improvement, with motor function recovery by day 6 and becoming ambulatory with mild ataxia by week 3. This case highlights the importance of considering underlying vertebral pathology in dogs with presumed ANNPE and emphasises that vertebral lesions detected on MRI may have clinical relevance and should not be overlooked.

INTRODUCTION

Acute non‐compressive nucleus pulposus extrusion (ANNPE) is a recognised cause of peracute spinal cord (SC) injury in dogs, resulting from the sudden extrusion of non‐degenerated nucleus pulposus (NP) of an intervertebral disc (IVD). The extruded NP strikes the SC, causing contusive injury with minimal or no compression (De Risio, 2015). While clinical signs and imaging features are well characterised (De Risio et al., 2009, 2015; Fenn et al., 2016), the exact triggers for NP extrusion remain unclear. Healthy IVDs usually tolerate biomechanical stress, but intense activity or trauma can lead to annular disruption and NP extrusion (Botsoglou et al., 2021; De Decker & Fenn, 2018). In dogs, it is unknown whether pathologies in the IVD or adjacent vertebrae predispose to ANNPE. In humans, disc abnormalities have been observed with vertebral metastasis mainly from carcinomas, possibly due to tumour‐related disruption of disc nutrition leading to degeneration (Kakitsubata et al., 2009; Resnick & Niwayama, 1978; Sasagawa et al., 2011). This case describes the clinical presentation, diagnostic imaging findings, histopathology, treatment and outcome of a dog with ANNPE at T13–L1 and concurrent T‐cell lymphoma in the T13 vertebral body.

CASE REPORT

An 8‐year‐old, 25.7 kg male neutered poodle cross dog was presented for peracute onset non‐ambulatory paraparesis. The dog was normal until the evening prior to presentation, when he exhibited sudden vocalisation while running to retrieve a ball, immediately followed by non‐ambulatory paraparesis. The dog was initially presented to an external veterinary emergency facility, where he was noted to have left pelvic limb paresis and right pelvic limb paralysis. Complete blood count (CBC), serum biochemistry panel and survey lateral radiographs of the entire vertebral column were performed. The CBC showed mild lymphopenia (1.01 × 10³/μL, reference range – RR: 1.05 to 5.10 × 10³/μL) with a normal total white blood cell count of 9.09 × 10³/μL (RR: 5.05 to 16.76 × 10³/μL). Serum biochemistry revealed mild hypercholesterolemia (cholesterol: 349 mg/dL, RR: 110 to 320 mg/dL). Radiographs showed multifocal intervertebral disc degeneration, with no fractures or other vertebral abnormalities. The dog was then referred to our hospital for neurological evaluation. On presentation, the dog was mentally appropriate, non‐ambulatory, with right pelvic limb paralysis and left pelvic limb paresis with strong motor function. Postural reactions were absent on the right, reduced on the left pelvic limb and normal in the thoracic limbs. Pelvic limb withdrawal reflexes were decreased bilaterally (more on the right), with normal patellar, perineal, cutaneous trunci and thoracic limb withdrawal reflexes. The dog showed no pain on spinal palpation; pain perception and tail function were intact, and the remainder of the neurological examination was normal. Neuroanatomical localisation was to the T3–L3 SC segments, accompanied by concurrent spinal shock. Main differential diagnoses included ANNPE, ischaemic myelopathy by a fibrocartilaginous embolism (FCE), Hansen type I intervertebral disc extrusion or hydrated nucleus pulposus extrusion (Fenn et al., 2020; Alcoverro et al., 2024).

The dog underwent magnetic resonance imaging (MRI) using a 3.0 Tesla unit (Siemens Medical Solutions USA, Inc., Malvern, PA) under general anaesthesia. Multiple sequences of the thoracolumbar vertebral column were acquired, including T2‐weighted (T2W), short‐tau inversion recovery, proton density‐weighted and Half‐Fourier acquisition single‐shot turbo spin echo (HASTE) in sagittal and transverse planes. Additionally, T1‐weighted (T1W), fat‐saturated transverse and sagittal plane sequences were obtained before and after intravenous administration of a gadolinium‐based contrast medium (gadoterate meglumine 0.1 mmol/kg IV, (Clariscan™, GE HealthCare, Oslo, Norway)). The signal intensity was assessed relative to that of the SC.

