Clinical signs, causes, and outcome of central cord syndrome in 22 cats

Carlos Ros Neurology and Neurosurgery Service, Memvet Referral Center, Palma de Mallorca, Spain

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Roberto José-López Small Animal Hospital, School of Veterinary Medicine, University of Glasgow, Scotland

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Cristina Font Hospital Veterinari Canis, Girona, Spain

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Anna Suñol Hospital for Small Animals, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Scotland

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Emili Alcoverro Chestergates Veterinary Specialists, Chester, UK

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Jasmin Nessler Department of Small Animal Medicine and Surgery, University of Veterinary Medicine Hannover, Hannover, Germany

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Alejandra García de Carellán Mateo Anaesthesia and Analgesia Service, Memvet Referral Center, Palma de Mallorca, Spain

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Vicente Aige Departamento de Sanidad y Anatomía Animal, Universidad Autónoma de Barcelona, Barcelona, Spain

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Rita Gonçalves Department of Veterinary Science, Small Animal Teaching Hospital, University of Liverpool, Neston, UK

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Abstract

OBJECTIVE

To describe the signalment, clinical findings, presumptive or definitive diagnosis, and outcome in cats with central cord syndrome (CCS).

ANIMALS

22 cats.

CLINICAL PRESENTATION

Cats evaluated for CCS at 7 referral hospitals between 2017 and 2021 were included. Information retrieved from medical records included signalment, physical and neurological examination findings, diagnostic investigations, definitive or presumptive diagnosis, treatment, and follow-up.

RESULTS

Median age at presentation was 9 years. Two neuroanatomical localizations were associated with CCS: C1-C5 spinal cord segments in 17 (77.3%) cats and C6-T2 spinal cord segments in 5 (22.7%) cats. Neuroanatomical localization did not correlate with lesion location on MRI in 8 (36.3%) cats. The most common lesion location within the vertebral column was over the C2 and C4 vertebral bodies in 6 (27.2%) and 5 (22.7%) cats, respectively. Peracute clinical signs were observed in 11 (50%) cats, acute in 1 (4.5%), subacute in 4 (18%), and chronic and progressive signs were seen in 6 (40.9%) cats. The most common peracute condition was ischemic myelopathy in 8 (36.3%) cats, whereas neoplasia was the most frequently identified chronic etiology occurring in 5 (22.7%) cats. Outcome was poor in 13 (59%) cats, consisting of 4 of 11 (36.6%) of the peracute cases, 3 of 4 (75%) of the subacute cases, and 6 of 6 of the chronic cases.

CLINICAL RELEVANCE

Central cord syndrome can occur in cats with lesions in the C1-C5 and C6-T2 spinal cord segments. Multiple etiologies can cause CCS, most commonly, ischemic myelopathy and neoplasia. Prognosis depends on the etiology and onset of clinical signs.

Abstract

OBJECTIVE

To describe the signalment, clinical findings, presumptive or definitive diagnosis, and outcome in cats with central cord syndrome (CCS).

ANIMALS

22 cats.

CLINICAL PRESENTATION

Cats evaluated for CCS at 7 referral hospitals between 2017 and 2021 were included. Information retrieved from medical records included signalment, physical and neurological examination findings, diagnostic investigations, definitive or presumptive diagnosis, treatment, and follow-up.

RESULTS

Median age at presentation was 9 years. Two neuroanatomical localizations were associated with CCS: C1-C5 spinal cord segments in 17 (77.3%) cats and C6-T2 spinal cord segments in 5 (22.7%) cats. Neuroanatomical localization did not correlate with lesion location on MRI in 8 (36.3%) cats. The most common lesion location within the vertebral column was over the C2 and C4 vertebral bodies in 6 (27.2%) and 5 (22.7%) cats, respectively. Peracute clinical signs were observed in 11 (50%) cats, acute in 1 (4.5%), subacute in 4 (18%), and chronic and progressive signs were seen in 6 (40.9%) cats. The most common peracute condition was ischemic myelopathy in 8 (36.3%) cats, whereas neoplasia was the most frequently identified chronic etiology occurring in 5 (22.7%) cats. Outcome was poor in 13 (59%) cats, consisting of 4 of 11 (36.6%) of the peracute cases, 3 of 4 (75%) of the subacute cases, and 6 of 6 of the chronic cases.

