Topic 2
Quantifying the Cognitive Aspects of Mental
Illness
In the Forensic patient
This section will discuss those neurophysiological
(e.g.-physical tests) and neuropsychological measurements that
are often used by mental health professionals to assess and
measure an individual's overall cognitive function, particularly
in the realm of the capacity to form specific criminal intent.
An Overview of Functional Neuroanatomy
The brain is divided into two specific anatomic regions, the
cortex and the brain stem. While the brain stem can be important
in regards to behavioral and cognitive abnormalities, this
section will concentrate on the role of the cortex in cognition.
The cortex is divided into four regions: the frontal lobes, the
temporal lobes, the occipital lobe, and the parietal lobes. The
frontal and temporal lobes of the brain are involved in (amongst
other cognitive functions) premeditation, deliberation, and the
formation of specific intent (both as regards critical and
non-critical decision-making). Specific abnormalities of these
brain regions can result in cognitive abnormalities that may be
important to a psychiatric defense. There are a variety of ways
to assess frontotemporal cortical brain functioning, and these
are discussed below.
In addition, many medical conditions (e.g. brain injury,
seizure disorder, cancer, dementia, etc.) can be associated with
specific abnormalities of the frontal and/or temporal lobes.
When assessing your client for psychiatric disease, it is
important to have an expert screen for pre-existing neurologic
disorders, which may affect frontal or temporal lobe
functioning.
The Limitations of DSM IV in the Forensic
Setting
While the DSM-IV is a nosological document that seeks to
categorize and subdivide mental illness by common
characteristics, the forensic aspects of mental illness are in
fact dimensional characterizations of cognition (at it's
essence, cognition is defined as an individual's ability to
think logically). Thus the legal definitions of an abnormal
cognitive state do not correlate to any particular DSM IV
diagnosis. That is to say that the law is often interested in
cognitive concepts such as "insanity", "diminished capacity",
and the like; which are really descriptions of a particular
cognitive state, but are not medical diagnostic terms.
Underlying these legal constructs is a specific definition of
"cognition", This is either the ability of an individual to
premeditate, deliberate, and form specific criminal intent (as
pertains to homicide), or the cognitive capacity of an
individual to understand and interact with others (as pertains
to informed consent, aiding in one's own defense, etc.). While
all of the DSM-IV mental illnesses discussed above can adversely
affect on "cognition", it is important to understand that the
measurement of "cognition" from a forensic standpoint (and also
from a neuropsychological and neurophysiological standpoint)
exists separate and apart from an specific DSM-IV diagnosis.
Neuropsychological and Medical Cognitive
Testing
Neuropsychological testing is generally not performed by all
psychologists, but is administered by a subset of Ph.D. degreed
psychologists termed neuropsychologists. Neuropsychologists have
specific training in the administration and interpretation of
specific cognitive assessment test batteries. In addition,
thorough neuropsychological testing has built into it paradigms
to assess for the presence of symptom amplification or
malingering for secondary gain, important issues when presenting
a psychiatric defense. While the nuances and subtleties of
neuropsychological testing are beyond the pall of this
particular document, there are other authoritative texts to
which the reader is referred.
Neuropsychological assessment is generally composed of a
battery of tests administered to an individual that measure
against statistical norms that person's ability to "think". A
neuropsychologist generally administers a battery of 10 - 12
tests that specifically key on certain domains of cognition,
such as attention, concentration, short-term memory, information
processing speed, visual memory, visual recall, executive
functioning and the like. The neuropsychologist then synthesizes
this information in the form of a report that seeks to
dimensionally categorize the presence or absence of specific
cognitive deficits in an individual and the degree of impairment
present in each of these cognitive domains.
It is important to note that cognitive deficits can exist
across the spectrum of psychiatric and neuropsychiatric disease,
such that individuals with schizophrenia, mood disorders,
dementia, delirium, and other neuropsychiatric disorders will
all to a greater or lesser extent exhibit cognitive deficiencies
on neuropsychological testing. In addition, many of the
medications used to treat psychiatrically impaired individuals
can cause cognitive deficits of their own. Finally, acute and
chronic drug and alcohol abuse can also result in demonstrable
cognitive deficits on this type of testing. Thus
neuropsychological assessment can statistically categorize the
presence and severity of key cognitive deficits in a criminal
defendant, and in many instances is necessary to demonstrate to
the court and/or a jury the presence and "cognitive" severity of
the psychiatric illness at issue.
