Open Veterinary Journal, (2025), Vol. 15(10): 5373-5382

Case Report

10.5455/OVJ.2025.v15.i10.55

Dynamic transition from spinal arachnoid diverticulum to syringohydromyelia in a cat: Correlation between computed tomography myelography and magnetic resonance imaging

Kohei Nakata^1*, Minoru Matsuno², Makoto Komatsu³, Takahiro Nagumo⁴, Yuki Hoshino¹ and Masaaki Katayama⁴

¹Laboratory of Small Animal Surgery, Department of Veterinary Medicine, School of Veterinary Medicine, Iwate University, Morioka, Japan

²Matsuno Pet Clinic, Akita, Japan

³Akita Komatsu Animal Hospital, Akita, Japan

⁴Laboratory of Small Animal Reconstructive Surgery, Department of Veterinary Medicine, School of Veterinary Medicine, Iwate University, Morioka, Japan

*Corresponding Author: : Fady E. AbdelKhalek. Department of Pharmacology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt. Email: Fady20_4 [at] yahoo.com

Submitted: 24/03/2025 Revised: 30/08/2025 Accepted: 22/09/2025 Published: 31/10/2025

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Abstract

Background: Diseases characterized by impaired spinal cord function due to fluid accumulation include syringohydromyelia (SHM) and spinal arachnoid diverticulum (SAD). SHM refers to fluid-filled cavities within the spinal cord, whereas SAD involves fluid accumulation in the subarachnoid space. Although the true incidence of SHM and SAD in cats is unknown, both conditions are rare based on the limited number of published case reports. Computed tomography (CT) myelography and magnetic resonance imaging (MRI) are regarded as the diagnostic gold standards.

Case Description: An approximately 1-year-old female Japanese domestic shorthair was referred for pelvic limb paresis. 4 months before presentation, CT myelography had revealed a teardrop sign suggestive of SAD. Subsequent MRI and CT myelography identified focal SHM at T13. T12–T13 dorsal laminectomy was performed, during which cerebrospinal fluid (CSF)-like leakage was observed. Durotomy was also performed, but no abnormalities were detected in the spinal arachnoid membrane. 5 months postoperatively, the cat regained ambulatory function, although mild residual ataxia persisted. Follow-up MRI revealed a T2-hyperintense region and a slit-like signal void on fluid-attenuated inversion recovery at T13.

Conclusion: This case demonstrates how the combination of MRI and CT myelography can effectively capture temporal changes in fluid accumulation within the spinal cord. Accurate imaging is essential for accurate diagnosis and treatment planning. Restoration of CSF perfusion and fluid drainage may contribute to clinical improvement in cats with focal SHM.

Keywords: Cat, CT myelography, MRI, Spinal arachnoid diverticulum, Syringohydromyelia.

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Introduction

Diseases characterized by impaired spinal cord function due to fluid accumulation include syringohydromyelia (SHM) and spinal arachnoid diverticulum (SAD). SHM is defined by the formation of fluid-filled cavities within the spinal cord (Rusbridge et al., 2000; Rusbridge et al., 2006). More specifically, syringomyelia refers to a syrinx located within the spinal cord parenchyma, whereas hydromyelia denotes dilation of the central canal. However, because definitive premortem differentiation between the two is difficult, the umbrella term SHM is commonly used regardless of syrinx location (Milhorat et al., 1995; Rusbridge et al., 2000). By contrast, SAD involves focal cerebrospinal fluid (CSF) accumulation within the subarachnoid space, leading to spinal cord compression and clinical signs of myelopathy (da Costa and Cook, 2016). Historically called spinal arachnoid cysts, the term SAD is now preferred because these lesions lack the epithelial lining characteristic of true cysts (Lowrie et al., 2014). The clinical signs of these conditions reflect the location of the myelopathy and are typically characterized by proprioceptive ataxia with varying degrees of tetraparesis or paraparesis, often accompanied by spinal-associated hyperpathia. Both SHM and SAD are rarely reported in dogs and are even less common in cats. To the best of our knowledge, reports of SHM and SAD in cats remain limited to isolated case reports and small case series, underscoring their rarity in the veterinary literature. Advanced imaging modalities, such as computed tomography (CT) myelography, and magnetic resonance imaging (MRI), are considered the gold standard for evaluating these diseases. On CT myelography, SAD appears as a teardrop-shaped expansion of the subarachnoid space filled with contrast medium, whereas SHM, which represents fluid retention within the spinal cord, is poorly visualized. Conversely, MRI is highly effective in detecting SHM but may be less reliable in assessing its continuity with the subarachnoid space. In this case, combining the two modalities allowed the initial identification of SAD and subsequent evaluation of SHM, clarifying the sequential transition between these conditions. This case report describes a rare presentation in which SAD and SHM developed at different times in the spinal cord of a cat, with both MRI and CT myelography aiding in their distinction. The findings emphasize the clinical relevance of combining imaging modalities to capture temporal changes in fluid accumulation and to guide appropriate treatment strategies in feline spinal myelopathy.

