Neurosurgical forum cord under the dura will ultimately fail. However, it would be helpful in building such evidence for the precise method of stimulation, either monopolar or bipolar, to be stated. In addition, it is extremely important to be specific about the pathological process associated with the pain syndrome. It is well known that pain may have many different characteristics and origins. Depending on these factors, there may be varying responses, not only initially, but over the long term. I am sure no one ever believed dorsal column stimulation would solve all problems of pain, no matter what the origin or type. I mention these special features since my experience with subdural and intradural placement of bipolar electrodes has been unsatisfactory with regard to permanent effectiveness in patients with primary nonneoplastic radicular syndromes. As a matter of fact, we have seen many cases in which back pain related to the region of the site of implantation by laminectomy and dorsal placement was troublesome. We now do not do permanent implantations by laminectomy in any position. However, the situation may be different with different methodology. Initially, we now employ temporary (percutaneous) stimulation and if a positive response is obtained in terms of pain relief, the percutaneously implanted electrodes are left in place epidurally and converted to a permanent assembly by subcutaneous anastomosis of the electrodes to the wires of the usual receiver. This is done under local anesthesia. We do not use cervical placement at C-2 but attempt to place epidural electrodes close to the segment felt to be related to the pain syndrome, particularly in the cervical area. For lumbar root syndromes we use vertebral levels in the lower thoracic area. Of interest is the fact that the level and distance between electrodes can be critical. We also try to use discontinuous stimulation. We specifically encourage patients to turn down stimulation for periods during the day so as to change polarization phenomenon. With time, the period without stimulation can be increased. Our experience in treating the central pain in some patients with multiple sclerosis is satisfactory so far; one has had relief from pain for over 4 years. Another category where pain relief is astonishing is in occlusive arterial disease of the legs and arms. J. Neurosurg. / Volume 44 / May, 1976
However, electrodes must be placed appropriately. I mention these special items since my experience is similar to that of others with the intradural and subdural placement of electrodes, but it is different with epidural electrodes, with smaller size electrodes, and greater distance between electrodes. Although our longest observations in many patients last over 1 year, we may still find increasing loss of effectiveness over more time. The fact remains that there is something very effective about spinal cord stimulation in certain pain states dependent upon the methodology employed. I don't think we should be too quick to discard a principle with inadequate evidence and without regard to the various factors involved. ALBERTW. COOK, M.D. Brooklyn, New York
Systemic Hypotension in Neurosurgery To THE EDITOR: Dr. Yashon and his associates are to be congratulated on their review of one of the most valuable recent advances in the field of operative neurosurgery (Yashon D, Magness AP II, Vise WM: Systemic hypotension in neurosurgery. J Neurosurg 43.'579-589, November, 1975). As a means of preventing permanent damage they have suggested "time constraining," hypothermia, and electroencephalographic (EEG) monitoring at least for cases in which longer hypotensive periods are anticipated. These theoretical considerations require further comments. The authors have correctly pointed out that lowering blood pressure below a level essential for cerebral autoregulation is dangerous. One needs to know the safe level and safe period. It has been shown that under ideal conditions autoregulation remains uninterrupted with blood pressure as low as 55 to 60 mm Hg systolic~ (mean pressure of 40) and that it fails below a pressure of 50 mm Hg systolic? Therefore a level of between 55 to 60 mm Hg systolic can be maintained in patients with normal blood pressure for a considerable period of time, which may be required for an unhurried dissection in such neurosurgical procedures as clipping of an intracranial aneurysm. We have used this low level of hypotension for as long as 5 hours in some difficult cases without any harmful effects? ,~ We have not found it necessary to 65]
Neurosurgical forum use hypothermia or EEG monitoring. Hypothermia is not only unnecessary3 but may be harmful. 1 It is essential to appreciate that under various conditions cerebral autoregulation can fail,5 causing a reduction in cerebral perfusion. Failure to recognize this factor is probably responsible for cerebral complications and hence the need for time constraining, hypothermia, or monitoring devices. Hypercapnia, hypoxia, posture, raised intracranial pressure, ischemic cortex, 1~ rapid lowering of blood pressure, 7 severe hemorrhage during surgery, cerebral vessels previously compromised by congenital anomaly, atheroma, or surgery are known to be responsible for upsetting autoregulation. The discussion of hypotensive agents is excellent. It is interesting that recent studies by Crockard, et al.? have found that sodium nitroprusside does disturb cerebral autoregulation. Rapid lowering of blood pressure by this agent may account for this. Finally it must be stressed that bypotensive anesthesia is a complicated technique and the success of surgery depends on its proper execution by a skilled anesthesiologist. RAM P. SENGUPTA, F.R.C.S.