Medical and neurophysiological testing
In addition to neuropsychological testing, cognitive
abnormalities can be demonstrated through neurophysiological
testing. These physical tests of actual brain anatomy and
function include:
The use of static testing, such as CAT scans (CT) and
Magnetic Resonance Imaging (MRI) to look for anatomic brain
abnormalities (atrophy, injury, stroke, brain malformation,
etc.).
The use of neurophysiological testing including
Electroencephalography, brain stem and visual evoked
responses, and P-300 neurophysiological testing to
demonstrate brain electrical conduction (e.g.- "wiring")
abnormalities.
The use of dynamic neuroimaging, such as Positron
Emission Tomography (PET) or Single Photon Emission
Tomography (SPECT) scanning, to delineate metabolic or blood
flow abnormalities in specific regions of the brain
associated with a specific cognitive deficiency.
Again, these tests are dimensional in nature and will detect
appropriate abnormalities in many of the psychiatric disorders
noted above. These types of tests are useful adjuncts in
characterizing the presence and cognitive severity of the
various psychiatric diseases discussed above. If any one test is
used alone to "prove" a specific psychiatric defense, this
over-reliance on a single medical technology may be subject to a
Daubert hearing.
Finally, there are a variety of common medical conditions
that can cause or augment specific cognitive abnormalities in
both psychiatrically ill and psychiatrically well individuals.
These would include:
The cognitive/brain effects of chronic heart and vascular
disease.
The cognitive/brain effects of endocrine disorders, such
as diabetes and thyroid disease.
The cognitive/brain effects of autoimmune disorders, such
as systemic lupus erythematosus.
The cognitive/brain effects of specific non-psychiatric
medications.
The cognitive/brain effects of neurotoxins (e.g.-lead,
solvents, etc.).
The cognitive/brain effects of other non-psychiatric
medical conditions (e.g.- cancer, HIV, etc).
Again, there are literally thousands of medical,
toxicological and medication-related cognitive effects that can
impinge on both "psychiatrically ill" and "psychiatrically well"
individuals, and may have pertinent ramifications in
demonstrating cognitive abnormalities in specific criminal
defendants. However the scope of this discussion is so broad,
that it cannot possibly be encompassed in this text.
In summary, the comprehensive dimensional assessment of a
criminal defendant's cognitive status should include not only
the rendering of the DSM-IV diagnosis and an appropriate report
by an expert, but should also include the judicious use of
neuropsychological and neurophysiological testing (and, where
appropriate, medical testing) to buttress these conclusions.
The expert's report and the dimensional
assessment of Cognition
When engaging a mental health expert to evaluate a client,
you should ask the expert the following questions:
Does the patient have a medical/neurological condition
that could affect cognitive functioning?
Does the patient take any medications that could affect
cognitive functioning?
Does the patient have a history of toxin exposure that
could affect cognitive functioning?
Have you done, or will you refer the patient for
cognitive testing by a bonafide neuropsychologist?
Have you done, or will you refer the patient for
neuroimaging and/or neurophysiologic testing to demonstrate
brain physiologic abnormalities?
Have you requested the patient's past medical records
and/or ordered current medical tests to evaluate for
non-psychiatric disease related causes for any cognitive
abnormalities?
Not every defendant will require all of these tests, and none
of these tests can stand alone as "proof" of a particular type
of cognitive deficit. However, this type of ancillary testing is
reflective of the modern age of mental health, and should be
part of any comprehensive psychological/psychiatric evaluation
of a mentally ill defendant.
Topic 1
...... Topic 2
Pain
Perception and Serum Beta-Endorphin in Trauma Patients
Lawson Bernstein, M.D., Pamela D. Garzone, Ph.D.
Thomas Rudy, Ph.D., Bruce Kramer, M.D.
Dwight Stiff, Ph.D., Andrew Peitzman, M.D.
Acute traumatic injuries engenders the
production of beta-endorphin (BE) and other endogenous opioids.
Elevated BE concentration putatively correlates with pain
perception in trauma patients. The authors examined traumatic
injury severity, pain perception, and BE concentration in
patients admitted to an urban trauma center. Brief rating
instruments for pain and unpleasantness were administered, and
blood was drawn for BE analysis in 48 trauma admissions and 33
age-, gender, and race-matched control subjects for comparison.
The authors found no correlation between the severity of pain
perception and BE, but a significant correlation was found
between BE and patient body weight (P<0.005), physician pain
rating (P<0.01), and the Injury Severity Score (P<0.001). The
results suggest that past findings associating trauma pain
perception and BE concentration are spurious.
