Depression

in Patients

With

Acute

Traumatic

Brain

J.

Paul Fedoroff, M.D., Sergio E. Starkstein, M.D., W. Forrester, M.D., Fred H. Geisler, M.D., Ricardo Stephan V. Arndt, Ph.D., and Robert G. Robinson,

Alfred

Objective:

This

study

was

undertaken

to examine

patients

with

Ph.D., E. Jorge, M.D.

closed

head

Injury

M.D.,

injuries

for

the

presence ofdepressive disorders. Method: A consecutive series of66 patients with closed head injuries but no significant spinal cord or other organ system injury were examined by means ofa semistructured psychiatric interview. The Hamilton Rating Scale for Depression as well as scales measuring impairment in activities ofdaily living, intellectualfunctioning, and social fi4 nctioning were administered. The patients’ CTscans were also examined. Results: Seventeen patients had major depression and two had minor depression. The presence ofleft dorsolateral

f rontal

lesions

right

and/or

hemisphere

depression.

left

lesions

Compared

basal

was

ganglia

lesions

associated

with

to the

nondepressed

and,

to a lesser

an increased group,

the

extent,

parietal-occipital

and

probability

of developing

major

group

with

major

depression

had

a

higher frequency ofprevious psychiatric disorder and showed evidence ofpoorer social functioning. Conclusions: Major depression occurs in about one-quarter ofpatients after traumatic brain injury. This is the same frequency as in other major disorders such as stroke. Major depression appears to be provoked by one or more factors that include poor premorbid social functioning

and

previous

(Am J Psychiatry

W

ith an annual is the

most

incidence common

1992;

psychiatric

of2 million cause

disorder

of brain

cases, trauma injury

in the

United States (1). In approximately 500,000 of these cases, the patients require hospitalization, and 80,000 have long-term sequelae of their brain injuries (1). The observation that brain injury leads to a variety of neuropsychiatnic disorders has been reported in the medical literature for many years. Adolf Meyer (2), for example, identified a number of disorders that he referred to as the “traumatic insanities,” and he associ-

Received

May 30, 1991; revision received Nov. 6, 1991; accepted From the Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore, Md.; the Shock Trauma

Dec. 5, 1991. University

Center of the Maryland Institute of Emergency Medical Services System, Division of Neurosurgery, Department of Surgery, University of Maryland, Baltimore, Md.; the Department of Psychiatry, University of Iowa College of Medicine; the Institute of Neurological Investigation Raul Carrea, Buenos Aires, Argentina; and the Division of Forensics,

The Clarke

Institute

of Psychiatry,

Toronto.

Address

reprint

requests to Dr. Robinson, Department of Psychiatry, University of Iowa, Medical Education Building, 500 Newton Rd., Iowa City, IA 52242. Supported in part by NIMH Research Scientist Award MH-00163 to Dr. Robinson and grant MH-40355, grant NS-151178 from NIH, a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression to Dr. Starkstein, and a grant from the Instituto Di Ida. The authors thank Ms. Andrea Michael for assistance with the data analysis. Copyright

918

© 1992

American

Psychiatric

or injury

to certain

critical

brain

locations.

149:918-923)

Association.

ated these disorders with specific lesion locations. Our knowledge about the behavioral and emotional effects of frontal lobe injury is largely the result of studying patients with traumatic brain injury. For instance, one of the best-known and earliest examples of behavioral and emotional changes associated with traumatic injury is Phineas Gage (3). His penetrating frontal lobe injury, caused by a railroad spike, led to a variety of emotional and personality changes, including disinhibition, apathy, loss of appropriate social behavior, and lability of mood. The quantitation of severity of traumatic brain injury by Teasdale and Jennett (4) led to a large number of studies examining the neurobehavioral consequences of mild, moderate, and severe head injuries (5-7). These studies

have

identified

numerous

behavioral

and

emo-

tional consequences of brain injury as well as numerous prognostic factors related to long-term outcome. There have been relatively few studies of mood disorders associated with traumatic brain injury, however, and most of these studies have used rating scales, questionnames, or relatives’ reports rather than structured mental status examinations and well-established diagnostic criteria to determine the existence of depression (8, 9). For several years, we have been reporting on the incidence (10), phenomenology ( 1 1 ), course (12), and treatment (13) of mood disorders in patients with focal brain injury due to stroke. We have reported that depression occurs more frequently in patients with either

