Similarly, the extensive histological analysis
has revealed a degenerative neurological phe-
nomenon associated with impact events of both
test conditions. With only one exception, all
traumatized subjects in both test series demon-
strated alterations of the large nerve cells and
elements as shrunken, misshapen and pyknotic
nuclei and classic loss of nuclear detail. It is
usually agreed that such degenerative changes
require a number of hours to manifest following
insult. These cell changes occurred within 60
minutes or less after impacts in this study. Con-
siderations of viral problems and other predis-
posing factors were not confirmed after a lengthy
and detailed analysis. Control subjects, both
laboratory-bred and fresh-colony imports of
different origin, were analyzed for possible
sources of artifacts with negative results and a
re-evaluation of potential test conditions for
sources of anoxia had the same result. In a
detailed analysis of over 300 other histological
surveys of traumatized baboons without direct-
head impact, no degenerative changes similar to
those were found. Only two other sources of
experimental work, by Snyder (1972) and Port-
noy (1970), have confirmed similar findings and
were, in fact, produced under similar impact
conditions.

V. Conclusions

On the basis of these initial tests, there appear
to be certain combinations of physiological re-
sponses and associated injury mechanisms that
may be either contradictory in part to current
theories now held by a number of investigators
or may actually indicate additional phenomena
not previously documented. Of greatest signifi-
cance, the contrecoup injury has been produced
by direct occipital impact to heads supported and
not free to respond kinematically to the impact
force. Further, this type of indirect injury has
been produced by only translational forces in
both the supported heads and heads free to move
in a controlled anterior-posterior plane with rela-
tively similar force inputs. Degenerative nerve
cell changes have also been consistently produced
under the conditions of acute head impact in less
than one hour and, without benefit of further
experimental evidence, appear to be trauma re-
lated. It is suggested that the experimental
evidence presented here is sufficient to seriously
question the absolute adequacy of current injury
tolerance data that are being offered and used to
establish tolerance standards. Additional ex-
perimental testing will be necessary to statistic-
ally evaluate these potentially conflicting theories
and provide realistic tolerance values for design
standards.


ACKNOWLEDGMENTS

The authors gratefully acknowledge the invaluable contributions of
D. E. Rowlan, E. M. Trout, M. A. Allgood, B. G. Nixon, Dr. G. D. Hanne-
man, Dr. A. M. Revzin, and C. K. Reed, all of the Civil Aeromedical Insti-
tute; and of Dr. S. Deutsch, Chairman of the Department of Anesthesiology,
the University of Oklahoma Health Sciences Center, in support of this study.
Special acknowledgment is made to Mr. Alan Greenberg and the Greenberg
Neurosurgical Trust Fund for technical support and international travel to
present a summary of this work at the International Congress on the Bio-
kinetics of Impact, Amsterdam, The Netherlands.




the hour after death, additional immediate fixing
of the brain and cord was not considered neces-
sary to inhibit autolysis.

III. Results

Summaries of test results for both test vari-
ables of supported- and moving-head series are
outlined in Tables 1 and 2. Difficulties in achiev-
ing mechanical stability of instrumentation im-
plants during impact resulted in certain data
artifacts and, in some instances, data loss. The
continuity of EEG electrode and carotid flow
transducer interfaces was momentarily disrupted
in all tests with artifactual or partial data loss.
Although EEG signals did recover in part as
stable signals, both flow transducers failed to
stabilize for meaningful data records. Similarly,
signal output from the transducers measuring
intracranial pressure appeared to be artifactual
and will not be considered for analysis in this
paper. The design limits of accelerometers
bonded to the anterior calvarium were exceeded
by impact velocities and were not used thereafter.
Blood gas values obtained were not considered
significant for the purposes of this study. Al-
though post-impact monitoring continued for as
long as one hour in isolated cases, data analysis
for this paper will consider only the first 30-
minute period following impact.

Supported-Head Series

Subject CP 110. Pupil dilation occurred bi-
laterally and returned to normal in 14 seconds
on only the right side. Conversely, only the left
corneal reflex was functional after 35 seconds
following bilateral loss. EEG patterns demon-
strated slowed activity post-impact. No signifi-
cant changes in the ECG pattern were observed,
but both pulse rate and arterial pressure levels
dropped after impact and recovered to baseline
values at 40 and 30 seconds respectively. Gross
autopsy findings were subcutaneous hemorrhage
at the impact site, a simple non-depressed linear
fracture from the occiput parasagittally into the
foramen magnum and contused areas intra-
durally in the inferior-frontal, temporal and oc-
cipital areas and the cerebellum. Subarachnoid
hemorrhages were histologically confirmed in the
same areas and a few isolated hemorrhages were
found deep in the temporal and cerebellar sub-
stance. Degenerative nerve cell changes were
observed among normal, healthy cells in the

frontal and occipital areas. These cell changes
were manifested as shrunken and pyknotic with
loss of nuclear detail.