(Psychosomatics 1995: 36:276-284)
Traumatic injury is a pervasive medical and
public health problem that costs billions of health care dollars
each year. Concomitant with injury is the perception of pain,
with and without tissue damage. A great variability in pain
response is common in persons with similar injuries, and it
appears that both physiologic and psychologic factors play
important roles in pain modulation. Unmodulated pain has been
shown to have a deleterious effect on patient surgical outcome,
including post operative morbidity and increased mortality when
compared with more adequately treated control subjects.
Psychiatric sequelae, including
mood and anxiety disorders, have been noted in patients with
traumatic injury and sever pain. Research and clinical
experience suggest that early aggressive pain treatment
correlates with better analgesic efficacy and later psychiatric
outcome, yet adequate pain assessment and treatment remains an
ongoing issue of debate in managing the trauma patient.
Acute traumatic injury
engenders a variety of physiologic changes involving the
cardiovascular, endocrine, and inflammatory systems.
Concomitant with the injury are the phenomena of pain and
“stress-induced analgesia” and neuroendocrine modulation of pain
perception. Tissue production of corticotropin-releasing
hormone (CRH)-like substances after injury appear to mediate
stress-induced analgesia through increased hypothalamic
production of proopiomelanocortinin, the precursor protein of
adrenocorticotropin and beta-endorphin (BE). BE, along with
other endogenous opioids, attenuates the neurophysiologic
response to acute pain. Cardiovascular collapse associated with
the hypotension parallels the acute rise in BE levels and can be
attenuated by opioid antagonists such as naloxone. BE returns
to baseline or subnormal levels after 5 to 14 days, and BE has
been correlated with increases pain behaviors in the rat
trauma-injury model.
Transient elevation of BE also
accompanies ethanol use, a frequent comorbid condition with
traumatic injury. In addition, obese people have greater
baseline serum concentrations of BE compared with normal weight
people.
BE serum concentrations have
been used as a measure of acute pain and a measure of the
efficacy of opiate analgesia in postoperative, cancer, and
pediatric burn patients. It has been postulated that
unmedicated acute injury pain proportionally correlates with
increased BE concentration. However, studies with human and
animal models of pain and opiate efficacy have presented varying
inconclusive results and have not controlled for other
physiologic variables associated with BE production.
MATERIALS AND
METHODS
This study was conducted in 1992 at the
University of Pittsburgh Trauma Center, where there are
approximately 2,000 adult trauma injury evaluations a year.
Forty-eight consecutive patients admitted for trauma who met the
inclusion criteria (systolic blood pressure [SBP] greater than
90 mmHg and Glasgow Coma Scale [GCS] score greater that 8) were
evaluated. The GCS is a standardized continuous rating scale to
assess consciousness level, and it is an accepted measure of
mental status abnormality in the acute trauma setting. A GCS of
8 or higher generally indicates that a patient is able to follow
commands and respond appropriately to questions. An SBP of less
than 90 mmHg is accepted as clinical evidence of significant
hypotension in the trauma patient, and for the purpose of this
study we used this standard as a measure of hypotension. The
lowest documented SBP was the standard used to determine
significant hypotension. Patients given medication in the field
or with significant pre-hospital hypotension were excluded from
the study.
After initial evaluation by the
trauma team, but before the treatment, the patients who met the
protocol criteria were asked by the principal
investigator/coinvestigator (LB/BK) to participate in a brief
(1-minute) pain assessment and to permit the investigator to
withdraw a 5-cc aliquot of blood for BE measurement. With
increasing evidence that two dimension of acute pain should be
assessed, two Visual Analog Scales (VAS)-one for pain intensity
and one for pain unpleasantness- were administered to the
patient. A blinded physician VAS co-rating was done by the
investigator (LB/BK) before patient recruitment or review of
clinical data, but after blood had been drawn for BE analysis.
The physician-raters relied on assessment pain behaviors (e.g.,
grimacing) to derive VAS scores. The VAS is a well-validated
pain rating instrument used in a number of pain studies in
trauma patients. The patient marks a point on a 10-cm line that
best reflects his or her current level of pain. The left side
of the line is marked “no pain” and the right “extreme pain.”
The score (0-10) is measured by the distance in centimeters from
the extreme left of the line to the patients mark.
