This topic keeps coming up in the SAQs. One notable appearance was in Question 5 from the first paper of 2010, where the candidates needed to not only identify the features, but also the causes of the partial spinal cord injury syndrome. This was again repeated in the identical  Question 15 from the first paper of 2015. The college also asked about the anterior spinal artery syndrome in Question 23 from the first paper of 2018, where much detail was expected regarding the management of a poorly perfused spinal cord.

The canonical resource for this would have to be Ch.78 from Oh's Manual, Spinal injuries by Sumesh Arora and Oliver J Flower. Specifically, on page 798, cord syndromes are discussed with enough detail to pass Question 5. If one happens to not own the Manual, one may find a similar amount of detail in the "International standards for neurological and functional classification of spinal cord injury" from 1997, and in a similar article on classifying partial cord syndromes from 2000. And if one were for some reason in need of a massive amount of detail, one might instead wish to purchase a copy of Diseases of the Spine and Spinal Cord By Thomas N. Byrne, which remains a definitive text on this subject.

The information from these abovementioned resources has been mixed, boiled and condensed into the table below.

Causes and Characteristic Features of Spinal Cord Syndromes

Syndrome

Characteristic features

Causes

There are some causes which are generic for all these syndromes, and they will not be repeated in each box. These are:

  • Trauma
  • Infarction
  • Abscess
  • Tumour or metastatic compression
  • Haematoma
  • AVM/haemorrhage

Any of these can cause any of the spinal syndromes, anywhere. Instead of these, the causes listed below are the characteristic pathological processes which usually give rise to a specific spinal cord syndrome, eg. anterior spinal artery occlusion causing anterior spinal syndrome.

Cord transection

  • Lost bilateral motor
  • Flaccid areflexia
  • Lost bilateral sensory
  • Transverse Myelitis

Cord hemisection

  • Lost ipsilateral motor
  • Lost ipsilateral proprioception
  • Lost ipsilateral light touch
  • Lost contralateral pain and temperature
  • Penetrating spinal injury
  • Radiation inury
  • Spinal metastases

Anterior cord injury

  • Preserved bilateral proproception, vibration and touch
  • Lost bilateral pain and temperature
  • Lost bilateral motor control

Interruption of the blood supply to the anterior spinal cord:

  • Aortic dissection
  • IABP complication
  • Surgery on the aorta; prolonged cross-clamp time

Posterior cord injury

  • Lost proprioception
  • Other sensation preserved bilaterally
  • Preserved power bilaterally
  • Ataxia results
  • Hyperextension injury
  • Posterior spinal artery injury
  • Tertiary syphilis
  • Friedrich's ataxia
  • Subacute degeneration (Vitamin B12 deficiency)
  • Atlantoaxial subluxation

Central cord syndrome

  • Sacral sensation preserved
  • Greater weakness in the upper limbs than in the lower limbs.
  • Hyperextension injury with pre-existing canal stenosis
  • Ependymoma
  • Syringomyelia

Conus medullaris syndrome

  • symmetrical paraplegia
  • Mixed upper and lower motor neuron
    findings
  • The same sort of pathologies can give rise either to a cauda equina syndrome or a conus medullaris syndrome; the difference is the level.

Cauda Equina syndrome

  • asymmetrical, lower motor neuron lower limb weakness
  • saddle area paraesthesia
  • bladder and bowel areflexia

*Discriminating conus medullaris from cauda equina lesions can be tricky.

Thomas N. Byrne's textbook offers a table on page 77, which answers this question in some detail. The relevant features are reproduced below:

Conus Medullaris vs. Cauda Equina Disease

Conus Medullaris

Cauda Equina

  • Mild motor deficits
  • Symmetrical deficits
  • Impaired pain and temperature sensation in a saddle distribution, with intact light touch sense
  • Achilles tendon reflex is present
  • Sphincters are impaired early and the impairment is severe
  • Onset is sudden and bilateral
  • Severe motor deficits
  • Asymmetrical deficits
  • Saddle sensory loss is complete; no dissociation of sensory loss
  • Absent reflexes
  • Sphincters are impaired late and the impairment is relatively mild
  • Onset is gradual and unilateral

Relevant neuroanatomy

Remember this diagram?

spinal cord labelled cross-section of ascending and descending tracts

This diagram hopefully makes it easier to understand the stereotypical cord section syndromes.

