Bifrontal decompressive craniectomy in the management of head trauma JOAN L. VENES, M.D., AND WILLIAM F. COLLINS, M.D.
Section of Neurological Surgery, Yale University School of Medicine, New Haven, Connecticut ~" Retrospective analysis of 13 patients who had bifrontal decompressive craniectomy for the management of posttraumatic cerebral edema shows a significant decrease in expected mortality, but severe morbidity in the survivors. Only one patient returned to the pretrauma level of neurological functioni No correlation could be found between the quality of survival and the neurological or operative findings.The need for more accurate prognostic criteria in the evaluation of severely head-injured patients is discussed. KEy WORDS cerebral edema "
head injury 9 decompressive craniectomy 9 intracranial pressure
A
RETROSPECTIVE analysis of 13 patients admitted following head trauma and treated by bifrontal, bitemporal decompressive craniectomy was undertaken in an attempt to determine the value of the procedure and to define the clinical parameters that might identify those patients most likely to benefit from this procedure.
9
devitalized tissue if it is present, the dural opening is closed with a graft of pericranium or temporal fascia. Acrylic and steel wire cranioplasty is done 3 months to 1 year following the injury.
Selection o f Patients
Eleven patients who had on admission, or later developed, evidence of progressive brain stem dysfunction as defined by the Technique appearance of decerebrate posturing, and in The operative procedure used is similar to whom no evidence of localized mass could be the one described by Kjellberg and Prieto. 1~ demonstrated, were selected for this The bifrontal excision of bone extends from procedure. Two other patients whose the supraorbital ridge to behind the coronal preoperative examination had shown no sutures and into the squamous portion of the evidence of brain stem dysfunction were intemporal bone to the floor of the middle cluded because massive cerebral swelling that fossa. The dura is opened along the supraor- developed at operation warranted decompresbital ridge and the incision carried into the sion. Patients whose initial injury was felt to middle fossa; the falx and sagittal sinus are be less severe were analyzed as a separate divided. Following inspection of the brain, group, since they should represent those in removal of hematoma, and removal of whom the best results might be expected. Method
J. Neurosurg. / Volume 42 / April, 1975
429
J. L. Venes and W. F. Collins Results
remained unchanged. One patient remained stable for 7 days and then had progressive loss Group 1: Moderately Severe Neurological of extraocular muscle function, the explanaDeficit tion for which was not determined. Three of This group included five patients who could the eight patients died, a mortality of 37.5%. either verbalize or respond semi-purposefully Of the remaining five, three are neuroto pain following injury (Table 1), indicating logically devastated and incapable of any selfthat significant neurological function of the care. Two have made a functional recovery brain stem and cerebral hemispheres but with marked decline in intellectual remained after the initial insult. In none of capacity and profound personality disturthese patients was the associated injury severe bance. No patient in this group returned to enough to cause hypotension, and although his normal status before injury. one patient was noted to have stertorous respirations, none were apneic or cyanotic. Discussion Three of these five patients progressed rapidly Markedly elevated intracranial pressure to decerebration while the other two were unfollowing head trauma is associated with a changed at the time of surgery. Extensive significant increase in mortality and morfractures of the vault and base of the skull bidity. 4,9,21 When this increased pressure is were present in the latter two; we believed caused by a mass effect from hematoma or craniectomy was indicated because of localized cerebral contusion, direct surgical massive cerebral swelling at the close of the attack for removal of the mass is usually incraniectomy for depressed skull fracture. dicated. Not infrequently, however, diagOne of the patients in this group died and nostic studies fail to demonstrate a focal letwo remain severely retarded with bilateral sion and cerebral edema is considered the motor involvement several years following incause of the increased intracranial pressure. jury. The 21/2-year-old child (Case 1) who demonstrated purposeful response to pain Bifrontal, bitemporal craniectomy (Fig. 1), with enlargement of the intradural space by a and no extraoculomotor paresis at the time of surgery now appears to have made a full fascial graft