Subject CP 111. Both pupil dilation and
corneal reflex loss were bilateral with return ex-
cept for continuous dilation of the left pupil.
Corneal reflexes were active after 46 seconds.
EEG activity was briefly slowed and ECG dem-
onstrated a continuous bradycardia and loss of P
wave. Both pulse rate and arterial pressure
levels were depressed post-impact and did not
return to normal baseline values. Coincident
with a small laceration and subcutaneous hemor-
rhage, a complex, fragmented fracture pattern
was centered around the impact site with occipi-
tal and post-parietal involvement. Occasional
subarachnoid hemorrhages in the frontal, occipi-
tal and cerebellar areas were confirmed histo-
logically, but deep micro-hemorrhages were
found only in the occipital portion of the cere-
brum and the cerebellum. In the frontal, tem-
poral and occipital portions of the cerebrum,
some of the large nerve cells were shrunken and
misshapen and presented altered staining reac-
tion. Their nuclei were indistinct with absence
of chromatin and nucleoli. Cells in the occipital
portion showed more intense degenerative
changes with pyknotic nuclei or indistinct struc-
ture and increased number of glial elements.

Subject CP 112. Pupils dilated bilaterally
with normal return in 60 seconds. Corneal re-
flexes were extinguished and became functional
after 12 and 20 seconds post-impact. EEG
activity slowed intermittently and the ECG pat-
tern changed significantly with distinct brady-
cardia and premature ventricular contractions.
Pulse rate and arterial pressure increased briefly,
then decreased to remain below baseline levels.
Pathologically, a scalp laceration with subcuta-
neous hemorrhage and a multi-fragmented frac-
ture pattern was centered around the impact site.
Gross examination revealed isolated areas of
contusion on the inferior surfaces of the frontal
lobes, temporal, occipital and posterior cerebel-
lum. Subarachnoid hemorrhages were observed
in microscopic sections from the frontal and
temporal areas and the cerebellum. The only
internal hemorrhages were located throughout
the cerebellum. A majority of the large nerve cells
presented the same degenerative changes as de-
scribed in the other test subjects. Although


EXPERIMENTAL TRAUMA OF OCCIPITAL IMPACTS

I. Introduction

Head injury is acknowledged to be one of the
more serious safety and medical management
problems in both air and ground vehicle acci-
dents. Although certain physiological phenom-
ena and injuries are predictively observed in
accident situations, little is known of the more
basic mechanisms producing these phenomena
and even less is known of the relationships be-
tween viable responses, trauma and impact char-
acteristics.

Early injury tolerance standards were based
on best estimates from isolated classical physio-
logical experiments and judgments of clinical
observations. In more recent years, revisions in
injury tolerances have, unfortunately, been de-
fined primarily in terms of fracture characteris-
tics of cranial and facial bones with little
emphasis on, or serious acknowledgment of, more
critical physiological problems. The philosophy
of this approach had been generally discredited
more than 100 years ago when Abernathy (1852),
Hutchinson (1877) and Bergmann (1880), among
others, supported the view that traumatic dis-
order of the brain can occur without structural
damage. The fact that more recent investigators,
such as Haynes and Lissner (1961), specifically
conclude that serious and fatal brain injuries can
occur without fracture has not significantly
changed the existing injury tolerance standards,
because of inadequate information. Following
Holbourn’s major work (1943), Ommaya’s over-
view of head injury (1966) and subsequent work
have again emphasized a more realistic trend in
experimental head injury to define the basic
mechanisms and correlate the events of impact
responses with controlled-impact characteristics.
Such data are relative to the real accident situa-
tion where physiological responses are direct
correlating factors of injury and survival status.

This report documents the physiological re-

sponses, trauma pathology and dynamic events
of head impact experiments that produced a

clinically defined state of cerebral concussion.
It was anticipated that a better understanding
of the relationships of trauma mechanisms would
result in a more effective early clinical manage-
ment of head injuries and more efficient methods
to prevent or reduce serious head injury with
meaningful tolerance standards for design. Pre-
vention or reduction of incapacitating head in-
juries that would preclude effective escape
procedures in survivable transportation accidents
is considered a priority safety problem.

II. Methods

Experimental Philosophy

The purpose of this study was to produce head
trauma at cerebral concussive levels with alert
primate test subjects to measure and correlate
physiological responses, histopathology, head
kinematics and the dynamic events associated
with impact forces. This study was the initial
phase of a comprehensive head injury program
planned for a series of head trauma experiments.
Within the scope of this phase, only the acute
trauma conditions were considered for a two-
variable study.