Anterior spinal artery syndrome

Though this has exam relevance (Question 23 from the first paper of 2018) it is in fact a very rare syndrome, appearing in 2% of patients undergoing ruptured aortic aneurysm repair, and in only 0.4% of elective AAA repairs (Gialdini, 2017).

Sensory signs of anterior spinal cord syndrome are:

  • Preserved bilateral proproception and vibration
  • Lost bilateral pain, temperature
  • Usually, preserved light touch sensation (Triggs & Beric, 1992)

Motor signs of anterior spinal cord syndrome are:

  • Early flaccid paralysis
  • Incontinence
  • Bilaterally absent deep tendon reflexes
  • Later, spasticity and hyper-reflexia

Perioperative risk factors for anterior spinal artery syndrome are

  • Perioperative hypotension
  • Prolonged aortic crossclamp time
  • Other instrumentation of the atheromatous aorta (eg. angiography, IABP, VA ECMO)
  • Inadequate heparinisation of the bypass circuit
  • Air emboli

Apart from "perioperative factors", Djurberg & Haddad (1995) list "conditions affecting blood flow in the anterior spinal artery":

  • Arteriosclerosis
  • Vascular malformations (aortic aneurysms, haemangioma etc.)
  • Tumour
  • Infection (tuberculosis)
  • Haematological disorders (polycythaemia, hypercoagulability)
  • Trauma of the spine (fracture. haematoma, foreign body etc.)
  • Chronic respiratory disease with polycythaemia
  • Anatomical changes of the spine (kyphoscoliosis, spondyloarthrosis, disc herniation etc.)

Management of an infarcted anterior cord involves maximising the perfusion of the cord via collaterals. The best information about this about this seems to come from Hnath et al (2007), who published a fairly successful protocol. This consisted of:

  • Increasing perfusion pressure
    • Hnath et al maintained the MAP  at ≥90 mm Hg. In their answer to Question 23, the college recommend cranking the vasopressors until symptoms resolve or complications develop. This comes from the "Spinal Cord Infarction" UpToDate article by Mullen et al (2016).
  • Decreasing spinal CSF pressure 
    • Hnath et al actively drained the CSF to maintain pressures <15 mm Hg. The college recommend simply draining to a positive pressure of no more than 8-12 mmHg, which is again from the same UpToDate source. The systematic review by Cina et al (2004) suggests that if you're going to do this, you should aim to decrease the CSF pressure to at least below 10 mmHg, for at least 48-60 hours. The rationale for this is that the lower CSF pressure minimise the resistance to afferent spinal cord blood flow, thereby increasing perfusion of at-risk regions (Strohm et al, 2017)

Hnath et al reported a 60% improvement, but their series had only 5 patients in the treatment arm, which somewhat dampens the enthusiasm of anybody following their footsteps. Chiesa et al (2005) list several other possible strategies:

  • Distal aortic perfusion by bypass of the left heart (i.e. piping oxygenated blood into the distal aorta), which doesn't seem to work according to Coselli et al (2004)
  • Deep hypothermic circulatory arrest which should theoretically protect the cord perioperatively (Safi et al, 1998)
  • Regional cooling of the cord by infusing normal saline at 4° C into a thoracic epidural (Cambria et al, 1997)
  • Protective pharmacological agents, used perioperatively (steroids, naloxone, barbiturates, papaverine, magnesium sulfate)

References

Oh's Manual: Chapter 78 (pp. 795) Spinal injuries by Sumesh Arora and Oliver J Flower

Wagner, Robert, and Andy Jagoda. "Spinal cord syndromes." Emergency medicine clinics of North America 15.3 (1997): 699-711.

Lin, Vernon W., et al. "Spinal Cord and Cauda Equina Syndromes." (2003).

Maynard, Frederick M., et al. "International standards for neurological and functional classification of spinal cord injury." Spinal cord 35.5 (1997): 266-274.

