Neurosurgical forum Letters
to
the
editor
On the Subject of Double Publication To THE EDITOR: We have long regarded the Journal of Neurosurgery as an interesting and alive journal with strong clinical relevance and high standards. Natura21y with our hospital's high proportion of accident and emergency cases, we have a special interest in articles that bear on trauma and its outcome. We therefore read with particular attention the article by Wilberger, et al. (Wilberger JE Jr, Harris M, Diamond DL: Acute subdural hematoma: morbidity, mortality, and operative timing. J Neurosurg 74.'212-218, February, 1991). However, the work seemed familiar. On further investigation, the material appeared to be the same as that in an article published in the Journal of Trauma) We find an extensive similarity between these two articles. They appear to be published from the same data base with very little difference. We are very concerned that this appears to be multiple publication. Apart from damaging the reputation of your journal, we object to the waste of resources which duplication causes and the waste of time which is imposed on all interested in the field. R. CAPFS,M.D. W. J. RUSSELL,M.D. Adelaide Hospital Adelaide, South Australia Reference 1. WilbergerJE Jr, Harris M, Diamond DL: Acute subdural hematoma: morbidity and mortality related to timing of operative intervention. J Trauma 30:733-736, 1991 RESPONSE: The concerns raised by Drs. Capps and Russell are serious ones that deserve appropriate response. As best as we can dctermine at this point in timc, this appears to havc occurred through a seriesof misunderstandings and miscommunications, for which the authors must assume primary responsibility.As the correspondents correctly point out, the data base for these two articles is indeed similar. However, the Journal of Neurosurger): article has significantly more information; additional data are presented, statistically analyzed, and evaluated. In this context we feel that the Journal of Neurosurgery article gives the neurosurgical reader a better opportunity to critically review and potentially validate or refute the data. Nevertheless, we apologize to these fine journals and their readers for what Drs. Capps and Russell, not inappropriately, term a "waste of resources and time." JACKE. WILBERGER,JR., M.D. Allegheny General Hospital Pittsburgh, Pennsylvania
.I. Neurosurg. / Volume 76/April 1992
EDITORIALCOMMENT:The issue of "double publication" is not taken lightly by the Journal of Neurosurgery. Currently, we receive well over 1000 manuscripts per year and we can publish only a very small portion of these. Accordingly, many very fine contributions must be declined, simply due to lack of space. Space limitations are imposed because of the cost of publishing the Journal of Neurosurgery and the feedback from our readership that they want a carefully edited journal, rather than one of great length. It should be clearly understood by our contributors that double publication is not acceptable. This is the policy followed by all major medical journals today. Had this Editor been informed of the earlier publication, this manuscript would have been rejected out of hand, irrespective of the value of its content. The question about the current article of the Journal of Neurosurgery presenting significantly more information is a matter of opinion, and will be dependent on the eye of the beholder. To the Editor, there does not appear to be a significant difference between these two contributions, and other members of the Editorial Board felt likewise. The Journal of Neurosurgery is extremely proud of the reputation it has earned throughout the neurosurgical and neuroscientific communities worldwide. The Editor and the Editorial Board will remain devoted to presenting original and unpublished work of substantial significance to our community. Exceptions to these fundamental criteria will not be made. Authors interested in publishing in the Journal of Neurosurgery are asked to keep this fact firmly in mind and not ~vary from the midline." THORALF M. SUNDT,JR., M.D. Editor, Journal of Neurosurgery Rochester, Minnesota
Posttraumatic Secondary Spinal Cord Trauma To THE EDITOR: WC read with interest the review article by Drs. Tator and Fehlings (Tutor CH, Fehlings MG: Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 75.'15-26, July, 1991). The authors state that Chehrazi, et al., 1found no reduction in spinal cord blood flow in cats after cord injury produced by the weight-drop technique. Elsewhere they imply that our study is one of the few that failed to support the vascular theory because we did not find evidence of posttraumatic ischemia. In fact, utilizing the H2 clearance technique, we did demonstrate a significant drop in the regional spinal cord blood flow after an initial transient increase) This delay in the onset of the posttraumatic white matter 723
