Neurosurgical forum to be determined more precisely, as well as the optimum technique for locating the target. We would argue that this can only be done with microelectrode or semi-microelectrode recordings. ROY A. E. BAKAY,M.D. MAHLONR. DELONG, M.D. JER~OLD L. VITEK,M.D., Ph.D. Emory University School of Medicine Atlanta, Georgia References
1. Aebischer P, Goddard M: Treating Parkinson's disease with lesions of the subthalamic nucleus. Science 252: 133-134, 1991 (Letter) 2. Alexander GE, Crutcher MD, DeLong MR: Basal gangliathalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal" and "limbic" functions. Prog Brain Res 85:119-146, 1990 3. Bergman H, Wichmann T, DeLong MR: Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 249:1436-1438, 1990 4. DeLong MR: Primate models of movement disorders of basal ganglia origin. Trends Neurosci 13:281-285, 1990 5. DeLong MR, Crutcher MD, Georgopoulos AP: Primate globus pallidus and subthalamic nucleus: functional organization. J Neurophysiol 53"530-543, 1985 6. DeLong MR, Georgopoulos AP: Motor functions of the basal ganglia as revealed by studies of single cell activity in the behaving primate. Adv Neuroi 24:131-140, 1979 7. Sellal F, Hirsch E, Lisovoski F, etal: Contralateral disappearance of parkinsonian signs after subthalamic hematoma. Neurology 42:255-256, 1992 8. Svennilson E, Torvik A, Lowe R, etal: Treatment of parkinsonism by stereotactic thermolesions in the pallidal region: a clinical evaluation of 81 cases. Acta Psychiatr Neuroi Scand 35:358-377, 1960 RESPONSE: I thank Dr. Bakay and his colleagues for their important letter that deserves some discussion. They are right in pointing out that our present target may not be the final one. In 1985, we had no justification to begin with experimental pallidotomy; therefore, we started by testing Leksell's method from 1956 to 1957. 5 Gradually we moved the target in a lateral direction. Today the standard target lies 2 m m in front of the midcommissural point, 6 m m below the intercommissural line, and 21 m m (in female patients) or 22 m m (in male patients) from the midline of the third ventricle. This change seems to have further improved the clinical effect and diminished the risk of optic tract lesions, which was 8% in the whole series of the first 100 pallidotomies and 4% in the last 25 patients. We had a motor/verbal complication in one case, as we reported in our paper. Since then, no other motor or verbal side effects have been observed. We now call our approach a "ventroposterolateral (VPL) pallidotomy." Surgical lesions in the VPL pallidum seem to be equally effective for the three cardinal parkinsonian symptoms and the levodopa-induced dyskinesias. Fortunately, no patient has been available for autopsy. The verification of the lesions is based on stereotactic computerized tomography and magnetic resonance imag488
ing. ~ These postoperative studies indicate that the effective target lies between the medial and the lateral pallidum, very close to the putamen. Thus, it is most likely that the medial conus of the pallidum is left intact (see Plate LXXVIII H.v -3.5 of Schaltenbrand and Wahren's atlas4). Contrary to the opinion of Dr. Bakay and his coworkers, I believe that the initiation of the movement is programmed in, or mediated by, the most medial part of the pallidum. Therefore, surgical lesions there and anywhere in the ascending pallidothalamocortical pathway most likely increase the bradykinesia. This was documented after thalamic lesions by Laitinen and Vilkki 3 two decades ago and was reconfirmed in our paper. Electrophysiological and positron emission tomography studies are needed, of course, for improved understanding of the pallidal mechanisms of parkinsonian symptoms and their optimal treatment. We are convinced that VPL pallidotomy radically improves the quality of life in some selected parkinsonian patients. Most important is that the previously "untreatable" bradykinesia can be abolished completely. It may be that surgical lesions in the subthalamic nucleus (STN), as demonstrated in animals by DeLong, z would be as effective as our pallidotomy. However, the vicinity of the STN to the pallidothalamic pathways, the ansa and the fasciculus lenticularis, may in man make this approach too risky. Furthermore, STN lesions may cause hemiballismus. I agree with Dr. Bakay and his coworkers that the new approach needs technical improvement and wellcontrolled prospective clinical studies. LAORI V. LAmNEN, M.D., PH.D. Sophiahemmet Hospital Stockholm, Sweden References