The inherent problems of accounting for all
influencing factors on test responses and selection
of test controls in experimental design were no
less critical to this study. Since specific neuro-
logical responses would be measured and a va-
riety of response phenomena would be expected
to occur as unknown factors with unknown in-
fluences, certain test conditions were considered
essential. Critical to this experimental design
was a pre-impact condition of normal neurologi-
cal responsiveness, As the measure of any test
response would be questionable under the influ-
ence of residual effects from anesthesia or medi-
cations that alter normal functions, the subject
could not be tested until the prolonged effects of
medication had disappeared. Such delay be-
tween surgical preparation and impact test would
present difficult maintenance problems with the




to contact the dura. Sterile normal saline solu-
tion was placed extradurally in both preparations
to maintain a fluid interface with the transducer.
The transducers were aligned in an an‘erior-
posterior plane five millimeters parasagittally to
the left. An array of two miniature accelerom-
eters (Endevco 2000 Series) was aligned and
mounted as a unit midsagittally in the post-
orbital ridge area to measure anterior-pos‘erior
and check vertical accelerations during the im-
pact sequence.

Although difficult to accurately measure with-
out more sophisticated gas or isotope techniques,
attempts to measure cerebral blood flow were
made with Biotronex BL flow transducers. Flow
rates were measured by placing a transducer at
the distal part of each common carotid artery
through a single, anterior midline incision on the
neck. Both external carotid branches were ligated
but no attempt was made to occlude the paired
vertebral artery source. ECG measurements
were obtained with a standard array of three
needle electrodes and stabilized by taping the
leads.

Arterial and venous blood pressures were
measured with Konigsberg catheter type (P
model) pressure transducers positioned in the
thoracic portion of the descending aorta and in-
ferior vena cava respectively. These implants
were accomplished by passing the catheter
through the right femoral artery and vein via
accessory branches. Entry through and subse-
quent ligation of the accessory vessels were made
to avoid interruption of the primary limb cir-
culation. A catheter tube was likewise placed
via the left femoral artery for an external Sta-
tham type pressure transducer as a backup
measurement of arterial blood pressure. The
left femoral vein was fitted with a cannula to
draw internal blood samples for analysis with a
Radiometer, Model BMS-3 acid-base analyzer.
Dual, small-diameter air tubes were positioned
on the head restraint to direct air flow into the
eyes as a continuous stimulus for eye reflexes.

Test Procedures

All test procedures were arranged and exe-
cuted in a standardized, chronological sequence
to assure compatibility with test control require-
ments of critical procedural time limits, Two
days prior to the test, a set of head and neck
x-rays, shaving of the surgical surface areas and

preparations for restraint sizing were completed.
The intervening day was required to permit the
subject to completely recover from the effects of
phencyclidine hydrochloride and sodium penta-
barbital used in preparation procedures.

Surgical preparation of the test subject was
accomplished as the first procedure the following
day. An initial 75 mg sodium methohexital so-
lution was administered intramuscularly with
atropine prior to surgical anesthesia, then tra-
cheal intubation was performed and anesthesia
was accomplished with a nitrous oxide-oxygen
mixture with halothane (per cent ratio of 6:4:2).
A maintenance dosage rate was continued with
decreased halothane volume of one-half to one
per cent. After completion of all implant pro-
cedures, the subject was positioned and secured
in the restraint system. Anesthetic agents were
immediately withdrawn and the subject allowed
to regain consciousness with continued oxygen
support. The subject was monitored until all
vital signs and responses were considered normal,
then placed in the test position. Following a
brief clinical evaluation, the endotracheal tube
was removed and bioinstrumentation connected
to start baseline monitoring and recording. In-
strumentation continuity checks were made with
viable signals for amplifying and recording
equipment; then data sampling at five-minute
intervals began at 30 minutes before impact with
activation of the automatic switching timer for
camera, lights and impact countdown. At five
minutes pre-impact, recorders were set on con-
tinuous run for data sampling until 30 minutes
post-impact. Euthanasia solution was adminis-
tered following this monitoring period through
the venous catheter to terminate the subject.

Within one hour after death, a comprehensive
necropsy protocol was conducted to identify and
describe gross trauma of all head and neck struc-
tures. All observations were recorded on tape
and by color photography. Autopsy procedures
were completed with the removal of the intact
brain and cervical cord for histological prepara-
tion and study. A standardized plan of brain
and cord sectioning was followed to assure com-
parison of similar sections in all test subjects.
Typical fixing procedures with buffered formalin
solutions were followed for routine staining with
hematoxylin-eosin and galocyanin blue agents.
Since autopsy procedures were initiated within




thage was coincident with the occipital impact
site and the origin of a linear fracture passing
parasagitally into the foramen magnum. Areas
of intradural hemorrhage were found on the
anterior aspect of the temporal lobes, posterior
aspects of the occipital poles and cerebellum.
Subarachnoid hemorrhages were confirmed in the
frontal and temporal areas and deep hemor-
rhages were revealed in the substance of the pons
and cerebellum. Typical degenerative nerve cell
changes were manifest, with some difference. A
few well-formed cells showed only indistinct
nuclear detail with some loss of chromatin, but
many more of the severely affected cells presented
satellitosis and early garyolysis. Most of these
changes were confined to the cerebrum.