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Case Details

An approximately 7-month-old female Japanese domestic shorthair was referred to Matsuno Pet Clinic with paresis of both pelvic limbs and a history of back trauma since adoption. The cat had previously been treated with antibiotics for trauma, but pelvic limb paresis persisted. Approximately 1 month later (day −118), CT myelography was performed at Akita Komatsu Animal Hospital using a Brivo CT 385 scanner (GE Healthcare, Chicago, IL, USA) (slice thickness, 1.25 mm; reconstruction kernel, BONEPLUS). Iohexol (Omnipaque 240, 240 mg I/ml; GE Healthcare) was administered via lumbar puncture at a dose of 0.5 ml/kg under the guidance of C-arm fluoroscopy (Brivo OEC 785; GE Healthcare). Scans were obtained approximately 5 minutes after the injection. Contrast distribution and the presence or absence of extradural/intradural filling defects were assessed. A bone tissue window (window width, 3000 HU; window level, 500 HU) was used for analysis. These studies revealed spinal cord compression caused by a T13 vertebra fracture and a “teardrop sign” in the contrast column at the same site (Fig. 1A–C). Although no obvious fracture line was observed in T12, spinal cord compression due to dorsal lamina thickening was noted.

Fig. 1. Computed tomography (CT) myelography of the thoracolumbar vertebrae obtained 4 months prior (day−118). (A) Reconstructed sagittal CT myelography shows dorsal compression of the spinal cord (black arrow), a T13 vertebral fracture (white arrow), and teardrop-shaped fluid accumulation (asterisk) at the dorsal aspect of T13. (B) Transverse image at the T12–T13 level demonstrates spinal cord flattening. (C) Transverse image at the T13 level shows fluid accumulation (asterisk) compressing the dorsal spinal cord. Images were acquired using a bone tissue window (window width, 3,000 HU; window level, 500 HU). Orientation markers: h=head, f=foot, r=right, l=left. Scale bar=1 cm.

Four months later, the cat was referred to the Iwate University Veterinary Teaching Hospital for evaluation of surgical suitability (day 1). On presentation, the cat was alert and exhibited ataxia in both pelvic limbs. Neurological examination showed loss of postural responses and decreased sensation of superficial pain in the pelvic limbs, along with lumbar spinal tenderness. Spinal reflexes were unremarkable. The neurological status of the cat corresponded to a grade 4 modified Frankel score (MFS) (Levine et al., 2006). The lesion was clinically localized to the T3–L3 spinal cord segments.