Hayes, Keith C., et al. "Classifying incomplete spinal cord injury syndromes: algorithms based on the International Standards for Neurological and Functional Classification of Spinal Cord Injury Patients." Archives of physical medicine and rehabilitation 81.5 (2000): 644-652.

McDonald, John W., and Cristina Sadowsky. "Spinal-cord injury." The Lancet 359.9304 (2002): 417-425.

Djurberg, H., and M. Haddad. "Anterior spinal artery syndrome." Anaesthesia 50.4 (1995): 345-348.

Eltorai, Ibrahim M. "Anterior Spinal Artery Syndrome." Rare Diseases and Syndromes of the Spinal Cord. Springer, Cham, 2016. 437-440.

Foo, Dominic, and Alain B. Rossier. "Anterior spinal artery syndrome and its natural history." Spinal Cord 21.1 (1983): 1.

Zuber, William F., Max R. Gaspar, and Philip D. Rothschild. "The anterior spinal artery syndrome--a complication of abdominal aortic surgery: report of five cases and review of the literature.Annals of surgery 172.5 (1970): 909.

TRIGGS, WILLIAM J., and ALEKSANDAR BERIĆ. "Sensory abnormalities and dysaesthesias in the anterior spinal artery syndrome." Brain 115.1 (1992): 189-198.

Aydin, A. "Mechanisms and prevention of anterior spinal artery syndrome following abdominal aortic surgery." Angiologiia i sosudistaia khirurgiia= Angiology and vascular surgery 21.1 (2015): 155-164.

Santamato, Andrea, et al. "Paraplegia due to Anterior Spinal Artery Stroke: Rehabilitative Program on Lower Extremity Weakness and Locomotor Function." Int J Phys Med Rehabil1.118 (2013): 2.

Ullery, Brant W., et al. "Risk factors, outcomes, and clinical manifestations of spinal cord ischemia following thoracic endovascular aortic repair." Journal of vascular surgery 54.3 (2011): 677-684.

Cheshire, William P., et al. "Spinal cord infarction Etiology and outcome." Neurology 47.2 (1996): 321-330.

Gialdini, Gino, et al. "Retrospective analysis of Spinal Cord Infarction after Aortic Repair (P6. 300)." Neurology 88.16 Supplement (2017): P6-300.

Hnath, Jeffrey C., et al. "Strategies to improve spinal cord ischemia in endovascular thoracic aortic repair: outcomes of a prospective cerebrospinal fluid drainage protocol." Journal of vascular surgery 48.4 (2008): 836-840.

Chiesa, Roberto, et al. "Spinal cord ischemia after elective stent-graft repair of the thoracic aorta." Journal of vascular surgery 42.1 (2005): 11-17.

Coselli, Joseph S., et al. "Left heart bypass during descending thoracic aortic aneurysm repair does not reduce the incidence of paraplegia." The Annals of thoracic surgery 77.4 (2004): 1298-1303.

Safi, Hazim J., et al. "Thoracic and thoracoabdominal aortic aneurysm repair using cardiopulmonary bypass, profound hypothermia, and circulatory arrest via left side of the chest incision." Journal of vascular surgery 28.4 (1998): 591-598.

Cambria, Richard P., et al. "Clinical experience with epidural cooling for spinal cord protection during thoracic and thoracoabdominal aneurysm repair." Journal of vascular surgery 25.2 (1997): 234-243.

Cinà, Claudio S., et al. "Cerebrospinal fluid drainage to prevent paraplegia during thoracic and thoracoabdominal aortic aneurysm surgery: a systematic review and meta-analysis." Journal of vascular surgery 40.1 (2004): 36-44.

Taira, Yutaka, and Martin Marsala. "Effect of proximal arterial perfusion pressure on function, spinal cord blood flow, and histopathologic changes after increasing intervals of aortic occlusion in the rat." Stroke 27.10 (1996): 1850-1858.

Strohm, Tamara, Seby John, and Muhammad Hussain. "Cerebrospinal Fluid Drainage for Acute Spinal Cord Infarction (P1. 301)." Neurology 88.16 Supplement (2017): P1-301.