Which of the following statements regarding spinal motion restriction is accurate?

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Overview[edit | edit source]

Also known as spinal shock syndrome, spinal shock is the loss of muscle tone and spinal reflexes below the level of a severe spinal cord lesion[1]. This "shock" does not imply a state of circulatory collapse but of suppressed spinal reflexes below the level of cord injury[2]. It takes between days and months for spinal shock to completely resolve and when it does, the flaccidity that was once seen gradually becomes spasticity[3]. It usually is consequent to severe spinal cord injury (SCI) that is either traumatic or ischaemic, with traumatic spinal shock occurring more in young people and mostly among males than females[4]. Spinal shock is characterized by a temporary rise in blood pressure that is proceeded by hypotension, flaccid paralysis, urinary retention and fecal Urinary Incontinence[4]. If reversal of symptoms does not occur within 24hrs, it may call for protracted recovery time and lengthened stay in rehabilitation[4].

[5]

Differential Diagnoses of Spinal Shock[edit | edit source]

These include:

• Vertebral fracture
• Spinal abscess
• Sepsis
• Cardiogenic shock[4]

Complications of Spinal Shock[edit | edit source]

• Neurological deterioration
• Pressure sores
• Fecal incontinence
• Urinary retention
• Deep vein thrombosis
• Aspiration pneumonitis[4]

Differences between Neurogenic Shock and Spinal Shock[edit | edit source]

Neurogenic shock[edit | edit source]

• Also known as vasogenic shock
• Defined as systolic blood pressure less than 100 mm Hg with a heart rate less than 80 bpm[6]
• Consequent to SCI with associated autonomic dysregulation[6]
• Common with cord injuries above T6 level. In other words, it is associated with cervical and high thoracic spine injury.
• Occurs at anytime from the onset of injury
• Frequently follows a traumatic SCI[6], but may also occur in non-traumatic cord lesions[7]
• Characterized by:
  • Systemic hypotension and bradycardia
  • Respiratory insufficiency and pulmonary dysfunction
  • Temperature dysregulation vis-à-vis hypothermia; flushed, warm skin
• Lasts between 1 to 6 weeks post the initial injury
• Managed by administering fluids and vasopressors with appropriate temperature monitoring[8]

Spinal shock[edit | edit source]

• Defined as a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of sensorimotor functions[9]
• Is a reversible reduction or loss in sensory and motor function after an acute SCI
• Rarely occurs in spinal cord lesions of gradual onset
• Involves reflex depression of cord function below the level of injury[10]
• When reflexes return, they follow a pattern where superficial ones show up before deep tendon reflexes[9].
• Characterized by:
  • Flaccid paralysis
  • Anaesthesia
  • Areflexia or hyporeflexia[8]
• Lasts between days to months
• Most often resolves on its own

[11]

Stages of Spinal Shock[edit | edit source]

The resolution of spinal shock does not occur abruptly but in phases. Ditunno et al (2004)[12] proposed a four-phase model of the syndrome.

Phase 1[edit | edit source]

• Lasts between 0 to 1 day
• Characterized by loss of descending facilitation
• Presents as areflexia or hyporeflexia

Phase 2[edit | edit source]

• Occurs between 1 to 3 days post injury
• Shows as denervation supersensitivity
• Leads to initial re-emergence of reflexes

Phase 3[edit | edit source]

• Lasts between 4 days to 1 month
• Axon-supported synapse growth occurs at this stage
• Initial hyper-reflexia is elicited here

Phase 4[edit | edit source]

• Lasts between 1 to 12 months
• Soma-supported synapse growth occurs
• Presents as spasticity

Autonomic Effects[edit | edit source]

• Neurogenic shock may occur in spinal cord injuries above T6, from the loss of autonomic innervation from the brain.
• In cervical and high thoracic SCI lesions, the synergy between sympathetic and parasympathetic system is lost but the parasympathetic system is preserved.
• There may be sacral parasympathetic loss encountered in lesions below T6 or T7.
• Cervical lesions cause total loss of sympathetic innervation. It leads to vasovagal hypotension and bradyarrhythmia's which resolve in 3–6 weeks.
• Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It leading to extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.[12]

Conclusion[edit | edit source]

While spinal shock may not be easily prevented, it can be managed and often requires a multidisciplinary team effort to do so. Its understanding and that of its mechanisms will enable the application of interventions that will facilitate recovery.

Additional Information[edit | edit source]

Physiotherapy Management of Individuals with Spinal Cord Injury

Bed Mobility and Transfers in Spinal Cord Injury

Prognosis and Goal Setting in Spinal Cord Injury

References[edit | edit source]

1. ↑ Smith PM, Jeffery ND. Spinal Shock-Comparative Aspects and Clinical Relevance. Journal of Verterinary Int Med 2008; 19(Iss 6)
2. ↑ Singhal V, Aggarwal R. Spinal Shock. In: Prabhakar H. Complications in Neuroanesthesia. Academic Press: Science Direct, 2016. p89-94.
3. ↑ Ko HY. Spinal Shock. In Management and Rehabilitation of Spinal Cord Injuries. Singapore: Springer, 2019. pg123-134.
4. ↑ 4.0 4.1 4.2 4.3 4.4 Ziu E, Mesfin FB. Spinal Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. p1-11.
5. ↑ Em Quattrocchi. What is SPINAL SHOCK? Available from: https://www.youtube.com/watch?v=DlJWQOtLWnM [last accessed 24/3/2021]
6. ↑ 6.0 6.1 6.2 Dave S, Cho JJ. Neurogenic Shock. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020; p1-10.
7. ↑ Flanagan EP, Pittock SJ, Diagnosis and Management of Spinal Cord Emergencies. In: Wijdicks EFM, Kramer AH editors. Handbook of Clinical Neurology. Elsevier, 2017. p319-335.
8. ↑ 8.0 8.1 Volski A, Ackerman DJ, Neurogenic Shock. In: Stawicki SP, Swaroop M editors. The Science and Art of Physiological Restoration. IntechOpen, 2019.
9. ↑ 9.0 9.1 Singhal V, Aggarwal R, Spinal Shock. In: Prabhakar H editor. Complications in Neuroanaesthesia. Academic: Science Direct, 2016. p89-94.
10. ↑ Graells XS, Benato ML, del Santoro PG, et al. Spinal Cord Injury. In: Nasr A, Saavedra TF, Collaço I, Abreu P, Namias N, Marttos. The Trauma Golden Hour. Cham: Springer, 2020. p65-72.
11. ↑ ACLS Certification Association. Neurogenic shock vs. Spinal shock. Available from: https://youtu.be/nPu7RW2JBkw [last accessed 10/1/2021]
12. ↑ 12.0 12.1 Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal cord. 2004 Jul;42(7):383-95.

What is spinal motion restriction?

Which of the following indicate the definite need for spinal immobilization?

Which of the following is the most common mechanism for spinal trauma?

Which of the following signs would indicate a spinal cord injury?