Based on our review of the literature, generalized CAPD associated with SAD has not been reported in non-brachycephalic breeds. This report describes a case of thoracolumbar myelopathy secondary to SAD associated with CAPD in a non-brachycephalic dog.

A 5-month-old, 3.6 kg, intact female, non-brachycephalic mixed-breed dog was presented to Chungbuk National University Veterinary Teaching Hospital with ambulatory paraparesis and urinary and fecal incontinence. Clinical signs had first appeared one month prior, initially presenting as acute reluctance to rise without any identifiable preceding event. The dog received conservative treatment with tramadol (5 mg/kg, per oral every 12 hours), gabapentin (10 mg/kg, per oral every 12 hours), and famotidine (1 mg/kg, per oral every 12 hours) at a local clinic; however, neurological signs progressively worsened.

Neurological examination revealed proprioceptive ataxia and postural reaction deficits in both pelvic limbs, with normal thoracic limbs. The modified Frankel score (MFS) was grade 4, defined as follows: grade 0, paraplegia without deep nociception; grade 1, paraplegia without superficial nociception; grade 2, paraplegia with nociception; grade 3, nonambulatory paraparesis; grade 4, ambulatory paraparesis and ataxia; grade 5, spinal hyperesthesia only or no neurologic dysfunction [11]. No pain was elicited on vertebral palpation, and the perineal reflex was intact despite incontinence. Neuroanatomical localization was consistent with T3-L3 myelopathy [12]. Based on the dog’s age and clinical signs, differential diagnoses included inflammatory, traumatic, anomalous, neoplastic, and degenerative conditions.

As conventional radiographs showed no abnormalities, magnetic resonance imaging (MRI) of the T3-L3 region was performed using a 1.5 T scanner (SIGNA Creator; GE Healthcare, USA). Sequences included sagittal T2-weighted (T2W), T1-weighted (T1W), contrast-enhanced T1W (T1CE), and fluid-attenuated inversion recovery (FLAIR); transverse T2W, T1W, T1CE, T2-weighted gradient echo (T2*); and dorsal T2W. MRI showed a teardrop-shaped intradural-extramedullary lesion (8 × 2.5 mm), located in the left dorsolateral region of the spinal cord, extending from T8 to T9 vertebra. The lesion was hyperintense on T2W and hypointense on T1W and FLAIR, without contrast enhancement. Moderate spinal cord compression and central canal dilation (cranial and caudal) were evident (Fig. 1). Additionally, ill-defined, patchy, intramedullary changes were identified caudally from the lesion mostly over T10 vertebra, which was hyperintense on T2W, T2* and FLAIR sequences, and hypointense on T1W sequences. No significant degenerative changes were present in the thoracolumbar spine. MRI findings were consistent with SAD causing adjacent spinal cord edema. Less likely differentials included synovial cysts, infectious cysts, and cystic neoplasia (e.g., cystic meningioma).

To rule out trauma and to further evaluate vertebral abnormalities potentially associated with SAD, a whole-body CT scan was performed using a 16-slice scanner (Revolution ACT; GE Medical Co., USA; 1 mm slices, 120 kVp, 125 mAs). CT revealed no fracture or trauma-related abnormalities but identified generalized CAPD from T2 to T9 vertebras (Fig. 2), including right aplasia at T2, left aplasia at T3, left hypoplasia and right aplasia at T6, bilateral aplasia from T4 to T8, and right aplasia with left hypoplasia at T9.

The dog’s symptoms were attributed to spinal cord compression caused by SAD secondary to generalized CAPD. Surgical decompression via left-sided hemilaminectomy at T8-T9 was performed. Following durotomy, a cyst-like lesion was visualized, after which partial resection and drainage were performed (Fig. 3). The dura mater was subsequently closed, and a fat graft was placed over the repair site. Histopathological evaluation of the resected tissue was not performed. Postoperative care included rehabilitation, analgesics, and antioxidant therapy. Gradual neurological improvement was observed from the first postoperative day. At one-month follow-up, ambulation had further improved and fecal incontinence was reduced, although urinary incontinence persisted. The MFS remained at grade 4.

