Cervical Disc Disease, Part 3: Cervical Spondylotic Myelopathy

In the last post I discussed cervical radiculopathy in which one or more nerve roots are affected by cervical degenerative disc disease (DDD) and spondylosis.  I explained that while we don’t fully understand the natural history of cervical radiculopathy most patients get better without surgery.  Surgery for cervical radiculopathy truly is elective barring severe pain or progressive weakness.  In this post, the final post in the cervical disc disease series, I’ll discuss cervical spondylotic myelopathy (CSM) which as you’ll see is a much more urgent problem.   In contrast to radiculopathy in which only nerve roots are compressed or injured, myelopathy refers to compression and injury of the spinal cord.  

As I mentioned in a previous post, degenerated cervical discs will dry out, collapse and lose height.  This leads to disc bulging and bone spur formation in front of the spinal cord as well as buckling of the ligamentum flavum behind the spinal cord.  Also, the facet joints behind the spinal cord degenerate which leads to bony overgrowth (the spondylosis of spondylotic myelopathy).  All of these factors lead to circumferential narrowing, or stenosis, of the cervical spinal canal, which in turn leads to compression and injury of the spinal cord (see figure 1).  The constant jarring and movement of one’s spinal cord within the spinal canal throughout the day exacerbates the injury.  This injury is seen as high signal within the spinal cord on MRI (see figure 2).

The true cause of spinal cord injury in CSM is still largely unknown.  Grossly, we see severe loss of neurons in the grey matter as well as degeneration of the white matter of the spinal cord.  This is similar to what would be seen if the spinal cord experienced a period of time in which it wasn’t getting enough blood/oxygen, i.e. your spinal cord having a stroke.  In fact, microscopic studies of spinal cords with CSM show microscopic destruction to the blood vessels that supply the spinal cord with oxygen.  This lack of oxygen then triggers a cascade of “secondary” insults such as inflammation and cell death that leads to more cellular damage.  These secondary insults can persist after surgical decompression although they are slowed somewhat.   

The natural history of CSM is also unclear.  A recent comprehensive analysis of studies on CSM states that 20%-62% of patients will have neurological deterioration with CSM.  This is quite a wide range and indicates the diversity in the quality of data that has been published on the subject.  If you look at that same data you’ll also see that 50-60% of patients will either remain stable or will improve slightly.  So in essence, if you’re diagnosed with CSM there’s a 50/50 chance that you’ll deteriorate neurologically.  Those are the odds that you must consider when considering surgery to decompress your spinal cord.  

Ligamentum flavum buckling  Google Search 1

Figure 1: An axial view of the spinal canal (note, this is a lumbar vertebra and is only used here to demonstrate anatomy.)  On the left, there is no narrowing of the spinal canal and it contains a normal diameter spinal cord (in green).  On the right, the spinal canal is severely narrowed by facet joint overgrowth, disc bulging and buckling of the ligamentum flavum (seen here in yellow.)  Note the severe compression of the spinal cord (in red). (adapted from  Kim DH, Albert TJ: Interspinous Process Spacers. J Am Acad Orthop Surg. April 2007 ;15:200-207.)

Estes Charles J MR MRI CERVICAL SPINE WITHOUT CONTRAST  Wind

Figure 2: Sagittal MRI of a patient with CSM.  Note the high signal in the spinal cord indicating ongoing spinal cord injury (red arrow).  

If some patients deteriorate while some don’t how do you make the decision to proceed with surgery?  Well, there are a lot of smart people working on this exact question.  Here’s what we know:  we know that the cellular destruction that occurs in CSM, once it’s triggered, will likely progress.  We also know that except in cases of mild CSM, conservative management such as physical therapy doesn’t slow the patient’s neurological decline.  Finally, we know that patients with a longer duration of symptoms or those with severe symptoms are more likely to deteriorate.  Patients with CSM will typically present with weakness and decreased dexterity in their hands, balance difficulties, difficulty walking and urinary disturbances.  I would argue that if you have any of these more advanced symptoms (versus, say, occasional numbness in your hands) you’re already at the stage where your symptoms are “severe” and you will likely worsen.  In these cases I boil it down for my patients like this: your neurological function is only as good at is now and it will likely continue to deteriorate if your CSM is left untreated.  Because of this, CSM is one of the few spinal conditions for which I am aggressive in recommending surgery as the first and only treatment.

J. Alex Thomas, M.D.

Sources: 

1)Karadimas SK, Erwin WM, Ely CG, Dettori JR, Fehlings MG: The Pathophysiology and Natural History of Cervical Spondylotic Myelopathy. Spine (Phila Pa 1976):2013 Aug 16 Epub ahead of print.

2)Matz PG, Anderson PA, Holly LT, Groff MW, Heary RF, Kaiser MG, et al.: The natural history of cervical spondylotic myelopathy. J Neurosurg Spine 11:104–11, 2009. 

 

 

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