Newcastle upon Tyne, England
References 1. Albert SN, Fazekas JF: Cerebral hemodynamics and metabolism during induced hypothermia. Curr Res Anesthesiol Analg 35:381-385, 1956 2. Crockard HA, Brown FD, Mullan JF: Effects of trimethaphan and sodium nitroprusside on cerebral blood flow in Rhesus monkeys. Presented at the Fifth Congress of the European Association of Neurosurgical Societies, Oxford, England, September 1975 3. Drake CG: The surgical treatment of vertebral-basilar aneurysms. Clin Neurosurg 16:114-169, 1968 4. Finnerty FA Jr, Witkin L, Fazekas JF: Cerebral hemodynamics during cerebral ischemia induced by acute hypotension. J Clin Invest 33:1227-1232, 1954 5. Harper AM: Physiology of cerebral blood flow. Br J Anaesthesiol 37:225-235, 1965 6. Saunders JW: Effect of controlled hypotension on cerebral function and circulation. Lancet 1:1156-1158, 1954 7. Schneider M: Critical blood pressure in the cerebral circulation, in Schade JP, McMenemy WH: Selective Vulnerability of the Brain in Hypoxaemia. Oxford: Blackwell, 1963, pp 7-20 652
8. Sengupta RP: Direct surgery of intracranial aneurysms using induced hypotension. Presented at the 24th Meeting of the Scandinavian Neurosurgical Society, Odense, Denmark, 1972 9. Sengupta RP, Chiu JSP, Brierley H: Quality of survival following direct surgery for anterior communicating aneurysms. J Neurosurg 43:58-64, 1975 10. Waltz AG, Sundt TM Jr: Influence of systemic blood pressure on blood flow and microcirculation of ischemic cerebral cortex. Failure of autoregulation. Prog Brain Res 30:107-112, 1968
Survey of Tetraplegia Resulting from Anterior Cervical Discectomy and Fusion To THE EDITOR: Patients undergoing anterior cervical discectomy and fusion may suffer a sudden onset of myelopathy, that is, may become partially or completely tetraplegic. This complication is recognized as a possible outcome of surgery in patients who already have the myelopathy of cervical spondylosis. The risk must be weighed against the probability that the patient will continue to lose spinal cord function without surgery. The patient without preoperative spinal cord dysfunction is also at some risk to his spinal cord when he has an anterior cervical discectomy and fusion. The literature does not reveal whether the complication of tetraplegia has ever occurred following an anterior cervical fusion in a patient without myelopathy, although many neurosurgeons have heard of isolated cases. The events leading to these disasters have not been documented. Has a recognizable accident occurred during the operation? Were there anesthetic or postoperative nursing problems? Can the complication occur when no untoward events occur during or after surgery? A survey is required to answer these questions. Anyone having knowledge of this complication is asked to communicate with the writer. All information will be regarded as confidential. A report will be prepared to provide information about this catastrophic complication. Please write to Dr. Ian Turnbull, 700 West 10th Avenue, Vancouver, British Columbia, Canada. IAN TURNBULL,M.D.
Vancouver, British Columbia J. Neurosurg. / Volume 44 / May, 1976
However, electrodes must be placed appropriately. I mention these special items since my experience is similar to that of others with the intradural and subdural placement of electrodes, but it is different with epidural electrodes, with smaller size electrodes, and greater distance between electrodes. Although our longest observations in many patients last over 1 year, we may still find increasing loss of effectiveness over more time. The fact remains that there is something very effective about spinal cord stimulation in certain pain states dependent upon the methodology employed. I don't think we should be too quick to discard a principle with inadequate evidence and without regard to the various factors involved. ALBERTW. COOK, M.D. Brooklyn, New York
Systemic Hypotension in Neurosurgery To THE EDITOR: Dr. Yashon and his associates are to be congratulated on their review of one of the most valuable recent advances in the field of operative neurosurgery (Yashon D, Magness AP II, Vise WM: Systemic hypotension in neurosurgery. J Neurosurg 43.'579-589, November, 1975). As a means of preventing permanent damage they have suggested "time constraining," hypothermia, and electroencephalographic (EEG) monitoring at least for cases in which longer hypotensive periods are anticipated. These theoretical considerations require further comments. The authors have correctly pointed out that lowering blood pressure below a level essential for cerebral autoregulation is dangerous. One needs to know the safe level and safe period. It has been shown that under ideal conditions autoregulation remains uninterrupted with blood pressure as low as 55 to 60 mm Hg systolic~ (mean pressure of 40) and that it fails below a pressure of 50 mm Hg systolic? Therefore a level of between 55 to 60 mm Hg systolic can be maintained in patients with normal blood pressure for a considerable period of time, which may be required for an unhurried dissection in such neurosurgical procedures as clipping of an intracranial aneurysm. We have used this low level of hypotension for as long as 5 hours in some difficult cases without any harmful effects? ,~ We have not found it necessary to 65]