at the site of the bifrontal dural neurological recovery and 4 years following incision, has been proposed as a means of lowering intracranial pressure in these inher injury competes on equal footing with her peers; however, she remains on anticonvul- stances? ~,~ Unlike solute diuretics or sant medication because of a persistent fron- hyperventilation, craniectomy for decomprestal spike focus on the electroencephalogram. sion does not rely on any intrinsic property of the brain itself but is designed to permit upThe fifth patient in this group (Case 2) has also made a good recovery except for a ward migration and outward expansion of sociopathic personality disorder which in a supratentorial structures to prevent transtenmilder form may have antedated the injury. torial herniation of the medial temporal lobe He had an epidural hematoma; his case is and the upper brain stem, and to protect the similar to those described by Ransohoff, et cerebral vascular perfusion pressure. This review demonstrates the difficulty in al., ~6 who demonstrated the usefulness of assessing the degree of reversible injury in decompressive craniotomy in the manageseverely head-injured patients. Mortality in ment of lateralized extraaxial lesions in which this series is significantly less than that the rotational acceleration forces producing reported by Kjellberg and PrietC z in a recent injury are probably somewhat less severe. article, but there is a high morbidity of severe disabling neurological sequelae in the surGroup 2." Very Severe Neurological Deficit viving patients. These eight patients were all decerebrate at The pathophysiology of severe craniothe time of admission and probably had been cerebral trauma remains poorly understood, rendered immediately unconscious by their and until more definitive knowledge is gained injuries. Seven were operated on within 6 in this area, therapy must remain empirical. hours; three had progressive neurological Although methods vary, intracranial pressure defects consisting of loss of extraocular motor monitoring of patients is now an accepted function, one had a brief response to mannitol procedure. 2,s'~a,14,2~ Unfortunately, no (1.5 gm/kg intravenously), and three precise clinical correlation between elevated 430
J. Neurosurg. / Volume 42 / April, 1975
Bifrontal decompressive craniectomy TABLE 1
Summary of 13 cases of head trauma treated by bifrontal decompressive craniectomy* Case No.
Age (yrs)
Initial Examination
Preoperative Examination
Operative Findings
Results (Follow-up duration)
Group 1 1
2
2
36
3t
9
4t
35
5t
30
pupil asymmetry; unchanged EOMs full; nonpurposeful to pain; It Babinski PERRL; EOMs full; rt CN 1II palsy; spontaneous and decerebrate purposeful to pain; no Babinski midposition pupils, unchanged light fixed; decerebrate pinpoint pupils; unchanged EOMs full, purposeful to pain; bilateral Babinski PERRL; bilateral It CN III palsy; palsy; CN VI bilateral CN VI rt flaccid, palsies; It semipurposeful decerebrate to pain
edema; comminuted fractures
full recovery; seizure disorder (5 yrs)
rt extradural hematoma; edema
personality disorder; no motor deficit (18 mos)
edema; bilateral subdural hematoma; cortical lacerations; comminuted, depressed fractures edema
profound retardation; rt hemiplegia; hydrocephalus, shunted (3 yrs)
bilateral extradural hematoma; edema; compound fracture
died 5 wks, neurovegetative state
died 48 hrs
Group 2 6t
7t
9
8t
3
9
15
10
19
11t
51
12
13
13t
21
PERRL; decerebrate CN III palsy; EOMs absent; decerebrate
edema; depressed fracture
bilaterally fixed and CN III palsy; dilated pupils; decerebrate EOMs full; flaccid; apneic bilaterally fixed and unchanged dilated pupils; EOMs absent; decerebrate PERRL; e y e s decerebrate deviated; decerebrate bilaterally fixed and transient response dilated pupils; to mannitol EOMs absent; decerebrate pinpoint pupils; unchanged EOMs full; rt flaccid; It decerebrate PERRL; EOMs full; bilaterally fixed decerebrate and dilated pupils; decerebrate PERRL; EOMs full; unchanged decerebrate
edema; no fracture
severe personality disturbance; retardation seizure disorder; It hemiparesis, mild (7 yrs) severe personality disturbance; retardation (51/2 yrs)
edema; depressed fracture
neurovegetative; hydrocephalus (24 mos)
edema; no fracture
rt hemiplegia and global aphasia (6 yrs) neurovegetative state (3 yrs)
edema; tetrapolar contusions; no fracture edema; comminuted, depressed fracture
neurovegetative state; hydrocephalus (17 mos)
edema; no fracture
died 7wks; neurovegetative; hydrocephalus
edema; no fracture
died 1 wk; decerebrate
* Abbreviations: EOM = extraocular eye movement; PERRL= pupils equal, round, react to light. t Angiography, pneumoencephalogram, or postmortem examination showed no postoperative evidence of a mass lesion.