Thoracic and abdominal radiographs revealed no abnormalities. MRI was performed using an AIRIS Vento 0.3-T scanner with a knee coil (Fujifilm, Tokyo, Japan) under general anesthesia. Sequences acquired included the following: T2-weighted sagittal and transverse sequences [repetition time (TR), 3000 ms; echo time (TE), 120 ms; slice thickness, 2.5 mm; gap, 0 mm; field of view (FOV), 300 mm; matrix, 256 × 256; number of excitations (NEX), 8]; T1-weighted sagittal and transverse sequences (TR, 300 ms; TE, 15 ms; slice thickness, 2.5 mm; gap, 0 mm; FOV, 300 mm; matrix, 256 × 256; NEX, 5); pre- and post-gadolinium (Omniscan; GE Healthcare) (dose, 0.1 mmol/kg; delay after injection, approximately 1 minute); and fluid-attenuated inversion recovery (FLAIR) sagittal and transverse sequences (TR, 9,000 ms; TE, 100 ms; slice thickness, 2.5 mm; gap, 0 mm; FOV, 300 mm; matrix, 256 × 256; NEX, 2). The total imaging time was 100 min. MRI revealed a lesion on the dorsal aspect of the T13 spinal cord that appeared hyperintense on T2-weighted images (T2WI) (Fig. 2A and C) and hypointense on both T1-weighted and FLAIR images (Fig. 2B and D). The lesion measured 6.0 mm × 5.0 mm × 18.3 mm and showed no enhancement following gadolinium intravenous administration. These findings indicated a fluid-filled lesion; however, it was not possible to determine whether the lesion was intramedullary or intradural–extramedullary.

Fig. 2. Magnetic resonance imaging (MRI) of the thoracolumbar spinal cord on day 1. (A) Sagittal T2-weighted imaging (T2WI) reveals hyperintensity within the spinal cord. (B) Sagittal fluid-attenuated inversion recovery (FLAIR) imaging displays hypointensity at the same site (asterisk). (C) Transverse T2WI at the T13 level reveals hyperintensity involving nearly the entire spinal cord. (D) Transverse FLAIR imaging at the T13 level shows hypointensity in the same region, consistent with a fluid-filled lesion. However, it was not possible to determine whether the lesion was intramedullary or intradural-extramedullary because its signal characteristics were indistinguishable from the subarachnoid space. Orientation markers: h=head, f=foot, r=right, l=left. Scale bar=1 cm.

CT myelography was performed using an Alexion CT scanner (Canon Medical Systems, Otawara, Japan) to evaluate the relationship of the fluid-filled lesion (slice thickness, 1.0 mm; reconstruction kernel, FC30). Iohexol (Omnipaque 240) was administered via lumbar puncture at a dose of 0.4 ml/kg under CT guidance. Scans were obtained approximately 5 minutes after the injection. The contrast distribution and the presence or absence of extradural/intradural filling defects were assessed. A bone tissue window (window width, 3,000 HU; window level, 500 HU) was used for analysis. CT revealed thickening of the dorsal vertebral arch associated with the T13 fracture, but no vertebral misalignment. CT myelography showed no narrowing or rupture of the contrast medium column (Fig. 3A–C), suggesting an intramedullary lesion.

Fig. 3. CT myelography of the thoracolumbar vertebrae on day 1. (A) Sagittal reconstructed CT myelography shows no obvious spinal cord compression. (B) Transverse image at the T12–T13 level shows an intact contrast medium column without deformation. (C) Transverse image at the T13 level shows an expanded contrast medium column. Images were acquired using a bone tissue window (window width, 3,000 HU; window level, 500 HU). Orientation markers: h=head, f=foot, r=right, l=left. Scale bar=1 cm.

Based on the diagnostic imaging findings, the cat was diagnosed with focal SHM. To the best of our knowledge, there are no published reports on the medical treatment of SHM in cats. Drawing from experience in dogs with syringomyelia associated with Chiari-like malformation, oral isosorbide (70% Isobide Syrup; Kowa, Tokyo, Japan) was empirically administered at 1 ml/kg twice daily until re-evaluation. On day 47, no adverse effects were noted in the cat’s general condition, complete blood count, or biochemical tests. However, ataxia persisted without obvious improvement or deterioration. Neurological examination again revealed loss of postural responses and decreased sensation of superficial pain in the pelvic limbs, along with tenderness in the lumbar spine. The MFS of the cat remained at grade 4. Follow-up MRI showed no significant change in the fluid-filled lesion, and surgery was performed due to the lack of improvement. T12–T13 dorsal laminectomy for spinal cord decompression and fluid drainage was performed under a standard anesthetic protocol.

