What Is Your Neurologic Diagnosis?

Demia J. de Tonnerre Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610.

Search for other papers by Demia J. de Tonnerre in
Current site
Google Scholar
PubMed
Close
 BVSc
,
L. Chris Sanchez Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610.

Search for other papers by L. Chris Sanchez in
Current site
Google Scholar
PubMed
Close
 DVM, PhD
, and
Robert J. MacKay Department of Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610.

Search for other papers by Robert J. MacKay in
Current site
Google Scholar
PubMed
Close
 BVSc, PhD

A 12-year-old 510-kg (1,122-lb) Thoroughbred mare was evaluated because of an 8-week history of sudden-onset nonprogressive hind limb ataxia. There had been minimal to no clinical improvement following multiple treatments (administration of ponazaril, toltrazuril, decoquinate, and levamisole) for equine protozoal myeloencephalitis (EPM). Heart and respiratory rates were within reference limits, and rectal temperature was slightly high (38.7°C [101.7°F]). The remainder of the physical examination findings were unremarkable.

What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.

Assessment Anatomic diagnosis

ProblemRule out location
Negative thoracolaryngeal reflex response (slap test) bilaterallySensory nerves and roots of T7-T11 spinal cord segments, central pathways to nucleus ambiguus (medulla), or efferent fibers of cranial nerve X via the recurrent laryngeal nerve innervating laryngeal adductor muscles
Hind limb paresis and ataxiaT3-S2
Abnormal postural responsesT3-S2
Abnormal walking tail-pull response (with normal standing tail-pull response)Upper motor neuron lesion from brainstem motor nuclei to S2 (lower motor neuron problem was unlikely because of normal resistance to standing tail pull)

Likely location of 1 lesion

The observed neurologic signs are explained by a single spinal cord lesion affecting upper motor neuron and general proprioceptive tracts between and including the T3 and T11 spinal cord segments

Etiologic diagnosis—Differential diagnoses included conditions resulting in extradural spinal cord compression such as neoplasia, abscess, synovial cyst, hematoma, or granuloma. Other differential diagnoses included EPM, spinal cord trauma with or without vertebral fracture, infarct attributable to fibrocartilaginous embolization, and verminous meningoencephalomyelitis. The diagnostic plan consisted of CSF analysis with cytologic examination of a sample to assess for verminous or protozoal inflammation or neoplasia. Paired serum and CSF samples were assessed for antibodies against Sarcocystis neurona with an ELISAa to test for EPM. Potential diagnostic imaging included plain cervical radiography to assess for vertebral fractures and cervical contrast myelography to assess for dorsoventral spinal cord compression. Endoscopic examination of the upper respiratory tract could also be used to confirm the negative bilateral thoracolaryngeal reflex.

Diagnostic test findings—None of the aforementioned diagnostic testing was performed, and the horse was euthanized (by means of IV administration of pentobarbital sodium) because of the chronicity and severity of clinical signs coupled with a lack of response to multiple treatments for EPM. Necropsy was performed with the consent of the owner and revealed an extradural hematoma extending along the ventral portion of the spinal cord, corresponding with the second to the eighth thoracic spinal cord segments. There was locally extensive hemorrhage in the epaxial muscles dorsal to the T2 vertebra. Histologic examination of the associated spinal cord segments was not performed.

Comments

To the authors' knowledge, there are limited reports of extradural spinal hematomas in horses, and all have been associated with the mid to caudal cervical segments (C4-C6) and brachial intumescence.1,2 The pathogenesis of cervical extradural spinal hematomas in horses remains poorly understood. It is hypothesized that hematoma development is induced by stress on vasculature associated with the high range of motion of the vertebral column within this region.1,2 Three reported equine cases of extradural hematomas were thought to have been associated with damage to the ventral internal venous plexus, spinal branch of the vertebral artery, or intervertebral vein.1

Extradural spinal hematomas in humans due to trauma (accidental or iatrogenic), abnormal vasculature, epidural venous plexus defects, pachymeningitis, neoplasia (vertebral hemangioma or metastatic carcinoma), coagulopathies (inherited or acquired), and spontaneous (idiopathic) causes have been reported.3 An association of extradural spinal hematomas with prolonged Valsalva maneuvers (ie, sneezing, defecation, or coitus) has been recognized.3,4 In humans, postulated risk factors include sickle cell anemia, anticoagulant treatments, dual antiplatelet therapy, elevated venous pressure (eg, during pregnancy), and recent trauma.3,4 These lesions are most often associated with the caudal cervical portion of the spinal cord or brachial intumescence; however, lesions affecting the thoracic spinal cord segments also develop.4,5 Compared with cervical extradural hematomas, those affecting thoracic segments are more likely to be associated with profound neurologic deficits.5,6 Both conservative management and surgical decompressive techniques for the treatment of spinal hematomas have been described. In the presence of marked spinal cord compression, prompt surgical evacuation is recommended.3,4

There is minimal information regarding treatment outcomes of cervical extradural spinal hematoma in horses. In 2 reports,1,2 4 of 5 affected horses were euthanized within 21 days after presumptive diagnosis because of their guarded prognosis and chronicity of neurologic signs. Reported treatments include administration of NSAIDs (flunixin meglumine or phenylbutazone) or corticosteroids (dexamethasone) as well as mannitol and dimethyl sulfoxide.