AmJPsychiatry

149:7,July

1992

FEDOROFF,

left dorsolateral frontal cortical lesions (14) or left basal ganglia lesions than in patients with lesions in any other location (15). In addition, for both coitical and subcortical lesions, the proximity of the lesion to the frontal pole was significantly correlated with severity of depression (14). One of the major questions, however, is whether these findings in stroke patients are generalizable to other brain-injured populations or whether there is something unique about the stroke population that contributes to the prevalence of depression. For examplc, compared to patients with traumatic brain injury, stroke patients tend to be older, to have potentially necurrent cardiovascular illnesses, and, frequently, to be taking multiple medications for various illnesses. Any of these factors or other variables might influence the expression of depression and its neuropathological correlates. In addition, the nature of the brain injury is different following stroke than following trauma. Traumatic injury is associated with diffuse axonal shear injury,

contusions,

and

both

arterial

and

venous

bleed-

ing, while ischemic infarction and intraparenchymal hemorrhage are the neuropathological mechanisms associated with stroke. We have conducted one previous study comparing the severity of depressive symptoms in patients who had had strokes and patients with closed head injuries (16). We found that although the stroke patients were more severely depressed than the patients with traumatic brain injury, the difference in severity of depressive symptoms was explained in large part by differences in the location of CT-visualized lesions in the left hemisphere. In addition, for both traumatic brain injury and stroke there was a significant correlation between proximity of the largest lesion to the left frontal pole and severity of depression. In the present study, patients with acute traumatic brain injury but without multiple system injury (e.g., patients without multiple fractures or intra-abdominal lesions) were examined with the use of structured interviews and diagnostic criteria to determine whether similar lesion locations or other clinical variables would be associated with major depression.

METHOD

Sixty-six patients with acute closed head injuries who had been consecutively admitted to a shock trauma centen were included in the study. Patients were excluded if they

had

significant fractures, dition,

open

head

injuries,

spinal

cord

injuries,

or

multiple system injuries such as multiple rupture of the spleen, or lung collapse. In adpatients

were

excluded

if they

had

a decreased

level of consciousness or aphasia that interfered with their ability to comprehend questions administered duning a verbal interview (i.e., patients had to be able to follow at least a two-stage command). Questions regarding personal and family history of psychiatric

Am

J

disorder

Psychiatry

were

149:7,

included

July

1992

in the structured

inter-

view. disorder

Information as well

about as alcohol

STARKSTEIN,

the existence or other

FORRESTER,

of previous substance

El AL.

