The first 2 articles in this issue are about some basic science concepts that have clinical applications. The first is by Mammis et al from the United States on erythropoietin—which not only serves as a red cell production stimulator, but also has neuroprotective effects in animal models. The authors review the macro- and microscopic events that occur in traumatic brain injury and the associated cellular and molecular changes that occur. Then, they briefly summarize the evidence for the action of erythropoietin as a neuroprotective agent, and suggest that the molecule may be ready for clinical testing. In his comments on the article, Dusick at the UCLA Brain Injury Research Program, provides a perspective on why clinical studies of promising agents do not work, with some speculation on how the treatments of brain injury will evolve in the future. I have written a brief introduction to this article to help the reader understand the concepts.
The next article is by Hokari et al from Japan who examine the physiologic events that lead to infarction in the brain using positron emission tomography (PET) scanning and single-photon emission computed tomography (SPECT) scanning methods. Their study helps us predict those patients who have a higher risk of cerebral infarction. Using patients with severe carotid or middle cerebral stenosis or occlusion, the authors identified those patients with regionally decreased cerebral blood flow (CBF) and reduced cerebral vascular reserve (CVR) to acetazolamide challenge. The CBF and CVR are measured using the SPECT imaging system. With a PET scanner, they identified those patients with an elevated oxygen extraction fraction (OEF). These patients with increased OEF had a 10.6% annual risk of developing an infarction in the compromised region compared with those who had normal (OEF). So, those patients in whom a brain region had diminished CBF and increased vasodilatation (CVR), but who were under metabolic stress requiring more oxygen extraction from the diminished blood flow, were at risk of infarction. So, by using SPECT, and in this case, PET scanning, we can now determine those patients at higher risk for infarction. This is an excellent study. Read the comments at the end.
Nakamura et al from Japan describe an interesting case to follow the article above in which they used near infrared spectroscopy to determine regional brain ischemia transcutaneously. The technology involves the emission of a narrow spectrum of near-infrared light that penetrates the skull and the brain tissue to be absorbed by the oxygenated hemoglobin. The remaining light is reflected off the brain tissues at a depth of 1 to 2 cm, and then—as it passes back through the skull to the scalp detector—is measured by a sensor that transmits the information to a computer. The computer, with a predetermined program, measures the oxygen saturation of the blood from the region penetrated by the light. The authors compared 2 technologies: first, the INVOS system, in which a single sensor was placed over the frontal lobe, and second, a system using multichannel emitters and detectors from the frontal to the parietal region. The multichannel detector was able to reveal ischemia in the parietal region that the static sensor could not detect frontally. They used these systems in doing a carotid endarterectomy. I have used the single detector system in carotid endarterectomy and it is far more sensitive than electroencephalogram monitoring and did register drops in cerebral oxygenation in the patients I operated. It is very sensitive to decreases in oxygen saturation. It is reasonable that the single sensor cannot detect events that occur beyond the area sampled by the sensor. The multichannel system allows a wider area of sampling. I have not used the multichannel system. The technology is excellent for use in carotid endarterectomy. I would not do a case without it.
The article by Dashti et al from Finland and “The Rainbow Team” describes their experience using indocyanine green video angiography during microsurgery of intracranial aneurysms to determine the patency of the major vessels to and from the aneurysm. I have written a brief editorial on the history of occlusion of aneurysms by clips and what can be done to determine if the proper placement of clips is being performed in countries all over the world.
Strutt et al from the United States analyzed the cognitive decline in patients who had a unilateral pallidotomy. Although some of the cognitive decline can be explained by a natural progression of the disease, other features of the neurocognitive decline are apparently related to the effect of the pallidotomy itself.
Chen et al from China report that with 16-slice CT angiography, the detail of cerebral aneurysm morphology and 3-dimensional anatomy can be shown as well as by conventional subtraction angiography.
Is non aneurysmal perimesencephalic or non-perimesencephalic subarachnoid hemorrhage (SAH) a benign disease? Gupta et al from India studied 61 patients whose initial presentation did not reveal an aneurysmal cause of SAH. The authors waited 6 weeks to repeat angiography and found that 2 patients had aneurysms. An additional 7 patients died while waiting for the second angiogram. No autopsies were performed to determine the cause of death in these patients. So was an aneurysm missed in these cases? We do not know. One lesson from this study is to perform a second angiogram within a shorter time after the initial bleed. Seven days is the time I usually use. The other conclusion is that if a patient survives until a second angiogram—performed 6 weeks after the initial bleed—94% of those patients with non-aneurysmal SAH have a good recovery.
Cansever et al from Turkey have performed an experiment in rats to determine which blood component causes vasospasm. The authors found that arterial blood, arterial vessel homogenate, or both together, had a significant vasospastic effect. Venous blood and venous vessel homogenate did not have the same effect on the blood vessels of the brain. As Macdonald indicates in his comments, this experiment provides further encouragement to investigate the differences seen by the authors.
Tanriover et al, working with Rhoton, have described an elegant approach to the internal acoustic meatus through the middle fossa. As the authors describe, there is a posterior fossa approach to this region, a trans-labyrinthine approach, and a middle fossa approach that has fallen in to disfavor because of its complications. The authors use anatomical dissections in cadavers to develop a middle fossa approach that logically avoids those complications. This is another example of Rhoton's influence that provides anatomically- based logic to surgical approaches to achieve success. The authors are to be congratulated for their work.
Cappabianca and Magro (editorial), and Malkasian (commentary) have written their thoughts on the importance of anatomy in developing surgical approaches for the readers.
Hauck and Samson from the U.S. report an interesting case of an A1-A2 anterior cerebral artery interposition vein graft they used after removing a giant aneurysm of the anterior cerebral artery. In our report, in 1986, we had not performed this surgical option in patients, but had done this type of interposition grafting in cadaver experiments. The authors, experience in approaching this challenge and in their use of a vein graft are good contributions for others to know if they encounter such a problem.
Surdell et al from the U.S. report the use of an endovascular expanding stent to treat a patient with intracranial carotid artery dissection.
Matsumura et al from Japan describe a simple method of training neurosurgeons and others to perform microvascular anastomosis without using animals. It is a useful first step in learning this technique.
July et al from Canada describe the value of using awake craniotomy to resect brain tumors particularly in resource-restricted countries of the world. This concept applies to developing and developed countries alike.
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