Subject CP 115. Bilateral pupil dilation oc-
curred and corneal reflexes extinguished without
recovery of either. EEG waves were flattened
and slowed and pulse rate, arterial pressure and
carotid flow all depressed without return to nor-
mal baseline levels. A scalp laceration and sub-
cutaneous hemorrhage attended a complex,
multi-fragmented fracture pattern of the occipi-
tal and parietal bones. Depressed fragments
were the cause of sagittal sinus lacerations and
subsequent loss of a large volume of blood. This
subject was terminated after a 15-minute moni-
toring period without regaining consciousness.
Gross contusion areas were observed over the
anterior temporal lobe, occipital and cerebellar
areas. Subarachnoid hemorrhage was extensive
in the temporal, occipital, pons, cerebellum and
cervical areas. Degenerative nerve cell changes
were confined to the occipital and cerebellar
areas.

Subject CP 116. There was no pupil dilation
and bilaterally extinguished corneal reflexes re-
turned after two seconds. There was a question-
able area of slowed EEG activity and pulse rate
and arterial pressure depressed for only 12 and
25 seconds respectively. A small subcutaneous
hemorrhage and short linear fracture were found
at the impact site. Although dural congestion
was evident on the anterior surfaces of the tem-
poral lobes, occipital and cerebellar surfaces,
subarachnoid and deep hemorrhages were con-
fined to the cerebellum. Conversely, degenerative
nerve cell changes were found in all histological
sections with the exception of the pons.

Subject CP 117. The bilateral pupil dilation
did not fully return to normal; however, both
corneal reflexes were extinguished for only two
seconds. Slowed activity was suggested in the
EEG patterns, but the ECG was not remarkable.
Pulse rate was depressed for 39 seconds and
arterial pressure returned to normal after in-
creasing for 25 seconds. The inferior frontal,
occipital and cerebellar areas showed dural con-
tusions; however, only the cerebellum had both
subarachnoid and deep hemorrhages. An iso-
lated temporal area of subarachnoid hemorrhage
was confirmed. Degenerative nerve cell changes
were found in the frontal, temporal, occipital
and cerebellum areas. There appeared to be
gradations of changes with slightly misshapen
and altered nuclear detail in many cells.

Subject CP 118. Although bilateral pupil di-
lation never recovered on the right side, and the
left remained dilated for 113 seconds, both cor-
neal reflexes were active after only two seconds.
EEG activity slowed and the P wave in the
ECG was depressed. The pulse rate remained
elevated for 220 seconds and, conversely, the ar-
terial pressure depressed for only 60 seconds
before recovery to normal baseline level. A
simple linear fracture in the occipital bone was
found with superficial subcutaneous hemorrhage
and scalp laceration. Grossly observed areas of
contusion were located along the -anterior tem-
poral, occipital and cerebellar surfaces. De-
generative nerve cell changes were confined to
the temporal, occipital and cerebellar sections
with clear zones surrounding these misshapen
cells to suggest edema. Intense areas of sub-
arachnoid hemorrhages were found in the front
and temporal portions and deep micro hemor-
rhages only in the cerebellum.

Subject CP 120. Similar to CP 117, there was
no recovery of normal pupil diameter but corneal
reflexes returned bilaterally within 13 seconds.
Slowed EEG activity is suggested and P wave
remained depressed for most of the monitoring
period. A depressed pulse rate recovered after
25 seconds post-impact and arterial pressure de-
creased to baseline levels after 80 seconds. A
complex, multiple fracture pattern in the occipi-
tal bone and parietals was not depressed and
associated with the typical lacerated scalp and
subcutaneous hemorrhage. Gross contusion areas
of the dura were most extensive in this group


nerve cells in the cervical cord section were
largely well formed with distinct nuclei, Nissl
substance appeared to be absent.

Subject CP 121. Pupil dilation was bilateral
with return on the right side only at 35 seconds.
Bilateral corneal reflex loss was very brief for
four seconds. EEG showed a delayed, but brief,
slowed activity and bradycardia with premature
ventricular contractions disappearing by the end
of the monitoring period. Pulse rate and ar-
terial pressure decreased and recovered at 40 and
35 seconds, respectively. A drop in the carotid
flow rates was observed for a few seconds, then
became unstable with neck movement. Isolated
hemorrhages were found subcutaneously at the
impact site, superficial to the origin of a single
linear fracture that continued into the foramen
magnum. Gross contusions were observed within
the dura over the temporal, pons, cerebellar and
post-cervical areas. Subarachnoid hemorrhages
were scattered along the surfaces of the temporal
lobes, posterior cerebellum, pons and the cervical
cord. This is the only test subject that did not
demonstrate degenerative nerve cell changes.