There was a reduction in size and T2W signal intensity of the T13–L1 intervertebral disc, with narrowing of the disc space. A subtle, right‐sided, ill‐defined intramedullary T2W hyperintensity was observed overlying the disc space. Within the epidural space at T13–L1, a small amount of non‐compressive, circumferential and predominantly right‐sided heterogeneous T2W iso‐ to hypointense and T1W hypointense material was noted, resulting in mild leftward displacement of the SC. Additionally, a centrally located, longitudinal T2W intramedullary hyperintensity extending from T10 to T12, consistent with SC oedema or gliosis, was observed. These findings were mostly consistent with ANNPE at T13–L1 (Fig 1).

FIG 1.

Magnetic resonance imaging of the thoracolumbar vertebral column and associated structures showing T13 vertebral body changes and findings consistent with acute non‐compressive, nucleus pulposus extrusion (ANNPE). Sagittal (A–D, G) and transverse (E, F) HASTE (A), STIR (B), T2W (C, E), pre‐contrast T1W (D) and post‐contrast T1W fat‐saturated (F, G) MRI images of the thoracolumbar vertebral column. The T13 vertebral body (asterisk) is mildly heterogeneously T2W hypointense (C) and strongly homogeneously T1W and STIR hyperintense (B, D), with homogeneous contrast enhancement (G). Ill‐defined intramedullary T2W hyperintensity at T13–L1 (C, E) and mild disc volume loss (C, arrow), suggestive of ANNPE. L indicates the left side of the transverse images.

Separate from these changes, the T13 vertebral body was mildly heterogeneously hypointense on T2W and strongly, homogeneously hyperintense on T1W and STIR sequences, with marked homogeneous contrast enhancement. The osseous architecture was preserved, with no signs of osteolysis or osteoproliferation. These features were most consistent with a round cell neoplasm, such as lymphoma or plasmacytoma (Auger et al., 2021; Kornder et al., 2016). Following diagnosis, the dog was hospitalised for supportive management, which included intravenous fluids (NaCl 0.45%) for the initial 24 hours and ongoing administration of gabapentin 12.7 mg/kg PO q8h (Gabapentin, CSPC Ouyi Pharmaceutical Co., Hebei, China), diazepam 0.35 mg/kg PO q8h (Mylan Laboratories Limited, Hyderabad, India) and maropitant 1 mg/kg IV q24h (Cerenia 10 mg/mL, Zoetis, Girona, Spain). Bladder expression was performed q8h when tolerated by the patient, and intermittent catheterisation with a urethral catheter (Kendall, Cardinal Health, Dublin, USA) was undertaken for bladder decompression when manual expression was unsuccessful or not tolerated. Passive range of motion exercises were also performed q12h. On day 4, the dog was discharged to await the scheduled surgical biopsy but was readmitted the morning of day 5 due to urinary retention and maintained hospitalised for continued monitoring and supportive care. Over his hospitalisation, gradual neurological improvement was observed. On day 6, the dog remained non‐ambulatory but had regained moderate motor function in the right pelvic limb. On that day, a surgical aspirate of the bone marrow was obtained from the right T13 lamina. Under general anaesthesia, the patient was placed in sternal recumbency, and the surgical site was prepared and draped in a routine aseptic manner. Intraoperative C‐arm fluoroscopy (Siremobil Compact L, Siemens, Munich, Germany) was used to accurately identify the T13 vertebra by placing a 22‐g × 3.5 in spinal needle (BD Spinal Needle; Becton, Dickinson and Company, Franklin Lakes, USA) over the spinous process. A right dorsolateral approach was performed to access the T12–T13 vertebrae. The right epaxial muscles were reflected to expose the T13 vertebral lamina and pedicle, and a bone marrow aspirate was obtained by drilling through the cortex and using a Jamshidi Bone Marrow Biopsy and Aspiration Needle (11G × 10 cm; Carefusion, San Diego, USA) for sample collection.