J. Neurosurg. / Volume 42 / April, 1975
431
J. L. Venes and W. F. Collins
Fro. 1. Skull film following extensive craniectomy in patient with comminuted fracture. Temporal decompression extends to floor of middle fossa to prevent laceration of upwardly migrating temporal lobes.
Fro. 2. Skull film following extensive craniectomy shows severe frontal lobe atrophy and calcifications in dura. This degree of frontal lobe damage is typical of that seen in all but one of the survivors in this series.
intracranial pressure and prognosis exists, except in cases in which perfusion pressure fails? ,1~ Stritch 18 has described a group of patients who died in a neurovegetative state 5 to 18 months following injury without clinical evidence of increased intracranial pressure; autopsy demonstrated severe widespread degeneration of white matter with no cortical laceration or significant intracranial hematoma. Since degeneration was so widespread, with sparing of some areas within a gyrus while adjacent areas were severely damaged, she postulated that rotational shearing forces were the etiological agent, x9 Such a shear-strain force would be most injurious to a body with the physical properties of brain, that is, incompressible but easily distorted. Thus, increased intracranial pressure, hematoma, and transtentorial herniation may in certain cases be only epiphenomena, the successful treatment of which does not alter the quality of survival as determined by the initial shearing injury to white matter? ,~ The greater benefit of decompression in patients with acute subdural or epidural hematomas might be anticipated from the experimental evidence that rotational-acceleration forces in blows directed to the side of the head, as seen in injuries producing extraaxial hematomas, are much less effective in producing concussion.7 It is quite probable that neuroaxonal disruption is significantly less in these cases, so that relief of increased intracranial pressure and prevention of herniation allows recovery of function.
Monitoring of intracranial pressure and regional blood flow may permit evaluation of the efficacy of surgical intervention or conservative therapy, such as mannitol and/or hyperventilation. Although monitoring of this sort can serve as an indicator of when therapy should be instituted and whether it has effectively controlled intracranial pressure, unless some method is devised that permits early recognition of patients in whom the initial injury is irreversible, a significant number of survivors will remain mentally and physically incapacitated. The degree of involvement of frontal lobe structures is interesting, considering the marked personality disturbances seen in three of the four survivors whose recovery was considered functional. Frontal lobe softening and widespread cerebral edema were constant autopsy findings, and atrophy of the frontal lobes demonstrated radiographically (Fig. 2) or noted at time of cranioplasty was present in all but one of the survivors.
432
References
1. Brendler SL, Selverstone B: Recovery from decerebration. Brain 93:381-392, 1970 2. Brock M: A modified equipment for the continuous monitoring of epidural or subdural pressure, in Brock M, Dietz H (eds): Intracranial Pressure: Experimental and Clinical Aspects. Berlin/Heidelberg/New York,
Springer-Verlag, 1972, pp 21-26 3. Bruce DA, Langfitt TW, Miller JD, et al: Regional cerebral blood flow, intracranial J. Neurosurg. / Volume 42 / April, 1975
Bifrontal decompressive craniectomy 4.
5.
6. 7. 8.
9.
10. 11. 12. 13.
14.