Subject CP 122. Post-impact pupil dilation
was bilateral with one of the greatest durations
of 120 seconds. Conversely, the bilateral loss of
corneal reflexes was only two seconds. Both the
EEG slowing and ECG patterns of bradycardia
and premature ventricular contractions remained
for only 45 seconds. The pulse rate stabilized
after 55 seconds and arterial pressure and carotid
flow rates returned to baseline after 180 seconds
from depressed levels. A small subcutaneous
hemorrhage was confirmed at the impact site,
but there was no fracture in the cranial vault.
This was the only subject without fracture. Two
small areas of dural contusions were found over
the inferior aspect of the frontal lobes and pos-
terior surface of the occipital lobes. Subarach-
noid hemorrhages were confined to the occipital
and pons areas and internal hemorrhage only in
the substance of the cerebellum and superior
cervical cord. A number of large nerve cells in
all cerebral areas were typically degenerative in
nature, most without nuclear detail and Nissl
substance. The Purkinje cells in the cerebellum
were not remarkable but few ganglion cells in
the cervical cord demonstrated degenerative
changes. None of the cells possessed Niss] sub-
stance.

Subject CP 124. Bilateral pupil dilation re-
mained for 48 seconds post-impact and corneal
reflexes were functional within 16 seconds. The
EEG patterns typically demonstrated slowed
activity. Premature ventricular contractions
were consistent throughout the monitoring pe-
riod, but only a brief interval of bradycardia
appeared immediately post-impact. Pulse rate,
arterial pressure and carotid flow rate decreased
immediately after impact, then recovered to
normal values after 20 seconds. A subcutaneous
hemorrhage overlying a single non-depressed
occipital fracture was coincident with the impact
site. The entire anterior surface areas of the
frontal lobes were contused, unlike all other sub-
jects. Subarachnoid hemorrhages were found in
the sub-frontal and inferior temporal surfaces
and along the posterior aspects of the occipital
lobes and cerebellum. Internal hemorrhages were
located in the pons and deep throughout the
cerebellum and typical degenerative neural alter-
ations were confirmed in the temporal and oc-
cipital areas.

Moving-Head Series

Subject CP 113. Bilateral pupil dilation and
loss of corneal reflex occurred immediately post-
impact with recovery within 20 seconds. Slowed
EEG activity occurred briefly and the ECG pat-
terns were not remarkable. Arterial pressure
increased for 20 seconds with similar carotid flow
shifts, but the pulse rate depressed 120 seconds.
Typical scalp laceration and subcutaneous hemor-
rhage were associated with a short linear fracture
of the occipital bone at the impact site. Contused
areas were found on the inferior surfaces of the
frontal lobes, anterior aspects of the temporal
lobes and posterior occipital areas. Diffuse
subarachnoid hemorrhages were confined to cor-
responding frontal and temporal areas and a
single area of internal hemorrhage was located
in the right occipital lobe. Among normal cells,
degenerative changes were found in the frontal,
temporal and occipital areas.

Subject CP 114. Pupil dilation and corneal
reflex loss were bilateral with short term recov-
ery time at 12 and 2 seconds respectively. As in
Subject CP 113, the ECG patterns were not re-
markable and only a brief few-second slowed
activity was evident. Both pulse rate and ar-
terial pressure were depressed for 25 and 80
seconds respectively. Local subcutaneous hemor-


awake subject and preclude documentation of
pre-impact baseline values. The use of a nitrous
oxide-oxygen mixture with halothane for surgi-
cal anesthesia and local anesthesia blocks periph-
eral to the occipital impact site was considered
essential to avoid residual effects and assure ex-
perimental validity.

Experimental Design

The experimental design for this study con-
sidered procedures and techniques that had been
used in other applications and represent the best
combinations to achieve program objectives.

Test Factors

An acute two-variable test series was conducted
with Savannah baboons (Papio cynocephalus)
as the initial phase of the comprehensive head
injury study. The test variables were (1) oc-
cipital impacts to supported heads (supported
series) and (2) occipital impacts to heads free
to move in a controlled linear, posterior-anterior
direction (moving series). These variables were
selected to control certain head-neck kinematics
that could be potentially related to physiological
responses and to identify the relationships, if
any, of associated injuries. The direction of
impact, relative to head orientation, was parallel
to the subject’s horizontal Frankfort plane. This
orientation of head-to-impactor interface in the
midsagittal plane was maintained for all impact
tests. The occipital type impact was selected as
the optimal condition to assure the greatest pos-
sible shock input to head structures with least
trauma of hard and soft tissues. Similarly, the
impact profile and impactor characteristics se-
lected to produce traumatic physiological changes
provided optimal factors of shape, mass and ve-
locity to create a relatively high shock input to
the head with the least amount of structural
damage. Based on previous occipital impacts
that considered factors of cranial geometry and
fracture patterns, impactor velocities averaging
43, 45 and 50 feet per second were selected using
similar x-ray analyses for each test subject.

Test subject responses and conditions clinically
observed and evaluated were pupillary and
corneal reflexes, lid closure, gross trauma and
histopathology. Instrumented and measured test
responses were electroencephalographic (EEG)
and electrocardiographic (ECG) patterns, pulse
rates, arterial and venous blood pressures, cere-

bral blood flow rates, blood gas levels, head ac-
celeration and head kinematic patterns.

