Important spinal cord injury syndromes

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, and then again in Question 4 from the first paper of 2021.  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. In Question 30 from the first paper of 2020, they wanted the difference between a high (C6/C7) and very high (C3/C4) spinal cord injury.

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?

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)