pressure and brain metabolism in comatose patients. J Neurosurg 38:131-144, 1973 Carlson CA, yon Essen C, Lofgren J: Factors affecting the clinical course of patients with severe head trauma. Part 1. Influence of biological factors. Part 2. Significance of posttraumatic coma. J Neurosurg 29:242-251, 1968 Cronqvist S, Ingvar D, Lassen N: Quantitative measurements of regional CBF related to neuroradiological findings. Acta Radiol (Diag) (Stockh) 5:760-766, 1966 Friede RL: Experimental concussion acceleration. Pathology and mechanics. Arch Neurol 4:449-462, 1961 Holbourn AHS: Mechanics of head injuries. Lancet 2:438-441, 1943 Hulme A, Chawla JC, Cooper R: Monitoring of intracranial pressure in neurosurgical patients. J Neurol Neurosurg Psychiatry 34:108-109, 1971 Ingvar DH, Lundberg N: Paroxysmal symptoms in intracranial hypertension studied with ventricular fluid pressure recording encephalography. Brain 84:446-459, 1961 Johnston IH, Johnston JAF, Jennet B: Intracranial pressure changes following head injury. Lancet 2:433-436, 1970 Kerr FWL: Radical decompression and dural grafting in severe cerebral edema. Mayo Clin Proc 43:852-864, 1968 Kjellberg RN, Prieto A Jr: Bifrontal decompressive craniotomy for massive cerebral edema. J Neurosurg 34:488-493, 1971 Lundberg N: Continuous recording and control of ventricular fluid pressures in neurosurgical practice. Acta Psyehiatr Stand 36: Suppi 149:1-193, 1960 Numoto M: Minute by minute intracranial pressure monitoring as a guide to management of pathological intracranial pressure, in Brock
J. Neurosurg. / Volume 42 / April, 1975
M, Dietz H (eds): Intracranial Pressure: Experimental and Clinical Aspects. Berlin/
Heidelberg/New York, Springer-Verlag, 1972, pp 217-221 15. Oppenheimer DR: Microscopic lesions in the brain following head injury. J Neurol Neurosurg Psychiatry 31:229-306, 1968 16. Ransohoff J, Benjamin MV, Gage EL Jr, et al: Hemicraniectomy in the management of acute subdural hematoma. J Neurosurg 34:70-76, 1971 17. Robertson RCL, Pollard C Jr: Decerebrate state in children and adolescents. J Neurosurg 12:13-17, 1955 18. Stritch S: Diffuse degeneration of the cerebral white matter in severe dementia following head injury. J Neurol Neurosurg Psychiatry 19:163-185, 1956 19. Stritch SJ: Shearing of nerve fibers as a cause of brain damage due to head injury. Lancet 2:443-448, 1961 20. Tindall GT, McGraw CP, Iwata K: Subdural pressure monitoring in head injured patients, in Brock M, Dietz H (eds): Intracranial
Pressure: Experimental and Clinical Aspects. Heidelberg~Berlin~New York, Springer-
Verlag, 1972, pp 9-13 21. Troupp H: Intraventricular pressure in patients with severe brain injury. 2. J Trauma 7:875-883, 1967 22. Vries JK, Becker DP, Young HF: A subarachnoid screw for monitoring intracranial pressure. Technical note. J Neurosurg 39:416-419, 1973
Address reprint requests to." Joan L. Venes, M.D., Section of Neurological Surgery, Yale University School of Medicine, New Haven, Connecticut.
433
Section of Neurological Surgery, Yale University School of Medicine, New Haven, Connecticut ~" Retrospective analysis of 13 patients who had bifrontal decompressive craniectomy for the management of posttraumatic cerebral edema shows a significant decrease in expected mortality, but severe morbidity in the survivors. Only one patient returned to the pretrauma level of neurological functioni No correlation could be found between the quality of survival and the neurological or operative findings.The need for more accurate prognostic criteria in the evaluation of severely head-injured patients is discussed. KEy WORDS cerebral edema "
head injury 9 decompressive craniectomy 9 intracranial pressure
A
RETROSPECTIVE analysis of 13 patients admitted following head trauma and treated by bifrontal, bitemporal decompressive craniectomy was undertaken in an attempt to determine the value of the procedure and to define the clinical parameters that might identify those patients most likely to benefit from this procedure.
9
devitalized tissue if it is present, the dural opening is closed with a graft of pericranium or temporal fascia. Acrylic and steel wire cranioplasty is done 3 months to 1 year following the injury.