1. DeLong MR: Primate models of movement disorders of basal ganglia origin. Trends Neurosci 13:281-285, 1990 2. Hariz M[: Correlation between clinical outcome and size and site of the lesion in computed tomography guided thalamotomy and pallidotomy. Stereolact Funet Neurosurg 54/55:172-185, 1990 3. Laitinen L, Vilkki J: Measurement of parkinsonian hypokinesia with Purdue pegboard and motor reaction time tests, in Siegfried J (ed): Parkinson's Disease. Berlin: Hans Huber, 1973, Vol 2, pp 185-192 4. Schaltenbrand G, Wahren W: Atlas for Stereotaxy of the Human Brain. Stuttgart: Georg Thieme, 1977 5. Svennilson E, Torvik A, Lowe R, etal: Treatment of parkinsonism by stereotactic thermolesions in the pallidal region: a clinical evaluation of 81 cases. Acta Psychiatr Neurol Stand 35:358-377, 1960
Head Injuries in Golf: Think First
To THE EDITOR: .4 propos of the very admirable "Think First" campaign, the following note may be of some interest. There are many neurosurgeons who play golf and possibly they could call attention to the Rule J. Neurosurg. / Volume 77/September, 1992
Neurosurgical forum Book at their Club, or institute some other form of warning about practice swings. Several years ago a classic article by Lindsay, et al.,J pointed out that the percentage of severe head injuries in sports per participant was highest in golf (boxing was a weak seventh, tied with skating). Having seen several such injuries, they initiated an effort to promulgate some form of warning. Most of these injuries are doubly compounded depressed fractures occurring on the first tee during warm up. Practice swings are taken with no regard for an individual who might be standing out of range of the swing but directly in line should the club slip out of the swinger's hands or the club head come off. (At least three deaths have been recorded from broken metal shafts flying up and striking a player in the neck: an extremely rare occurrence, but three too many.) In addition, players may not look behind and may strike some unsuspecting individual on the back swing. Not infrequently small stones, broken tees, or other small hard objects are propelled, resulting in severe eye injuries. Including something in the Rule Book, 2 which is published every 4 years by the Royal and Ancient Golf Club of St. Andrews and The United States Golf Association, is almost like getting something into the Bible. Eventually, with the supporting documentation of the Lindsay article, however, the warning was placed as the very first item in the Rule Book under ETIQUETTE, subsection Safety, advising that, "prior to playing a stroke or making a practice swing, the player should ensure that no one is standing close by or in a position to be hit by the club, the ball or any stones, pebbles, twigs or the like which may be moved by the stroke or swing." Whether this will reduce the incidence of golf-related head injuries remains to be seen, possibly in a follow-up study by Lindsay and his colleagues. Unfortunately, very few golfers ever look at the Rule Book and very few Clubs take any preventative steps. DWIGHTPARKINSON,M.D. University of Manitoba Winnipeg, Manitoba, Canada
the United States Golf Association: The Rules of Golf. 1988, p 1
Selection Bias, Survival, and Brachytherapy for Glioma: Correction To THE EDITOR:We wish to correct two minor errors in our recent paper (Florell RC, Macdonald DR, Irish WD, et al: Selection bias, survival, and brachytherapy for glioma. J Neurosurg 76:179-183, February, 1992). First, the curves in Fig. 1 right are incorrectly labeled: the top line should have been solid, as it depicts the survival of brachytherapy-eligible patients with anaplastic glioma, and the bottom line should have been hatched, as it depicts those ineligible for brachytherapy. I enclose a corrected Fig. 1 right. Second, the first sentence in the last paragraph of the "Results" section should read " . . . two patients died at 18.53 and 27.03 months and three were alive...", as none of the patients in this analysis received adjuvant brachytherapy implants. We regret these mistakes and any confusion they may have caused your readers. J. GREGORYCAIRNCROSS,M.D., F.R.C.P.(C) University of Western Ontario London, Ontario, Canada
References 1. Lindsay KW, Greig M, Jennett B: Serious head injury in sport. Br Med J 281:789-790, 1980 2. The Royal and Ancient Golf Club of St. Andrews and
J. Neurosurg. / Volume 77/September, I992
FIG. 1. Survival curves for 33 patients with anaplastic glioma (malignant glioma other than glioblastoma).