The 5-cc aliquot of blood drawn
at admission was placed in a vacutainer tube containing
ethylenediaminetetracetic acid and aprotinin and immediately
placed on ice. The time of sample collection was recorded.
Blood sample were decanted and frozen until analysis for BE.
The elapsed time from admission to assessment was approximately
10 minutes in most cases. In most instances, when it did not
interfere with clinical care (i.e. critical illness, “stat”
transfer to intensive care unit, etc.), informed consent was
obtained before the interview. Otherwise, informed consent was
obtained after the patient was stabilized medically. The
protocol was approved by the University of Pittsburgh Medical
Center Institutional Review Board and is in accordance with its
established guidelines on the treatment of human subjects.
The medical record was screened
for demographic data such as age, gender and weight. In
addition, the Injury Severity Score (ISS) was recorded. The ISS
is a point-system test that yields a hierarchical rating for
various injury types, thus allowing for comparison of injury
severity between patients with different traumas. At admission,
blood alcohol level and toxicology screen results were recorded
and scored categorically (positive/negative) for the primary
analysis.
Thirty-three healthy volunteers
served as the control group. They were recruited through a
local newspaper that asked for subject without an acute or
chronic illness or currently on prescription medication.
Patients were also interviewed as to health status before study
entry. These healthy and un medicated volunteers, matched to
the trauma patients for age, gender, height and race, also had a
5-cc aliquot of blood drawn, and the VAS was administered to
them in the manner previously described. This ensured that both
groups experienced in minor trauma of phlebotomy prior to VAS
rating. These blood samples were centrifuged, plasma decanted,
and frozen until assay.
BETA-ENDORPHIN ASSAY PROCEDURE
Plasma concentrations or immunoreactive
BE (I-BE) were determined with a commercially available
radioimmunoassay (RIA) kit (INC-STAR Corp., Stillwater, MN.).
Blood samples were collected as described. The samples were
immediately centrifuged for 15 minutes at 760 x g (4 C), and the
serum was removed and stored at –85 C until assayed. The RIA
used the double-antibody technique. BE was extracted from the
plasma by passage through a column containing anti-BE-coated
sepharose particles. Bound BE was subsequently eluted from the
column and incubated with the beta-endorphin antiserum, followed
by I-BE. Phase separation was done with a precipitated complex
of second antibody and carrier. All samples and standards were
subsequently counted in an 1272 CliniGamma gamma counter with a
calculation method of %B/B (percent bound/free) vs. log
concentration.
The antibody to BE has a cross
reactivity of 100% to human BE, less than 5% cross-reactivity to
B-lipotropin, and essentially no cross reactivity to other
peptides or proteins such as dynorphin, enkephalin,
adrenocorticotropic hormone, luteinizing hormone, or
follicle-stimulating hormone. The range of quantitation for the
assay is 5-80 pmol/L, with the limit of detection being
approximately 3 pmol/L. The intra-assay coefficient of
variation (CV) is <10%, except at the limit of quantitation,
which has a CV of 13.7%. Concentration values for quality
control samples analyzed with each set of study samples
consistently fell within the range specified for each kit. In
addition, the calculated value of the control group was always
within 10% of its theoretical value.
In addition to performing the
standard validation described, several other factors and plasma
constituents were evaluated for their effects on the accurate
determination of plasma BE. Because trauma patients could
potentially have had their injury precipitated through the use
of ethanol or other drugs of abuse, it was of interest to
evaluate the effects of these agents on the assay. In addition,
these subjects may have experienced posttraumatic metabolic
disturbances that produced changes in plasma components such as
albumin and alpha-1 acid glycoprotein (AAG), as well as changes
in plasma pH, which could potentially affect accurate analysis
of BE. These factors also required evaluation of their possible
effects on the assay. To 1-ml aliquots of control plasma was
added 100μg each of morphine, D-amphetamine, cocaine, and
tetrahydrocannabinol. This concentration is well above that
reported to cause toxicity and the level that would be expected
to occur after extensive abuse of these agents. Ethanol (2.5
μl) was added to a plasma sample to give a concentration of 200
mg percent. Forty mg of albumin was added to plasma containing
4.5 g/dL to give a final concentration of 8.5g/dL, whereas
8.2mg of AAG was added to a plasma containing 7.8 mg to give a
final concentration of 160 mg/dL. Plasma pH was adjusted by
adding 25 μl of either 1 mol/L hydrochloric acid or 1 mol/L
sodium hydroxide toa 1 ml sample to give final pH values of 6.5
and 9.4, respectively.
