What Is Your Neurologic Diagnosis?

Yael Merbl Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA

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Carlos Valerio-López Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA

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Introduction

A 6-year-old castrated male indoor-outdoor domestic medium-hair cat was presented for evaluation of acute nonambulatory tetraparesis. On the day of presentation, the owners had found the cat outside vocalizing and laterally recumbent with stiff extended limbs, a left head turn, and no response to visual stimuli. The owners reported that the cat had been normal an hour earlier. The patient had been taken to an emergency clinic where radiographs of the spine and abdomen, hematologic testing, testing for FeLV and FIV infection, and testing for N-terminal pro-B-type natriuretic peptide (SNAP Feline proBNP Test; Idexx Laboratories Inc) had been performed. Hyperglycemia (305 mg/dL; reference range, 74 to 159 mg/dL) and hypokalemia (3.1 mmol/L; reference range, 3.5 to 5.8 mmol/L) were the only abnormalities. A single dose of buprenorphine (0.010 mg/kg, IM) was administered before referral for further diagnostic testing.

On admission, physical examination showed that the left limbs were subjectively colder than the right limbs. Additionally, 2 small puncture wounds < 1 cm apart without any accompanying skin lesions were observed on the rostral aspect of the right side of the neck. The patient seemed to be nonvisual. Open-mouth breathing was noted, but results of thoracic auscultation were unremarkable. Blood pressure was within reference limits.

Assessment

Anatomic diagnosis

The moderate decreased mentation could have been due to a lesion of the forebrain or brainstem or a result of systemic disease. The most common neurolocalization for a lesion causing acute nonambulatory tetraparesis would be the brainstem (midbrain through medulla) or cervical spinal cord (C1-C5 or C6-T2). Less frequently, peracute forebrain lesions can result in transient nonambulatory tetraparesis. The left head turn could have been due to a lesion of the left forebrain or a cervical lesion causing torticollis. The miosis of the right eye suggested right Horner syndrome with disruption of the right sympathetic pathway; because only miosis was apparent, the disruption would have been only partial. The bilaterally decreased menace and nasal stimulation responses were attributed to multifocal lesions involving cranial nerves II, V, and VII or a diffuse lesion involving the forebrain, brainstem, or both. Because menace and nasal stimulation are responses and not reflexes, mentation changes resulting from a forebrain ascending reticular activating system lesion or severe systemic disease could have caused the decreased responses. The bilateral decreases in the pupillary light responses with decreased consensual responses were most likely a result of bilateral lesions of cranial nerves II or III or may have been due to sympathetic innervation overriding the parasympathetic response.

Likely location of a single lesion

The neurologic findings did not indicate a straightforward neuroanatomic localization (Supplementary Video S1). On the basis of clinical findings, we suspected either multifocal brain lesions involving the forebrain (cranial nerve II deficits and head turn) and brainstem (cranial nerve III and V deficits, nonambulatory status, and Horner syndrome). An alternative neurolocalization was a right-sided C1-C5 myelopathy along with markedly increased sympathetic tone altering some of the cranial nerve reflexes and responses. Other considerations included the fact that the extensor rigidity in all 4 limbs supported an upper motor neuron lesion of the cervical or cranial thoracic spinal cord segments (ie, C1-C5 or C6-T2) or a lesion of the brainstem from the midbrain through the medulla. However, the disparity between the severe tetraparesis and mild cranial nerve deficits supported a cervical lesion. The normal withdrawal reflexes in both front limbs decreased the suspicion of a C6-T2 localization. Finally, the Horner syndrome resulting in both miosis and warmer extremities on the side ipsilateral to the lesion supported a loss of upper motor neuron innervation to the preganglionic sympathetic neurons. A C1-C5 lesion would not explain the decreased pupillary light and menace responses; however, cats with marked sympathetic tone can have decreased menace and pupillary light responses even if the animal is visual.