489
1. Aebischer P, Goddard M: Treating Parkinson's disease with lesions of the subthalamic nucleus. Science 252: 133-134, 1991 (Letter) 2. Alexander GE, Crutcher MD, DeLong MR: Basal gangliathalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal" and "limbic" functions. Prog Brain Res 85:119-146, 1990 3. Bergman H, Wichmann T, DeLong MR: Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 249:1436-1438, 1990 4. DeLong MR: Primate models of movement disorders of basal ganglia origin. Trends Neurosci 13:281-285, 1990 5. DeLong MR, Crutcher MD, Georgopoulos AP: Primate globus pallidus and subthalamic nucleus: functional organization. J Neurophysiol 53"530-543, 1985 6. DeLong MR, Georgopoulos AP: Motor functions of the basal ganglia as revealed by studies of single cell activity in the behaving primate. Adv Neuroi 24:131-140, 1979 7. Sellal F, Hirsch E, Lisovoski F, etal: Contralateral disappearance of parkinsonian signs after subthalamic hematoma. Neurology 42:255-256, 1992 8. Svennilson E, Torvik A, Lowe R, etal: Treatment of parkinsonism by stereotactic thermolesions in the pallidal region: a clinical evaluation of 81 cases. Acta Psychiatr Neuroi Scand 35:358-377, 1960 RESPONSE: I thank Dr. Bakay and his colleagues for their important letter that deserves some discussion. They are right in pointing out that our present target may not be the final one. In 1985, we had no justification to begin with experimental pallidotomy; therefore, we started by testing Leksell's method from 1956 to 1957. 5 Gradually we moved the target in a lateral direction. Today the standard target lies 2 m m in front of the midcommissural point, 6 m m below the intercommissural line, and 21 m m (in female patients) or 22 m m (in male patients) from the midline of the third ventricle. This change seems to have further improved the clinical effect and diminished the risk of optic tract lesions, which was 8% in the whole series of the first 100 pallidotomies and 4% in the last 25 patients. We had a motor/verbal complication in one case, as we reported in our paper. Since then, no other motor or verbal side effects have been observed. We now call our approach a "ventroposterolateral (VPL) pallidotomy." Surgical lesions in the VPL pallidum seem to be equally effective for the three cardinal parkinsonian symptoms and the levodopa-induced dyskinesias. Fortunately, no patient has been available for autopsy. The verification of the lesions is based on stereotactic computerized tomography and magnetic resonance imag488
ing. ~ These postoperative studies indicate that the effective target lies between the medial and the lateral pallidum, very close to the putamen. Thus, it is most likely that the medial conus of the pallidum is left intact (see Plate LXXVIII H.v -3.5 of Schaltenbrand and Wahren's atlas4). Contrary to the opinion of Dr. Bakay and his coworkers, I believe that the initiation of the movement is programmed in, or mediated by, the most medial part of the pallidum. Therefore, surgical lesions there and anywhere in the ascending pallidothalamocortical pathway most likely increase the bradykinesia. This was documented after thalamic lesions by Laitinen and Vilkki 3 two decades ago and was reconfirmed in our paper. Electrophysiological and positron emission tomography studies are needed, of course, for improved understanding of the pallidal mechanisms of parkinsonian symptoms and their optimal treatment. We are convinced that VPL pallidotomy radically improves the quality of life in some selected parkinsonian patients. Most important is that the previously "untreatable" bradykinesia can be abolished completely. It may be that surgical lesions in the subthalamic nucleus (STN), as demonstrated in animals by DeLong, z would be as effective as our pallidotomy. However, the vicinity of the STN to the pallidothalamic pathways, the ansa and the fasciculus lenticularis, may in man make this approach too risky. Furthermore, STN lesions may cause hemiballismus. I agree with Dr. Bakay and his coworkers that the new approach needs technical improvement and wellcontrolled prospective clinical studies. LAORI V. LAmNEN, M.D., PH.D. Sophiahemmet Hospital Stockholm, Sweden References