CLINICAL RELEVANCE

Central cord syndrome can occur in cats with lesions in the C1-C5 and C6-T2 spinal cord segments. Multiple etiologies can cause CCS, most commonly, ischemic myelopathy and neoplasia. Prognosis depends on the etiology and onset of clinical signs.

Introduction

A variety of myelopathies has been reported in feline patients.1 Previous studies reported that the most commonly diagnosed feline spinal cord disorders are lymphoma and other neoplastic diseases, followed by feline infectious peritonitis, spinal fracture and luxation, intervertebral disc disease, and ischemic myelopathy (IM), among other diseases.13 Despite the overlap of clinical signs between diseases, clinical reasoning using a combination of signalment and clinical and neurological examination findings can be used to prioritize the most common differential diagnoses in cats with myelopathies.3 However, none of these previous studies described central cord syndrome (CCS) in cats.

Central cord syndrome is a clinical presentation in which patients manifest more severe paresis (or even plegia) in the thoracic limbs (TLs) than in the pelvic limbs (PLs) or when clinical signs only involve the TLs.4 It is hypothesized that lesions causing CCS affect the central part of the spinal cord, where the motor neurons and the axons for the TLs are located, rather than in the periphery, where the white matter tracts to the PLs are found.5 There are no anatomical studies regarding the exact location of the cervical intumescence in cats; therefore, the spinal cord segments where the TLs’ motor neurons are located and their potential anatomical variability are unknown.

Recently, CCS has been described in dogs.6 To the authors’ knowledge, there are no previous studies in the veterinary literature describing CCS in cats. The aim of this study was to describe clinical and neurological signs, presumptive or definitive diagnosis, treatment, and outcome of cats with CCS as the main clinical sign.

Methods

This was a retrospective study using case populations obtained from 7 veterinary neurology referral centers. The medical records were reviewed from 2017 to 2021 for all cats presenting with clinical signs consistent with CCS that underwent MRI of the cervical spinal cord. Owner consent was obtained for all clinically indicated investigations. A patient with CCS was included when clinical signs were more severe in the TLs compared to the PLs or when clinical signs only involved the TLs. Patients were excluded from the study if clinical signs only involved the PLs or were more pronounced in the PLs, or if the patient did not undergo MRI.

For each case, the clinical data recorded included the following: signalment (breed, age, sex, and body weight), clinical history, physical and neurological examination findings, CBC and serum biochemistry, MRI findings, definitive or presumptive diagnosis, treatment, and follow-up information. Thoracic radiographs, abdominal ultrasound, and CSF analysis findings were recorded when performed. Information regarding the presence of concomitant diseases was also collected. The presence of cervical hyperesthesia, cervical ventroflexion, partial (miosis only) or complete (miosis, ptosis, enophthalmos, and protrusion of the third eyelid) sympathetic denervation of the eye (Horner syndrome), and signs consistent with respiratory failure or impaired ventilation on admission were also recorded.

Onset of clinical signs was categorized into peracute (< 2 days), acute (2 to 5 days), subacute (5 to 14 days), and chronic (> 14 days), as described in the veterinary literature.3

All cats had a full neurological examination performed by a board-certified neurologist or a neurology resident under the supervision of a European College of Veterinary Neurology specialist. Neurological status was categorized into 3 groups, as stated for dogs6: grade 1, minimally decreased proprioceptive and motor function in both TLs with normal PLs; grade 2, severe paresis in both TLs and minimally decreased proprioceptive and motor function in both PLs; and grade 3, absence of motor function in both TLs and paresis in both PLs.

The lesion was neuroanatomically localized to the C1-C5 spinal cord segments if the patient had postural reaction deficits with normal or increased spinal reflexes in all 4 limbs. The lesion was clinically localized to the C6-T2 spinal cord segments (ie, the cervical intumescence) if the patient had abnormal postural reactions in all 4 limbs and if the withdrawal reflex was decreased or absent in the TLs with normal or increased spinal reflexes in the PLs.

Imaging diagnosis was performed using MRI in all cases (Achieva 3.0 T MRI scanner, Philips Medical Systems; Essenza 1.5 T MRI scanner, Siemens Healthcare GmbH; Grande 0.3 Tesla Vet-MR, Esaote SPA; Magnetom Avanto 1.5 Tesla, Siemens Healthcare GmbH; and Ingenia 1.5T CX, Koninklijke Philips NV).