mood

abuse, in

the family history or the personal history, was specffically asked of each patient and relatives who were present at the time of interview. A psychiatric history was considered positive for a disorder if the patient or a relative appeared to meet the DSM-III criteria for that disorder. This diagnosis did not depend on the patient’s receiving treatment. None of the patients had a depressive disorder atthetime ofthetnaumatic brain injury, and none received the head injury as a result of a suicide attempt. After they gave informed consent, all patients received detailed psychiatric examinations approximately 1 month after injury. Symptoms of depression, mania, and anxiety were elicited with a modified version of the Present State Examination (PSE) (17) administered by a research psychiatrist (A.W.F.). This is a semistructured psychiatric interview that was modified to examine all symptoms used in the DSM-III criteria. Quantitative mood ratings were obtained with the observer-rated Hamilton Rating Scale for Depression (18), a 17-item scale that measures psychological and physiological symptoms of depression. Cognitive function was measured with the Mini-Mental State examination (19), which has been shown to be a reliable and valid means of assessing a limited range of cognitive functions in several medically ill or brain-injured populations (16). Mini-Mental State scores range from 0 to 30, with scores below 24 indicative of clinically significant cognitive impairment. Impairment in activities of daily living was measured with the Johns Hopkins Functioning Inventory (16). Scores on this scale range from 0 to 27, with higher scores indicating a greater degree of functional impairment. Social functioning was quantitatively assessed with the Social Functioning Exam and the Social Ties Checklist (20). The Social Functioning Exam, which has been shown to be reliable and valid for patients with stroke, assesses patients’ satisfaction with their social functioning by means of a structured interview. Scores range from 0.00 (greatest satisfaction) to 1.00 (least satisfaction). The Social Ties Checklist assesses the number of social connections available to the patient. Scores may range from 0 to 10, with higher scores indicating less social support. All neurological examinations were conducted by a neurosurgeon (F.H.G.) who was blind to the results of the psychiatric examinations. Results of the neurological examinations were recorded by using the standardized neurological examination form of the Traumatic Coma Data Bank (21). CT scans were obtained as part of the standard clinical evaluation of patients admitted to the emergency medical services system that administers the shock trauma center. Scans were usually done within the first day after trauma and repeated 1-2 weeks later. All scans were done on a GE-lOb scanner with standard 10-mm axial cuts parallel to the canthomeatal line. The nature of the lesion (e.g., contusion, intraparenchymal bleeding, subarachnoid hemorrhage) was deter-

919

DEPRESSION

AND

TRAUMATIC

BRAIN

INJURY

TABLE 1. Characteristics of 64 Depressed tients With Traumatic Brain Injury

and Nondepressed

Patients With Major Depression

Patients Without Depression

(N=17)

(N=47)

Pa-

data were excluded from further small number in this category.

mean

Variable

N

%

N

%

Malesex Blackrace

14 S 1 7

82.4 29.4 5.9 41.2

41 11 4 21

87.2 23.4 8.5 44.7

Left-handedness Married Hollingshead socioeconomic class IV or V Family history of psychiatric disorder

Personal

history

psychiatric

Personal history of alcohol and other substance abuse asignificant

difference

of lesion

rest

of the

view

was

36.6

tients

and

32.1

(SD=S.8), mood

number depressed

of years group

subjects.

The

days

(SD=1S.8)

days

the mean was

29.5

age (SD=

of education was 12.4 and 12.3 (SD=2.1) for

time

(SD=20.7)

from

injury

for the for the

to inter-

depressed

patients

pa-

without

8

47.1

23

48.9

the

12

70.6

17b

23.9

There were no significant differences between the depressed and nondepressed groups in terms of age, sex, race, marital status, education, socioeconomic class, or

groups

47.1 (2=4.38,

df=1,

1 1L p=O.O4).

locations

mood

Other

population

medication

background are

taken

shown

at the

time

RESULTS

Seventeen subjects met the DSM-III duration criteria for major depression,

symptom and and 47 had no

characteristics in table

1

of

.

of interview.

The

study

group consisted primarily of men in Hollingshead’s socioeconomic class IV who were in their late 20s. There were no significant differences between the depressed and nondepressed patients in the frequency of a past family history of psychiatric disorder. There was a significantly greaten frequency of a previous

personal

history

of psychiatric

disorder

in the

group with major depression (table 1 ). When patients with histories of alcohol or other substance abuse were excluded, this difference was no longer significant. There was no significant difference between groups in the frequency of a personal past history of alcohol and! on other substance abuse. There

were

no significant

differences

between

the two

groups in the frequency of any neurological findings. Twenty-six patients (seven with major depression and 19 without depression) had some motor impairment, 1 3 (seven depressed and six nondepressed) had sensory impairment, and 14 (three depressed and 11 nondepressed) had ocular palsies. Only one of the 1 7 patients with major depressed patients