1. DeLong MR: Primate models of movement disorders of basal ganglia origin. Trends Neurosci 13:281-285, 1990 2. Hariz M[: Correlation between clinical outcome and size and site of the lesion in computed tomography guided thalamotomy and pallidotomy. Stereolact Funet Neurosurg 54/55:172-185, 1990 3. Laitinen L, Vilkki J: Measurement of parkinsonian hypokinesia with Purdue pegboard and motor reaction time tests, in Siegfried J (ed): Parkinson's Disease. Berlin: Hans Huber, 1973, Vol 2, pp 185-192 4. Schaltenbrand G, Wahren W: Atlas for Stereotaxy of the Human Brain. Stuttgart: Georg Thieme, 1977 5. Svennilson E, Torvik A, Lowe R, etal: Treatment of parkinsonism by stereotactic thermolesions in the pallidal region: a clinical evaluation of 81 cases. Acta Psychiatr Neurol Stand 35:358-377, 1960
Head Injuries in Golf: Think First
To THE EDITOR: .4 propos of the very admirable "Think First" campaign, the following note may be of some interest. There are many neurosurgeons who play golf and possibly they could call attention to the Rule J. Neurosurg. / Volume 77/September, 1992
Neurosurgical forum Book at their Club, or institute some other form of warning about practice swings. Several years ago a classic article by Lindsay, et al.,J pointed out that the percentage of severe head injuries in sports per participant was highest in golf (boxing was a weak seventh, tied with skating). Having seen several such injuries, they initiated an effort to promulgate some form of warning. Most of these injuries are doubly compounded depressed fractures occurring on the first tee during warm up. Practice swings are taken with no regard for an individual who might be standing out of range of the swing but directly in line should the club slip out of the swinger's hands or the club head come off. (At least three deaths have been recorded from broken metal shafts flying up and striking a player in the neck: an extremely rare occurrence, but three too many.) In addition, players may not look behind and may strike some unsuspecting individual on the back swing. Not infrequently small stones, broken tees, or other small hard objects are propelled, resulting in severe eye injuries. Including something in the Rule Book, 2 which is published every 4 years by the Royal and Ancient Golf Club of St. Andrews and The United States Golf Association, is almost like getting something into the Bible. Eventually, with the supporting documentation of the Lindsay article, however, the warning was placed as the very first item in the Rule Book under ETIQUETTE, subsection Safety, advising that, "prior to playing a stroke or making a practice swing, the player should ensure that no one is standing close by or in a position to be hit by the club, the ball or any stones, pebbles, twigs or the like which may be moved by the stroke or swing." Whether this will reduce the incidence of golf-related head injuries remains to be seen, possibly in a follow-up study by Lindsay and his colleagues. Unfortunately, very few golfers ever look at the Rule Book and very few Clubs take any preventative steps. DWIGHTPARKINSON,M.D. University of Manitoba Winnipeg, Manitoba, Canada
the United States Golf Association: The Rules of Golf. 1988, p 1
Selection Bias, Survival, and Brachytherapy for Glioma: Correction To THE EDITOR:We wish to correct two minor errors in our recent paper (Florell RC, Macdonald DR, Irish WD, et al: Selection bias, survival, and brachytherapy for glioma. J Neurosurg 76:179-183, February, 1992). First, the curves in Fig. 1 right are incorrectly labeled: the top line should have been solid, as it depicts the survival of brachytherapy-eligible patients with anaplastic glioma, and the bottom line should have been hatched, as it depicts those ineligible for brachytherapy. I enclose a corrected Fig. 1 right. Second, the first sentence in the last paragraph of the "Results" section should read " . . . two patients died at 18.53 and 27.03 months and three were alive...", as none of the patients in this analysis received adjuvant brachytherapy implants. We regret these mistakes and any confusion they may have caused your readers. J. GREGORYCAIRNCROSS,M.D., F.R.C.P.(C) University of Western Ontario London, Ontario, Canada
References 1. Lindsay KW, Greig M, Jennett B: Serious head injury in sport. Br Med J 281:789-790, 1980 2. The Royal and Ancient Golf Club of St. Andrews and
J. Neurosurg. / Volume 77/September, I992
FIG. 1. Survival curves for 33 patients with anaplastic glioma (malignant glioma other than glioblastoma).
489
