Posterior Cord Syndrome

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Introduction[edit | edit source]

Posterior Cord Syndrome (PCS) is the rarest form of incomplete spinal cord injury. An individual with this form of spinal cord injury (SCI) will have intact motor function and sensations of pain, light touch, and temperature, but impairments in proprioception, vibration, kinesthesia, and combined cortical functions below the level of the lesion (see: Sensation).

Clinically Relevant Anatomy[edit | edit source]

As the name implies, the vast majority of damage with this form of incomplete spinal cord injury is towards the posterior aspects of the spinal cord. As a result, the common location of injury in Posterior Cord Syndrome is to the posterior columns and dorsal horns of the spinal cord, which are part of the Dorsal Column Medial Lemniscal Pathway (DCML). The DCML provides the sensory information of discriminative touch (two point discrimination, stereognosis, localization of touch), deep touch, vibration, conscious proprioception, and information for combined cortical functions such as graphesthesia for all body regions except the head.[1] The end destination of this information is then carried to the primary somatosensory cortex of the Parietal Lobe for central processing.[1]

However, when considering the vascular anatomy of the spinal cord, specifically the posterior spinal arteries, there may be some alterations to the Corticospinal Tract or even aspects of the Spinothalamic tract due to a border zone of infusion. [2]As there is generally not extensive damage to the corticospinal or spinothalamic tracts, voluntary motor function (corticospinal tract), and sensations of pain, crude touch, and temperature (spinothalamic tract) are preserved.[3] [4]

Incidence/Prevalence[edit | edit source]

There is a wide variance in global reports of incident rates for spinal cord injury. Recent estimates from the Global Burden of Disease suggest an incidence rate of 0.9 million spinal cord injuries, 20.6 million prevalent cases, and 6.2 million years lived with disability (YLD) in 2019. [5] On average, spinal cord injuries appear to be more commonly afflicting males based on age standardized incidence rate (ASIR) and age standardized YLD rate (ASYR) , and injuries at neck level had higher ASYR than injuries below the neck.[5] No readily available global reports suggest incidence/prevalence rates of incomplete spinal cord injury; however, the United States National Spinal Cord Injury Statistical Center reports that 67.2% of traumatic spinal cord injuries are incomplete.[6] See Epidemiology of Spinal Cord Injury for more information.

Reports of Posterior Cord Syndrome incidence rates vary; however it is believed to be the least prevalent SCI, with estimates of 2% or less.[2] [7]

Pathophysiology[edit | edit source]

The pathophysiology of spinal cord injury appears to follow mechanisms of primary and secondary injury. Primary injury refers to the resultant physical trauma to the spinal cord anatomy due to impingement from fractured bone or surrounding soft tissue. This damage then disrupts components of the nervous system, such as destruction of the neural parenchyma, disruption of the axonal network, and hemorrhagic disruption to glial membranes. Secondary injury is the component which generates the most damage to the spinal cord, and involves a series of chemical and mechanical changes ultimately leading to necrosis, neural apoptosis, and glial scar formation.[8]

It is unclear what the most common mechanism of injury (MOI) is for Posterior Cord Syndrome due to its rarity. Common causes of PCS include posterior spinal artery ischemia, tumor, herniated disc, Vitamin B12 deficiency, and trauma.[7] Trauma appears to be the least common MOI for PCS, but is thought to be associated with hyperextension injuries, though this MOI is more commonly associated with Central Cord Syndrome.[7]

Clinical Presentation[edit | edit source]

For a comprehensive clinical examination overview, see: Assessment of Spinal Cord Injury and Neurological Assessment

Although individuals with PCS retain their motor function, a lack of proprioception can elevate their fall risk and increase the ability to perform ambulation and other Activities of Daily Living. As a result, ataxic gait, falls, and impaired coordination below the level of lesion are common presentation characteristics. [9] Additionally, the patient may experience paresthesia throughout the levels below the site of lesion; a lack of appropriate sensation may contribute to the development of Pressure Injuries.[2][9]

On clinical examination, the following components may be utilized, not only to identify functional deficits, but to rule out additional locations of injury:

Diagnostic Procedures[edit | edit source]

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Differential Diagnosis[edit | edit source]

add text here relating to the differential diagnosis of this condition

Management / Interventions[edit | edit source]

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Prognosis[edit | edit source]

Outcome Measures[edit | edit source]

For all suspected spinal cord injuries, the American Spinal Injury Association (ASIA) Impairment Scale is performed to assess long-term prognosis. General standards of practice are to perform this assessment within 72 hours of suspected injury to reliably predict the likelihood of recovery.

See Spinal Cord Injury Outcome Measures Overview for all relevant outcome measures for SCI. (Note: based on typical PCS presentation, they will likely be within the ASIA Impairment Scale category of D - Motor Incomplete. Refer to the pertinent outcome measures for a patient's respective ASIA level.

Resources[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 Al-Chalabi M, Reddy V, Alsalman I. Neuroanatomy, Posterior Column (Dorsal Column). StatPearls [Internet]. 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507888/ (accessed 31 January 2024).
  2. 2.0 2.1 2.2 McKinley W, Hills A, Sima A. Posterior cord syndrome: Demographics and rehabilitation outcomes. J Spinal Cord Med. 2021;44(2):241
  3. Welniarz Q, Dusart I, Roze E. The corticospinal tract: Evolution, development, and human disorders. Dev Neurobiol. 2017;77(7):810-829
  4. Waxman SG. Clinical Neuroanatomy 27th ed. New York: McGraw Hill, 2013.
  5. 5.0 5.1 Ding W, Hu S, Wang P, Kang H, Peng R, Dong Y, Li F. Spinal Cord Injury: The Global Incidence, Prevalence, and Disability From the Global Burden of Disease Study 2019. Spine (Phila Pa 1976). 2022;47(21):1532-1540.
  6. National Spinal Cord Injury Statistical Center. Traumatic Spinal Cord Injury Facts and Figures at a Glance. Birmingham, AL: University of Alabama at Birmingham, 2023
  7. 7.0 7.1 7.2 Kennamer BT, DelPino BJ, Lettieri SC, Gridley DG, Hollingworth AK, Feiz-Erfan I. Blunt traumatic posterior cord syndrome. Spinal Cord Ser Cases. 2022;8:52
  8. Anjum A, Yazid MD, Fauzi Daud M, Idris J, Ng AMH, Selvi Naicker A, Ismail OHR, Athi Kumar RK, Lokanathan Y. Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms. Int J Mol Sci. 2020;21(20):7533.
  9. 9.0 9.1 Lanzieri P, Carneiro Ramos R, Mocarzel LO, Gismondi RA. Posterior Cord Syndrome and Trace Elements Deficiency as an Uncommon Presentation of Common Variable Immunodeficiency. Case Rep Med. 2017;2017:9870305.