Etiologic diagnosis

Differential diagnoses for acute nonambulatory tetraparesis with a left head turn and cranial nerve deficits included trauma, a vascular disorder such as an ischemic event (eg, secondary to hypertrophic cardiomyopathy or hyperthyroidism), and a hemorrhagic disorder (eg, a coagulation factor deficiency). Other differential diagnoses considered less likely owing to the acute onset of clinical signs included infectious disease (eg, feline infectious peritonitis, bacterial or fungal encephalomyelitis, and Cuterebra larval migration), neoplasia, and inflammatory disease (eg, autoimmune encephalitis, which has been reported in cats but is much less common than in dogs).

Diagnostic Test Findings

On admission, blood glucose and lactate concentrations were measured in samples obtained from all 4 limbs to evaluate for circulatory deficits, but results were unremarkable. Results of thoracic focused assessment with sonography were consistent with possible hypertrophic cardiomyopathy; results of abdominal focused assessment with sonography were normal. Serum electrolyte concentrations and results of blood gas testing were within reference limits. Thoracic radiographs from the referring veterinarian were considered normal.

To rule out cardiovascular, metabolic, and coagulation disorders, thyroxine concentration and coagulation times (prothrombin time and activated partial thromboplastin time) were measured and echocardiography was performed. Thyroxine concentration was within reference limits (1.51 µg/dL; reference range, 1 to 4 µg/dL), as was the prothrombin time (9.0 seconds; reference range, 8.7 to 12.9 seconds), but the activated partial thromboplastin time (28.3 seconds; reference range, 11 to 16.7 seconds) was mildly prolonged. Echocardiography revealed asymmetric septal hypertrophy, increased left ventricular dimensions, and mild (considered incidental) atrioventricular valve dysplasia. Creatine kinase activity was measured to assess for muscle damage potentially associated with trauma and was high (1,578 U/L; reference range, 0 to 368 U/L). Magnetic resonance imaging of the brain and cervical spine with CSF analysis was recommended.

Results of MRI of the brain were unremarkable. Magnetic resonance imaging of the cervical vertebral column revealed a solitary, oval, well-defined intramedullary lesion at the level of C1 and C2 (Figure 1). The lesion was hypointense on T1- and T2-weighted images, with a signal void on fast field echo (gradient echo) images and ill-defined perilesional hyperintensity on T2-weighted and FLAIR images. Mild contrast enhancement of the lateral aspect of the neck was seen on T1-weighted images following gadolinium administration. This signal intensity change extended caudally along the jugular furrow and right lateral subcutaneous tissues of the neck to the level of C2-C3.

Figure 1
Figure 1

Transverse fast field echo (A), sagittal T2-weighted (B), and transverse postcontrast T1-weighted (C) MRI images of a 6-year-old domestic medium-hair cat evaluated because of acute tetraparesis. Notice the solitary, oval, well-defined intramedullary lesion at the level of C1 and C2, surrounded by perilesional hyperintensity. The lesion appears as a signal void on the fast field echo image (A; arrowhead), indicating that it was a result of hemorrhage. The white line on the sagittal image (B) indicates the level of the transverse images. Soft tissue contrast enhancement is evident (C; arrow).

Citation: Journal of the American Veterinary Medical Association 260, 11; 10.2460/javma.21.01.0052

The MRI findings were consistent with intramedullary hemorrhage with surrounding edema. The multifocal subcutaneous and fascial hyperintensity could have been secondary to trauma. Cerebrospinal fluid was analyzed to rule out potential pathogens, and results included neutrophilic pleocytosis (336 nucleated cells/µL), an RBC count of 6 RBCs/µL, and a microprotein concentration of 21.6 mg/dL (reference interval, < 25 mg/dL). No pathogens were seen, and the changes were considered likely to have been associated with the intramedullary hemorrhage seen on MRI images.

Treatment

Treatment included supportive care, fluid therapy with a balanced electrolyte solution (12 mL/h, IV), and buprenorphine (20 μg/kg, oral transmucosally, q 6 h) for pain management; clindamycin (12.5 mg/kg, IV, q 12 h) was administered because of the puncture wounds and was subsequently changed to ampicillin-sulbactam (30 mg/kg, IV, q 8 h). Maropitant (Cerenia; 1 mg/kg, IV, q 24 h) was given because of initial inappetence, and eye lubrication (q 6 h) was also provided. Physical rehabilitation was started while the cat was hospitalized and continued at home after discharge and once a week in our hospital.