Selection o f Patients
Eleven patients who had on admission, or later developed, evidence of progressive brain stem dysfunction as defined by the Technique appearance of decerebrate posturing, and in The operative procedure used is similar to whom no evidence of localized mass could be the one described by Kjellberg and Prieto. 1~ demonstrated, were selected for this The bifrontal excision of bone extends from procedure. Two other patients whose the supraorbital ridge to behind the coronal preoperative examination had shown no sutures and into the squamous portion of the evidence of brain stem dysfunction were intemporal bone to the floor of the middle cluded because massive cerebral swelling that fossa. The dura is opened along the supraor- developed at operation warranted decompresbital ridge and the incision carried into the sion. Patients whose initial injury was felt to middle fossa; the falx and sagittal sinus are be less severe were analyzed as a separate divided. Following inspection of the brain, group, since they should represent those in removal of hematoma, and removal of whom the best results might be expected. Method
J. Neurosurg. / Volume 42 / April, 1975
429
J. L. Venes and W. F. Collins Results
remained unchanged. One patient remained stable for 7 days and then had progressive loss Group 1: Moderately Severe Neurological of extraocular muscle function, the explanaDeficit tion for which was not determined. Three of This group included five patients who could the eight patients died, a mortality of 37.5%. either verbalize or respond semi-purposefully Of the remaining five, three are neuroto pain following injury (Table 1), indicating logically devastated and incapable of any selfthat significant neurological function of the care. Two have made a functional recovery brain stem and cerebral hemispheres but with marked decline in intellectual remained after the initial insult. In none of capacity and profound personality disturthese patients was the associated injury severe bance. No patient in this group returned to enough to cause hypotension, and although his normal status before injury. one patient was noted to have stertorous respirations, none were apneic or cyanotic. Discussion Three of these five patients progressed rapidly Markedly elevated intracranial pressure to decerebration while the other two were unfollowing head trauma is associated with a changed at the time of surgery. Extensive significant increase in mortality and morfractures of the vault and base of the skull bidity. 4,9,21 When this increased pressure is were present in the latter two; we believed caused by a mass effect from hematoma or craniectomy was indicated because of localized cerebral contusion, direct surgical massive cerebral swelling at the close of the attack for removal of the mass is usually incraniectomy for depressed skull fracture. dicated. Not infrequently, however, diagOne of the patients in this group died and nostic studies fail to demonstrate a focal letwo remain severely retarded with bilateral sion and cerebral edema is considered the motor involvement several years following incause of the increased intracranial pressure. jury. The 21/2-year-old child (Case 1) who demonstrated purposeful response to pain Bifrontal, bitemporal craniectomy (Fig. 1), with enlargement of the intradural space by a and no extraoculomotor paresis at the time of surgery now appears to have made a full fascial graft at the site of the bifrontal dural neurological recovery and 4 years following incision, has been proposed as a means of lowering intracranial pressure in these inher injury competes on equal footing with her peers; however, she remains on anticonvul- stances? ~,~ Unlike solute diuretics or sant medication because of a persistent fron- hyperventilation, craniectomy for decomprestal spike focus on the electroencephalogram. sion does not rely on any intrinsic property of the brain itself but is designed to permit upThe fifth patient in this group (Case 2) has also made a good recovery except for a ward migration and outward expansion of sociopathic personality disorder which in a supratentorial structures to prevent transtenmilder form may have antedated the injury. torial herniation of the medial temporal lobe He had an epidural hematoma; his case is and the upper brain stem, and to protect the similar to those described by Ransohoff, et cerebral vascular perfusion pressure. This review demonstrates the difficulty in al., ~6 who demonstrated the usefulness of assessing the degree of reversible injury in decompressive craniotomy in the manageseverely head-injured patients. Mortality in ment of lateralized extraaxial lesions in which this series is significantly less than that the rotational acceleration forces producing reported by Kjellberg and PrietC z in a recent injury are probably somewhat less severe. article, but there is a high morbidity of severe disabling neurological sequelae in the surGroup 2." Very Severe Neurological Deficit viving patients. These eight patients were all decerebrate at The pathophysiology of severe craniothe time of admission and probably had been cerebral trauma remains poorly understood, rendered immediately unconscious by their and until more definitive knowledge is gained injuries. Seven were operated on within 6 in this area, therapy must remain empirical. hours; three had progressive neurological Although methods vary, intracranial pressure defects consisting of loss of extraocular motor monitoring of patients is now an accepted function, one had a brief response to mannitol procedure. 2,s'~a,14,2~ Unfortunately, no (1.5 gm/kg intravenously), and three precise clinical correlation between elevated 430
J. Neurosurg. / Volume 42 / April, 1975
Bifrontal decompressive craniectomy TABLE 1
Summary of 13 cases of head trauma treated by bifrontal decompressive craniectomy* Case No.
