Spinal shock after acute spinal cord injury
Spinal shock is a temporary loss of spinal cord function below an acute injury: the limbs start floppy with absent reflexes, then become stiff with exaggerated reflexes.
Remember
Spinal shock begins with floppy, weak muscles and absent reflexes below an acute cord injury, then over days to weeks it turns into the upper motor neurone picture of raised muscle tone and exaggerated reflexes.
Spinal shock follows an acute injury to the spinal cord that damages the upper motor neurone pathway (the damage that later gives raised tone and exaggerated reflexes). It occurs immediately after the injury and can last days to weeks.
In the first phase the reflex circuits below the injury go quiet. That gives flaccid paralysis, where the muscles are floppy and weak with no tone, and areflexia, where reflexes are absent. The paralysis affects the whole of the body below the level of the injury, and is not limited to the distal muscles. A complete transection (a cut right through the cord) is the classic cause of spinal shock: the cord below the cut is cut off from the brain.
That early picture mimics lower motor neurone damage (the peripheral kind), even though the injury lies in the upper motor neurone pathway. It is a common trap to read the early floppy phase as proof of lower motor neurone damage.
Over the following days to weeks, muscle tone rises (hypertonia) and reflexes become exaggerated (hyperreflexia), the classic upper motor neurone picture. The mechanism is not fully understood. It is related to neuroplasticity (the nervous system rewiring itself), here in the spinal cord.
Key facts
- Cause
- an acute injury to the spinal cord that damages the upper motor neurone pathway, with a complete transection as the classic cause.
- Early phase
- flaccid paralysis with absent reflexes below the injury.
- Later phase
- hypertonia and hyperreflexia, the classic upper motor neurone picture.
- Duration
- it can last days to weeks.
- Paralysis
- the paralysis affects the whole of the body below the level of the injury, and is not limited to the distal muscles.
- Mechanism
- not fully understood, but related to neuroplasticity in the spinal cord.
Exam traps
- Spinal shock does not begin with spastic paralysis and exaggerated reflexes, because the early state is flaccid paralysis with absent reflexes; raised tone and brisk reflexes appear only later.
- Reflexes are not preserved from the onset of spinal shock, because they are lost at once and come back exaggerated later, as the tone rises.
- Persistent flaccid paralysis with areflexia would suggest lower motor neurone destruction, but the flaccid, areflexic phase of spinal shock is temporary and gives way to hypertonia and hyperreflexia.
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