None of these perturbations
produced a statistically significant effect on the measured
concentration of BE in a control subject’s plasma sample. In
addition, a 2-cycle freeze thaw of a plasma sample and allowing
it to sit at room temperature for up to 2 hours was without
effect. The results of these validation studies prove that he
BE assay is sensitive and specific and that is also not easily
influenced by several psysiological factors that may be present
in trauma patients.
Statistical Methods
Chi-square tests and analysis of variance
were used to evealuate significant differences between the
control and patient samples. Linear regression analyses and
Pearson correlations were used to determine the association
between posttrauma beta-endorphin concentration (PBEC) and
selected predictor variables. Partial correlations were used to
further clarify the association between patients’ and
physicians’ pain ratings, injury severity, and PBEC. Only P
values less than 0.05 were considered statistically significant.
RESULTS
Forty-eight patients, 28 men (mean age =
42,43 years, SD = 20.21), and 20 women (mean age = 34.95, SD =
10.15) completed the study, Thirty-three subjects, 14 men and 19
women, with the mean age of 35.57 (SD = 18.73) and 36.68 (SD =
15.37), respectively, served as control subjects. The control
group was not significantly different from the patient group
with respect to age, gender, race and heights. The patients and
control subjects differed as to weight: the patients mean weight
was 170.26, lb (SD = 37.43), compared with the control group’s
weight of 147.33 lb (SD = 23.48) (P< 0.001).
Comparison of Beta-Endorphin
Concentration in Trauma
Patients and Control Subjects
The control subjects had
significantly lower posttrauma PBEC than the patients (P< 0.001,
Table 1). The mean PBEC for the control subjects and patients
was < 5 pmol/L (SD = 1.25, range = < 5-8.6 pmol/L
and 16.39 pmol/L (SD = 16.83, range = 5 < 66.2 pmol/L),
respectively. However because the weight of the subjects was
found to be significantly correlated with PBEC (r = 0.385, P
<0.001). and because the control group weighed significantly
less than the patient group (P < 0.01), and analysis of
convariance was done to test whether significant PBEC group
differences remained after statistically controlling for body
weight. This analysis indicated the patient group still had a
significantly higher PBEC than the control subjects after
convarying for body weight (P <0.01).
Predictors of Posttrauma
Beta-Endorphin Concentration
Twelve variables were
hypothesized as being potential predictors of posttrauma PBEC.
The variables and mean values are also presented in Table 1.
Separate regression analyses were computed to evaluate the
contribution of these 12 variables to PBEC. The results of the
regression analyses are presented in Table 2. As shown in Table
2, the patient’s weight, the physician’s rating of the patient’s
pain severity, and the ISS were significantly associated with
PBEC. These three significant predictors accounted for 51.3% of
the variance in PBEC (P < 0.001). The patients’ pain severity
of unpleasantness ratings were not significant predictors of
PBEC.
Additional analyses were done
to further clarify the apparent discrepancy between the
patients’ and physicians’ pain ratings. Results of these are
presented in Table 3. As shown in Table 3, the patients’ and
physicians’ pain severity and pain unpleasantness were
significantly correlated. However, the physicians’, but not
patients’, pain severity and pain unpleasantness ratings were
significantly associated with the ISS. Controlling for the
significant association between the ISS and pain severity score,
the partial correlation between the physician’ rating of pain
severity and PBEC was not satistically significant (r = 0.12,P =
0.39).
DISCUSSION
The production of BE in the acute trauma
setting is a complex physiologic event. In addition, other
psychologic and pharmachologic varialbles also affect the BE
response to injury. Previous human studies examining the
BE-acute pain relationship have not taken this multivariate
pathophysiologic approach. In this study, an association
between patient pain intensity and/or unpleasantness perceptions
and elevated BE could not be demonstrated.
As noted, local tissue response
to injury produces CRH-like factors that augment physiologic
secretion of BE from the hypothalamus and the adrenals. The
positive correlation between BE and the body weight may be
attributable to increased local tissue response to injury (more
soft tissue to injure), augmented by hypothalamic response to
CRH, or increased adrenal production of BE in heavier persons.
Because the hypothalamic-pituitary-adrenal axis may react
differently in the obese, and because BE concentrations are
generally higher in the over-weight as compared with normal
weight persons, these factors would seem a likely explanation.
Likewise, obesity itself could be a risk factor for greater
tissue damage caused by blunt trauma, because there is a
relationship between force of the impact and weight. However,
neither of these conclusions are substantiated by our study.