Age (yrs)
Initial Examination
Preoperative Examination
Operative Findings
Results (Follow-up duration)
Group 1 1
2
2
36
3t
9
4t
35
5t
30
pupil asymmetry; unchanged EOMs full; nonpurposeful to pain; It Babinski PERRL; EOMs full; rt CN 1II palsy; spontaneous and decerebrate purposeful to pain; no Babinski midposition pupils, unchanged light fixed; decerebrate pinpoint pupils; unchanged EOMs full, purposeful to pain; bilateral Babinski PERRL; bilateral It CN III palsy; palsy; CN VI bilateral CN VI rt flaccid, palsies; It semipurposeful decerebrate to pain
edema; comminuted fractures
full recovery; seizure disorder (5 yrs)
rt extradural hematoma; edema
personality disorder; no motor deficit (18 mos)
edema; bilateral subdural hematoma; cortical lacerations; comminuted, depressed fractures edema
profound retardation; rt hemiplegia; hydrocephalus, shunted (3 yrs)
bilateral extradural hematoma; edema; compound fracture
died 5 wks, neurovegetative state
died 48 hrs
Group 2 6t
7t
9
8t
3
9
15
10
19
11t
51
12
13
13t
21
PERRL; decerebrate CN III palsy; EOMs absent; decerebrate
edema; depressed fracture
bilaterally fixed and CN III palsy; dilated pupils; decerebrate EOMs full; flaccid; apneic bilaterally fixed and unchanged dilated pupils; EOMs absent; decerebrate PERRL; e y e s decerebrate deviated; decerebrate bilaterally fixed and transient response dilated pupils; to mannitol EOMs absent; decerebrate pinpoint pupils; unchanged EOMs full; rt flaccid; It decerebrate PERRL; EOMs full; bilaterally fixed decerebrate and dilated pupils; decerebrate PERRL; EOMs full; unchanged decerebrate
edema; no fracture
severe personality disturbance; retardation seizure disorder; It hemiparesis, mild (7 yrs) severe personality disturbance; retardation (51/2 yrs)
edema; depressed fracture
neurovegetative; hydrocephalus (24 mos)
edema; no fracture
rt hemiplegia and global aphasia (6 yrs) neurovegetative state (3 yrs)
edema; tetrapolar contusions; no fracture edema; comminuted, depressed fracture
neurovegetative state; hydrocephalus (17 mos)
edema; no fracture
died 7wks; neurovegetative; hydrocephalus
edema; no fracture
died 1 wk; decerebrate
* Abbreviations: EOM = extraocular eye movement; PERRL= pupils equal, round, react to light. t Angiography, pneumoencephalogram, or postmortem examination showed no postoperative evidence of a mass lesion.
J. Neurosurg. / Volume 42 / April, 1975
431
J. L. Venes and W. F. Collins
Fro. 1. Skull film following extensive craniectomy in patient with comminuted fracture. Temporal decompression extends to floor of middle fossa to prevent laceration of upwardly migrating temporal lobes.
Fro. 2. Skull film following extensive craniectomy shows severe frontal lobe atrophy and calcifications in dura. This degree of frontal lobe damage is typical of that seen in all but one of the survivors in this series.
intracranial pressure and prognosis exists, except in cases in which perfusion pressure fails? ,1~ Stritch 18 has described a group of patients who died in a neurovegetative state 5 to 18 months following injury without clinical evidence of increased intracranial pressure; autopsy demonstrated severe widespread degeneration of white matter with no cortical laceration or significant intracranial hematoma. Since degeneration was so widespread, with sparing of some areas within a gyrus while adjacent areas were severely damaged, she postulated that rotational shearing forces were the etiological agent, x9 Such a shear-strain force would be most injurious to a body with the physical properties of brain, that is, incompressible but easily distorted. Thus, increased intracranial pressure, hematoma, and transtentorial herniation may in certain cases be only epiphenomena, the successful treatment of which does not alter the quality of survival as determined by the initial shearing injury to white matter? ,~ The greater benefit of decompression in patients with acute subdural or epidural hematomas might be anticipated from the experimental evidence that rotational-acceleration forces in blows directed to the side of the head, as seen in injuries producing extraaxial hematomas, are much less effective in producing concussion.7 It is quite probable that neuroaxonal disruption is significantly less in these cases, so that relief of increased intracranial pressure and prevention of herniation allows recovery of function.
Monitoring of intracranial pressure and regional blood flow may permit evaluation of the efficacy of surgical intervention or conservative therapy, such as mannitol and/or hyperventilation. Although monitoring of this sort can serve as an indicator of when therapy should be instituted and whether it has effectively controlled intracranial pressure, unless some method is devised that permits early recognition of patients in whom the initial injury is irreversible, a significant number of survivors will remain mentally and physically incapacitated. The degree of involvement of frontal lobe structures is interesting, considering the marked personality disturbances seen in three of the four survivors whose recovery was considered functional. Frontal lobe softening and widespread cerebral edema were constant autopsy findings, and atrophy of the frontal lobes demonstrated radiographically (Fig. 2) or noted at time of cranioplasty was present in all but one of the survivors.
