The Lucite Calvarium—A Method for Direct Observation of the Brain

II. Cranial Trauma and Brain Movement

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INTRODUCTION

In a previous report23 an experimental surgical technic in which the convex portion of the monkey skull is replaced by a transparent lucite calvarium was described. Because a large area of both cerebral hemispheres is exposed through the lucite window, the method is ideally suited for the study of intracranial phenomena under “closed box” conditions. It may be of interest to mention that the technic was developed primarily to study the effects of cranial trauma on the underlying brain. The patterns of brain motion resulting from blows to both the freely movable and the immobile

INTRODUCTION

In a previous report23 an experimental surgical technic in which the convex portion of the monkey skull is replaced by a transparent lucite calvarium was described. Because a large area of both cerebral hemispheres is exposed through the lucite window, the method is ideally suited for the study of intracranial phenomena under “closed box” conditions. It may be of interest to mention that the technic was developed primarily to study the effects of cranial trauma on the underlying brain. The patterns of brain motion resulting from blows to both the freely movable and the immobile head were recorded by high-speed cinematography.

It is stressed that these experiments were conducted to study the motion patterns of the cerebral mass and any other visible physical change. It is not a study of cerebral concussion. Although brain movement and concussion are probably closely interrelated the mechanism of concussion is not explainable in the light of our findings. It is hoped, however, that this study may furnish additional data toward the eventual solution of the problem of cerebral concussion.

HISTORICAL BACKGROUND

A review of the literature of the past century and a half discloses that the efforts of investigators have been directed principally toward explaining the phenomenon of concussion. Comparatively few studies have been undertaken with a primary objective of explaining the mechanics involved in the production of focal and contrecoup brain injury. In establishing the historical background for this presentation these studies of cerebral movement and damage are emphasized. Reference to studies of concussion is made only insofar as these studies contribute to the subject under discussion. Excellent reviews of the development of our current knowledge of cerebral concussion may be found in the writings of Polis,20 Miller,18 Denny-Brown and Russell,7 and Denny-Brown.6

According to Polis,20 Fallopius was first to describe cerebral damage on the side of the brain opposite the site of impact. However, the term “contrecoup” did not come into popular use until 1766, at which time a series of papers on the subject was presented by various members of the Paris Academy of Surgery. Since this time many explanations of the mechanism of focal and contrecoup cerebral damage have appeared in the literature. These theories, which may be classified under six separate mechanisms (Fig. 1), explain brain damage on the basis of: (a) vibrations transmitted from the skull to the underlying brain; (b) passage of waves of force through the brain; (c) brain displacement at the pole opposite the site of impact; (d) deformation of the skull; (e) pressure gradients set up within the brain as a result of the blow; (f) rotation of the cerebral mass within the confines of the skull.

Fig. 1.
Fig. 1.

Theories concerning the mechanism of coup and contrecoup cerebral damage. The skull deformation shown in the diagram representing the theory of transmitted waves of force has not been described in all of the writings on this theory but is included for the sake of simplicity.

Vibration Theory. This theory, which is the oldest, was originally formulated in 1766 as the consensus of the various members of the Paris Academy of Surgery who postulated the mechanism of contrecoup damage. According to these observers the brain damage was attributed to vibrations originating in the skull at the site of the blow and transmitted throughout the entire skull, arriving at a point diametrically opposite the site of origin. Depending on their intensity, these vibrations would or would not fracture the skull at the contrecoup point but the brain at this point would supposedly be subjected to a force greater than in other areas.

In 1835 Gama12 gave a new impetus to the vibration theory by conducting the first experiments designed to explain contrecoup lesions. His investigations were carried out on models consisting of glass flasks containing ichthyocol in which colored threads were dispersed. When the flask was struck the threads vibrated, the pattern of vibration depending on the site and force of the blow. The vibration theory was short-lived but as late as 1888, Bryant2 noted that a severe blow on the head may not fracture the skull but nevertheless may cause vibrations that are transmitted to the brain and lacerate its substance.

Theories Based on Transmitted Waves of Force. In the latter part of the nineteenth century the first theories explaining contrecoup on the basis of transmission of waves of force through the brain substance made their appearance. In 1873 Félizet10 demonstrated the momentary depression of the skull resulting from blows by dropping skulls filled with paraffin and coated with ink onto a hard surface. The resulting mark on the surface struck was larger than any possible point of contact of the calvarium and could only be explained by flattening of the skull.

These findings were elaborated in 1878 by Duret9 who explained contrecoup as due to a bulging outward of the skull at the pole opposite the point depressed by the trauma. The bulging outward (soulevement) produced a vacuum which ruptured surface blood vessels. The studies of Miles17 published in 1892 were purported to confirm Duret's theory. This observer coated one side of the heads of fresh cadavers with vaseline or putty and struck the opposite side. The resulting indentation of the putty and vaseline suggested a “cone of bulging.” He therefore concluded that the vacuum produced beneath the bulging tore the superficial cerebral vessels. Miles further noted that Erichsen believed contrecoup damage was due to a wave of force being transmitted through the brain substance and “breaking” against the inner table of the skull on the opposite side.

In 1895 Chipault and Braquehaye4 employed a tambour arrangement to demonstrate momentary rises and falls in intracranial pressure at the sites and opposite points of blows respectively. The tambours were screwed into the skulls of large dogs and the detached heads of fresh cadavers. These findings have been confirmed recently by Walker, Kollros and Case25 with an improved method of manometric recording.

Courville's recent report5 lends additional support to the theory of transmission of lines and waves of force through the brain. According to this observer the head in motion resembles a bullet in flight since both have a line of force in their trajectory. When the forward motion of the head is suddenly arrested the line of force is immediately reversed and extends backward through the nervous tissue to a point opposite the site of impact. Presumably, waves of force spread outward from the main line of force. The lines and waves of force are modified by the angle of impact and by the deflection and diffusion resulting from their contact with structures of different densities, such as the falx and tentorium. Courville concludes that the “ultimate lesion depends on the relation of the waves of force along this line to the cortex and the subcortex which lie against the inflexible bony wall, on the degree of resilience of the blood vessels in the areas affected by the waves of force and on the anatomic structure of the brain in the area involved.” In support of his theory Courville mentions that cerebral lesions are occasionally demonstrable along the path of force at autopsy.