Bone marrow aspirate smears were prepared, stained with Diff‐Quik and submitted for cytologic evaluation. Approximately 70% of the cells were monomorphic intermediate to large lymphocytes (Fig 2). The lymphocytes had a round to oval nucleus, up to three prominent nucleoli, fine chromatin and expanded mid‐blue cytoplasm. Rare mitotic figures were noted. Low numbers of small lymphocytes and plasma cells were seen. No infectious organisms were observed. These findings were consistent with lymphoid neoplasia, suggestive of stage V lymphoma or acute lymphoid leukaemia. The slides were submitted for a polymerase chain reaction for antigen receptor rearrangement (PARR) assay to assess for clonality, which revealed a clonal T‐cell population, confirming the diagnosis of T‐cell lymphoma.

FIG 2.

Cytologic features of lymphoid neoplasia in bone marrow aspirate from the vertebral body of T13. Diff‐Quik stain, 50× objective. The smear is dominated by a monomorphic population of intermediate to large neoplastic lymphocytes (arrow), characterised by fine chromatin and prominent nucleoli. These cells are notably larger than a non‐degenerate neutrophil (asterisk) and display minimal size variability. Occasional small lymphocytes are present in the background (arrowhead). The findings are consistent with infiltration by a lymphoid malignancy.

The day following the surgical biopsy, a CHOP (cyclophosphamide, doxorubicin [hydroxydaunorubicin], vincristine [Oncovin®] and prednisone) protocol was initiated, and the dog was discharged on the same day. This protocol consists of four 4‐week cycles: vincristine (0.7 mg/m² IV, week 1; vincristine 1 mg/mL, Hospira, Lake Forest, USA), cyclophosphamide (250 mg/m² PO, week 2; cyclophosphamide 25 mg capsule, West‐Ward Pharmaceuticals, Columbus, USA; and cyclophosphamide 50 mg capsule, Alembic Pharmaceuticals, Panchmahal, India), doxorubicin (30 mg/m² IV, week 3; doxorubicin 2 mg/mL, Pfizer, New York, USA) and a rest period (week 4). During the first cycle, the dog received an oral tapering course of prednisone (prednisone 20 mg tablet, Strides Pharma Science Limited, Bengaluru, India), administered at 30, 20 and 10 mg/m² PO q24h, with each dose maintained for 1 week. At his week‐3 visit for doxorubicin administration, the dog was ambulatory with strong motor function in both pelvic limbs and mild hindlimb ataxia.

After one cycle of CHOP, chemotherapy was paused for transition to radiation therapy. Stereotactic radiotherapy was planned using 11 coplanar 6‐MV X‐ray beams and the sliding window technique (Eclipse v.18; Varian Medical Systems, Palo Alto, USA), and delivered with a clinical linear accelerator (Novalis TX; Varian Medical Systems, Palo Alto, USA) and a robotic 6 degrees‐of‐freedom couchtop (Protura; CIVCO, Coralville, USA) after plan‐specific quality assurance testing (Portal Dosimetry, Varian Medical Systems, Palo Alto, USA) and daily cone beam CT‐based image guidance. The prescription was 40 Gy total (in five consecutive daily fractions) to the gross tumour volume (i.e., T13 vertebral body lesion as visualised on MRI), with simultaneous delivery of 35 Gy to a high‐priority clinical target volume that included the entire T13 vertebra, and 30 Gy to a lower‐priority clinical target volume encompassing the T13/L1 disc, L1 vertebral endplate and the enclosed SC segment plus an isotropic planning target volume expansion of 5 mm. For each radiotherapy fraction, the dog was anaesthetised without respiratory motion management. Twenty days later, chemotherapy was resumed, and the dog completed three additional cycles of CHOP. Eight months after diagnosis, and 2.5 months after completing chemoradiotherapy, the dog remains ambulatory with mild paraparesis and pelvic limb ataxia, and his neurological status has been static since the initial improvement.