Four days after presentation, the cat’s neurologic status had markedly improved. The cat was still nonambulatory, but pupillary light and menace responses were present (although decreased), suggesting that the cat was visual, and the cat appeared mentally appropriate. Four weeks after discharge, the cat was strongly ambulatory and postural reactions were substantially improved, although still absent in the right thoracic limb. Cranial reflexes and spinal reflexes were normal. The cat was visual, and mentation was considered normal (Supplementary Video S2).

Comments

The present report describes recovery of a cat following cervical intramedullary hemorrhage (hematomyelia). A previous report1 described hematomyelia in a cat secondary to hemophilia, with multifocal hemorrhages in the thoracolumbar spinal cord. Unfortunately, that cat lost deep pain sensation and was euthanized.

Hematomyelia is a rare cause of myelopathy in veterinary as well as human medicine.24 The condition is subdivided on the basis of nontraumatic versus traumatic causes. Nontraumatic hematomyelia can be further subdivided into primary (idiopathic) and secondary5 and represents most cases reported in veterinary medicine.6 Several underlying secondary causes have been identified, including coagulation disorders, vascular malformations, syrinx formation, and neoplasia.710

In this case, the possibility of cardiovascular abnormalities and coagulation impairments was assessed prior to MRI. Echocardiographic findings were not supportive of disease progression severe enough to cause thrombotic events. Coagulation testing showed a mild increase in activated partial thromboplastin time. This assay is an indicator of the function of coagulation factors in the intrinsic and common pathways; however, a nonspecific mild increase is sometimes seen in cats.11 Therefore, the clinical importance of the increase in our cat was unknown.

The puncture wounds found on physical examination coincided with soft tissue swelling and edema seen on MRI in this area. The combination of history, imaging, and physical findings all supported traumatic hematomyelia. High-field MRI allows early diagnosis of this condition.12 The decreased menace, nasal stimulation, and pupillary light responses may have resulted from the cat’s altered mentation status in conjunction with high sympathetic tone, which can interfere with menace13 and pupillary light14 response testing in cats. The head turn seen on initial presentation could potentially be explained by the asymmetric spinal cord lesion on the contralateral side causing disruption of the afferent proprioception tracts. A similar hypothesis has been described for dogs with syringomyelia that have cervicothoracic torticollis, a corkscrew deviation of the neck and head that causes the head to be twisted ventrally, contralateral to the side of dorsal horn involvement.15

Surgical intervention for spinal cord hemorrhage has been sporadically reported in the veterinary literature6,16; however, no management guidelines exist in human or veterinary medicine.4 Therefore, management remains dependent on clinical considerations.17 In the case reported here, surgical intervention was not pursued because of the high potential for severe spinal cord injury associated with a surgical approach to the lesion. To the best of our knowledge, there are no reports of surgical approaches to treat cervical hematomyelia in cats, and its prognosis has not been established.

To summarize, hematomyelia is a rare presentation in veterinary medicine with limited published information regarding treatment and prognosis. Conservative management and time to heal may yield a favorable outcome.

Supplementary Materials

Supplementary materials are posted online at the journal website: avmajournals.avma.org

References

  • 1.

    Barnard LR, Leblond G, Nykamp SG, Gaitero L. Spontaneous thoracolumbar hematomyelia secondary to hemophilia B in a cat. JFMS Open Rep. 2015;1(2):2055116915597239. doi:10.1177/2055116915597239

    • Search Google Scholar
    • Export Citation
  • 2.

    Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003;26(1):149. doi:10.1007/s10143-002-0224-y

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3.

    Akpınar A, Celik B, Canbek I, Karavelioğlu E. Acute paraplegia due to thoracic hematomyelia. Case Rep Neurol Med. 2016;2016:3138917. doi:10.1155/2016/3138917

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4.