Brain Displacement at Pole Opposite Impact. Russell, in 1932,22 objected to the theory of transmitted force. He recognized that trauma caused movement of the brain within the skull but held that contrecoup was due to the brain tearing itself away from its covering by the force of its own momentum. Thus, when the moving head is suddenly arrested the brain at the pole opposite the point of impact is moving in a forward direction whereas the skull has been arrested. The degree of skull and brain damage is proportional to the suddenness with which the momentum is altered.

In their classical experiments on cerebral concussion published in 1941, Denny-Brown and Russell7 note that contrecoup lesions occurred infrequently but attributed them to the fling of the brain creating a momentary vacuum under the membranes opposite the point struck.

Similarly, Rowbotham21 and Dott8 describe an area of diminished pressure at the pole opposite the site of impact due to movement of brain away from skull. The suction created by this movement may rupture not only the surface vessels but also those more deeply placed.

Contrecoup Injury by Skull Deformation. This theory, which is related to the vibration theory, explains contrecoup damage on the basis of flattening of the skull at the time of impact. Skull deformation, as noted above, had been demonstrated experimentally by both Félizet and Miles. According to Munro19 the mechanism is as follows:

With the skull and brain both in motion in the same direction, the brain lags slightly behind the skull, because of a difference in inertia. When the skull is struck and its motion arrested, the force of the blow is transmitted throughout the bone. The flattest arch in the skull leading from the point of impact is mechanically the weakest. Its apex will either bend outward or break and allow the distal extremity to move inward in the direction of the center of the head. The lag in the forward progress of the brain within the skull places it momentarily where the inward shift of the bone collides with and, as it were, slaps its surface. The amount of damage done will depend upon the inertia of the brain, the weakness of the bony arch and the abruptness with which motion is arrested.

This explanation is likewise offered by Rowbotham in addition to the vaccuum theory.

Pressure Gradient Theory. This theory of contrecoup was proposed by Goggio13 in 1941. He draws objections to both the compression wave and elastic body theories. His objection to the former theory is that the brain damage should always be greatest at the site of origin of the wave of force. He furthermore objects to alternate lengthening and shortening of the skull as the explanation of cerebral damage because the bony buttresses do not make it an elastic body and because contrecoup occurs in the presence of fractures which should lessen the deformation. The pressure gradient theory treats contrecoup as a problem in intracranial hydrodynamics in which the maximum fall in intracranial pressure occurs at a point diametrically opposite the point of impact. The sudden diminution of pressure in the contrecoup area causes rupture of blood vessels.

Rotation Theory. Although rotation of the cerebral mass as a whole was suspected as early as 1865 its relationship to contrecoup was not clearly explained and fully appreciated until Holbourn15 presented his physical interpretations in 1943.

In 1865 Alquié1 conducted experiments designed to test the vibration theory which had been supported by the experimental work of Gama in 1835.12 Alquié conducted his studies with glass models filled with gelatin, with dry skulls, and with the skulls of cadavers and live animals. He observed that a blow caused a centrifugal rotation of the brain which flung it against the inner table of the skull, particularly in the direction of the blow, following which there was a rebound. The surface convolutions sustained the greatest damage since they were subjected to the greatest rotary force.

Further evidence for cerebral mass movements was reported by Ferrari11 in 1882. This observer filled skulls with gelatin and cerebral tissue in which glass capillary tubing or cover glasses were embedded at various depths. When these models were struck on the vertex with falling weights, the glass objects near the surface of the brain were fragmented even though the skull was not fractured.

It is noteworthy that many writers on the subject of contrecoup have recognized that the brain moved with relation to the skull. Goggio, in particular, stressed the rotation of the brain within the skull as an explanation for the increased frequency of the brain damage in the frontotemporal region. Others have recognized this movement and used it to explain the tearing of the cortical veins from the longitudinal sinus leading to the development of a subdural hematoma.

Holbourn's explanation of contrecoup is based on the physical principles applicable to confined masses of cerebral density and elaborated by experiments on gelatin models. He believes that brain damage is due to rotational acceleration forces and not to transmitted waves of compression and rarefaction. He states that the prime requisite for contrecoup damage is that the head be set in rotation by the blow. This rotation may be in the coronal, sagittal and horizontal planes or their combinations. The rotation is transmitted to the brain which glides in its dural compartments. The gliding motion is relatively free except where the brain is confined by bony structures, namely, in the frontal and middle fossae of the skull. In these areas shear strains occur which lacerate cerebral tissue and tear blood vessels. Damage is less in those areas of the brain that are free to glide, or under conditions where rotation is minimal. Holbourn's theory accounts more satisfactorily than any of the others for the distribution of contrecoup lesions as seen in fatal cases of head injury. It is also supported by the direct observations of brain movement as seen in the high speed motion pictures of this study.

Gunshot Wounds of the Brain. Although many writings on experimental gunshot wounds of the brain appear in the literature, the background for our study was established by the studies of Butler, Puckett, Harvey and McMillen.3 By means of both high speed cinematography and a microsecond roentgenographic technic these observers had demonstrated that the passage of a high velocity missile through the heads of experimental animals produces a large, rapidly expanding and pulsating temporary cavity within the brain. The pressure within this cavity increases in direct proportion to the velocity of the missile and may be sufficient to cause extensive comminution and disarticulation of the bones of the skull. These workers furthermore demonstrated that the extensive fracturing of the skull was due to the high radial velocity imparted to the cerebral tissue. When the brain was removed through the foramen magnum prior to the wounding only minor skull damage occurred.