Neurosurgical forum ischemia has been well known. 2 Our study, however, does not lend support to the theory of secondary injury from posttraumatic spinal cord ischemia because we found no improvement in the outcome of the animals in which we maintained posttraumatic regional spinal cord blood flow at or above baseline by spinal stimulation. We concluded that amelioration of the posttraumatic ischemia is of no benefit and that this ischemia may be an epiphenomenon of injury. I hope these comments are useful in clarifying our experimental findings. B. BARRYCHEHRAZI,M.D. University of California. Davis, Medical Center Sacramento, California
References 1. Chehrazi BB, Scremin O, Decima EE: Effect of regional spinal cord blood flow and central control in recover)' from spinal cord injury. J Neurosurg71:747-753. 1989 2. Senter HJ, Venes JL: Altered blood flow and secondary injury in experimental spinal cord trauma. J Neurosurg 49:569-578, 1978
RESPONSE: Dr. Chehrazi has quite correctly identified our misinterpretation of their data on posttraumatic spinal cord blood flow. In our review article we should have included the paper by Chehrazi, et al., among the many studies demonstrating posttraumatic ischemia of the spinal cord. They showed that spinal cord blood flow declined to about 60% of normal 5 hours after a weight-drop injury in cats. It should be noted that this reduction is much less severe than in any of our studies of severe spinal cord injury. The authors are grateful to Dr. Chehrazi for clarifying this matter and apologize for our misinterpretation of his data. Dr. Chehrazi's letter also comments on the significance of posttraumatic ischemia and the therapeutic value of treatment to restore spinal cord blood flow. Our paper reviews this point extensively, and concludes that the balance of evidence indicates that severe posttraumatic ischemia is of major importance and that efforts to elucidate the exact pathophysiology of this secondary mechanism of injury should continue. It is our thesis that further knowledge of the molecular and biochemical events causing posttraumatic ischemia will lead to better ways of counteracting the ischemia and to enhance recovery of patients with acute spinal cord
Eosinophilia Following Shunting To THE EDITOR: The recent article by Tung, el aL, regarding cerebrospinal fluid (CSF) eosinophilia in shunted hydrocephalic children (Tung H, Raffel C, McComb JG: Ventricular cerebrospinal fluid eosinophilia in children with ventriculoperitoneal shunts. J Neurosurg 75:541-544, October, 1991 )brought to mind two recent patients on our service. Both had initial shunts placed within the first months of life, with baseline normal CSF profiles and cell counts. Both patients received the routine single 4-mg dose of intrathecal gentamicin at the time of shunt placement, as did the patients in the paper by Tung and colleagues. Within the first few days after shunt surgery, both developed low-grade fever and were found to have elevated CSF white cell counts with marked eosinophilia (53% and 50%), as well as elevated CSF protein levels. Neither had intraventricular hemorrhage. All cultures and stains for bacteria, fungus, and tuberculosis were negative. The cell counts, protein levels, and proportion of eosinophils returned to normal over several weeks. Cerebrospinal fluid eosinophilia has been reported after intrathecal administration of gentamicin.~ Could it be that our patients, as well as some of the those in Dr. Tung's series, have shown a reaction to the gentamicin? The correlation between the number of shunt operations and the finding of eosinophilia could be related to a dose-dependent or exposure effect. Alternatively, the probability of discovering a transient eosinophilia induced by the drug would be increased if the shunt coincidentally malfunctioned while the cell count was elevated. Finally, the drug reaction itself and the inflammatory pleocytosis so induced could increase the risk of shunt obstruction. In either case, the fact that the eosinophilia resolves spontaneously in these eases suggests that a temporary stimulus, rather than an ongoing process such as a reaction to the shunt material itself, may be responsible. ANN-CHRISTINEDUHAIME,M.D.
Children's Surgical Associates, Ltd. Philadelphia, Pennsylvania
Reference 1. Mine S, Solo A, Yamaura A, et al: Eosinophilia of the cerebrospinal fluid in a case of shunt infection: case report. Neurosurgery 19:835-836, 1986
injury.
CEARLESH. TATOR,M.D., F.R.C.S.(C) MICHAELG. FEHLINGS,M.D.