Wernicke’s

depression were given

aphasia.

and four a diagnosis

with

pressed

In the remaining

of the 47 nonof Broca’s or

preand 14 nondepressed), there was mild global aphasia, transcortical sensory or motor aphasia, or severe anomia. The Glasgow coma scale scores 24 hours after injury were not significantly different between groups (desented

language

patients,

patients

impairment

mean=9.2,

(five

SD=3.4;

jury

(Glasgow

and 26%

coma

score=8-1

(Glasgow

coma

patients),

scone=3-7;

.

pa-

there a significant head injury (Glasthe depressed and moderate head in-

1; 24%

of the nondepressed

who

depressed

nondcpressed

tients, mean=10.0, SD=3.4), nor was difference in the distribution of mild gow coma score=12-1S; 35% of 43% of the nondepressed patients),

injury

considered.

disorder. study

and 32% of the nondepncssed Multivaniate discniminant

920

and

disorder

72.3

mined from the CT scan. All scans were read by a neurologist (S.E.S.) who was blind to the results of the psychiatnic examination. All lesion locations were determined and transposed onto templates according to the procedure described by Levine and Grek (22). Subjects with specific lesion locations (e.g., left anterior lesions) were defined as patients whose CT scans showed lesions in those locations (e.g., left dorsal lateral frontal cortex and/or left basal ganglia) regardless of whether lesions were also seen in other locations. Several of the rating scale scores and other variables showed abnormal distributions. For consistency, we used nonpanametnic procedures throughout our statistical analyses. For instance, when we compared the depressed and nondepressed groups for differences on the demographic variables (e.g., age, sex), we used MannWhitney U or chi-square tests. When we analyzed scones on the six psychiatric rating scales, we conducted an overall multivaniate test of significance in order to 1) account for the interconnelations among scones on the rating scales and 2) control the overall probability of obtaining a significant result by chance (alpha error). This was accomplished with a nonparametnic analog of discniminant analysis based on ranks (23). The overall test of significance was taken as the test for the full model including all scales. Logistic regression was used to test for an association between the diagnosis of depression and lesion location. Again, an overall test was used to control for alpha inflation and interrelations among the lesion locations. Following the significant likelihood ratio test for the full model, backward selection was used to reduce number

1 0.7). The mean (SD=2.0) fonthe the

years

without

34

bN46

the

26.8

subjects

76.4

8

between

age was

of the

analysis because of the The depressed subjects’

13

of

disordera

diagnosis of mood disorder. Two additional patients met the DSM-III symptom criteria for dysthymia (we have referred to this as minor depression), but their

of the depressed

on severe

head

41 % of the depressed

patients). analysis showed

an overall

significant difference between the group with major depression and the nondepressed group in psychiatric rating scale scores (Wilks’s lambda=0.38, F=1S.4, df=6, 56, p=O.0001 ). Univaniate test statistics disclosed sig-

AmJPsychiatry

149:7,July

1992

FEDOROFF,

TABLE

2.

Scores on Psychiatric Rating Scales of 64 Depressed

and Non depressed

Patients With Traumatic

FORRESTER,

El AL.

Bra in Injury

Score

-

Patients

PatientsWith

Major

STARKSTEIN,

Depression

Without

Analysis

Depression F

(N=47)

(N=17)

Mean

.

SD

(df=1, 61)

p

Scale

Mean

SD

Hamilton Rating Scale for Depression Present State Examination Mini-MentalState Johns Hopkins Functioning Inventory Social Ties Checklist Social Functioning Exam