For the T12–T13 dorsal laminectomy, the cat was positioned prone, and the spinous processes of T12–L1 were exposed. The T13 spinous process was resected, and a dorsal laminectomy was performed. Upon entering the spinal canal, CSF-like fluid leakage was observed even before the dural incision. The laminectomy was extended caudally to include the spinous processes of T12–T13, followed by a dural incision. No obvious adhesions or dilation of the spinal arachnoid membrane was identified. The incision was closed without dural reattachment because no residual spinal cord compression remained. The procedure was completed without significant intraoperative complications. The cat received fentanyl citrate (1–3 μg/kg/hour) via continuous-rate infusion for analgesia postoperatively.

Postoperative MRI confirmed resolution of the fluid-filled lesion, although detailed assessment of the spinal cord was limited by air artifacts. The cat recovered uneventfully and was discharged 2 days later. Postoperative monitoring revealed no signs of pain, such as vocalization or abnormal posture. Neurological deficits, including pelvic limb ataxia and proprioceptive loss, remained unchanged at the time of discharge; however, the general condition and appetite of the cat had improved. Oral cephalexin (Rilexipet A; Virbac, Carros, France) was administered at 25 mg/kg twice daily and prednisolone (Predonine; Shionogi, Osaka, Japan) at 0.3 mg/kg once daily for 2 weeks postoperatively. Postoperative rehabilitation was not feasible because of the temperament of the cat.

On day 91, follow-up neurological examination revealed no change in gait or postural responses of the pelvic limbs; however, superficial pain sensation had returned, and lumbar tenderness was no longer present. The MFS of the cat remained at grade 4. MRI showed hyperintensity of the T13 spinal cord on T2WI and a slit-shaped signal void on FLAIR imaging. By day 188, the cat demonstrated improved mobility, including the ability to walk with mild ataxia and jump onto a table. Neurological examination revealed loss of postural responses, and the MFS remained at grade 4. MRI findings were unchanged, showing mild hyperintensity on T2WI and a slit-shaped hypointensity on FLAIR imaging (Fig. 4A–D).

Fig. 4. MRI of the thoracolumbar spinal cord on day 188. (A) Sagittal T2WI shows hyperintensity within the spinal cord (asterisk). (B) Sagittal FLAIR imaging shows hypointensity at the corresponding site (arrow). (C) Transverse T2WI at the T13 level shows mild hyperintensity. (D) Transverse FLAIR imaging at the T13 level shows a slit-shaped hypointensity (arrow), suggesting dorsal spinal cord rupture during surgery. Orientation markers: h=head, f=foot, r=right, l=left. Scale bar=1 cm.

Ethical approval

This study was conducted with written informed consent from the owner. Clinical management and the use of diagnostic procedures followed institutional guidelines. Ethics committee approval was not required because this was a single case managed as part of routine clinical care. Written consent for publication was obtained from the owner on day 1.

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Discussion

SHM is a rare condition in cats and has been reported in association with neurologic feline infectious peritonitis (Kitagawa et al., 2007; Okada et al., 2009; Crawford et al., 2017), traumatic spinal cord injury (Wessmann et al., 2015), hydrocephalus (Tani et al., 2001; Okada et al., 2009), brain tumors (Tomek et al., 2008; Okada et al., 2009), and intervertebral disc disease linked to spinal deformities (Crowe et al., 2019). Similarly, SAD is also uncommon in cats and has been reported in association with trauma and spinal deformities (Vignoli et al., 1999; Schmidt et al., 2007; Sugiyama and Simpson, 2009). Both conditions involve abnormal CSF accumulation, either within or outside the spinal cord. The co-occurrence of SAD and SHM has been documented in both dogs and cats, with SHM more often found cranial to SAD in dogs (Slanina, 2016) and more frequently caudal to SAD in cats (De Frias et al., 2025). Although MRI is generally effective for diagnosing these disorders, the use of a low-field MRI system in this case limited spatial resolution, making it difficult to distinguish intramedullary from extramedullary lesions, particularly in the context of marked fluid accumulation. To overcome this limitation, CT myelography with a higher spatial resolution was also performed. The results revealed no subarachnoid fluid accumulation, unlike the findings 4 months earlier (day −118), suggesting an intramedullary lesion consistent with focal SHM. The absence of the previously observed teardrop sign may indicate the resolution of SAD; however, the lack of dynamic CSF flow assessment prevents definitive interpretation. To the best of our knowledge, a shift in the location of CSF accumulation within the spinal cord of a cat over such a short interval has not been previously documented.