METHODS AND MATERIALS

Macaque monkeys fitted with lucite calvaria were used in all of the experiments. The method for preparing the experimental animals was described in the previous report.23 Since this, several improvements in technic have been introduced.

Most important of the technical changes is that the holes originally placed to drain the space between the lucite plate and the brain are no longer used. The xanthochromic fluid that forms in this space is absorbed within a 7–14 day period. An additional important step is the re-suturing of the scalp with tantalum wire (0.007 inch) after each observation of the brain rather than resecting the scalp at the end of the second stage. By this means the incidence of wound and meningeal infection has been appreciably lowered and the method better adapted to a long period of observation. Finally, the lucite calvarium is now fastened to the skull with the standard 5/16 inch vitallium skull screws rather than the ⅜ inch bone screws which have a much larger diameter.

Method for Delivering Blows to the Head. Blows on the head were delivered by means of a special apparatus operating with compressed air which was designed for this study by Captain R. H. Draeger (MC), U.S.N. The apparatus (Fig. 2) has four essential parts:

  1. A cylindrical chamber that contains the compressed air charge.

  2. A vertical mercury manometer for recording the air pressure.

  3. A horizontal barrel leading from the chamber through which projectiles are propelled.

  4. Cylindrical aluminum projectiles weighing 100, 200, 300, and 500 gm.

Fig. 2.
Fig. 2.

Compressed air gun designed for delivering calibrated blows to the head. Note the vertical mercury manometer, the compressed air chamber, the horizontal barrel through which the projectiles are propelled and two of the four projectiles in the front rack. The vents near the end of the barrel release the compressed air charge behind the projectile and thereby permit a sharp, instantaneous blow to be struck.

Compressed air can be obtained from either the usual laboratory outlet or from a cylinder. The charge is built up gradually behind the projectile which is suddenly released by a trigger mechanism. Air vents in the end of the barrel release the driving pressure and allow an instantaneous blow to be struck.

The velocity, energy and momentum of each projectile at a given air pressure were calibrated with a ballistics pendulum at the Naval Research Laboratory, Anacostia, D. C. The force of the blow can be considerably altered by varying the weight of the projectiles and pressure. The maximum blows delivered by the apparatus have been calibrated at a pressure of 800 mm. mercury (Table 1).

TABLE I

Velocity and energy of blows at a pressure of 800 mm. mercury

Weight ofVelocityEnergy
Projectile (grams)(ft./sec.)(ft./lb.)
1007720.4
2005722.4
3004420.0
50034.516.3

These maximal values for the 100, 200, and 300 gm. projectiles exceed the velocity of 28.3 ft./sec. and energy of 17.83 ft./lb., which Denny-Brown and Russell found necessary to produce concussion in the cat and monkey.

Due to its lightness in weight and portability the apparatus is ideal for experiments that require working in different laboratories. A further advantage is that by varying the weights of the projectile and the compressed air pressures one is able to deliver blows of constant velocity and variable energy or vice versa.

In all of the experiments recorded in this investigation a blow having a velocity of 30 ft./sec. and an energy of 6.6 ft./lb. was used. This blow was obtained by propelling the 200 gm. projectile with a charge of air compressed to 300 mm. mercury. In repeated experiments on conscious animals this blow failed to cause any objective evidence of concussion. It is therefore a subconcussive blow. In the cinematographic studies the blows were delivered to the frontal, temporal, parietal, and occipital regions of the rigidly fixed or freely movable head. Fixation of the head was obtained by binding it to a heavy steel angle-iron with adhesive tape. The angle-iron, in turn, was bolted to the rigid oak frame of the animal holder. By this means the head was immobilized satisfactorily although not perfectly.

Cinematographic Recording of the Blow. Cinematographic recordings of the pattern of brain movement resulting from the blow were made on 16 mm. color film with an Eastman High Speed Camera. In these experiments a rate varying from 2000 to 3000 frames per second was used. Since intense illumination is necessary to obtain proper film exposure, a battery of two 13,800 watt and two 16,000 watt arc lamps was used to illuminate the animal's head. The intensity of the illumination could not be measured but was estimated at 3,000,000–4,000,000 foot candles. The blow was timed to fall within the period of maximum camera speed.

The pattern of brain movement was analyzed in a Movieola and by repeated projection of a film loop on the screen. Animated drawings were made from the films of one blow so that the movement pattern could be analyzed in greater detail. When these films are projected at a speed of 16 frames per second the brain movement is prolonged from 125 to 185 times its normal duration. Even under these conditions of slow motion the movement does not occupy more than a few seconds and it is difficult to be certain of the finer patterns of motion.

Gunshot Wounds of the Brain. Observations of the effects of perforating missiles on the brains of two monkeys were made in the laboratories of the Department of Biology of Princeton University. The perforating missiles consisted of steel spheres, ⅛ inch in diameter, weighing 130 mgm., which were fired at velocities of 1121 and approximately 1800 ft./sec. Perforating bitemporal wounds were obtained in both instances. The path of the missiles was identical in both instances (Fig. 3).

Fig. 3.
Fig. 3.

Perforating gunshot wound of the brain with an ⅛ inch steel sphere having a velocity of approximately 1800 ft. per sec. Note the hemorrhagic softening along the path of the missile.

The cinematographic recording and analysis of the trauma was carried out according to the method described for the blow experiments excepting that black and white motion picture film was used.

RESULTS

It was clearly demonstrated that the subconcussive blows used in this study gave rise to gliding movements of the brain within the cranial cavity. The brain movement lagged behind the motion of the skull, apparently due to the inertia of the cerebral mass.

Movement of the brain and skull is probably most clearly visualized if both are considered as spheroid. As such both are subject to motion in a horizontal, coronal or sagittal plane or combinations thereof (Fig. 1). The skull rotates on the cervical axis whereas rotation of the cerebral mass occurs within the cranial cavity.

In this study the rotatory movements of the cerebral convolutions were chiefly in a sagittal or horizontal plane. Distinct movements through a coronal arc were not seen. This is apparently due to the falx cerebri serving as a baffle between the lateral compartments of the cranial cavity.