13.8

3.2

6.8

2.6

37.79

0.0001

19.6

4.2

6.8

3.6

78.70

0.0001

27.5

2.3

26.5 1.4 3.6 0.11

3.1 1.8 1.5 0.10

1.74 0.31 2.49 4.92

2.2

3.3

4.2 0.19

1.2 0.16

nificant between-group differences in Hamilton depression scores, PSE scores, and Social Functioning Exam scones (table 2). There were no significant intergroup differences in intellectual impairment as measured by the Mini-Mental State examination, impairment in activities of daily living as measured by the Johns Hopkins Functioning Inventory, or social connectedness as measured by the Social Ties Checklist. According to the resulting discriminant function, 1 8 (29% ) of 63 patients were classified into the depressed group and 45 (71%) were classified into the nondepressed group (three patients were excluded from the analysis because of missing data). These findings indicate’a 100% sensitivity and a 98% specificity. Of the 47 nondepressed patients, 41 had abnormal findings on CT scans, and of the 17 patients with majon depression, 15 had CT scan abnormalities. Of the total of 56 subjects who exhibited abnormal CT scans, 22 had single focal lesions and 23 had multiple or bilateral lesions. In addition, 13 patients had extraparenchymal hemorrhages (epidural, subdunal, on subanachnoid bleeding) or CT evidence of brain edema, brain atrophy, on hydrocephalus. Most of the patients (71% of the depressed and 62% of the nondepressed patients) had CT evidence of brain contusions. There were no significant differences in the frequency of vanous types of injury between the depressed and nondepressed groups. To analyze the relation between lesion location and the presence of major depression, a logistic regression model was used. The model included the following location variables: left hemisphere, right hemisphere, cortical, subcortical, single, multiple, frontal, onbitofrontal, temporal, temporobasal, left anterior (i.e., left donsolatenal frontal cortex and/or left basal ganglia), and panietal-occipital. There was an overall significant association between lesion location and the development of major depression (X2=33.64, df=12, p= 0.0008). A backward selection procedure was used to remove the nonsignificant variables (p>O.OS). After their removal, the reduced model included the following lesion locations: left hemisphere only, right hemisphere only, cortical, frontal (i.e., right, left, on bilateral frontal excluding onbitofrontal involvement), left antenor, and parietal-occipital (X2=3i.39 df=6, p=O.0001). The parameter estimates and probabilities of each of

Am

J

Psychiatry

149:7,

July

1992

0.19 0.58 0.12 0.03

TABLE 3. Maximum Likelihood Estimates for Regression Coefficients of Lesion Locat ions and Dep ression in 64 Patients With Traumatic

Brain

Injury

Analysis

Parameter Lesion

Location

Estimate

Left hemisphere Right hemisphere Cortical

-2.84 2.40 -3.67

Frontal Left anterior

-3.58 5.90

Parietal-occipital

3.75

Standard Error

Wald x2 (df=1)

1.44 1.12 1.45 1.38

4.08 4.74 6.28 6.56

1.64

12.97

1.44

6.91

p 0.04 0.03 0.01 0.01

0.0003 0.009

these six individual variables are shown in table 3. The presence of a left anterior lesion was by far the strongest correlate of major depression. To a lessen degree, panietal-occipital and night hemisphere lesions increased

the probability

of developing

major

depression.

On the other hand, the presence of left hemisphere, contical, and frontal lesions was associated with a decreased probability of developing major depression. If we compare the predicted and observed events, the model shows a 70% sensitivity and an 83% specificity.

DISCUSSION

This study for the first time examined patients with traumatic brain injury for depressive disorder with the use of a structured psychiatric interview and DSM-III diagnostic criteria. We found that 27% of the patients whose data were analyzed met the criteria for major depression. This frequency is within the wide frequency range for depression reported by other investigators who have used cutoff scones on self-rated depression scales (8) and is close to the frequency of major depression found in patients with stroke (10). Perhaps the failure to use structured psychiatric interviews and defined diagnostic criteria is the reason that the reported frequency of depression following traumatic brain injury has varied from 10% to 60% (24). This study also found that major depression following traumatic brain injury was significantly associated with lesion location. The presence of left anterior lesions (i.e., left dorsolateral frontal and/or left basal gan-