Tt was anticipated that resistance by the sub-
ject to body restraint would indirectly influence
both observed and measured responses during
sequential test procedures. The entire body was
enclosed in a restraint system, except for certain
head and neck areas, to control this resistance
and reduce the isometric stress. The head was
enclosed separately in a rigid form-fitting cast
and secured to a holding device that controlled
head motion for each test condition and pre-
vented gross deformation of the cranial vault
during impact. An erect sitting position of the
test subject was considered a best compromise
for impactor-subject orientation and subject
maintenance during extended periods.

Environmental control of the test area was
planned and maintained to assure duplication
of conditions for each test. Temperature, light,
noise and motion factors that provided external
sensory cues to the subject were controlled to
reduce spontaneous excitement responses during
data measurement. Test subjects were laboratory-
conditioned, adult, female baboons in a weight
range of 22 to 28 pounds. All subjects were held
in quarantine and clinically monitored for at
least six weeks before testing to assure behavioral
and physiological stability.

Bioinstrumentation

Conventional and modified bioinstrumentation
techniques and equipment were selected on the
basis of state-of-the-art availability to this lab-
oratory.

A standard array of three bilaterally paired
EEG signal leads was positioned parasagittally
within the exposed frontal and parietal bone
areas via a single midline scalp incision. Each
lead, shielded and insulated, was attached to a
gold-plated electrode implanted through the
calvarium to permit a direct extradural fluid
interface. A single ground lead was implanted
midsagittally on the superior aspect of the ex-
posed supraorbital ridge. All extracranial tis-
sues, including the periosteum, were removed
from the implant sites to reduce signal interfer-
ence. Two Konigsberg pressure transducers
(P model) were placed extradurally to measure
intracranial pressure. Each transducer was ce-
mented in place deep in the trephined hole but
did not extend through the inner table of bone




a

. Denny-Brown,

'. Holbourn,

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Snyder, R. G.: Personal communication, 1972,
Tindall, G. T.: Personal communication, 1972.
Vance, B. M.: ARCH. SURG., 14:1022, 1927.


TABLE 2. Summary of Moving-Head Impact Responses

POSTIMPACT

CONDITIONS cP 113 cP 114 cP 115 cP 116 cP 117 cP 118 cP 120
-

PUPIL oy | Bilateral | Bilateral |Bilateral | None [Bilateral [Bilateral [Bilateral
PUPILS 1 Both at Both at None Bilateral | None R= None None
NORMAL 20 sec 12 sec L=113 sec

CORNEAL || pitaterai | Bilateral |Bilateral [Bilateral [Bilateral |Bilateral |Bilateral
REFLEX OUT

CORNEAL Both at Both at None Both at Both at Both at |R=13 sec
REFLEX IN 20 sec 2 sec 2 sec 2 sec 2 sec L=10 sec
EEG Slowed Slowed Slowed Slowed Slowed Slowed Slowed
ECG P Wave P Wave

Depressed |Depressed

PULSE Rate |] Down:Norm | Down:Norm |Down: No |Down:Norm |Down:Norm |Up:Norm Down:Norm
at 120sec | at 25 sec | Return at 12 sec |at 39 sec |at 220sec |at 25 sec

ARTERIAL Up:Norm Down:Norm |Up-Down: |Down:Norm |Up:Norm Down:Norm |Up:Norm
PRESSURE at 20 sec | at 80 sec |No Return |at 25 sec jat 25 sec {at 60 sec jat 80 sec

CAROTID

FLOW Increase | Decrease [Decrease {Increase Decrease

GROSS: | simple: Simple: Complex: |Simple: Complex: |Simple: Complex:
CRANIAL Occipital | Occipital |Occipital |Occipital [Occipital [Occipital |Occipital

FRACTURE Parietal Parietal Parietal
GROSS: Inf Front | Ant Temp |Ant Temp |Ant Temp [Inf Front |Ant Temp |Inf Front
BRAIN Ant Temp | Occipital |Occipital |Occipital [Occipital |Occipital | Temporal
CONTUSION || Occipital | Cerebellum] Cerebellum|Cerebellum|Cerebellumj Cerebellum Occipital
| Cerebellum
HISTOLOGY: || Frontal Frontal Temporal |Cerebellum|Temporal /|Frontal Frontal
EXT BRAIN | Temporal | Temporal | Occipital Cerebellum] Temporal |Temporal
HEMORRHAGE Pons Occipital
Cerebellum Cerebellum
Cervical Cervical
HISTOLOGY: || Occipital | Pons Frontal Cerebellum |Cerebellum|Cerebellum|Occipital
INT BRAIN Cerebellum| Temporal Cerebellum
HEMORRHAGE Occipital
Pons
Cerebellum
Cervical
HISTOLOGY: || Frontal Frontal Occipital |Prontal Frontal Temporal |Frontal
NERVE CELL|| Temporal | Temporal |Cerebellum|Temporal [Temporal |Occipital | Temporal
CHANGES Occipital | Occipital ‘Occipital |Occipital |Cerebellum|Occipital
Cerebellum |Cerebel lum} Cerebellum
Cervical
IMPACTOR 43.6 45.3 50.2 43.7 45.7 48.8 51.6
VELOCITY ft/sec ft/sec ft/sec ft/sec ft/sec ft/sec ft/sec
IMPACTOR 700 925 400 1125 800 875 850
LoaD ||__1bs lbs lbs lbs lbs lbs lbs
IMPACTOR 840 1100 800 1325 900 1050 1020
PEAK g g 8 8g 8 g g &