The degree of convolutional glide varied considerably in the different areas of the brain. It was invariably of greatest amplitude in the parietal and occipital lobes, irrespective of the site of the blow. Frontal lobe motion, while present, was minimal. Movement of the temporal lobe could not be seen through the lucite plate.

Movement of the brain was affected considerably by the mobility or immobility of the head. A blow that routinely caused a substantial amount of convolutional displacement in the freely movable head produced little or no movement when the head was immobile. This point was demonstrated repeatedly.

An additional observation of interest was the dampening effect of cerebrospinal fluid pressure on brain displacement. An identical blow delivered to the head of the same animal after withdrawal of cerebrospinal fluid was attended by considerable increase in the amplitude of convolutional glide.

Perforating gunshot wounds of the brain caused a sudden outward displacement of the cerebral mass without visible rotation evidenced by flattening of the convolutions against the inner surface of the lucite plate.

Each of these findings is elaborated in the ensuing data.

Midline Frontal Blows. The pattern of brain movement resulting from blows in this area was visualized from two directions. In two experiments the camera was focused on the convex surface of both hemispheres. In the third trial the head was photographed in profile so that only the cerebral hemisphere of the same side was visualized.

In each instance the midline frontal blow caused the head to be moved through a sagittal plane of rotation with the neck serving as a pivot (Fig. 4). The rotational glide of the surface convolutions was through the same plane.

Fig. 4.
Fig. 4.

Head displacement and convolutional rotation patterns resulting from midline frontal blows.

Because of the inertia of the brain described above there was a momentary pause before the surface convolutions followed the skull through the sagittal plane of displacement. However, before the head proper had begun its reverse motion to the starting position the brain had already commenced its anterior rotation. The final movements of the brain consisted of anteroposterior undulations of diminishing amplitude.

Maximal convolutional displacement occurred in the parietal lobes. Motion of the frontal convolutions, while present, was considerably less in degree.

When a blow was delivered to the frontal region of the immobilized head, brain motion was considerably reduced.

Midline Occipital Blows. Blows in this region of the freely movable head caused a rotational pattern which was the reverse of that noted with the midline frontal blows. Again convolutional glide was greater in the parietal region and minimal in the frontal lobes.

Parietal Blows. Since blows in the parietal region cause a displacement of the head in a combined horizontal, coronal and sagittal plane, movement of the brain is of a similarly complicated pattern. Brain movement was much greater following blows in the parietal and temporal regions than in the frontal and occipital regions.

Despite the displacement of the head through a coronal arc, a coronal rotation of the brain was not seen. In other words the cerebral hemisphere on the side of the blow was not flung against the falx nor was the contra-lateral hemisphere displaced away from it. Cerebral rotation occurred principally in a horizontal plane. When the head was displaced anteriorly and to the right side (clockwise) by blows in the left parietal region, the first movement of the brain was similarly clockwise. The reverse was true for right parietal blows. Following the original displacement the rotation of the brain was counterclockwise, finally ceasing after diminishing clockwise-counterclockwise oscillations (Fig. 5). Convolutional motion was invariably greater in the parieto-occipital region than in the frontal region but was equally extensive in the two hemispheres.

Fig. 5.
Fig. 5.

Patterns of head and convolutional motion resulting from parietal blows.

The decreasing oscillations of the brain as it comes to a state of rest are particularly striking with the parietal and temporal blows. These settling movements are especially prominent in the parietal lobes, where maximum cerebral movement is located. During the phase of greatest brain rotation there is considerable stretching of the surface veins. In two experiments parietal veins entering the longitudinal sinus were torn, leading to the development of a subdural (“sublucite”) hematoma.

Following a parietal blow in one animal the intracranial pressure was reduced by removing 2 cc. of cerebrospinal fluid by lumbar puncture. This is equivalent to the removal of approximately 20 cc. in humans. Repetition of the blow under these conditions caused a considerable increase in the amplitude of brain rotation. Furthermore, the final oscillations of the brain were especially striking in this case. Thus the role of the cerebrospinal fluid as a baffle was clearly demonstrated.

In contrast to the experiment in which a blow was delivered under conditions of reduced intracranial pressure were those in which blows were delivered to the immobile head. Under these conditions the amplitude of brain movement was either considerably reduced or absent. The pattern of rotation, however, was similar to that which occurred with the freely movable head.

Temporal Blows. The pattern of brain movement with blows in this region was similar to that noted with the parietal blows. Because the amplitude of head rotation was greatest in the horizontal plane the brain rotation was likewise most marked in this plane (Fig. 6). Clockwise and counterclockwise horizontal rotation of the brain was initially dependent on the original displacement of the head. Blows to the temporal area of the freely movable head were followed by considerable cerebral motion. The final undulations of the brain were particularly prominent. In contrast, temporal blows to the fixed head caused only a slight rotatory motion, although the pattern of motion was similar.

Fig. 6.
Fig. 6.

Nature of displacement of the head and of the cerebral convolutions resulting from temporal blows.

Gunshot Wounds of the Head. In the two experiments in which the ⅛ inch steel spheres traversed the frontotemporal region of the skull at velocities of approximately 1100 and 1800 ft/sec., the effects on the brain were similar but more intensified in the instance of the greater velocity. The considerable increase in intracranial pressure resulting from the passage of the missile caused a sudden flattening of the brain against the inner surfaces of the lucite plate and the skull. This flattening was particularly striking along the edge of the bone supporting the falx where a ridge of cerebral tissue formed momentarily on each side (Fig. 7). Considerable hemorrhagic softening was noted along the path of the missile when the brain was cut in horizontal section.

Fig. 7.
Fig. 7.

Gunshot wound of the brain. The intense flattening of the convolutions at the height of intracranial pressure is shown.