921

DEPRESSION

AND

TRJMATIC

BRAIN

INJURY

glia lesions) and, to a lessen degree, panietal-occipital and right hemisphere lesions was associated with a higher probability of developing major depression. On the other hand, the presence of left hemisphere lesions, frontal (i.e., right, left, or bilateral frontal excluding orbitofrontal) lesions, and purely cortical lesions diminished the probability of developing a major depressive disorder. A previous personal history of psychiatric disorder (including alcohol and other substance abuse) was more frequent in the group with major depression. This group also showed evidence of poorer premonbid social functioning. Before further discussion of this study, several methodological limitations should be acknowledged. First, only patients who were alert and cognitively able to be interviewed were included. Second, only patients with relatively minor injury to other body systems were included, so that a more uniformly injured population, without major disability due to non-CNS injury, could be studied. In addition, the patients were primarily young white men from the lower socioeconomic classes who had histories of alcohol or drug abuse. Although this

demographic

profile

ported in epidemiologic jury (1), our findings tient

populations

is typical

studies may not

with

of the population

of traumatic be applicable

traumatic

brain

ne-

brain into all pa-

injury.

Closed

head injuries involve trauma to the entire brain, and it would be misleading to assume that the only areas that have been injured are the ones visible on CT scan. While

it is certain

that

the

extent

of brain

injury

was

underestimated in this study (we did not have information from magnetic resonance imaging), it is unlikely that there was any systematic undenrepresentation among patients who met the criteria for major depression, since the mean scones on the Glasgow coma scale, the Johns Hopkins Functioning

Inventory,

and

the Mini-Mental

State

exami-

nation and the distribution of mild, moderate, and severe head injuries were not significantly different between groups. In addition, we did not examine the patients for neglect, disturbances in prosody, unawareness of deficits, or denial of illness (disturbances that are usually associated with nighthemispherelesions). It is possible that some patients with these disturbances may not have been able to recognize their inner mental state appropriately. Given these cautions, what are the implications of this study?

First,

the

study

supports

our

previous

finding

in

patients with stroke of an increased frequency of depression among those with left donsolateral cortical and left basal ganglia lesions (14, 15). This finding is consistent with a previous study of patients with chronic brain injuries in which anterior left hemisphere lesions were found to be associated with the most severe depressive symptoms in both stroke and traumatic brain injury (16). It is interesting that the association between major

depression

and

left

anterior

lesions

was

highly

significant despite the “protective” effect associated with the presence of both left hemisphere and frontal lesions. This finding suggests that the left dorsolatenal frontal cortex and the left basal ganglia are critical structures in the left hemisphere as far as mood is con-

922

cerned, and they may represent strategic lesion locations for the initiation of major depression. The probability of developing major depression was also associated with the presence of panietal-occipital lesions and with the presence of right hemisphere lesions. Gnafman et al. (25) reported that depressive symptoms were associated with penetrating injuries that involved the night hemisphere (night orbitofrontal lesions). Their subjects, however, were studied years after the penetrating injuries, without the use of structured psychiatric interviews, and are not comparable to the patients in this study. Lishman (26) also reported that several years after penetrating brain injury, depressive symptoms were more common among patients with night hemisphere lesions. We previously examined the correlates of depression following acute-stroke lesions of the night hemisphere (27). Patients who developed major or minor depression during the in-hospital evaluation for acute stroke had a higher frequency of panietal lobe lesions than the nondepressed or unduly cheerful patients. Finset (28) reported the occurrence of depression following right hemisphere panietal lobe damage. In the present study, we also found that purely cortical lesions were associated with a decreased probability of developing major depression. This indicates that subcortical and basal ganglia lesions may have the strongest correlation with major depression. We have previously suggested (14) that the mechanism of depression following anterior brain injury may involve the interruption of biogenic amine-containing neurons as they pass through the basal ganglia on frontal

subcortical

consistent This

white

with study

also

our

matter.