ll


TECHNICAL REPORT STANDARD TITLE PAGE

T. Report No. | 2. Government Accession No. 3. Recipient's Catalog No.
FAA-AM-74-4 |
Title and Subtitle 3. Report Date

March 1974
EXPERIMENTAL TRAUMA OF OCCIPITAL IMPACTS 6. Performing Organization Code
7. Author(s)

8. Performing Orgonization Report No.
Joseph W. Young, Robert G. Fisher,

G. Townley Price _and Richard F. Chandler
9. Performing Organization Name and Address

FAA Civil Aeromedical Institute

P. 0. Box 25082 TT. Contract or Grant No.
Oklahoma City, Oklahoma 73125

0. Work Unit No.

13. Type of Report and Period Covered

12. Sponsoring Agency Name and Addres

Office of Aviation Medicine
Federal Aviation Administration
800 Independence Avenue, S. W. 14."Sponsoring Agency Code
Washington, D.C. 20591

15. Supplementary Notes

OAM Report

Research leading to preparation of this report was performed under
Project AM-B-72-PRS-40,

16. Abstract

This paper presents clinical observations, physiological data and pathological
findings that have been collected on a series of baboons exposed to controlled
occipital impacts under local anesthesia. This acute experimental trauma study
was accomplished to establish trauma mechanisms and compare the relative effects
of impact with supported heads and heads capable of responding to impact in a
controlled horizontal A-P plane, Fourteen laboratory-conditioned test subjects
were surgically instrumented to obtain EEG, bilateral carotid blood flow and
aortic and venous blood pressures. Standard ECG and pulse and respiration
rates were recorded in addition to the clinical observations of pupillary
responses and corneal reflexes that were documented with high-speed movies.
Pre-impact and post-impact data baselines were continuously recorded with the
impact event, Occipital blows were delivered in the midsagittal plane (parallel
to the Frankfort plane) with a pneumatic piston containing load cells and
accelerometers. The piston was programmed for a stepped-impact profile of

42 to 52 feet per second velocity.

In all tests with the supported and mobile heads, there was apparent reversible
stunning, mydriasis, bradycardia, absence of corneal reflexes and EEG slowing.
Anterior (opposite) surface contrecoup trauma was observed in all tests with
controlled-head motion and contrecoup trauma was produced with the supported-
head tests. A unique degenerative nerve cell change was found in all trauma-
tized subjects.

17. Key Words 18. Distribution Statement
Brain Damage, Experimental Pathology, Document is available to the public
Impact Trauma, Injury Potential through the National Technical

Information Service, Springfield,
Virginia 22151

19. Security Classif. (of this report) 20. Security Classif. (of this page) 21. No. of Pages | 22. Price

Unclassified Unclassified 11 $3.00

Form DOT F 1700.7 (8-69)




covering the sub-frontal, temporal, occipital,
cerebellar areas. Subarachnoid hemorrhage was
extensive in the frontal, temporal, occipital,
cerebellar and cervical surfaces with deep hemor-
rhage only in the occipital and cerebellar sections.
Shrunken and misshapen cells with pyknotic
nuclei were again found among normal cells in
the frontal, temporal, occipital and cerebellar
areas.

IV. Discussion

The relatively small number of subjects in this
initial test series precludes a detailed statistical
analysis of data values; however, trends of cer-
tain response phenomena are distinct and appear
to be predictable. The general nature of clinic-
ally observed and measured acute responses to
direct occipital impact was not unlike systemic
responses that have been observed and docu-
mented by others. The results do suggest that
certain functional and structural changes are oc-
curring under these particvlar impact conditions
which may not conform to the more popular
explanations of injury mechanisms or which
have not been experimentally produced by others.
In general, the relatively higher levels of shock
input resulting in the supported-head series pro-
duced more intense injury and more pronounced
changes in systemic response than found in the
test with controlled-head motion. Although
there was an average difference in impactor ve-
locity of 4 ft./sec. faster and relatively higher
inputs to the heads of the moving-head series,
the type and intensity of cranial vault fracture
were not significantly different, with two excep-
tions. In Subject CP 122 there was no fracture
in a predicted worse case condition and, ironic-
ally, multiple depressed fractures occurred in a
moving-head subject (CP 115) that made arti-
factual most of the physiological response data.