To describe the lesion location within the vertebral column, the vertebral body over which the lesion was located was used as a reference. If the lesion was directly over the intervertebral disc space, the caudal vertebral body was used (eg, lesion located in the C2-C3 intervertebral disc space = C3) to facilitate statistical analysis.

To the authors’ knowledge, there are no current studies in the veterinary literature describing where the cervical intumescence begins in cats. On the basis of a cadaveric anatomical study (Figure 1), the cervical intumescence was considered to start at the level of the C5 vertebral body, and therefore lesions located cranially were considered to be cranial to the cervical intumescence.

Figure 1
Figure 1
Figure 1

Neuroanatomical study of a cat that was euthanized due to an ischemic myelopathy (black arrow; A). Note that the C6 spinal cord segment lies over the C5 vertebral body (white arrow; B).

Citation: Journal of the American Veterinary Medical Association 262, 3; 10.2460/javma.23.08.0478

The reliability of the neuroanatomical localization based on the neurological examination (C1-C5 or C6-T2 spinal cord segments) was compared with the exact anatomical lesion location observed on the MRI study.

In cases for which CSF was collected, the results were recorded. Depending on the patient’s geographical area and clinical suspicions, the most common infectious diseases were evaluated.

Treatment interventions (surgical or medical) were recorded. Outcome was considered good when the patient’s neurological grade improved after treatment. Within this group, time to improve one neurological grade and/or time to recover completely were recorded in days when available. Outcome was considered poor when the cat did not improve neurologically or was euthanized.

Descriptive statistics were calculated using Excel (Microsoft Corp), and categorical variables were summarized in frequencies and percentages, parametric data as mean and SD, and nonparametric data as median and minimum and maximum when appropriate. Normality of distribution was evaluated by the Shapiro-Wilk test and histogram inspection.

Results

Twenty-two cats were included in the study. Breed distribution was 19 (86.5%) domestic shorthair cats, 2 (9%) domestic longhair cats, and 1 (4.5%) British shorthair cat. Gender distribution was 12 females (11 neutered) and 10 males (8 neutered). Median age at presentation was 9 years (range, 3 months to 17 years), and median body weight was 4.65 kg (range, 1 to 7.2 kg).

Physical examination on presentation was unremarkable in all but 5 cats (2 had hypothermia [35.5 °C], 2 had a heart murmur with gallop rhythm on cardiac auscultation, and 1 had bradycardia [60 beats/min]). Hematology and biochemistry were unremarkable in all cats except 1, in which moderate anemia was observed (Hct, 19.7%; reference interval, 30% to 45%). Thoracic radiographs or abdominal ultrasound were performed in 6 cats, and in 1 cat, bilateral renomegaly was observed on the abdominal ultrasound.

On the basis of neurological examination, the lesion was localized to the C1-C5 spinal cord segments in 11 (50%) cats and C6-T2 spinal cord segments in 11 (50%) cats. Partial Horner syndrome was observed in 1 (4.5%) cat, and cervical hyperesthesia was detected in 10 (45.5%) cats. Cervical ventroflexion was observed in 1 (4.5%) cat. None of the patients had impaired ventilation or signs consistent with respiratory failure on admission.

Clinical signs of CCS were peracute in 11 (50%) cats, acute in 1 (4.5%) cat, subacute in 4 (18%) cats, and chronic and progressive in 6 (27.5%) cats. Of the 22 cats with CCS, 1 (4.5%) was considered grade 1, 10 (45.5%) grade 2, and 11 (50%) grade 3.

The definitive or presumptive diagnosis associated with CCS was IM in 8 (36.3%) cats, neoplasia in 5 (22.7%), inflammatory immune-mediated or infectious meningomyelitis in 4 (18.2%), vertebral fracture and luxation in 2 (9%), and acute noncompressive nucleus pulposus extrusion (ANNPE), vertebral angiomatosis, and syringomyelia (suspected to be secondary to frontal lobe meningioma) in 1 (4.5%) cat each. In the cats with neoplasia, mast cell tumor was histopathologically confirmed in 1 case, lymphoma was suspected in 1 case (as part of a multicentric lymphoma as lymphoma was confirmed on hepatic and splenic cytology), and in the other 3 cases a mesenchymal neoplasia was suspected on the basis of imaging findings (Figure 2).

