C5 Syndrome

For patients who undergo cervical myelopathy/radiculopathy surgery,  surgeons always have concern for developing the so called C5 Syndrome.   Some patients do wake up with weakness to the deltoid and biceps muscles.  Typically, however,  patients will not experience the weakness for a few days after the surgery.  You can imagine the concern for both the patient and the surgeon.   A deteriorating neurological situation is an emergent situation.  Usually,  a workup,  with diagnostic imaging is initiated soon after discovery of the weakness.

But,  in the C5 syndrome,  usually,  there is no evidence of any direct neural compression on the diagnostic studies.  In addition,  neuro diagnostic studies such as EMG/NCV’s are inconclusive to the cause of the C5 syndrome.

The cause of this C5 Syndrome has yet to be well defined.  But,  most agree the vast majority of the isolated upper extremity weakness will be associated specifically to the C5 nerve, and corresponding muscle groups.

There is some thoughts to the following scenarios:

1. C5 nerve injury during surgical unroofing of the nerves.  The nerves may also be kinked by shifting bone windows in the so called laminoplasty procedures.  Usually,  the patients do have identified weakness immediately after surgery.   While this explanation may explain patients with a posterior laminectomy approach,  it is difficult to explain for anterior discectomy patients as it is rare to directly expose any of the nerve roots with the anterior approach.

2. C5 nerve root tethering after posterior shifting of the spinal cord after decompression.  Some anatomic studies suggest the C5 nerve is shorter than other nerves.  In addition,  the C4-5 facet joint is more anterior than other joints,  so the cord, and the nerve is oriented more anteriorly before decompression.  After posterior decompression,  the cord does orient more posteriorly.  In that more posterior orientation,  the C5 nerve will act as a tether,  thus causing stretch of the nerve.  This may explain the subsequent development of C5 nerve manifestations.  Again,  this does not explain the C5 Syndrome in anterior surgery.

3.  Spinal Cord ischemia by the tethering effect of the radicular artery to the spinal cord.  Similar to the C5 nerve tethering effect above,  the radicular artery associated with the C5 nerve root, and C5 spinal cord area can be compromised by the tethering effect.  A transient spinal cord ischemia may explain the temporary loss of C5 nerve function.

4. Segmental spinal cord disoder.  Some patients with C5 syndrome have evidence of signal intensity changes on MRI imaging of the C5 areas.  While this scenario may be possible,  it does not adequately explain the unilateral findings on most C5 Syndromes.

5.  Reperfusion Injury of the spinal cord.    Paradoxically,  rapid reperfusion with oxygenated cells may be associated with increased cellular injury,  and decreased perfusion.

Certainly,  these scenarios continue to be investigated,  and conflicting studies have draw conclusions on the validity of the theory.

What we do know is that the vast majority of the C5 syndromes are temporary,  with almost complete return of nerve function for the vast majority of patients.  Still,  surgeons always have concerns about the development of the C5 syndrome, as it has been reported in up to 5% of patients who had cervical myelopathy surgery.  If you have cervical surgery,  please understand this is a concern,  although the vast majority of patients recover with little residual deficits.

Last modified: January 5, 2018