The Toronto Hospital and University of Toronto Toronto, Ontario, Canada
Reference 1. Chehrazi BB, Scremin O, Decima EE: Effect of regional spinal cord blood flow and central control in recovery from spinal cord injury. J Neurasurg 71:747-753, 1989 724
RESPONSE: Dr. Duhaime's comments are of particular interest with regard to our study, as all patients in the study routinely received an intraventricular injection of gentamicin at the time of any shunt insertion or revision. However, data from our study also strongly suggest that gentamicin in the cerebrospinal fluid (CSF) is not the sole cause of eosinophilia. The association of infection with eosinophilia is not easily explained if the cause is the intraventricular injection of a single dose
J. Neurosurg. / Volume 76/April 1992
to
the
editor
On the Subject of Double Publication To THE EDITOR: We have long regarded the Journal of Neurosurgery as an interesting and alive journal with strong clinical relevance and high standards. Natura21y with our hospital's high proportion of accident and emergency cases, we have a special interest in articles that bear on trauma and its outcome. We therefore read with particular attention the article by Wilberger, et al. (Wilberger JE Jr, Harris M, Diamond DL: Acute subdural hematoma: morbidity, mortality, and operative timing. J Neurosurg 74.'212-218, February, 1991). However, the work seemed familiar. On further investigation, the material appeared to be the same as that in an article published in the Journal of Trauma) We find an extensive similarity between these two articles. They appear to be published from the same data base with very little difference. We are very concerned that this appears to be multiple publication. Apart from damaging the reputation of your journal, we object to the waste of resources which duplication causes and the waste of time which is imposed on all interested in the field. R. CAPFS,M.D. W. J. RUSSELL,M.D. Adelaide Hospital Adelaide, South Australia Reference 1. WilbergerJE Jr, Harris M, Diamond DL: Acute subdural hematoma: morbidity and mortality related to timing of operative intervention. J Trauma 30:733-736, 1991 RESPONSE: The concerns raised by Drs. Capps and Russell are serious ones that deserve appropriate response. As best as we can dctermine at this point in timc, this appears to havc occurred through a seriesof misunderstandings and miscommunications, for which the authors must assume primary responsibility.As the correspondents correctly point out, the data base for these two articles is indeed similar. However, the Journal of Neurosurger): article has significantly more information; additional data are presented, statistically analyzed, and evaluated. In this context we feel that the Journal of Neurosurgery article gives the neurosurgical reader a better opportunity to critically review and potentially validate or refute the data. Nevertheless, we apologize to these fine journals and their readers for what Drs. Capps and Russell, not inappropriately, term a "waste of resources and time." JACKE. WILBERGER,JR., M.D. Allegheny General Hospital Pittsburgh, Pennsylvania
.I. Neurosurg. / Volume 76/April 1992
EDITORIALCOMMENT:The issue of "double publication" is not taken lightly by the Journal of Neurosurgery. Currently, we receive well over 1000 manuscripts per year and we can publish only a very small portion of these. Accordingly, many very fine contributions must be declined, simply due to lack of space. Space limitations are imposed because of the cost of publishing the Journal of Neurosurgery and the feedback from our readership that they want a carefully edited journal, rather than one of great length. It should be clearly understood by our contributors that double publication is not acceptable. This is the policy followed by all major medical journals today. Had this Editor been informed of the earlier publication, this manuscript would have been rejected out of hand, irrespective of the value of its content. The question about the current article of the Journal of Neurosurgery presenting significantly more information is a matter of opinion, and will be dependent on the eye of the beholder. To the Editor, there does not appear to be a significant difference between these two contributions, and other members of the Editorial Board felt likewise. The Journal of Neurosurgery is extremely proud of the reputation it has earned throughout the neurosurgical and neuroscientific communities worldwide. The Editor and the Editorial Board will remain devoted to presenting original and unpublished work of substantial significance to our community. Exceptions to these fundamental criteria will not be made. Authors interested in publishing in the Journal of Neurosurgery are asked to keep this fact firmly in mind and not ~vary from the midline." THORALF M. SUNDT,JR., M.D. Editor, Journal of Neurosurgery Rochester, Minnesota
Posttraumatic Secondary Spinal Cord Trauma To THE EDITOR: WC read with interest the review article by Drs. Tator and Fehlings (Tutor CH, Fehlings MG: Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 75.'15-26, July, 1991). The authors state that Chehrazi, et al., 1found no reduction in spinal cord blood flow in cats after cord injury produced by the weight-drop technique. Elsewhere they imply that our study is one of the few that failed to support the vascular theory because we did not find evidence of posttraumatic ischemia. In fact, utilizing the H2 clearance technique, we did demonstrate a significant drop in the regional spinal cord blood flow after an initial transient increase) This delay in the onset of the posttraumatic white matter 723