The gunshot wounds caused no visible rotation of the cerebral hemispheres. If rotation did occur, it was masked by the sudden outward displacement of the brain. The lucite plate remained firmly fixed to the skull following both woundings although in the second experiment it was extensively fractured at the point of exit.

DISCUSSION

In an experiment of this type it is necessary to determine if the data accumulated from observations on the experimental animals may be interpreted as representing the conditions that exist in the human being. We believe that this is permissible because:

  1. The intracranial anatomic relationships are similar in the macaque and the human skull.

  2. The “closed box” conditions of the cranial chamber have been maintained.

  3. The cushioning of the brain by the cerebrospinal fluid was preserved.

  4. Removal of the dura overlying the convexity would not permit motion not normally present since the brain is not attached to it except when the cortical veins enter the sagittal sinus. The smooth inner surface of the dura provides an ideal surface on which the convolutions can glide.

Movement of the brain resulting from blows on the head has been clearly demonstrated in these experiments. It has been shown that the surface movement has a gliding rotatory quality which is modified by the site and direction of the blow, by fixation or mobility of the head and by certain other factors. For purposes of simplification rotation is considered as occurring in the horizontal, coronal and sagittal planes or combinations of these planes. Blows that cause the skull to move through a simple sagittal arc cause a pure type of brain movement in the same plane. On the other hand temporal and parietal blows cause rotation of the skull and brain through a combination of planes. In these latter blows the sagittal and horizontal convolutional glides were most pronounced whereas coronal rotation was not evident. Nevertheless, it is possible that coronal rotation did occur but was either masked by the other motion patterns or was not visible under the conditions of these experiments.

Indentation of the skull resulting from the blow was noted in some of the experiments. However there was no obvious outward bending of the opposite pole of the skull as surmised by previous investigators. Furthermore there was no grossly visible change in the cerebral circulation.

The most interesting observations of this study concern:

  1. The variation in the degree of motion in different areas of the brain.

  2. The relationship between the amplitude of rotation and the distribution of cerebral lesions.

  3. The effect of fixation of the head at the time of the blow.

  4. The tamponade effect of the cerebrospinal fluid.

  5. The explanation of subdural hematoma on the basis of cerebral rotation.

Each of these points may now be considered in detail.

Rotation of the cerebral mass was maximal in the parieto-occipital region and minimal in the frontal area irrespective of the site and direction of the blow. In the pure sagittal types of rotation induced by frontal and occipital blows the convolutional motion was equal on the two sides. However, when the blows were delivered to the temporal and parietal areas of the skull the amplitude of movement in all planes was slightly greater on the side of the blow.

Since the frontal lobes are subjected to the same rotational forces as the parietal and occipital lobes, their comparatively slight motion can be explained only on their anatomical position. Free motion must be inhibited by the more rigid anterior fossa as compared to the less confining posterior portion of the supratentorial space. This restraining effect of the anterior fossa on the frontal lobes must lead to strains within the cerebral tissue. Holbourn has postulated that it is these shear strains that lead to laceration and hemorrhagic softening of the cerebral tissue. Although the temporal lobes were not visualized through the lucite calvarium it is not unlikely that similar strains occur in these regions since these lobes are similarly confined by the middle cranial fossae. On the other hand the parietal and occipital lobes are less restricted in their gliding and therefore less subject to shear strains.

These observations are in accord with the actual distribution of cerebral lesions in fatal cases of head injury. In Vance's24 series of 512 necropsies, contrecoup lesions were generally confined to the under surface of the frontal and the temporosphenoidal lobes. Blows to posterior areas of the head usually caused damage to both frontotemporal areas. Blows to the lateral areas of the skull damaged the opposite temporosphenoidal area. However, frontal blows rarely caused contrecoup lesions. Similarly, Le Count and Apfelbach16 noted the rarity of occipital lobe injury with trauma to the frontal region.

In Courville's5 series of 206 consecutive cases of fatal head injuries, the sites of cerebral damage were temporal lobe in 145 cases and frontal lobe in 84. Injuries to the occipital lobes were rare unless by direct contusion from a depressed fracture.

Fixation of the head at the time of the blow resulted in a considerable diminution of the rotatory motion. Apparently under the conditions of fixation the flinging movement imparted to the brain by the moving skull does not occur. Because of this, contrecoup lesions should be unusual under these conditions. This is similarly supported by the experiences of Vance,24 Le Count and Apfelbach,16 Munro,19 Denny-Brown and Russell,7 Gurdjian and Webster.14 Vance was unable to demonstrate contrecoup lesions at autopsy in the brains of 40 individuals whose heads were crushed by an automobile on a roadway. Le Count and Apfelbach state that when the cranial bones are broken with the head in a fixed position contrecoup damage is reduced to a minimum. Munro notes that contrecoup lesions occur only when the head is struck and arrested while in motion. In their experiments on cerebral concussion Denny-Brown and Russell, and Gurdjian and Webster noted a greater degree of cerebral damage when the head was freely movable, rather than fixed, at the time of impact.

The cushioning of the brain by the cerebrospinal fluid was demonstrated in the experiment in which blows of equal force were delivered before and after the withdrawal of the fluid. Under the conditions of reduced intracranial pressure the amplitude of convolutional glide was considerably greater. This point probably has no clinical significance other than to demonstrate the supportive role of the cerebrospinal fluid. However, this finding encourages further investigation of the relationship between brain movement and concussion. If concussion is at all related to brain rotation it should be more easily obtainable under conditions of reduced intracranial pressure.

Finally, the pathogenesis of the subdural hematoma may be considered. It has long been taught that the subdural bleeding is due to the tearing of cortical veins from the sagittal sinus by the displacement of the brain. Although the actual tearing of the veins was not visualized, massive subdural (“sublucite”) venous bleeding occurred following parietal blows in two animals. The bleeding occurred from parietal veins in the region where convolutional glide was greatest. This experimental finding is in harmony with the location of subdural hematomas as found in clinical practice.