DISCUSSION

This case highlights an unusual presentation of ANNPE occurring concurrently with adjacent vertebral T‐cell lymphoma in a dog. While a causal relationship cannot be established, the presence of vertebral neoplasia raises important questions about whether structural or metabolic changes in adjacent bone could alter disc integrity and predispose to NP extrusion.

In this case, a diagnosis of ANNPE at T13–L1 was supported by the characteristic clinical signs; vocalisation followed by peracute onset of lateralised, non‐painful neurological deficits during exercise (Fenn et al., 2016), together with imaging features including intramedullary T2W hyperintensity over the disc space, reduced IVD volume and the presence of a small amount of non‐compressive extradural material (Chang et al., 2007; De Risio, 2015). A definitive diagnosis can only be confirmed by histopathology, which was not performed in this case.

In addition to these findings, additional sequences revealed changes in the T13 vertebral body that were later confirmed as lymphoma on surgical biopsy, underscoring the value of STIR and post‐contrast T1W MRI sequences in detecting subtle vertebral pathology. On initial T2W imaging, T13 showed only mild, heterogeneous hypointensity, easily overlooked in the context of presumed ANNPE. However, STIR revealed marked hyperintensity, and contrast‐enhanced T1W images showed diffuse, homogeneous enhancement, findings most consistent with neoplasia.

The concurrent vertebral lymphoma was considered incidental, as no osseous changes that could result in SC compression were observed on MRI. The dog’s rapid improvement was typical of ANNPE and the clinical and imaging features make neoplastic myelopathy unlikely.

This co‐occurrence raises questions about the underlying pathophysiological mechanisms of ANNPE. The presence of vertebral neoplasia could have contributed to structural and biomechanical impairment of the IVD through multiple mechanisms. In human oncology, metastatic vertebral tumours have been linked to IVD degeneration and endplate changes (Kakitsubata et al., 2009; Resnick & Niwayama, 1978; Sasagawa et al., 2011; Yasuma et al., 1989). In this case, no endplate changes were observed on MRI; however, in people such alterations may be subtle and often only confirmed histopathologically rather than reliably detected on imaging (Kakitsubata et al., 2009). As IVDs rely partly on nutrient diffusion from adjacent vertebral bone marrow, tumours may disrupt this process, leading to degeneration and weakening. Although direct disc invasion is rare, it has been reported (Sasagawa et al., 2011). Three primary mechanisms have been proposed: (1) direct infiltration of the annulus fibrosus from the exposed rim of the vertebral endplate, (2) penetration into the outer annulus via the subspace between the longitudinal ligaments and the vertebral edge and (3) hematogenous spread through subligamentous vessels (Yasuma et al., 1989). These tumour‐associated changes could compromise the disc’s structural integrity, reducing its ability to withstand normal biomechanical stresses and thereby increasing susceptibility to ANNPE.

A limitation of this case report is the lack of follow‐up MRI, which could have clarified whether intramedullary changes evolved over time. However, given the marked clinical improvement observed after initial treatment, repeat imaging was not pursued.

In conclusion, while the co‐occurrence of ANNPE and vertebral lymphoma in this case may be incidental, it raises the important question of whether vertebral neoplasia could predispose to ANNPE. This case also highlights the value of evaluating all MRI sequences, as STIR and contrast‐enhanced T1W sequences revealed pathology not evident on T2W sequences. Incorporating these sequences into MRI protocols for dogs with myelopathy may improve diagnostic accuracy and clinical management. Further studies are needed to explore possible associations between vertebral pathology and ANNPE, and the impact of vertebral neoplasia on disc integrity.

Author contributions

A. Mondino: Conceptualisation, data curation, visualisation, writing (original draft and review and editing), J. Macri: writing (data curation, review and editing), R. Mokhtari: data curation, visualisation, writing (review and editing), W. Patterson: data curation, visualisation, writing (review and editing), A. Tauro: writing (review and editing), N. J. Olby: Conceptualisation (supporting); writing (original draft supporting), writing (review and editing).

Conflict of interest

None of the authors of this article has a financial or personal relationship with other people or organisations that could inappropriately influence or bias the content of the paper.

Data availability statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.