In 1 equine case1 of presumptive cervical extradural spinal hematoma, initial neurologic assessment revealed grade 3/5 ataxia and tetraparesis, and myelography confirmed spinal cord compression (at the level of C5 through T1). Treatments included administration of dimethyl sulfoxide, mannitol, and flunixin meglumine. Reevaluation after 9 months revealed mild-to-moderate atrophy of muscle groups associated with the neck and forelimbs (rhomboid cervicis, splenius, and subclavius muscles) and minimal gait improvement. However, myelography revealed resolution of spinal cord compression. That horse's gait improved over a period of several years, and evaluation 5 years after onset of clinical signs revealed only grade 1 to 2/5 ataxia. The fact that clinical improvement did not correlate with myelographic findings suggests that spinal cord compression may not be the sole cause of neurologic dysfunction in horses with cervical extradural spinal hematoma. The more favorable outcome in that specific case (compared with other published reports) may have been associated with the lesser neurologic grade at time of diagnosis.

To the authors' knowledge, an exclusively thoracic extradural spinal hematoma in horses has not been previously described. In the horse of the present report, the lesion extended along the ventral aspect of the spinal cord from T2 to T8, which correlated well with the neurologic findings and resultant neuroanatomic localization. There was no history or evidence of trauma associated with the onset of neurologic signs and no evidence of trauma to the thoracic vertebrae; thus, the hemorrhage observed grossly in the dorsal epaxial muscles was unlikely to have been related to an inciting cause. Histologic examination of the spinal cord segments or extradural hematoma was not performed. Nonetheless, given the duration, stability, and severity of the horse's neurologic signs, return to normal function seemed unlikely regardless of treatment.1,2 The case described in the present report has highlighted the use of clinical neurologic assessment to accurately localize a lesion in a situation where antemortem contrast myelography or cross-sectional imaging were unavailable.

Footnotes

a.

EPM Sarcocystis neurona SAG2/4/3 ELISA, Equine Diagnostic Solutions, Lexington, Ky.

References

  • 1. Gold JR, Divers TJ, Miller AJ, et al. Cervical vertebral spinal hematomas in 4 horses. J Vet Intern Med 2008;22:481485.

  • 2. Cunha dos Santos FC, de Lourdes Adrien Delgado M, Fernades CG, et al. Cervical extradural hematoma in an ataxic horse. Equine Vet Educ 2014;26:306309.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Adamson DC, Bulsara K, Bronec PR. Spontaneous cervical epidural hematoma: case report and literature review. Surg Neurol 2004;62:156159.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Sai Kiran NA, Kasliwal MK, Kale SS, et al. Two children with traumatic thoracic spinal epidural hematoma. J Clin Neurosci 2009;16:13561358.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Rosenberg O, Itshayek E, Israel Zvi. Spontaneous spinal epidural hematoma in a 14-year-old girl. Pediatr Neurosurg 2003;38:216218.

  • 6. Hsieh CT, Chiang YH, Tang CT, et al. Delayed traumatic thoracic spinal epidural hematoma: a case report and literature review. Am J Emerg Med 2007;25:6971.

    • Crossref
    • Search Google Scholar
    • Export Citation

Contributor Notes

Address correspondence to Dr. de Tonnerre (ddetonnerre@ufl.edu).
  • 1. Gold JR, Divers TJ, Miller AJ, et al. Cervical vertebral spinal hematomas in 4 horses. J Vet Intern Med 2008;22:481485.

  • 2. Cunha dos Santos FC, de Lourdes Adrien Delgado M, Fernades CG, et al. Cervical extradural hematoma in an ataxic horse. Equine Vet Educ 2014;26:306309.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Adamson DC, Bulsara K, Bronec PR. Spontaneous cervical epidural hematoma: case report and literature review. Surg Neurol 2004;62:156159.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Sai Kiran NA, Kasliwal MK, Kale SS, et al. Two children with traumatic thoracic spinal epidural hematoma. J Clin Neurosci 2009;16:13561358.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Rosenberg O, Itshayek E, Israel Zvi. Spontaneous spinal epidural hematoma in a 14-year-old girl. Pediatr Neurosurg 2003;38:216218.

  • 6. Hsieh CT, Chiang YH, Tang CT, et al. Delayed traumatic thoracic spinal epidural hematoma: a case report and literature review. Am J Emerg Med 2007;25:6971.

    • Crossref
    • Search Google Scholar
    • Export Citation

Advertisement