SUMMARY AND CONCLUSIONS

  1. High-speed cinematography has been used to observe the effects of subconcussive blows and gunshot wounds of the head on the brains of macaque monkeys fitted with lucite calvaria.

  2. Blows on the head cause swirling, rotatory movements of the brain within the cranial cavity.

  3. The patterns of convolutional motion are determined by the direction in which the head is displaced by the blow.

  4. Midline frontal and occipital blows displace the head through a sagittal arc and produce convolutional gliding through the same arc.

  5. In contrast, temporal and parietal blows rotate the head through a combination of sagittal, horizontal and coronal planes and cause a complicated type of brain movement in which convolutional glide in the sagittal and horizontal planes is striking. Coronal rotation of the brain was not visualized distinctly.

We are indebted to the staffs of the Audio-Visual Branch of the Bureau of Medicine and Surgery and of the Photographic Science Laboratory, U. S. Naval Air Station, Anacostia, D. C. for their excellent cooperation in the cinematographic studies. The cooperation of Professors E. N. Harvey and E. G. Butler and their colleagues in the Department of Biology, Princeton University, was invaluable in the study of gunshot wounds of the head. J. G. Wisda, PhM1c, V6, U.S.N.R., rendered valuable technical assistance in all of the experiments.

REFERENCES

  • 1.

    Alquié. Étude clinique et expérimentale de la commotion traumatique ou ébranlement de l'encéphale. Gaz. méd. Paris186520: 226; 254; 314; 382; 396; 463; 500.Alquié. Étude clinique et expérimentale de la commotion traumatique ou ébranlement de l'encéphale. Gaz. méd. Paris 1865 20: 226; 254; 314; 382; 396; 463; 500.

  • 2.

    BryantT. Lecture on cranial and intracranial injuries. Lancet18882: 404408; 507–510.Bryant T. Lecture on cranial and intracranial injuries. Lancet 1888 2: 404–408; 507–510.

  • 3.

    ButlerE. G.PuckettW. O.HarveyE. N. and McMillenJ. H. Experiments on head wounding by high velocity missiles. J. Neurosurg.19452: 358363.Butler E. G. Puckett W. O. Harvey E. N. and McMillen J. H. Experiments on head wounding by high velocity missiles. J. Neurosurg. 1945 2: 358–363.

  • 4.

    ChipaultA. and BraquehayeJ. Études graphiques sur les fractures indirectes de la base du crâne (définition et mécanisme). Arch. gén. Méd.1895176: 279296; 394–404; 665–701.Chipault A. and Braquehaye J. Études graphiques sur les fractures indirectes de la base du crâne (définition et mécanisme). Arch. gén. Méd. 1895 176: 279–296; 394–404; 665–701.

  • 5.

    CourvilleC. B. Coup-contrecoup mechanism of craniocerebral injuries. Some observations. Arch. Surg. Chicago194245: 1943.Courville C. B. Coup-contrecoup mechanism of craniocerebral injuries. Some observations. Arch. Surg. Chicago 1942 45: 19–43.

  • 6.

    Denny-BrownD. Cerebral concussion. Physiol. Rev.194525: 296325.Denny-Brown D. Cerebral concussion. Physiol. Rev. 1945 25: 296–325.

  • 7.

    Denny-BrownD. and RussellW. R. Experimental cerebral concussion. Brain194164: 93164.Denny-Brown D. and Russell W. R. Experimental cerebral concussion. Brain 1941 64: 93–164.

  • 8.

    DottN. M. Injuries of the brain and skull. In: Surgery of modern warfare. H. Bailey ed. Baltimore: Williams & Wilkins Co.19422nd ed.1: 259287.Dott N. M. Injuries of the brain and skull. In: Surgery of modern warfare. H. Bailey ed. Baltimore: Williams & Wilkins Co. 1942 2nd ed. 1: 259–287.

  • 9.

    DuretH. Traumatismes cranio-cérébraux. Paris: F. Alcan19201357 pp.Duret H. Traumatismes cranio-cérébraux. Paris: F. Alcan 1920 1357 pp.

  • 10.

    Félizet. Quoted by Polis A. and Miles A.Félizet. Quoted by Polis A. and Miles A.

  • 11.

    FerrariA. Sulla commozione cerebrale. Osservazione ed esperimenti. Spallanzani Riv. Sci. med. nat.1882 2 s. 11: 169196.Ferrari A. Sulla commozione cerebrale. Osservazione ed esperimenti. Spallanzani Riv. Sci. med. nat. 1882 2 s. 11: 169–196.

  • 12.

    GamaJ.-P. Traité des plaies de tête et de l'encéphalite principalement de celle qui leur est consécutive. Ouvrage dans lequel sont discutées plusieurs questions relatives aux fonctions du système nerveux en générale. Paris: Crochard18352nd ed.xxiv 616 pp. (see p. 94).Gama J.-P. Traité des plaies de tête et de l'encéphalite principalement de celle qui leur est consécutive. Ouvrage dans lequel sont discutées plusieurs questions relatives aux fonctions du système nerveux en générale. Paris: Crochard 1835 2nd ed. xxiv 616 pp. (see p. 94).

  • 13.

    GoggioA. F. The mechanism of contre-coup injury. J. Neurol. Psychiat.1941 n.s. 4: 1122.Goggio A. F. The mechanism of contre-coup injury. J. Neurol. Psychiat. 1941 n.s. 4: 11–22.

  • 14.

    GurdjianE. S. and WebsterJ. E. Experimental head injury with special reference to the mechanical factors in acute trauma. Surg. Gynec. Obstet.194376: 623634.Gurdjian E. S. and Webster J. E. Experimental head injury with special reference to the mechanical factors in acute trauma. Surg. Gynec. Obstet. 1943 76: 623–634.

  • 15.

    HolbournA. H. S. Mechanics of head injuries. Lancet19432: 438441.Holbourn A. H. S. Mechanics of head injuries. Lancet 1943 2: 438–441.

  • 16.

