What Is Your Neurologic Diagnosis?

Fenella E. Schmidli Division of Clinical Neurology, Vetsuisse Faculty, University of Bern, CH-3012 Bern, Switzerland.

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Blake D. Webb Southeast Veterinary Neurology, Boynton Beach, FL 33437.

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Julien J. Guevar Division of Clinical Neurology, Vetsuisse Faculty, University of Bern, CH-3012 Bern, Switzerland.

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Introduction

A 4-year-old 30-kg (66-lb) spayed female terrier mix was referred for evaluation because of a 1-day history of generalized weakness, which progressed to flaccid tetraplegia and difficulty breathing. The dog was treated with carprofen, maropitant, and enrofloxacin prior to the referral evaluation. General physical examination revealed bradycardia (60 beats/min) and an abnormal respiratory pattern with little thoracic movement during the inspiratory phase. The dog's peripheral capillary oxygen saturation as measured by pulse oximetry was 91% (reference value, > 95%).

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

Problem Rule out location
Tetraplegia C1-C5 or C6-T2 spinal cord segments or peripheral neuromuscular problem
Decreased withdrawal reflexes in all limbs Peripheral neuromuscular problem or C1-T2 and L6-S3 spinal cord segments

Likely location of 1 lesion

Cervical spinal cord segments (C1-C5 vs C6-T2) or neuromuscular disease

Etiologic diagnosis—Neuromuscular disease or cervical myelopathy was considered the most likely diagnosis for the dog's sudden onset of flaccid tetraplegia without spinal hyperesthesia and decreased withdrawal reflexes. The differential diagnoses for an acute, progressive cervical myelopathy were degenerative or vascular causes associated with spinal shock in light of the decreased spinal reflexes. An intervertebral disk disorder (Hansen type I, acute, noncompressive nucleus pulposus extrusion or acute, hydrated nucleus pulposus extrusion) was considered the most likely degenerative cause because of the acute and progressive nature of the disorder and the presence of the patellar reflexes. Possible vascular causes included ischemic (fibrocartilaginous embolization) and hemorrhagic (acquired or congenital coagulopathy) myelopathies. Differential diagnoses for rapidly progressing neuromuscular disease affecting all 4 limbs included acute fulminating myasthenia gravis, acute idiopathic polyradiculoneuritis, botulism, or tick paralysis. Although conservation of the patellar reflexes with such disorders would be unusual, it could not be ruled out that those reflexes would diminish at a later stage in the disease progression.

The diagnostic plan included a CBC, serum biochemical analysis, assessment of coagulation variables, and arterial blood gas analysis to evaluate the dog's ventilation and general health prior to anesthesia. The plan also included thoracic radiography to rule out metastatic disease and, subsequently, MRI of the C1-T2 region to identify potential myelopathy.

Diagnostic test findings—The results of the CBC, serum biochemical analysis, and coagulation profile were unremarkable. Findings of the arterial blood gas analysis included Pao2 of 77.0 mm Hg (reference interval, 75 to 100 mm Hg) and Paco2 of 37.6 mm Hg (reference interval, 35 to 45 mm Hg). Thoracic radiography revealed mild aerophagia. Magnetic resonance imaging was performed with a 1.5-T scanner.a Multiplanar T1- and T2-weighted images, STIR images, and T1-weighted fat-saturated pre- and postcontrast images of the cervical portion of the vertebral column were obtained. Within the right laterodorsal aspect of the vertebral canal, there was an amorphous accumulation of extradural material (predominantly iso- to hyperintense on T2-weighted images and hypointense on T1-weighted images) that extended from the caudal aspect of C3 to the caudal aspect of C5 and caused marked compression of the spinal cord and the right C4 spinal nerve root. The material had mottled and nonuniform T2* gradient recalled echo susceptibility artifact and intermittent, faint, peripheral contrast enhancement. All cervical intervertebral disks were hypointense on T2-weighted images, with the C3-4 intervertebral disk being the most hypointense. A diagnosis of C3-4 intervertebral disk extrusion with additional extensive extradural hemorrhage (Funkquist type 3) was made (Figure 1)

