Ron Pawl, Surgical Neurology's Editorial Board expert on pain and spine surgery, reviewed 2 articles published in The Spine Journal in Volume 7 for September-October 2007. The first article states that preoperative psychological assessment can reveal patients who will have poor outcomes from spine surgery. Ron discusses the tests that can be used to identify these people. The second article reported on the different complications and charges that occur across the United States from lumbar fusions. The use of lumbar fusion was 50% higher in one part of a state compared with that in another area. In the United States, back surgery is performed 5 times more commonly than in England and Scotland. In 10 years, from 1992 to 2003, lumbar fusions rose from 14% to 47% of spine surgeries. Even with degenerative spondylolisthesis, simple laminectomy resulted in good outcomes in more than 80% of the patients. Read Ron's editorial. It is probably the most useful message about spinal surgery you will read. The economic incentives to do more complex surgery are driving the market and the spine surgeons. We understand that. Most will ignore these warnings, but that will be a strategic mistake. (Remember that I told you so.) Note that the insurers also read the same studies and will come to the same conclusions Ron did. Ron and the articles he reviewed provide compelling evidence that the strategy for the future is to establish an integrated back, neck, and limb pain center—with multiple disciplines involved—to evaluate and treat the patient. With that strategy, you cannot lose regardless of what the government or insurers do. The patient will always be yours.
I am sure that many of you, as I, have wondered about the scientific progress being made in spinal cord regeneration. The following 2 articles provide good insight into the problems and a view of what is being done to understand spinal cord injury.
Karaoglan et al from Turkey performed a very nice experiment to study the histological damage after spinal cord injury, the number of dying cells that are found at the injury site, and the functional recovery of the animals. It is an easy article to read and provides a nice summary of what is happening histologically, molecularly, and functionally. After spinal cord injury, it is presumed that signaling molecules turn on genes that produce proteins called capsases. The capsases lead to a series of biochemical events that produce programed cell death. The Ac.YVAD.cmk molecule, which the authors used to treat the animals, inhibits the capsases and thus prevents cell death. In this experiment, the authors showed that, histologically and functionally, the rats treated with this molecular capsase and cell death inhibitor had better outcomes than the controls without the treatment. In addition, the treated animals had less dying cells at the injury site. This is an excellent article to read and serves as a nice introduction to the following article on spinal cord injury by Shields et al. Both articles point to a future when this problem will be better understood with more treatment options than in the past.
Chris Shields and his colleagues in the United States have one of the leading centers in research on spinal cord injury and recovery. In the introduction to their article in this issue, Shields et al described that there are molecular factors released after the injury that are both growth inhibitory and growth promoting to axons. The authors used an enzyme chondroitinase, which degrades various inhibitory factors known as chondroitins. There are also other inhibitory molecules of different types. The authors found that the administration of chondroitinase did reduce the inhibitory chondroitins at the site of the injury and allowed some axonal growth across the lesion site compared with controls. The comments at the end of the article are complimentary. The article is an example of the complexity of this area of research, and that progress in it is slow. I suggest that you read the Introduction and the Discussion sections to get a nice review of the work in this area. The experiment is well done. This and the preceding article are very good.
Oka et al from Japan have reviewed their experience with arterial dissection in the carotid territory. In their 6 cases, they divide the events into acute with a significant deficit, a single attack with a mild outcome, and a dissection that produces multiple attacks of ischemia. They suggest that an extracranial-intracranial (EC-IC) bypass would be of value in the last category—those with a progressing disease. One of the 2 cases they bypassed recovered. The other progressed so fast that the patient could not benefit from surgery. This is a nice report of a difficult problem to treat. Two thoughts come to mind. Firstly, the collateral circulation from other parts of the brain will be a significant factor in determining the outcome in these patients; however, embolizaton from the site of dissection can occur. Secondly, the potential for interventional therapy in which a stent is placed at the site of the dissection may offer the best treatment option in the future.
Hori et al from Japan have written a very interesting article analyzing the histology of the carotid bifurcation. What they found was that there is a transition from the elastic common carotid artery to the muscular internal carotid artery. The transition zone spans the area of the carotid bifurcation. Why carotid plaques form at these transition zones is not known. The formation of plaques is believed to be part of an inflammatory process. Biochemically, the monocytes are attracted to the endothelium by molecular signaling agents. The monocytes then migrate farther into the media of the vessel wall where they remain as macrophages. The macrophages then engulf the cholesterol lipid molecules that are circulating in the blood and diffusing into the vessel wall. These fat-laden macrophages accumulate cholesterol lipids, enlarge, and form a plaque. In this article, the authors described the location of the plaque at this transition zone from the elastic to the muscular artery. We do not know why the plaque locates at this area biochemically. The authors postulate that physical factors, such as wall shear stress, will cause the plaque to be formed at this location. This is an interesting article to read.