    Fiaschi P, Severino M, Ravegnani GM, et al. Idiopathic cervical hematomyelia in an infant: spinal cord injury without radiographic abnormality caused by a trivial trauma? Case report and review of the literature. World Neurosurg. 2016;90:3844. doi:10.1016/j.wneu.2016.01.094

    • Search Google Scholar
    • Export Citation
  • 5.

    Byrne TN, Benzel EC, Waxman SG. Syringomyelia and spinal hemorrhage. In: Byrne TN, Benzel EC, Waxman SG, eds. Diseases of the Spine and Spinal Cord. Oxford University Press Inc; 2000:341358.

    • Search Google Scholar
    • Export Citation
  • 6.

    Barker A, Williams JM, Chen A, Bagley R, Jeffery ND. Suspected primary hematomyelia in 3 dogs. Can Vet J. 2015;56(3):278284.

  • 7.

    Leep Hunderfund AN, Wijdicks EF. Intramedullary spinal cord hemorrhage (hematomyelia). Rev Neurol Dis. 2009;6(2):E54E61.

  • 8.

    Sharp N, Wheeler S. Miscellaneous conditions. In: Sharp N, Wheeler S, eds. Small Animal Spinal Disorders. 2nd ed. Elsevier Mosby Ltd; 2005:319337.

    • Search Google Scholar
    • Export Citation
  • 9.

    Cakirer S, Basak M, Galip GM. Cervical hematomyelia secondary to oral anticoagulant therapy: case report. Neuroradiology. 2001;43(12):10871088. doi:10.1007/s002340100626

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 10.

    Pullarkat VA, Kalapura T, Pincus M, Baskharoun R. Intraspinal hemorrhage complicating oral anticoagulant therapy: an unusual case of cervical hematomyelia and a review of the literature. Arch Intern Med. 2000;160(2):237240. doi:10.1001/archinte.160.2.237

    • Search Google Scholar
    • Export Citation
  • 11.

    Lisciandro SC, Hohenhaus A, Brooks M. Coagulation abnormalities in 22 cats with naturally occurring liver disease. J Vet Intern Med. 1998;12(2):7175. doi:10.1111/j.1939-1676.1998.tb02097.x

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 12.

    Chao CH, Tsai TH, Huang TY, Lee KS, Hwang SL. Idiopathic spontaneous intraspinal intramedullary hemorrhage: a report of two cases and literature review. Clin Neurol Neurosurg. 2013;115(7):11341136. doi:10.1016/j.clineuro.2012.09.004

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13.

    Quitt PR, Reese S, Fischer A, Bertram S, Tauber C, Matiasek L. Assessment of menace response in neurologically and ophthalmologically healthy cats. J Feline Med Surg. 2019;21(6):537543. doi:10.1177/1098612X18788890

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14.

    Taylor AR, Kerwin SC. Clinical evaluation of the feline neurologic patient. Vet Clin North Am Small Anim Pract. 2018;48(1):110. doi:10.1016/j.cvsm.2017.08.001

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15.

    Rusbridge C, McFadyen AK, Knower SP. Behavioral and clinical signs of Chiari-like malformation-associated pain and syringomyelia in Cavalier King Charles Spaniels. J Vet Intern Med. 2019;33(5):21382150. doi:10.1111/jvim.15552

    • Search Google Scholar
    • Export Citation
  • 16.

    Thibaud JL, Hidalgo A, Benchekroun G, et al. Progressive myelopathy due to a spontaneous intramedullary hematoma in a dog: pre- and postoperative clinical and magnetic resonance imaging follow-up. J Am Anim Hosp Assoc. 2008;44(5):266275. doi:10.5326/0440266

    • Search Google Scholar
    • Export Citation
  • 17.

    Shaban A, Moritani T, Al Kasab S, Sheharyar A, Limaye KS, Adams HP Jr. Spinal cord hemorrhage. J Stroke Cerebrovasc Dis. 2018;27(6):14351446. doi:10.1016/j.jstrokecerebrovasdis.2018.02.014

    • PubMed
    • Search Google Scholar
    • Export Citation
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