Figure 1
Figure 1

Magnetic resonance images obtained from a 4-year-old dog that was referred for evaluation because of a 1-day history of generalized weakness, which progressed to flaccid tetraplegia and difficulty breathing. In a midsagittal single shot fast spin echo image of the cervical portion of the vertebral column (A), there is an extensive area devoid of signal from the CSF (arrowheads). In transverse T2-weighted images (B and D), notice the focal extradural iso- to hypointense material compressing the spinal cord dorsolaterally at the level of the intervertebral disk space between C4 and C5. In a right para-sagittal T2-weighted image of the cervical portion of the vertebral column (C), there is a loss of the hyperintense CSF fluid and fat signal, along with the presence of multifocal punctate areas of hypointense material within the dorsolateral aspect of the vertebral canal (arrows).

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.579

Surgical decompression was achieved via C3-C5 partial dorsal laminectomy. The right lamina and part of the pedicle of C3 on the right were removed, preserving the spinous process. Dorsal laminectomy and right pediculectomy were performed at C4 and C5 (with preservation of the C3-C4 and C4-C5 articular facets). Additionally, a nasopharyngeal cannula was placed for oxygen support. Thoracic radiography was repeated 1 day after surgery because of the dog's continued difficulty breathing, and the findings were unremarkable. The dog's transient respiratory difficulties were attributed to diaphragmatic weakness given the lack of inspiratory motion. Whether the phrenic nerve dysfunction was secondary to the extradural compression or to spinal shock was unclear. The bradycardia was possibly related to reduced sympathetic activity; unopposed parasympathetic function could have been responsible for the bradycardia through the phrenic nerve.

Comments

Following surgery, there was progressive improvement in the dog's clinical condition. The withdrawal reflexes of the pelvic limbs returned to normal by the second day after decompressive surgery. The dog's respiration gradually improved; on the third day after surgery, provision of supplemental oxygen was discontinued. The postoperative medical treatment included prednisone to reduce inflammation, fentanyl to facilitate pain control, maropitant to control nausea, and methocarbamol to promote muscle relaxation. Furthermore, cage rest and daily physical therapy were implemented. Seven days after surgery, the dog had nonambulatory tetraparesis and was discharged from the hospital. At a recheck examination 4 weeks later, the dog had ambulatory tetraparesis with moderate generalized proprioceptive ataxia. The dog eventually recovered fully, both clinically and neurologically.

This case described in the present report highlighted an unusual presentation of a dog with flaccid tetraplegia and spinal shock affecting all 4 limbs. Spinal shock is defined as profound transient depression in segmental spinal reflexes caudal to a lesion, despite the reflex arcs remaining physically intact.1,2 This state is characterized by flaccid paralysis of skeletal muscles. If not recognized, lesion localization within the reflex arcs may be made incorrectly. Spinal shock appears to differ in duration between humans and small animals.1 In human medicine, 4 phases of spinal shock can be distinguished. Phase I is characterized by areflexia or hyporeflexia caudal to the spinal cord injury, which develops within 24 hours after the initial injury. In this phase, the bulbocavernosus reflex returns. Between 1 and 3 days following the spinal cord injury, phase II occurs. Phase II is associated with denervation hypersensitivity; during this phase, cutaneous reflexes become stronger and electrophysiologic testing reveals signs of recovery of the neuronal pathways responsible for the deep tendon reflexes. Phase III is a more protracted period of recovery, lasting 4 to 30 days, during which the deep tendon reflexes re-emerge followed by the recovery of the flexor withdrawal reflex. Phase IV can last up to 12 months, during which time exaggerated tendon reflexes and increased muscle tone develop.3 In dogs and cats, the recovery from spinal shock is far more rapid.4,5 The difference in duration of spinal shock signs in humans and small animals may be attributable to anatomic differences in the descending motor control pathway. In humans, the pyramidal tract projects directly to the ventral horn motor neurons of the spinal cord, whereas in nonprimates, the corticospinal tract axons project almost exclusively to the dorsal horn of the spinal cord and influence motor neurons indirectly by means of interneurons. Therefore, in small animals, there is a certain degree of plasticity mediated by interneuronal circuitry in this pathway.6,7,8