This

findings

suggests

hypothesis

in the present that

premonbid

remains

study. vulnerability

factors (personal history of psychiatric disorder and poor social functioning) may be operative in the development of major depression among patients with tnaumatic brain injury. This is consistent with our findings and those of other investigators in stroke and traumatic brain injury (10, 29) and suggests several areas for furthen investigation. Although other investigators have not found that severity

of depressive

symptoms

is significantly

correlated

with duration of loss of consciousness, duration of posttraumatic amnesia, or the presence of skull fracture (9), depression following traumatic brain injury has been associated with degree of neuropsychological impairment (9). We did not find a significant difference in degree of intellectual impairment between our depressed and nondepressed patients. This may be because we cxamined less severely injured patients (the mean MiniMental State examination scores for depressed and nondepressed patients were 27.5 and 26.5, respectively), and there may have been a “ceiling” effect that precluded demonstrating an influence of depression on intellectual function. The finding of relatively low Hamilton depression scale scores among the patients with major depression is another important issue. Although sion scores were not significantly

Am

J

these different

Psychiatry

total depresfrom those

1 49:7, July 1992

FEDOROFF,

we found previously among patients who developed major depression following stroke or myocandial infanction (30), we are examining this issue in more detail in another study (i.e., examining which symptoms are specific to depression following traumatic brain injury). Several facts, however, should be kept in mind. First, the diagnosis of depression was based on meeting the DSM-III criteria for depression and was made by nesearch psychiatrists using a semistructured interview. This remains the “gold standard” for depression, and all of the patients met these criteria. Second, the patients

were identified on the basis of the existence of traumatic brain injury and not depression and therefore might not have had symptoms as severe as those found in patients at psychiatric institutions. Moreover, the patients with traumatic

brain

Hamilton

depression

cantly tients.

injury

different Third,

Hamilton may

had

major

that

but not used

somewhat

had

highly

signifi-

nondepressed included

by DSM-III

different

and traumatic brain injury of patients with traumatic

depression

were

from those of the depressive symptoms

scale

be

who

scores

for diagnosis

in functional

depression, brain injury

pain the

depression

and subgroups may be identi-

fled on the basis of the presence of different symptom profiles on longitudinal course. There arc probably multiple etiologies for depression after traumatic brain injury. Some may involve single etiologic agents (e.g., genetic factors), while others may involve a complex interaction between organic and psy-

chosocial with

factors.

lesions

nomenology depression

come sions, their their kinds early

even

critical

within

brain

the

regions,

group

the

phe-

and the pathophysiological mechanisms of may be different (e.g., following left anterior

as compared

Future

Moreover,

in certain

with

studies

right

panietal

will need

lesions).

to examine

a variety

of out-

variables, including the course of these depresthe dynamic changes in their clinical correlates, effect on recovery from traumatic brain injury, etiology, and their response to treatment. These of investigations may ultimately facilitate the recognition and treatment or prevention of these

severe

mental

disorders. REFERENCES

1. Frankowski RF: Descriptive epidemiologic studies of head injury in the United States 1974-1984. Adv Psychosom Med 1986; 16: 153-1 72 2. Meyer A: The anatomical facts and clinical varieties of traumatic insanity. Am J Insanity 1904; 60:373-441 3. Harlow JM: Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society 1868; 2:327-346 4. leasdale G, Jennert B: Assessment of coma and impaired consciousness: a practical scale. Lancet 1974; 2:81-84 S. Teasdale G, Parker L, Murray G, KnillJones R, Jennert B: Predicting the outcome of individual patients in the first week after severe head injury. Acta Neurochir Suppl (Wien) 1979; 28:161-164 6. Alexandre A, Colombo F, Nertempi P, Benedetti A: Cognitive outcome and early indices of severity of head injury. J Neurosurg 1983; 59:751-761

Am

J

Psychiatry

1 49:7,

July

1992

STARKSTEIN,

FORRESTER,

El AL.

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