Neurosurgical forum ischemia has been well known. 2 Our study, however, does not lend support to the theory of secondary injury from posttraumatic spinal cord ischemia because we found no improvement in the outcome of the animals in which we maintained posttraumatic regional spinal cord blood flow at or above baseline by spinal stimulation. We concluded that amelioration of the posttraumatic ischemia is of no benefit and that this ischemia may be an epiphenomenon of injury. I hope these comments are useful in clarifying our experimental findings. B. BARRYCHEHRAZI,M.D. University of California. Davis, Medical Center Sacramento, California
References 1. Chehrazi BB, Scremin O, Decima EE: Effect of regional spinal cord blood flow and central control in recover)' from spinal cord injury. J Neurosurg71:747-753. 1989 2. Senter HJ, Venes JL: Altered blood flow and secondary injury in experimental spinal cord trauma. J Neurosurg 49:569-578, 1978
RESPONSE: Dr. Chehrazi has quite correctly identified our misinterpretation of their data on posttraumatic spinal cord blood flow. In our review article we should have included the paper by Chehrazi, et al., among the many studies demonstrating posttraumatic ischemia of the spinal cord. They showed that spinal cord blood flow declined to about 60% of normal 5 hours after a weight-drop injury in cats. It should be noted that this reduction is much less severe than in any of our studies of severe spinal cord injury. The authors are grateful to Dr. Chehrazi for clarifying this matter and apologize for our misinterpretation of his data. Dr. Chehrazi's letter also comments on the significance of posttraumatic ischemia and the therapeutic value of treatment to restore spinal cord blood flow. Our paper reviews this point extensively, and concludes that the balance of evidence indicates that severe posttraumatic ischemia is of major importance and that efforts to elucidate the exact pathophysiology of this secondary mechanism of injury should continue. It is our thesis that further knowledge of the molecular and biochemical events causing posttraumatic ischemia will lead to better ways of counteracting the ischemia and to enhance recovery of patients with acute spinal cord
Eosinophilia Following Shunting To THE EDITOR: The recent article by Tung, el aL, regarding cerebrospinal fluid (CSF) eosinophilia in shunted hydrocephalic children (Tung H, Raffel C, McComb JG: Ventricular cerebrospinal fluid eosinophilia in children with ventriculoperitoneal shunts. J Neurosurg 75:541-544, October, 1991 )brought to mind two recent patients on our service. Both had initial shunts placed within the first months of life, with baseline normal CSF profiles and cell counts. Both patients received the routine single 4-mg dose of intrathecal gentamicin at the time of shunt placement, as did the patients in the paper by Tung and colleagues. Within the first few days after shunt surgery, both developed low-grade fever and were found to have elevated CSF white cell counts with marked eosinophilia (53% and 50%), as well as elevated CSF protein levels. Neither had intraventricular hemorrhage. All cultures and stains for bacteria, fungus, and tuberculosis were negative. The cell counts, protein levels, and proportion of eosinophils returned to normal over several weeks. Cerebrospinal fluid eosinophilia has been reported after intrathecal administration of gentamicin.~ Could it be that our patients, as well as some of the those in Dr. Tung's series, have shown a reaction to the gentamicin? The correlation between the number of shunt operations and the finding of eosinophilia could be related to a dose-dependent or exposure effect. Alternatively, the probability of discovering a transient eosinophilia induced by the drug would be increased if the shunt coincidentally malfunctioned while the cell count was elevated. Finally, the drug reaction itself and the inflammatory pleocytosis so induced could increase the risk of shunt obstruction. In either case, the fact that the eosinophilia resolves spontaneously in these eases suggests that a temporary stimulus, rather than an ongoing process such as a reaction to the shunt material itself, may be responsible. ANN-CHRISTINEDUHAIME,M.D.
Children's Surgical Associates, Ltd. Philadelphia, Pennsylvania
Reference 1. Mine S, Solo A, Yamaura A, et al: Eosinophilia of the cerebrospinal fluid in a case of shunt infection: case report. Neurosurgery 19:835-836, 1986
injury.
CEARLESH. TATOR,M.D., F.R.C.S.(C) MICHAELG. FEHLINGS,M.D.
The Toronto Hospital and University of Toronto Toronto, Ontario, Canada
Reference 1. Chehrazi BB, Scremin O, Decima EE: Effect of regional spinal cord blood flow and central control in recovery from spinal cord injury. J Neurasurg 71:747-753, 1989 724
RESPONSE: Dr. Duhaime's comments are of particular interest with regard to our study, as all patients in the study routinely received an intraventricular injection of gentamicin at the time of any shunt insertion or revision. However, data from our study also strongly suggest that gentamicin in the cerebrospinal fluid (CSF) is not the sole cause of eosinophilia. The association of infection with eosinophilia is not easily explained if the cause is the intraventricular injection of a single dose
J. Neurosurg. / Volume 76/April 1992