    LeCountE. R. and ApfelbachC. W. Pathologic anatomy of traumatic fractures of cranial bones and concomitant brain injuries. J. Amer. med. Ass.192074: 501511.LeCount E. R. and Apfelbach C. W. Pathologic anatomy of traumatic fractures of cranial bones and concomitant brain injuries. J. Amer. med. Ass. 1920 74: 501–511.

  • 17.

    MilesA. On the mechanism of brain injuries. Brain189215: 153189.Miles A. On the mechanism of brain injuries. Brain 1892 15: 153–189.

  • 18.

    MillerG. G. Cerebral concussion. Arch. Surg. Chicago192714: 891916.Miller G. G. Cerebral concussion. Arch. Surg. Chicago 1927 14: 891–916.

  • 19.

    MunroD. Cranio-cerebral injuries. Their diagnosis and treatment. New York: Oxford University Press1938xxviii412 pp.Munro D. Cranio-cerebral injuries. Their diagnosis and treatment. New York: Oxford University Press 1938 xxviii 412 pp.

  • 20.

    PolisA. Recherches expérimentales sur la commotion cérébrale. Rev. Chir. Paris189414: 273319; 645–730.Polis A. Recherches expérimentales sur la commotion cérébrale. Rev. Chir. Paris 1894 14: 273–319; 645–730.

  • 21.

    RowbothamG. F. Acute injuries of the head. Their diagnosis treatment complications and sequels. Edinburgh: E. & S. Livingstone1942xii288 pp. (see pp. 12–19).Rowbotham G. F. Acute injuries of the head. Their diagnosis treatment complications and sequels. Edinburgh: E. & S. Livingstone 1942 xii 288 pp. (see pp. 12–19).

  • 22.

    RussellW. R. Cerebral involvement in head injury. A study based on the examination of two hundred cases. Brain193255: 549603.Russell W. R. Cerebral involvement in head injury. A study based on the examination of two hundred cases. Brain 1932 55: 549–603.

  • 23.

    SheldenC. H.PudenzR. H.RestarskiJ. S. and CraigW. M. The lucite calvarium—a method for direct observation of the brain. I. The surgical and lucite processing techniques. J. Neurosurg.19441: 6775.Shelden C. H. Pudenz R. H. Restarski J. S. and Craig W. M. The lucite calvarium—a method for direct observation of the brain. I. The surgical and lucite processing techniques. J. Neurosurg. 1944 1: 67–75.

  • 24.

    VanceB. M. Fractures of the skull. Complications and causes of death: a review of 512 necropsies and of 61 cases studied clinically. Arch. Surg. Chicago192714: 10231092.Vance B. M. Fractures of the skull. Complications and causes of death: a review of 512 necropsies and of 61 cases studied clinically. Arch. Surg. Chicago 1927 14: 1023–1092.

  • 25.

    WalkerA. E.KollrosJ. J. and CaseT. J. The physiological basis of concussion. J. Neurosurg.19441: 103116.Walker A. E. Kollros J. J. and Case T. J. The physiological basis of concussion. J. Neurosurg. 1944 1: 103–116.

The opinions or conclusions contained in this report are those of the authors. They are not to be construed as necessarily reflecting the views or the endorsement of the Navy Department.

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Headings

Figures

  • View in gallery

    Theories concerning the mechanism of coup and contrecoup cerebral damage. The skull deformation shown in the diagram representing the theory of transmitted waves of force has not been described in all of the writings on this theory but is included for the sake of simplicity.

  • View in gallery

    Compressed air gun designed for delivering calibrated blows to the head. Note the vertical mercury manometer, the compressed air chamber, the horizontal barrel through which the projectiles are propelled and two of the four projectiles in the front rack. The vents near the end of the barrel release the compressed air charge behind the projectile and thereby permit a sharp, instantaneous blow to be struck.

  • View in gallery

    Perforating gunshot wound of the brain with an ⅛ inch steel sphere having a velocity of approximately 1800 ft. per sec. Note the hemorrhagic softening along the path of the missile.

  • View in gallery

    Head displacement and convolutional rotation patterns resulting from midline frontal blows.

  • View in gallery

    Patterns of head and convolutional motion resulting from parietal blows.

  • View in gallery

    Nature of displacement of the head and of the cerebral convolutions resulting from temporal blows.

  • View in gallery

    Gunshot wound of the brain. The intense flattening of the convolutions at the height of intracranial pressure is shown.

References

1.

Alquié. Étude clinique et expérimentale de la commotion traumatique ou ébranlement de l'encéphale. Gaz. méd. Paris186520: 226; 254; 314; 382; 396; 463; 500.Alquié. Étude clinique et expérimentale de la commotion traumatique ou ébranlement de l'encéphale. Gaz. méd. Paris 1865 20: 226; 254; 314; 382; 396; 463; 500.

2.

BryantT. Lecture on cranial and intracranial injuries. Lancet18882: 404408; 507–510.Bryant T. Lecture on cranial and intracranial injuries. Lancet 1888 2: 404–408; 507–510.

3.

ButlerE. G.PuckettW. O.HarveyE. N. and McMillenJ. H. Experiments on head wounding by high velocity missiles. J. Neurosurg.19452: 358363.Butler E. G. Puckett W. O. Harvey E. N. and McMillen J. H. Experiments on head wounding by high velocity missiles. J. Neurosurg. 1945 2: 358–363.

4.

ChipaultA. and BraquehayeJ. Études graphiques sur les fractures indirectes de la base du crâne (définition et mécanisme). Arch. gén. Méd.1895176: 279296; 394–404; 665–701.Chipault A. and Braquehaye J. Études graphiques sur les fractures indirectes de la base du crâne (définition et mécanisme). Arch. gén. Méd. 1895 176: 279–296; 394–404; 665–701.

5.

CourvilleC. B. Coup-contrecoup mechanism of craniocerebral injuries. Some observations. Arch. Surg. Chicago194245: 1943.Courville C. B. Coup-contrecoup mechanism of craniocerebral injuries. Some observations. Arch. Surg. Chicago 1942 45: 19–43.