In veterinary medicine, the etiology of SAD is not fully understood and is considered multifactorial, involving both congenital and acquired factors. In congenital cases, a one-way valve mechanism caused by arachnoid proliferation may lead to progressive expansion of the diverticulum due to impaired CSF flow. Certain breeds, such as Rottweilers, Pugs, and French Bulldogs, are overrepresented in SAD cases, with Rottweilers being more commonly affected in the cervical region and Pugs and French Bulldogs, in the thoracolumbar region [6]. The role of concomitant diseases in SAD remains unclear; however, neurological disorders are often reported at or near SAD lesions, particularly in Pugs and French Bulldogs [13]. CAPD, especially in Pugs, has been suggested as a contributing factor [9], and a case of SAD secondary to CAPD has also been described in a Chow Chow, another brachycephalic breed [14]. Acquired causes include vertebral malformations, intervertebral disc herniation and its surgical correction, inflammation, and trauma. In this case, with the exception of generalized CAPD, no other congenital or acquired conditions that could explain spinal micromotion were identified. This report describes a case of thoracolumbar myelopathy in a non-brachycephalic dog, in which generalized CAPD was identified as a possible contributing factor to SAD formation. Given that CAPD is frequently observed in the cranial two-thirds (T1-T9) of the thoracic vertebral column in both brachycephalic and non-brachycephalic small-to-medium-sized breeds [15], CT was performed both to rule out trauma and to investigate the etiology of SAD despite the lack of breed predisposition. However, the exact causal relationship between CAPD and SAD remains unclear.

The dog’s clinical signs were consistent with thoracolumbar myelopathy due to SAD, with generalized thoracic CAPD considered a possible contributing factor. Fecal incontinence was likely due to dorsal spinal cord compression affecting ascending sensory pathways, as SADs typically occur in the dorsal subarachnoid space [6]. Surgical intervention was elected, as it has been associated with more favorable outcomes compared to medical management [16]. Recurrence is a significant long-term complication of SAD, with longer clinical duration associated with earlier postoperative relapse of neurological signs [17]. Additionally, the presence of concurrent intramedullary lesions has been reported as a negative prognostic indicator [8]. Despite the dog’s prolonged clinical history and intramedullary changes, neurological improvement was observed at the one-month follow-up.

Other spinal cord lesions associated with SAD may have been present in this case; however, distinguishing such conditions requires advanced MRI sequences, such as half-Fourier acquisition single-shot turbo spin-echo or 3-dimensional constructive interference in steady state sequences, which enhance CSF signal and improve visualization of SAD extent, arachnoid webs, and adhesions [18]. Although the clinical relevance of leptomeningeal adhesions remains unclear [6], they may arise from chronic vertebral instability or meningeal irritation and contribute to constrictive myelopathy [7]. Histopathological evaluation is also important when differentiating SAD from related conditions such as constrictive myelopathy and meningeal fibrosis, both of which may result from repetitive low-grade instability associated with CAPD. Severe meningeal fibrosis can impair spinal cord perfusion and obstruct CSF flow, emphasizing the need for accurate differentiation [7,19].

The main limitation of this case include the short follow-up period, which was limited to one month. Although clinical improvement was observed, the prolonged duration of signs, presence of CAPD at the SAD site, and intramedullary changes suggest a guarded prognosis requiring long-term monitoring. Another limitation is the absence of vertebral stabilization. While decompressive procedures such as laminectomy with durotomy, durectomy, or dural marsupialization are commonly used and have been associated with clinical improvement [20], decompression alone may be inadequate for CAPD-related instability. Tauro et al. [8] reported that decompression without stabilization can exacerbate vertebral instability and increase the risk of postoperative deterioration or recurrence. In this case, the lack of stabilization may predispose the patient to long-term complications. Additionally, the abscence of histopathology limits definitive differentiation from related conditions such as constrictive myelopathy or meningeal fibrosis. Finally, although CAPD was considered a contributing factor in the development of SAD, the exact causal relationship remains suggestive.

In summary, SAD was identified as the immediate cause of myelopathy, with generalized CAPD suspected as the underlying etiology. This case highlights the potential clinical relevance of generalized CAPD even in non-brachycephalic breeds. Given the possible association between CAPD and SAD, combined MRI and CT imaging is recommended for unexplained progressive thoracolumbar myelopathy regardless of breed. This combined imaging approach allows for a more complete evaluation of both soft tissue and vertebral structures, and can assist in determining optimal surgical planning. Further research is required to establish the relationship between CAPD and secondary spinal cord disorders, including SAD.