432
References
1. Brendler SL, Selverstone B: Recovery from decerebration. Brain 93:381-392, 1970 2. Brock M: A modified equipment for the continuous monitoring of epidural or subdural pressure, in Brock M, Dietz H (eds): Intracranial Pressure: Experimental and Clinical Aspects. Berlin/Heidelberg/New York,
Springer-Verlag, 1972, pp 21-26 3. Bruce DA, Langfitt TW, Miller JD, et al: Regional cerebral blood flow, intracranial J. Neurosurg. / Volume 42 / April, 1975
Bifrontal decompressive craniectomy 4.
5.
6. 7. 8.
9.
10. 11. 12. 13.
14.
pressure and brain metabolism in comatose patients. J Neurosurg 38:131-144, 1973 Carlson CA, yon Essen C, Lofgren J: Factors affecting the clinical course of patients with severe head trauma. Part 1. Influence of biological factors. Part 2. Significance of posttraumatic coma. J Neurosurg 29:242-251, 1968 Cronqvist S, Ingvar D, Lassen N: Quantitative measurements of regional CBF related to neuroradiological findings. Acta Radiol (Diag) (Stockh) 5:760-766, 1966 Friede RL: Experimental concussion acceleration. Pathology and mechanics. Arch Neurol 4:449-462, 1961 Holbourn AHS: Mechanics of head injuries. Lancet 2:438-441, 1943 Hulme A, Chawla JC, Cooper R: Monitoring of intracranial pressure in neurosurgical patients. J Neurol Neurosurg Psychiatry 34:108-109, 1971 Ingvar DH, Lundberg N: Paroxysmal symptoms in intracranial hypertension studied with ventricular fluid pressure recording encephalography. Brain 84:446-459, 1961 Johnston IH, Johnston JAF, Jennet B: Intracranial pressure changes following head injury. Lancet 2:433-436, 1970 Kerr FWL: Radical decompression and dural grafting in severe cerebral edema. Mayo Clin Proc 43:852-864, 1968 Kjellberg RN, Prieto A Jr: Bifrontal decompressive craniotomy for massive cerebral edema. J Neurosurg 34:488-493, 1971 Lundberg N: Continuous recording and control of ventricular fluid pressures in neurosurgical practice. Acta Psyehiatr Stand 36: Suppi 149:1-193, 1960 Numoto M: Minute by minute intracranial pressure monitoring as a guide to management of pathological intracranial pressure, in Brock
J. Neurosurg. / Volume 42 / April, 1975
M, Dietz H (eds): Intracranial Pressure: Experimental and Clinical Aspects. Berlin/
Heidelberg/New York, Springer-Verlag, 1972, pp 217-221 15. Oppenheimer DR: Microscopic lesions in the brain following head injury. J Neurol Neurosurg Psychiatry 31:229-306, 1968 16. Ransohoff J, Benjamin MV, Gage EL Jr, et al: Hemicraniectomy in the management of acute subdural hematoma. J Neurosurg 34:70-76, 1971 17. Robertson RCL, Pollard C Jr: Decerebrate state in children and adolescents. J Neurosurg 12:13-17, 1955 18. Stritch S: Diffuse degeneration of the cerebral white matter in severe dementia following head injury. J Neurol Neurosurg Psychiatry 19:163-185, 1956 19. Stritch SJ: Shearing of nerve fibers as a cause of brain damage due to head injury. Lancet 2:443-448, 1961 20. Tindall GT, McGraw CP, Iwata K: Subdural pressure monitoring in head injured patients, in Brock M, Dietz H (eds): Intracranial
Pressure: Experimental and Clinical Aspects. Heidelberg~Berlin~New York, Springer-
Verlag, 1972, pp 9-13 21. Troupp H: Intraventricular pressure in patients with severe brain injury. 2. J Trauma 7:875-883, 1967 22. Vries JK, Becker DP, Young HF: A subarachnoid screw for monitoring intracranial pressure. Technical note. J Neurosurg 39:416-419, 1973
Address reprint requests to." Joan L. Venes, M.D., Section of Neurological Surgery, Yale University School of Medicine, New Haven, Connecticut.
433
