Spinal shock was a term first coined in the 18th Century to describe the symptoms of acute spinal cord injury. These symptoms include a loss of sensation accompanied by motor paralysis and loss of reflexes which usually recover to some degree over time.
In those with spinal shock, reflexes in the spinal cord caudal (below the site of injury) are usually depressed or entirely absent; these states are known as hyporeflexia and areflexia, respectively. Rostral reflexes (above the site of SCI) are, however, usually unaffected by spinal shock.
Those with already narrowed spaces in the spine and conditions such as spondylolisthesis or other causes of spinal stenosis may be at a higher risk of spinal shock as even less severe injuries to the spine may impact the spinal cord when space is tight.
The reason spinal shock occurs is that there is a sudden loss of conductivity of electrical signals in the spinal cord as potassium ions move from the intracellular to the extracellular spaces (i.e. from inside cells to outside cells). When this happens the body can no longer effectively send nerve signal impulses to control automatic reflexes below the site of the SCI. In some cases the area above the SCI may also be affected, depending on the level of trauma and subsequent inflammation.
Symptoms of Spinal Shock
Patients with spinal shock may have complications such as low blood pressure (hypotension) as the sympathetic nervous system is unable to regulate vascular tone (the contraction of the blood vessels). This is only usually the case when the SCI is in the cervical spinal cord, and such injury may also cause bradyarrhythmias that usually correct themselves within 3-6 weeks of injury.
Severe Spinal Shock – A Medical Emergency
Injuries above T6 may create autonomic dysreflexia, which is permanent and is characterised by sympathetic nerve stimulation below the SCI that goes unchecked by the central nervous system. What this means is that the brain is no longer able to prevent these nerves being stimulated leading to symptoms such as extreme hypertension, bowel/bladder incontinence, sweating, headaches, and other issues.
Spinal cord injury that is followed by sudden paroxysmal hypertension (acute onset of severe high blood pressure) requires immediate medical attention, especially where the following symptoms are also present:
- Pounding headache
- Excessive sweating
- Flushing of the skin above the level of injury
- Slowing heart rate
- Nasal congestion (stuffiness)
- Cognitive impairment, confusion (in some cases)
As recovery progresses from spinal shock, patients often experience hyperreflexia and subsequent spasticity as the axons and synapses in the spinal cord are re-established. This has become known as the four-phase model of spinal shock, devised by Ditunno, et al, in 2004:
- Phase 1: 0-1 days – Areflexia/Hyporeflexia due to loss of descending facilitation
- Phase 2: 1-3 days – Initial reflex return and denervation supersensitivity
- Phase 3: 1-4 weeks – Hyperreflexia (initial) with axon-supported synapse growth
- Phase 4: 1-12 months – Hyperreflexia and spasticity through soma-supported synapse growth.
What this actually means for patients is that in the first phase of spinal shock there is a complete loss of, or weakening of all the reflex responses below the site of the spinal cord injury. This is caused by a loss of excitatory stimulation from the brain which means that the neurons in the area below the SCI become less responsive to stimuli.
Second Phase of Spinal Shock
In the second phase of spinal shock there is a gradual return of some reflexes below the SCI site. The polysnyaptic responses usually return first, including the bulbocavernosus reflex. Also known as the Osinski Reflex, the bulbocavernous reflex involves anal sphincter contraction in response to specific types of stimulation.
Monosynaptic reflexes do not normally return until the third phase of spinal shock. Reflexes return due to hypersensitivity of reflex muscles after denervation. This is because there are more receptors expressed for neurotransmitters, making nerves easier to stimulate.
In the third phase the deep tendon reflexes (monosynaptic reflexes) are restored and may become hyperreflexive, meaning that little stimulation is needed to provoke a response. The areas below the SCI begin to sprout interneurons and lower motor neurons to re-establish the synaptic connections. Shorter axons are usually the first to prompt these new synapses (in Phase 3) with soma-stimulated synaptic growth seen in Phase 4.
Recovery From Spinal Shock
While some patients experience almost a full recovery after spinal shock, abnormalities in reflexes, particularly autonomic reflexes, are extremely likely and rehabilitation necessarily focuses on working with the nerve regrowth that does occur. Symptoms of spinal shock usually arise in the first half hour to an hour after injury, be it physiologic or anatomic. The type of injury that causes spinal shock is usually acute but there are cases where the injury occurs over the longer term, usually a few hours. This may be the case where degenerative spine issues are a factor, including spinal stenosis.
J F Ditunno, J W Little, A Tessler, and A S Burns. Spinal shock revisited: a four-phase model, Spinal Cord (2004) 42, 383–395. doi:10.1038/sj.sc.3101603 Published online 23 March 2004
Atkinson PP, Atkinson JL. Spinal shock. Mayo Clin Proc. 1996 Apr;71(4):384-9.