In the veterinary medical literature, there are reports1,9,10,11 of naturally occurring spinal shock in small animals. However, these reports mostly describe spinal shock in association with thoracolumbar spinal cord injury.1,9 To our knowledge, there are only 2 reports10,11 (involving 1 cat and 1 dog) of transient, decreased, segmental spinal reflexes in all limbs after injury to the cervical portion of the spinal cord or brainstem. The dog of the present report had signs compatible with spinal shock that developed following cervical spinal cord injury. The presence of patellar tendon reflexes in this dog was attributed to the timing of the referral evaluation; in experimental settings in dogs, the patellar tendon reflex reappears between 30 minutes and 2 hours after spinal cord transection.4 This stage of spinal shock was therefore likely missed in the dog of the present report. The decreased withdrawal reflexes of the pelvic limbs returned to normal 3 days following the initial signs, which was in concordance with the reported return of the withdrawal reflex within 2 days to 6 weeks after experimental spinal cord transection in nonprimates.4,5 For the dog of the present report, the withdrawal reflex in the thoracic limbs remained decreased at a recheck examination 5 weeks after surgery. It is debatable whether this finding was associated with spinal shock or merely the cervical myelopathy itself. Decreased withdrawal reflexes in the thoracic limbs do not always indicate a lesion from C6 to T2 and may also be associated with C1-C5 spinal cord lesions.12 Cardiac arrhythmias secondary to sympathetic dysfunction and parasympathetic override following spinal cord injuries and spinal shock have been reported.13 For a dog with acute nonpainful flaccid tetraparesis or tetraplegia accompanied by abnormal spinal reflexes in all limbs, cervical spinal cord injury should not be overlooked.

Footnotes

a.

Signa Horizon LX 1.5T, GE Healthcare, Milwaukee, Wis.

References

  • 1.

    Smith PM, Jeffery ND. Spinal shock—comparative aspects and clinical relevance. J Vet Intern Med 2005;19:788793.

  • 2.

    Nacimiento W, Noth J. What, if anything, is spinal shock? Arch Neurol 1999;56:10331035.

  • 3.

    Ditunno JF, Little JW, Tessler A, et al. Spinal shock revisited: a four-phase model. Spinal Cord 2004;42:383395.

  • 4.

    Blauch B. Spinal reflex walking in the dog. Vet Med Small Anim Clin 1977;72:169173.

  • 5.

    Little JW. Serial recording of reflexes after feline spinal cord transection. Exp Neurol 1986;93:510521.

  • 6.

    Brouwer B, Ashby P. Corticospinal projections to upper and lower limb spinal motoneurons in man. Electroencephalogr Clin Neurophysiol 1990;76:509519.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Taylor JL, Gandevia SC. Noninvasive stimulation of the human corticospinal tract. J Appl Physiol 2004;96:14961503.

  • 8.

    Yang HW, Lemon RN. An electron microscopic examination of the corticospinal projection to the cervical spinal cord in the rat: lack of evidence for cortico-motoneuronal synapses. Exp Brain Res 2003;149:458469.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Full AM, Barnes Heller HL, Mercier M. Prevalence, clinical presentation, prognosis, and outcome of 17 dogs with spinal shock and acute thoracolumbar spinal cord disease. J Vet Emerg Crit Care (San Antonio) 2016;26:412418.

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

    Brocal J, Guevar J, Stalin C, et al. Intra-parenchymal brainstem haemorrhage secondary to iatrogenic needle injury after a parenteral injection in a cat. JFMS Open Rep 2016;2:2055116916631562.

    • Search Google Scholar
    • Export Citation
  • 11.