6.

Denny-BrownD. Cerebral concussion. Physiol. Rev.194525: 296325.Denny-Brown D. Cerebral concussion. Physiol. Rev. 1945 25: 296–325.

7.

Denny-BrownD. and RussellW. R. Experimental cerebral concussion. Brain194164: 93164.Denny-Brown D. and Russell W. R. Experimental cerebral concussion. Brain 1941 64: 93–164.

8.

DottN. M. Injuries of the brain and skull. In: Surgery of modern warfare. H. Bailey ed. Baltimore: Williams & Wilkins Co.19422nd ed.1: 259287.Dott N. M. Injuries of the brain and skull. In: Surgery of modern warfare. H. Bailey ed. Baltimore: Williams & Wilkins Co. 1942 2nd ed. 1: 259–287.

9.

DuretH. Traumatismes cranio-cérébraux. Paris: F. Alcan19201357 pp.Duret H. Traumatismes cranio-cérébraux. Paris: F. Alcan 1920 1357 pp.

10.

Félizet. Quoted by Polis A. and Miles A.Félizet. Quoted by Polis A. and Miles A.

11.

FerrariA. Sulla commozione cerebrale. Osservazione ed esperimenti. Spallanzani Riv. Sci. med. nat.1882 2 s. 11: 169196.Ferrari A. Sulla commozione cerebrale. Osservazione ed esperimenti. Spallanzani Riv. Sci. med. nat. 1882 2 s. 11: 169–196.

12.

GamaJ.-P. Traité des plaies de tête et de l'encéphalite principalement de celle qui leur est consécutive. Ouvrage dans lequel sont discutées plusieurs questions relatives aux fonctions du système nerveux en générale. Paris: Crochard18352nd ed.xxiv 616 pp. (see p. 94).Gama J.-P. Traité des plaies de tête et de l'encéphalite principalement de celle qui leur est consécutive. Ouvrage dans lequel sont discutées plusieurs questions relatives aux fonctions du système nerveux en générale. Paris: Crochard 1835 2nd ed. xxiv 616 pp. (see p. 94).

13.

GoggioA. F. The mechanism of contre-coup injury. J. Neurol. Psychiat.1941 n.s. 4: 1122.Goggio A. F. The mechanism of contre-coup injury. J. Neurol. Psychiat. 1941 n.s. 4: 11–22.

14.

GurdjianE. S. and WebsterJ. E. Experimental head injury with special reference to the mechanical factors in acute trauma. Surg. Gynec. Obstet.194376: 623634.Gurdjian E. S. and Webster J. E. Experimental head injury with special reference to the mechanical factors in acute trauma. Surg. Gynec. Obstet. 1943 76: 623–634.

15.

HolbournA. H. S. Mechanics of head injuries. Lancet19432: 438441.Holbourn A. H. S. Mechanics of head injuries. Lancet 1943 2: 438–441.

16.

LeCountE. R. and ApfelbachC. W. Pathologic anatomy of traumatic fractures of cranial bones and concomitant brain injuries. J. Amer. med. Ass.192074: 501511.LeCount E. R. and Apfelbach C. W. Pathologic anatomy of traumatic fractures of cranial bones and concomitant brain injuries. J. Amer. med. Ass. 1920 74: 501–511.

17.

MilesA. On the mechanism of brain injuries. Brain189215: 153189.Miles A. On the mechanism of brain injuries. Brain 1892 15: 153–189.

18.

MillerG. G. Cerebral concussion. Arch. Surg. Chicago192714: 891916.Miller G. G. Cerebral concussion. Arch. Surg. Chicago 1927 14: 891–916.

19.

MunroD. Cranio-cerebral injuries. Their diagnosis and treatment. New York: Oxford University Press1938xxviii412 pp.Munro D. Cranio-cerebral injuries. Their diagnosis and treatment. New York: Oxford University Press 1938 xxviii 412 pp.

20.

PolisA. Recherches expérimentales sur la commotion cérébrale. Rev. Chir. Paris189414: 273319; 645–730.Polis A. Recherches expérimentales sur la commotion cérébrale. Rev. Chir. Paris 1894 14: 273–319; 645–730.

21.

RowbothamG. F. Acute injuries of the head. Their diagnosis treatment complications and sequels. Edinburgh: E. & S. Livingstone1942xii288 pp. (see pp. 12–19).Rowbotham G. F. Acute injuries of the head. Their diagnosis treatment complications and sequels. Edinburgh: E. & S. Livingstone 1942 xii 288 pp. (see pp. 12–19).

22.

RussellW. R. Cerebral involvement in head injury. A study based on the examination of two hundred cases. Brain193255: 549603.Russell W. R. Cerebral involvement in head injury. A study based on the examination of two hundred cases. Brain 1932 55: 549–603.

23.

SheldenC. H.PudenzR. H.RestarskiJ. S. and CraigW. M. The lucite calvarium—a method for direct observation of the brain. I. The surgical and lucite processing techniques. J. Neurosurg.19441: 6775.Shelden C. H. Pudenz R. H. Restarski J. S. and Craig W. M. The lucite calvarium—a method for direct observation of the brain. I. The surgical and lucite processing techniques. J. Neurosurg. 1944 1: 67–75.

24.

VanceB. M. Fractures of the skull. Complications and causes of death: a review of 512 necropsies and of 61 cases studied clinically. Arch. Surg. Chicago192714: 10231092.Vance B. M. Fractures of the skull. Complications and causes of death: a review of 512 necropsies and of 61 cases studied clinically. Arch. Surg. Chicago 1927 14: 1023–1092.

25.

WalkerA. E.KollrosJ. J. and CaseT. J. The physiological basis of concussion. J. Neurosurg.19441: 103116.Walker A. E. Kollros J. J. and Case T. J. The physiological basis of concussion. J. Neurosurg. 1944 1: 103–116.

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