Loss of corneal reflexes and pupil dilation oc-
curred as expected and typically confirmed by
other researchers such as Denny-Brown and
Russell (1941), McCullough (1971) and Tindall
(1972). The duration of the reflex loss was
longer in the supported-head series and the pupil
dilation without recovery is attributed to the
more severe shock input based on_ histological
evidence. There also appears to be a significant
difference in the ECG responses with distinct
bradycardia and premature ventricular contrac-

tions occurring in five of the six supported-head
tests and only a marked P wave depression oc-
curring in two subjects of the moving-head
series. This phenomenon seems consistent with
the relative intensity of altered physiological
responses occurring with supported heads. These
levels are also consistently higher than produced
in other relatable work and cannot be effectively
compared.

Of greater significance, examination of patho-
logical findings reveals unusual combinations of
trauma that seem to contradict established con-
ventions of injury mechanisms. The conforma-
tion of such trauma by histological analysis was
not completely unexpected in some instances;
however, the distinct and intense hemorrhage in
the frontal and temporal areas of all subjects
with supported heads as well as those in the
moving-head series are, not regarded as typical
findings under these experimental conditions.
By conventional definition these trauma areas
are defined as contrecoup injuries and should
have only occurred in heads that were free to
move with the occipital blow. This definition of
contrecoup was well documented by LeCount and
Apfelbach (1920), Vance (1927) and Munro
(1938) with confirmed experimental and human
data. These same observations were confirmed
experimentally by Denny-Brown and Russell
(1941), among others, who failed to produce
contrecoup injury with supported-heads at im-
pact, but at lower levels of shock input.

It is interesting to note that while contrecoup
injuries and loss of consciousness were produced
in both moving and supported heads with trans-
lational motion-force orientation, the theory of
Holbourn (1943) and experimental evidence by
Ommaya (1966), Hirsch (1970) and Gennarelli
(1972) demonstrate that rotational, not transla-
tional, motion is the primary component asso-
ciated with concussion and brain injury for brief
shock inputs. Whether or not contrecoup trauma
can be expected to occur predictively under these
and similar conditions must await further ex-
perimental evidence. Since this study phase did
not consider the rotational component as an ex-
perimental variable, the relative significance of
the translational role in producing unconscious-
ness under other conditions is not known.


TABLE 1. Summary of Supported-Head Impact Responses

POSTIMPACT

CONDITIONS cP 110 cP 111 cP 112 cP 121 cP 122 CP 124
PUPTL Bilateral |Bilateral |Bilateral /Bilateral |Bilateral | Bilateral
DILATION
PUPILS R=14 sec |R=90 sec Both at |R=35 sec Both at Both at
NORMAL L= None L= None 60 sec L= None 120 sec 43 sec
cones OUT Bilateral |Bilateral |Bilateral |Bilateral |Bilateral | Bilateral
CORNEAL R= None Both at |R=20 sec Both at Both at |R=16 sec
REFLEX IN | L=35 sec 46 sec L=12 sec 4 sec 2 sec L=13 sec
EEG Slowed Slowed Slowed Slowed Slowed Slowed
ECG Bradycard |Bradycard |Bradycard |Bradycard |Bradycard
- No P Wave Pvc Pvc PVC Pvc
PULSE RATE] Down:Norm |Down: No |Up-Down: {Down:Norm |Down:Norm |Down:Norm
at 40 sec | Return No Return {at 40 sec |at 55 sec jat 20 sec
ARTERIAL Down:Norm |Down: No |Up-Down: Down:Norm |Up:Norm Down:Norm
PRESSURE at 30 sec | Return No Return |at 35 sec |at180sec {at 20 sec
CAROTID
FLOW Decrease |Increase | Decrease
beeen Simple: Complex: |Complex: |Simple: None Simple:
FRACTURE Occipital |Occipital |Occipital |Occipital Occipital
GROSS: Inf Front |Occipital |Inf Front |Temporal Inf Front |Frontal
BRAIN Temporal ({Cerebellum|Temporal [Occipital |Occipital |Temporal
CONTUSION | Occipital Occipital |Cerebellum Occipital
AREAS Cerebellum Cerebellum Cerebellum
HISTOLOGY: | Frontal Frontal Frontal Temporal Occipital |Frontal
EXT BRAIN | Temporal [Occipital |Temporal | Pons Pons Temporal
HEMORRHAGE | Occipital |Cerebellum|Cerebellum|Cerebellum Occipital
Cerebellum Cervical Cerebellum
HISTOLOGY: | Temporal [Occipital |Pons Pons Cerebellum] Pons
INT BRAIN | Cerebellum|Cerebellum|Cerebellum|Cerebellum|Cervical
HEMORRHAGE
HISTOLOGY: || Frontal Frontal Frontal None Frontal Temporal
NERVE CELL | Occipital |Temporal Temporal Temporal [Occipital
CHANGES Occipital |Occipital Occipital
IMPACTOR 43.7 43.7 43.0 41.9 43.5 42.0
VELOCITY ft/sec ft/sec ft/sec ft/sec ft/sec ft/sec
IMPACTOR 975 1025 930 750
LOAD lbs lbs lbs lbs
IMPACTOR 1260 1200 1100 900
PEAK g g g g g

10