Figure 2
Figure 2
Figure 2
Figure 2
Figure 2
Figure 2
Figure 2

Midline sagittal (A) and transverse (B) T2-weighted image (T2WI) MRI in a cat with an intramedullary hyperintense lesion at the level of the C2 vertebral body, suspected to be consistent with ischemic myelopathy (arrow). Midline sagittal (C) and transverse (D) T2WI in a cat with an intramedullary hyperintense lesion suspected to be consistent with a C3-C4 acute noncompressive nucleus pulposus extrusion (arrow). Midline sagittal image (E) and transverse (F) T2WI at the level of C5-C6 IVS in a cat with a diffuse intramedullary hyperintense lesion, suspected to be consistent with meningomyelitis (arrow).

Citation: Journal of the American Veterinary Medical Association 262, 3; 10.2460/javma.23.08.0478

Of those cats with abnormalities detected in the physical examination, 2 cats with heart murmur and gallop rhythm had IM, while the others had neoplasia or immunomediated or infectious meningomyelitis.

Peracute CCS was mainly observed with IM in 8 of 11 (72.7%) cats, vertebral fracture and luxation in 2 of 11 (18.1%) cats, and neoplasia in 1 (4.5%) cat; acute CCS was observed in 1 cat with ANNPE; subacute CCS was observed in 4 cats with immunomediated or infectious meningomyelitis; and chronic CSS was often associated with neoplasia in 4 of 6 (66.6%) cats and was also observed in 1 cat with vertebral angiomatosis and 1 cat with syringomyelia. Cervical hyperesthesia was evidenced in 4 cats with IM, 2 cats with immunomediated or infectious meningomyelitis, and 1 cat with neoplasia, syringomyelia, vertebral fracture and luxation, and vertebral angiomatosis, respectively.

On the basis of MRI findings, 17 (77.3%) cats had a lesion located cranial to the cervical intumescence, while 5 (22.7%) cats had a lesion located in the cervical intumescence.

The anatomical location of the lesion causing CCS was found at the level of the C2 vertebral body in 6 (27.2%) cats and over the C4 vertebral body in 5 (22.7%) cats. Other locations included a diffuse lesion cranial to the cervical intumescence in 4 (18.2%) cats, C6 vertebral body in 2 (9%) cats, diffuse lesion at the cervical intumescence in 2 (9%) cats, and at the level of the C1, C3, and C7 vertebral body in 1 cat (4.5%) each. Of those cats with a diffuse lesion cranial to the cervical intumescence, 1 cat had a lesion from the C1 to C6 vertebral bodies, 1 cat from the C2 to C4 vertebral bodies, and 2 cats from the C3 to C6 vertebral bodies. Of those cats with a diffuse lesion at the cervical intumescence, one cat had a lesion from the C7 to T1 vertebral bodies and the other had the lesion from the C6 to T1 vertebral bodies. In 8 (36.3%) patients, clinical neuroanatomical localization did not correlate with the location of the lesion observed on MRI.

Cerebrospinal fluid was analyzed in 12 (54.5%) cats. The results were normal in 2 cats, and there was AN increased total nucleated cell count (pleocytosis: median, 122 WBCs/µL [14 to 184 WBCs/µL]; normal value, < 5 WBCs/µL) and AN increased protein concentration (protein: 126 mg/dL [81 to 243 mg/dL]; normal values, 25 to 45 mg/dL cervical and lumbar, respectively) in 5 cats (in 1 cat with IM and 4 cats with immunomediated or infectious meningomyelitis). Albuminocytological dissociation was observed in 3 cats (median, 409 mg/dL)—1 cat with suspected neoplasia, 1 cat with IM, and 1 cat with vertebral angiomatosis—and iatrogenic blood contamination occurred in 2 cats. Serology for feline coronavirus and Toxoplasma gondii was tested in 3 cats and was negative in all cases.

With regards to treatment, surgery was performed in 1 cat (due to a vertebral fracture at the level of the dorsal lamina of C4, and surgical removal of the depressed lamina fracture was performed). Medical treatment (consisting of fluid therapy, glucocorticoids, and/or clindamycin depending on the suspected etiology) combined with rest, physiotherapy, and analgesia was elected in 21 (95.5%) cats.