In dogs, SAD is often associated with chronic spinal cord compression caused by intervertebral disc disease (Galloway et al., 1999; Rylander et al., 2002), inflammatory spinal cord disease (Chen et al., 2005), or spinal trauma (Skeen et al., 2003; Schneider et al., 2010). A recent report summarizing the clinical signs of SAD in 21 cats (De Frias et al., 2025) described a wide age range (18 weeks to 13 years). Neuroanatomical localization was consistent with T3–L3 myelopathy in 86% of cases (18 cats) and C1–C5 myelopathy in 14% of cases (3 cats). Most cats presented with chronic, progressive, non-lateral, and painless myelopathy. Interestingly, 48% of cases had no identifiable underlying or concurrent spinal disease, while three cats had a history of trauma. With medical management, 80% of the cats experienced long-term deterioration and 20% remained unchanged; notably, no cases of spontaneous resolution were reported, unlike in the present case. In humans, intracranial arachnoid cysts have occasionally been reported to resolve spontaneously (Yamauchi et al., 1999; Haddad et al., 2022); there was also a report of recurrent and spontaneously resolving SAD (Hayashi et al., 2018), in which CSF accumulation observed on initial CT myelography had resolved by the time of follow-up imaging 4 months later. Although pathological confirmation was not obtained in the present case, the initial CSF retention may have resulted from physical obstruction secondary to the spinal fracture, which subsequently resolved with fracture remodeling. Alternatively, traumatic SAD in cats may regress spontaneously, similar to trauma-associated intracranial arachnoid diverticula reported in humans.

To the best of our knowledge, no cases of focal SHM in cats similar to the present case have been reported. Previous reports of SHM in cats have been limited to individual case descriptions, with the clinical course largely determined by the underlying condition. In dogs, secondary SHM and SAD following trauma have been documented (Skeen et al., 2003; Schneider et al., 2010; Wessmann et al., 2015), but reports of shifting fluid retention are scarce. In humans, both focal and widespread SHM secondary to SAD have been described (Srinivasan et al., 2016), suggesting that altered CSF flow plays a contributory role. In the present case, it is plausible that trauma triggered an inflammatory or hemorrhagic response and that the spinal canal narrowing associated with the fracture led to a CSF perfusion disorder, resulting in SAD formation. Furthermore, trauma-induced expansion of the subarachnoid space or spinal canal narrowing may have disrupted CSF flow, contributing to the development of secondary SHM. We hypothesized that as the fracture healed, vertebral remodeling altered CSF dynamics, leading to the resolution of the arachnoid enlargement and progression to secondary SHM. Ultimately, remodeling likely restored CSF flow, leaving only SHM as the residual lesion (Fig. 5).

Fig. 5. Schematic diagram illustrating the proposed mechanism of secondary syringohydromyelia (SHM) formation in this case. (A) Four months prior, trauma-related injury or thickening of T12 caused a cerebrospinal fluid (CSF) perfusion disorder, leading to the formation of a spinal arachnoid diverticulum (SAD). (B) The resulting CSF flow disturbance contributed to the development of secondary SHM. (C) As the vertebral fracture healed and CSF flow dynamics were restored, the arachnoid expansion resolved, leaving only the secondary SHM.