When weight was removed as a
potential confound, the positive correlation between ISS and BE
remained, underscoring the robust relationship between the two.
This relationship is consistent with the role of tissue trauma
as the primary injury-associated variable responsible for
elevated BE in the trauma patients vs. control subjects.
Contrary to other studies, we did not find a positive
association between alcohol and elevated BE concentration,
although this effect may be undetectable when compared to the
overwhelming stimulus of tissue injury.
Almost 50% of the variance in
BE remains unexplained in this sample, highlighting the
complexity of BE production. The influence of alcohol and
other factors that affect BE (e.g.,head trauma, loss of
consciousness) are difficult to separate from the cascade of
physiologic events associated with the neurophormonal response
to acute injury. No correlation was found between the presence
of opiates (11.4% of the sample), cocaine (18%), marijuana (17%)
in the serum toxiocologies and elevated patient BE. In
addition, the effect of chronic vs. acute ethanol and illicit
substance use is not quantifiable from this study. Although six
cases experienced transient loss of consciousness at the scene,
none had elevated PBEC levels. The presence of premorbid
significant gastrointestinal (10.4%) or cardiac disease (14.6%)
in patients did not correlate with the changes in BE, nor did
the presence of current prescription drug use (35.3%). Other
medical diagnoses or illicit substance effects could not be
assessed because of the low presence these in the sample. These
other conditions may be related to perturbations in BE
physiology or premorbid pain experience, which could affect
acute injury BE response and/or pain perception.
The finding of a lack of
association between patient pain/unpleasantness and BE contrasts
with the studies cited before. Past studies have suggested that
elevated BE is a marker for pain and associated with pain
perceptions. One hypothesis suggests that elevated BE is a
associated with the undertreated acute or chronic pain and that
adequate analgesia is reflected in normalization of BE levels.
Another hypothesis suggests that BE itself has autonomous
analgesic properties that modulate the efferent limb of
cutaneous and possibly visceral pain perception. Thus, BE
levels, either elevated or depressed, should be positively or
inversely related to pain severity perception. Both hypothesis
require assumptions as to cause and effect and impute
mechanistic connections where none may exist.
This study assumes that
peripheral measurement of BE reflects central nervouse system
(CNS) levels of hormone. It is possible that there is a
dissociated response between CNS and peripheral production of BE
and that different physiological compartments reflect this
inequality. Acute CNS production of BE may significantly lag
behind that of the adrenal gland. Moreover, the ependymal
barrier between the brain and the systemic circulation is
discontinuous. One prominent locus of discontinuity is the
hypothalamic-pituitary stalk. This suggests that peripheral
measurements of BE may reflect some percentage of centrally
produced hormone, although the total amount is not known. A
dissociated response is difficult to document, however, and
requires simultaneous cerebrospinal fluid and serum assays.
Studies simultaneously sampling peripheral and central BE
concentrations are inconsistent in documenting any correlation
between the two.
An interesting and potentially
important finding from this study is the significant correlation
between physician related pain/unpleasantness assessment and ISS.
These findings suggest that the physicians’ ratings of pain
severity were determined, in part, by their assessment of the
degree of trauma present, followed by an influence about how
much pain the patient “should be” experiencing, based on the
behavioral observations (e.g. facial grimacing). This
replicates and extends previous findings form the nontrauma
literature indicating that physicians have great difficulty in
estimating patients pain from the physical examination. In
addition, these findings underscore the complex relationship
between injury and pain, which may encompass psychologic and
situational responses idiosyncratic to the patient. A
hypothesis inferred from this study is that physicians underrate
psychic experiences as compared to overt tissue trauma/physical
injury in their assessment of acute trauma injury pain.
CONCLUSION
Assessment and management of acute injury
pain remains a difficult clinical issue. Our study highlights
the problems inherent in correlating pain assessment to a single
BE assay and elucidates other confounding physiologic mechanisms
that affect BE production. It also demonstrates that physician
pain assessment may overlap only slightly with the patients
experience and may rely excessively on injury assessment alone.
This work was
supported by Western Pennsylvania Psychiatric Seed Grant No.
2-90871
This research was presented
at the American Psychiatric Association Meeting, May 1993, San
Francisco, Ca.
The authors thank Erin
Gordish for data entry and the housestaff from the Departments
of Surgery, Emergency, and Critical Care medicine for their help
in identifying study candidates.
