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Laurance Johnston, Ph.D.

Sponsor: Institute of Spinal Cord Injury, Iceland



Surgical decompression of the spinal cord is often carried out soon after injury and, in some cases, long after injury. Basically, with this surgery, various tissue or bone fragments that compress the spinal cord and, in turn, compromise cord function are removed. Depending upon the injury’s unique circumstances, decompression can be accomplished by a variety of surgical approaches, including, for example, approaching the compressed cord from either the front (anterior) or back (posterior).

Acute Injury

Although animal studies consistently suggest that spinal-cord decompression soon after injury minimizes neurological damage, human studies have been more ambiguous, i.e., some studies suggest benefits and others do not.  Results seem to depend upon numerous factors, such as the nature of the injury, the timing of the surgery, and specific outcome measures.

Earlier studies, including those carried out by some of the pioneers of modern SCI medicine, suggested that conservative, non-surgical approaches (e.g., postural techniques,  bed rest, etc), were the best way to fuse the injured spine and would avoid exposing the patient to surgery-associated risks and neurological complications.

However, as spinal surgery became more sophisticated over time, minimizing its downside, the pendulum increasingly swung towards the widespread use of surgical decompression in acute SCI.

There has been a plethora of studies attempting to address the effectiveness of surgical decompression. For example, Dr. Stephen Papadopoulos et al (USA) concluded that “immediate spinal column stabilization and spinal cord decompression…may significantly improve neurological outcome.”  In their study, 91 consecutively admitted patients with acute cervical injuries were prospectively evaluated. Of these patients, 66 had potential spinal-cord compression assessed by magnetic resonance imaging (MRI); if present (54% of patients), they underwent immediate surgical decompression and stabilization. For a variety of reasons, 25 patients were treated outside of this protocol (i.e., no surgical decompression) and served as a reference group.

The protocol-treated group fared better than reference patients on several criteria. For example, 50% of protocol patients improved from their initial Frankel grade compared to only 24% of reference patients (Like the ASIA scale, Frankel scale ranges from grade A, representing complete injury, to grade E, normal function). In addition, eight protocol, but no reference, patients improved from complete motor quadriplegia to independent ambulation. Finally, the protocol patients needed less intensive-care and hospital time.

Using a meta-analysis approach, a number of recent review articles have attempted to provide a big-picture assessment of the many decompression studies published over the years. Although these articles do not provide a thumbs-up or -down recommendation for the use of decompression surgery in acute SCI, cumulative evidence suggests that the procedure 1) does not increase the complication rate after acute SCI, as suggested in earlier studies, 2) provides benefit for certain types of injuries, and 3) reduces the time spent in intensive care. Because definite data indicating its superiority over conservative-management approaches are lacking, the procedure should be considered a valid practice option but not a standard of care.

In 2010, Dr. Michael Fehlings and associates (USA) published the results of a prospective survey, which asked 971 spine surgeons about the timing of their surgical decompression procedures after injury. Eighty percent preferred to decompress the spinal cord within 24 hours. In the case of complete and incomplete cervical injury, 46% and 73% would operate within six hours, respectively.

Apoptosis Inhibition: A compressed cord compromises spinal-cord cell viability by many potential mechanisms, including triggering apoptosis, a form of post-injury neuronal cell death in which a programmed sequence of events leads to cell elimination. This possibility was evaluated by Dr. Kan Xu and colleagues (China) in rats with an experimentally induced compression injury. Their results suggested that decompression reduces the number of neuronal cells dying from such a mechanism.  

Hypothermia Influence: As discussed later, cooling procedures may preserve some neurological function after injury. In animal studies, Dr. Peter Batchelor et al (Australia) demonstrated that cooling can also expand the time period in which surgical decompression remains effective. This is important because neurosurgeons generally believe that more function can be preserved if the cord is quickly decompressed; however, the desired timeliness can not always be achieved for a variety of logistical and other reasons.

After creating a compression injury in rats, the investigators cooled half of the animals to 33o C starting 30 minutes after injury. After 7.5 hours of cooling, decompression was carried out. Eight weeks later, functional recovery and preservation of spinal-cord tissue in the cooled rats were compared to the control rats whose body temperature was maintained at a normal level. Functional recovery was assessed by the commonly used BBB scale, which measures recovery of hind-limb function on a scale from 0 (no hind-limb movement) to 21 (normal walking).  The rats that had been cooled before decompression regained more function (9.5 BBB score) compared to the controls (5.3 BBB score). In addition, the amount of injury-site tissue spared was greater in the cooled rats. The investigators concluded that “hypothermia may be a useful bridging therapy to prevent neurological decline prior to decompressive surgery.”

Chronic Injury

As reviewed by Dr. Wise Young (New Jersey, USA), some studies suggest that delayed surgical decompression, even long after the acute injury phase, can produce some restored function.

The potential beneficial influence of such decompression is, however, a confounding factor in interpreting the results of new function-restoring SCI therapies that are emerging throughout the world. Specifically, if the supposed function-restoring intervention (e.g., cell transplantation) is structurally affecting the cord’s injury site, it may be relieving some of the compression caused by the injury. As such, it may be difficult to attribute any regained function to the intervention alone; it may be just a consequence of the decompression and the ensuing enhanced flow of blood and cerebrospinal fluid.

Dr. Henry Bohlman (photo) and colleagues (Ohio, USA) have published a number of studies suggesting that decompression may be beneficial for patients with SCI who are beyond the acute phase of injury.

One of their studies focused on patients with incomplete, cervical injuries. In these patients, myelography (a form of x-ray examination using an injected dye) was used to determine whether bone or vertebral disk fragments were compressing the spinal cord’s anterior side. If so demonstrated, the compression was alleviated through anterior-decompression surgery followed by stabilization using iliac bone grafts. The time between injury and decompression averaged 13 months (range, one month to nine years), and patients were followed on average six years (range, 2-17 years). Of the 55 followed patients, 29 became functional walkers, and 39 recovered additional upper-extremity function. Only nine regained no motor function. In general, the more time that had elapsed since injury, less improvement accrued.

A similar study focused on patients with complete quadriplegia. In this study, the injury-to-decompression time averaged 15 months (range, one month to eight years), and patients were followed on average five years (range, 2-13 years). Of the 46 followed patients, seven improved at least two functional levels, and 18 improved one level. No motor improvement was noted in 20 patients. Once again, more benefits were obtained by patients who were decompressed sooner after injury.