The cat underwent surgery to alleviate clinical symptoms by draining the intraspinal fluid and preventing re-accumulation through the restoration of CSF perfusion via laminectomy. During the procedure, fluid leakage was observed upon dorsal lamina resection. This leakage was interpreted as a rupture of the dura mater and dorsal spinal cord surface, possibly caused by elevated intraspinal pressure, spinal cord thinning, and minor mechanical stimulation.

In humans, the treatment of symptomatic SHM associated with SAD generally focuses on addressing the underlying filling mechanism of the SAD (Mallucci et al., 1997; Srinivasan et al., 2016). However, in the present case, it was not possible to determine whether CSF flow dynamics were restored postoperatively. Advanced imaging techniques capable of visualizing CSF flow, such as the time-spatial labeling inversion pulse method with high-field MRI (Ito et al., 2021; Ishikawa et al., 2024), may be useful for evaluating CSF dynamics in similar cases. If no abnormalities in CSF flow are detected, less invasive approaches, such as percutaneous fluid drainage by lumbar puncture, could be considered as alternatives to surgical interventions that impose additional stress on the compromised spinal cord. In this case, clinical improvement suggested that fluid drainage was beneficial; however, treatment options that minimize spinal cord invasiveness warrant consideration. Further evaluation of the consequences of spinal cord rupture, including long-term prognosis, is required.

This case report has several limitations. First, histopathological confirmation was not obtained, precluding a definitive diagnosis of the observed lesions. In future cases, tissue sampling, such as during postmortem examination, may help validate imaging findings and improve diagnostic accuracy. Second, low-field MRI was used, which may have limited spatial resolution and contrast differentiation, particularly in regions with extensive fluid accumulation. Detailed localization of fluid retention was achieved using high-spatial resolution CT myelography. However, the use of high-field MRI or advanced imaging techniques, such as contrast-enhanced MR myelography, could provide a more precise evaluation of CSF dynamics and a clearer delineation of intradural structures, thereby enhancing our understanding of the underlying pathophysiology. Additionally, differences in CT myelography techniques between facilities could potentially influence image appearance; however, given the inherently high spatial resolution of CT myelography, such differences would not be expected to alter intramedullary versus extramedullary localization. Finally, because this is a single case report, the ability to generalize the findings is limited. Nonetheless, the rarity and unusual clinical course described in this case report provide valuable insights for clinicians and underscore the importance of combining multiple imaging modalities, such as MRI and CT myelography, particularly when a single modality is insufficient for accurate lesion localization.

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Conclusion

Myelopathy caused by fluid accumulation within the spinal cord is an uncommon condition in cats, and this case demonstrated a unique temporal shift in the location of fluid retention. Accurate diagnosis through a combination of MRI and CT myelography is essential because the distribution of fluid provides important clues for classifying the pathology and selecting appropriate treatment strategies. In suspected cases, early CT myelography may help identify abnormalities in the subarachnoid space that are not visible on MRI alone. Moreover, even when clinical signs improve, follow-up imaging is recommended to monitor the potential development of secondary SHM. Although no established treatment protocol exists for focal SHM in cats, prioritizing fluid drainage and the restoration of CSF perfusion may lead to clinical improvement. This case contributes to a broader understanding of feline myelopathy and CSF dynamics. Further studies involving larger case numbers and advanced imaging modalities, such as contrast-enhanced MR myelography, are needed to clarify the underlying pathophysiology and refine diagnostic and therapeutic approaches.

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Acknowledgments

None.

Conflicts of interest

The authors have no conflicts of interest related to this work.

Funding

This study received no specific grant.

Authors’ contribution

KN: case management, imaging acquisition/interpretation, surgery, conceptualization, writing—original draft. MM: perioperative and postoperative care. MK: imaging acquisition and interpretation. TN, YH, and MK: writing—review and editing.

Data availability

The imaging DICOM files supporting the findings of this study are available from the corresponding author upon reasonable request. Clinical data have been included within the article, and all personal or owner-identifying information has been removed.

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