Outcome was considered good in 9 (41%) cats and poor in 13 (59%) cats. Of those with poor outcome, 4 of 11 (36.3%) had a peracute onset of CCS signs, 3 of 4 (75%) had a subacute onset, and 6 of 6 (100%) had chronic CCS signs.

In the group of cats with a good outcome, 6 cats had an IM, 1 cat an inflammatory/infectious meningomyelitis, 1 cat an ANNPE, and 1 cat a vertebral fracture and luxation. The most common condition associated with poor prognosis was neoplasia in 5 cats, followed by inflammatory/infectious meningomyelitis in 3 cats, IM in 2 cats, and vertebral fracture and luxation, cervical syringomyelia (secondary to intracranial meningioma), and vertebral angiomatosis in 1 cat each. Six cats were euthanized immediately after diagnosis, 5 cats were euthanized within the first week after diagnosis due to lack of improvement, and 2 cats were euthanized 1 and 3 months after diagnosis due to absence of improvement. Follow-up information was available in 5 cats with good outcome (22.7%; 3 of them had IM, 1 ANNPE, and 1 a vertebral fracture and luxation). Median time to improve 1 neurological grade was 4 days (range, 3 to 6 days).

Discussion

This multicentric retrospective study evaluated the signalment, neurological grade, neuroanatomical location, definitive or presumptive diagnosis, and outcome of cats presented with CCS. In this study, CCS was associated with 2 neuroanatomical localizations: C1-C5 and C6-T2 spinal cord segments. Patients with a C6-T2 myelopathy have lower motor neuron and upper motor neuron (UMN) signs in the TLs and PLs, respectively.7 Clinically, patients with a C6-T2 myelopathy show absent or delayed postural reactions in all 4 limbs with decreased or absent spinal reflexes and muscle tone in the TLs.7 These patients may show more paresis in the TLs than in the PLs and therefore signs consistent with CCS due to the involvement of the lower motor neurons of the TLs, which are in the gray matter of the cervical intumescence.

Central cord syndrome can also occur with lesions affecting the C1-C5 spinal cord segments,6 as described in the present study. Patients with C1-C5 myelopathy show absent or delayed postural reactions with normal spinal reflexes in all 4 limbs, causing UMN signs in all 4 limbs.7 It has been described that cervical injuries affecting tracts closer to the gray matter and sparing more superficial tracts cause more severe damage to the UMN tracts of the TLs than those of the PLs and, thus, signs consistent with CCS.8,9 In humans, it is believed that damage to the lateral corticospinal tracts causes bilateral weakness of the upper body, whereas patients retain strength in the lower limbs.8 These tracts are somatotopically arranged, with those involving the cervical spinal cord being most medial and those distributing to lumbosacral levels more lateral.9 As a result, clinical signs of CCS may be justified by a lesion affecting these descending pathways.

The most common condition associated with CCS in cats was IM, followed by neoplasia and meningomyelitis. Ischemic myelopathy was the most common peracute disorder associated with CCS in this study, while neoplasia was most commonly found in chronic cases. These findings differ from what has been reported for dogs, for which the most common condition associated with peracute CCS was Hansen type I intervertebral disc herniation, followed by hydrated nucleus pulposus extrusion.6 These differences may be explained by the low prevalence of intervertebral disc disease in cats compared to dogs.1,2,10 The incidence of intervertebral disc disease in cats is reported to be 0.12% to 0.24%,11,12 compared with 2% in dogs.13,14 Although most of the intervertebral disc disease described in cats corresponds to the thoracolumbar area, cervical intervertebral disc disease in cats has also been reported recently.15

The most common anatomical location of the lesion associated with CCS was over the C2 vertebral body, followed by C4 and diffusely in the cranial cervical spinal cord. It has been reported that IM has a predilection for the cranial cervical spinal cord in older cats,11,12 being more common at C2, the area where the ventral spinal artery is narrowest.16,17,18

One important point to consider is that there is lack of anatomical literature specifying the exact location of the cervical intumescence in cats. Additionally, in cats the variability of size and breed is not as marked as in dogs; therefore, the origins of the cervical intumescence might not be that different, unless there is an individual variation, but further research is needed.