    Beltran E, Dennis R, Doyle V, et al. Clinical and magnetic resonance imaging features of canine compressive cervical myelopathy with suspected hydrated nucleus pulposus extrusion. J Small Anim Pract 2012;53:101107.

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

    Forterre F, Konar M, Tomek A, et al. Accuracy of the withdrawal reflex for localization of the site of cervical disk herniation in dogs: 35 cases (2004–2007). J Am Vet Med Assoc 2008;232:559563.

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

    Berlowitz DJ, Wadsworth B, Ross J. Respiratory problems and management in people with spinal cord injury. Breathe (Sheff) 2016;12:328340.

Contributor Notes

Address correspondence to Dr. Schmidli (fenella.schmidli@vetsuisse.unibe.ch).
  • Figure 1

    Magnetic resonance images obtained from a 4-year-old dog that was referred for evaluation because of a 1-day history of generalized weakness, which progressed to flaccid tetraplegia and difficulty breathing. In a midsagittal single shot fast spin echo image of the cervical portion of the vertebral column (A), there is an extensive area devoid of signal from the CSF (arrowheads). In transverse T2-weighted images (B and D), notice the focal extradural iso- to hypointense material compressing the spinal cord dorsolaterally at the level of the intervertebral disk space between C4 and C5. In a right para-sagittal T2-weighted image of the cervical portion of the vertebral column (C), there is a loss of the hyperintense CSF fluid and fat signal, along with the presence of multifocal punctate areas of hypointense material within the dorsolateral aspect of the vertebral canal (arrows).

  • 1.

    Smith PM, Jeffery ND. Spinal shock—comparative aspects and clinical relevance. J Vet Intern Med 2005;19:788793.

  • 2.

    Nacimiento W, Noth J. What, if anything, is spinal shock? Arch Neurol 1999;56:10331035.

  • 3.

    Ditunno JF, Little JW, Tessler A, et al. Spinal shock revisited: a four-phase model. Spinal Cord 2004;42:383395.

  • 4.

    Blauch B. Spinal reflex walking in the dog. Vet Med Small Anim Clin 1977;72:169173.

  • 5.

    Little JW. Serial recording of reflexes after feline spinal cord transection. Exp Neurol 1986;93:510521.

  • 6.

    Brouwer B, Ashby P. Corticospinal projections to upper and lower limb spinal motoneurons in man. Electroencephalogr Clin Neurophysiol 1990;76:509519.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Taylor JL, Gandevia SC. Noninvasive stimulation of the human corticospinal tract. J Appl Physiol 2004;96:14961503.

  • 8.

    Yang HW, Lemon RN. An electron microscopic examination of the corticospinal projection to the cervical spinal cord in the rat: lack of evidence for cortico-motoneuronal synapses. Exp Brain Res 2003;149:458469.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Full AM, Barnes Heller HL, Mercier M. Prevalence, clinical presentation, prognosis, and outcome of 17 dogs with spinal shock and acute thoracolumbar spinal cord disease. J Vet Emerg Crit Care (San Antonio) 2016;26:412418.

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

    Brocal J, Guevar J, Stalin C, et al. Intra-parenchymal brainstem haemorrhage secondary to iatrogenic needle injury after a parenteral injection in a cat. JFMS Open Rep 2016;2:2055116916631562.

    • Search Google Scholar
    • Export Citation
  • 11.

    Beltran E, Dennis R, Doyle V, et al. Clinical and magnetic resonance imaging features of canine compressive cervical myelopathy with suspected hydrated nucleus pulposus extrusion. J Small Anim Pract 2012;53:101107.

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

    Forterre F, Konar M, Tomek A, et al. Accuracy of the withdrawal reflex for localization of the site of cervical disk herniation in dogs: 35 cases (2004–2007). J Am Vet Med Assoc 2008;232:559563.

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

    Berlowitz DJ, Wadsworth B, Ross J. Respiratory problems and management in people with spinal cord injury. Breathe (Sheff) 2016;12:328340.

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