Neurosurgical forum use hypothermia or EEG monitoring. Hypothermia is not only unnecessary3 but may be harmful. 1 It is essential to appreciate that under various conditions cerebral autoregulation can fail,5 causing a reduction in cerebral perfusion. Failure to recognize this factor is probably responsible for cerebral complications and hence the need for time constraining, hypothermia, or monitoring devices. Hypercapnia, hypoxia, posture, raised intracranial pressure, ischemic cortex, 1~ rapid lowering of blood pressure, 7 severe hemorrhage during surgery, cerebral vessels previously compromised by congenital anomaly, atheroma, or surgery are known to be responsible for upsetting autoregulation. The discussion of hypotensive agents is excellent. It is interesting that recent studies by Crockard, et al.? have found that sodium nitroprusside does disturb cerebral autoregulation. Rapid lowering of blood pressure by this agent may account for this. Finally it must be stressed that bypotensive anesthesia is a complicated technique and the success of surgery depends on its proper execution by a skilled anesthesiologist. RAM P. SENGUPTA, F.R.C.S.
Newcastle upon Tyne, England
References 1. Albert SN, Fazekas JF: Cerebral hemodynamics and metabolism during induced hypothermia. Curr Res Anesthesiol Analg 35:381-385, 1956 2. Crockard HA, Brown FD, Mullan JF: Effects of trimethaphan and sodium nitroprusside on cerebral blood flow in Rhesus monkeys. Presented at the Fifth Congress of the European Association of Neurosurgical Societies, Oxford, England, September 1975 3. Drake CG: The surgical treatment of vertebral-basilar aneurysms. Clin Neurosurg 16:114-169, 1968 4. Finnerty FA Jr, Witkin L, Fazekas JF: Cerebral hemodynamics during cerebral ischemia induced by acute hypotension. J Clin Invest 33:1227-1232, 1954 5. Harper AM: Physiology of cerebral blood flow. Br J Anaesthesiol 37:225-235, 1965 6. Saunders JW: Effect of controlled hypotension on cerebral function and circulation. Lancet 1:1156-1158, 1954 7. Schneider M: Critical blood pressure in the cerebral circulation, in Schade JP, McMenemy WH: Selective Vulnerability of the Brain in Hypoxaemia. Oxford: Blackwell, 1963, pp 7-20 652
8. Sengupta RP: Direct surgery of intracranial aneurysms using induced hypotension. Presented at the 24th Meeting of the Scandinavian Neurosurgical Society, Odense, Denmark, 1972 9. Sengupta RP, Chiu JSP, Brierley H: Quality of survival following direct surgery for anterior communicating aneurysms. J Neurosurg 43:58-64, 1975 10. Waltz AG, Sundt TM Jr: Influence of systemic blood pressure on blood flow and microcirculation of ischemic cerebral cortex. Failure of autoregulation. Prog Brain Res 30:107-112, 1968
Survey of Tetraplegia Resulting from Anterior Cervical Discectomy and Fusion To THE EDITOR: Patients undergoing anterior cervical discectomy and fusion may suffer a sudden onset of myelopathy, that is, may become partially or completely tetraplegic. This complication is recognized as a possible outcome of surgery in patients who already have the myelopathy of cervical spondylosis. The risk must be weighed against the probability that the patient will continue to lose spinal cord function without surgery. The patient without preoperative spinal cord dysfunction is also at some risk to his spinal cord when he has an anterior cervical discectomy and fusion. The literature does not reveal whether the complication of tetraplegia has ever occurred following an anterior cervical fusion in a patient without myelopathy, although many neurosurgeons have heard of isolated cases. The events leading to these disasters have not been documented. Has a recognizable accident occurred during the operation? Were there anesthetic or postoperative nursing problems? Can the complication occur when no untoward events occur during or after surgery? A survey is required to answer these questions. Anyone having knowledge of this complication is asked to communicate with the writer. All information will be regarded as confidential. A report will be prepared to provide information about this catastrophic complication. Please write to Dr. Ian Turnbull, 700 West 10th Avenue, Vancouver, British Columbia, Canada. IAN TURNBULL,M.D.
Vancouver, British Columbia J. Neurosurg. / Volume 44 / May, 1976