In this study, the correlation between clinical neuroanatomical localization (C1-C5 or C6-T2 myelopathy) and anatomical lesion location observed on MRI was 63.7%. This mismatch between clinical neurolocalization and anatomical location was also reported in a case series in 1 of 8 cats with IM.16 Neuroanatomical localization in the cervical spinal cord is based on the evaluation of the spinal reflexes in the TLs, mainly the withdrawal reflex.7 Patients with absence of postural reactions in all 4 limbs and normal spinal reflexes in the TLs are usually neurolocalized to the C1-C5 spinal cord segments, whereas patients with decreased or absent spinal reflexes in the TLs are usually neurolocalized to the C6-T2 spinal cord segments.7 Due to the multicentric and retrospective nature of this study, slight variations in the withdrawal reflex testing may have influenced the assessment. Furthermore, withdrawal reflex testing has limited accuracy for determining neuroanatomical localization in dogs (65.8%) and this is likely to be the case in cats.19 Suspected cervical spinal shock, consisting of transient hyporeflexia or areflexia caudal to the lesion in a patient with normal anatomical reflex arc, cannot be totally excluded; however, an absent or decreased withdrawal reflex in all 4 limbs would be expected as described in the literature for dogs.20

In this study, cervical hyperesthesia was detected in 10 (45.5%) cats. Conditions associated with cervical hyperesthesia were related to the primary disease such as meningomyelitis, vertebral fracture, and luxation, among others. Additionally, a previous study21 reported that 22% of cats with IM showed cervical discomfort on presentation, while in the present study, 50% of cases with IM had cervical hyperesthesia on presentation. Although pure intramedullary lesions (eg, IM, intramedullary neoplasia) should not cause spinal hyperesthesia, some animals may show discomfort within the first hours after the onset of clinical signs.22,23 This may be explained by the initial distention of the meninges or the remodeling and destruction or involvement of the dorsal horn, as previously described.22

In the present study, the outcome of cats with peracute CCS signs was poor in 36.3% of cases—substantially higher than what has been reported for dogs (7%).6 Ischemic myelopathy was the most common condition of peracute CCS and is generally associated with an underlying condition, such as systemic hypertension, chronic kidney disease, hyperthyroidism, or hypertrophic cardiomyopathy in cats.16,18,21 The presence of a concomitant primary condition may explain the worse prognosis in cats compared to dogs. In 1 study,21 an underlying disease was identified in 12 out of 19 cases of IM in cats, but in the present study only 2 cases of IM had an underlying cardiac disease, suspected to be the cause of the clinical signs. Regarding chronic conditions for CCS in cats, neoplasia was one of the main differential diagnoses, which was associated with poor outcome in 88.8% of cases.

The limitations of the present study included its retrospective nature, including cases from multiple institutions, the low case number, the lack of definitive diagnoses, and the lack of long-term follow-up information or repeated imaging studies. More anatomical studies to determine where the cervical intumescence is located in cats are needed.

Cats can have CCS with more paresis in the TLs than in the PLs, as described in dogs. Central cord syndrome can occur with 2 neuroanatomical localizations: the cervical intumescence and cranial to it. Main diseases associated with peracute and chronic CCS in cats were IM and neoplasia, respectively. In the present study, main anatomical location associated with CCS was over the C2 and C4 vertebral bodies. Cats with chronic CCS had a poorer prognosis than those with peracute CCS, as chronic CCS was usually associated with neoplasia.

Acknowledgments

None reported.

Disclosures

The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors have nothing to disclose.

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  • Figure 1

    Neuroanatomical study of a cat that was euthanized due to an ischemic myelopathy (black arrow; A). Note that the C6 spinal cord segment lies over the C5 vertebral body (white arrow; B).

  • Figure 2

    Midline sagittal (A) and transverse (B) T2-weighted image (T2WI) MRI in a cat with an intramedullary hyperintense lesion at the level of the C2 vertebral body, suspected to be consistent with ischemic myelopathy (arrow). Midline sagittal (C) and transverse (D) T2WI in a cat with an intramedullary hyperintense lesion suspected to be consistent with a C3-C4 acute noncompressive nucleus pulposus extrusion (arrow). Midline sagittal image (E) and transverse (F) T2WI at the level of C5-C6 IVS in a cat with a diffuse intramedullary hyperintense lesion, suspected to be consistent with meningomyelitis (arrow).

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