Kubo et al from Japan reported on the molecular events that occur in the endothelial side of the blood vessel in subarachnoid hemorrhage (SAH). What they found was that an inflammatory process occurs that is similar to that reported in the previous article on carotid plaques. SAH triggers the appearance of molecules that protrude from the endothelium and capture the circulating inflammatory cells. Then, another set of molecules attaches these inflammatory cells to the endothelium, so that the cells can migrate into the blood vessel wall. The first set of molecules that attract the inflammatory cells are called selectins, and the adhesion molecules are called intercellular adhesion molecule (ICAM). Compared with the controls without SAH, the ICAMS were increased in the SAH patients and were found in even higher amounts in patients who developed delayed ischemic deficits (DID) or delayed ischemic deficits. In addition, C reactive protein, a marker of inflammation, was also increased in SAH and in DID. The selectins did not appear to change in any of the groups. This is an interesting article. Its clinical use will take some time to be developed, but as in the previous article, they indicate the molecular level to which neurosurgery is going. There is work being done in atherosclerosis to stop the inflammation process and also in SAH and vasospasm at the molecular level. This is the future.
Wang et al from Taiwan have written about their experience in improving pedicle screw placement for fusions. The authors used image guidance at each vertebral level to locate the pedicle and to make certain the screw placement was accurate. Their system worked correctly in more than 99% of the cases. To me, the interesting statistic was that with manual screw placement, 14% to 42% of the pedicle screws penetrated the cortex of the pedicle bone. With image guidance, the figure declined to 3% to 8%. Obviously, even this low percentage of complications is not acceptable. It appears from this article that better screw placement can occur with the use of image guidance at each vertebral level.
Cansever et al from Turkey reported on their experience with cavernomas of the spinal canal over a 5-year period; 3 were intramedullary, 1 extradural, and 1 intradural but extramedullary. They advocate total surgical removal. Patients can be worse after surgery, but will improve later. Professor Zhou from Shanghai, China, has had the same experience with 15 similar lesions in 20 years. In my experience with cavernomas in the brain stem and spinal cord, it is important to reduce the size of the cavernoma by coagulation, so that the cavernoma is “shrunk” (reduced in size) from the surrounding tissues. This surgical technique, done with a Malis irrigating bipolar, reduces the transmission of electric current to the surrounding tissue and allows easier removal of the cavernomas. In addition, the use of a 0.5-mm tipped bipolar forceps allows pinpoint coagulation for small lesions in very difficult locations.
Zakaraia et al from Malaysia compared 2 different treatments of chronic subdural hematomas (CSDH). Burr holes were placed in all patients. In one group, a catheter was left in the subdural hematoma (SDH) space and attached to gravity drainage. In the second group, the SDH cavity was irrigated between both burr holes, and a catheter was left for drainage. There was no difference in the outcomes of either group. There are many myths about CSDH treatment. I suggest that you read the article by Sambasivan on his experience in treating 2300 CSDH (Surgical Neurology. 1997;47:379). He used a small temporal craniectomy, washed out the SDH, and left the dura open with the subdural space communicating with the subtemporal area. A subdural drain was left for 24 hours, and the patients were hydrated post operatively with 2000 mL of 0.5% saline to help obliterate the space. If there were membranes, he opened both. He had a significant reduction in recurrence of the hematomas and 0.5% mortality.
Inoue et al from Japan reported on their experience in reopening occluded common carotid arteries in 2 patients. In my experience, if the common carotid is occluded as these authors reported, it is important to do a detailed angiographic examination with delayed runs to demonstrate reflux from the vertebral artery to the external carotid and then through the bifurcation up the internal carotid to the head. Because the flow through these channels is slow, the internal carotid can only be seen on the delayed images. It is important to note the size of the internal carotid artery. If it appears normal, then there is an excellent chance that the removal of the common carotid obstruction will provide good flow to the internal carotid artery. However, in some cases, the internal carotid artery becomes narrow probably from recanalization of a previous occlusion, and in this case, the revascularization of the common carotid and internal carotid will not produce high flows.
Agrawal et al from India described their experience providing neurosurgical help to Nepal. They described the conditions that exist and what they did to improve the care. This article completes the span of this issue of the journal from the advanced molecular reports as in the articles on spinal cord injury and vessel and inflammatory cell factors in SAH to those areas of the world with primitive neurosurgery. There is no end to the opportunities available in medicine from helping those in need to the more sophisticated biological research. Both are advancing the frontier of medicine. Where will we be 100 years from now in regard to spinal cord injury and neurosurgery in Nepal?
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