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Homicide of an aggressive adolescent boy with right temporal lesion: A case report
Neuroscience & BiobehavioralReviews, Vol. 7, pp. 41%422, 1983. ©AnkhoInternationalInc. Printedin the U.S.A.
Homicide of an Aggressive Adolescent Boy with Right Temporal Lesion: A Case Reporf JOEST MARTINIUS M a x - P l a n c k - I n s t i t u t f u r P s y c h i a t r i e , Kraepelinstr. 10, D-8000 M u n c h e n 40, F R G
MARTINIUS, J. Homicide of an aggressive adolescent boy with right temporal lesion: A case report. NEUROSCI BIOBEHAV REV 7(3)419-422, 1983.---Thecase is reported of a 14-year-oldmale who killed an 8-year-old child following an alleged insult. The subject had been known to be aggressive throughout his school career. He had suffered one nocturnal seizure at the age of 13, but he never was amnesic for any of his fights. There was a history of possible hypoxic birth trauma. Neuropsychiatric investigation revealed developmental lags in speech and other psychosocial skills and, on computer tomography, a circumscribed lesion (cystic defect) lateral to the right nucleus amygdalae. Homicide
Brain lesion
Case report
hemispheres correlates with distinct psychopathological manifestations, in the dominant left hemisphere with paranoid states and in the non-dominant right hemisphere with dysphoria, excitability and manic-depressive states. In brief, the argument about aggression and localized or lateralized brain dysfunction in man is not settled. The case reported here may add to the argument, particularly because it presented a topological similarity with another unusual case of violent behavior who probably is well remembered by many working in the field. Our patient is a male who at the age of 14 years killed an 8 year old boy by beating, strangling and stabbing, following an alleged verbal insult by the young boy. The two had consented to enter a deserted house to make fire in the basement--which they did. There an argument arose. After the killing R.N. went home and only on the following morning when it became known that the child was missing indicated and finally confessed what had happened. He was not amnesic. R.N. is the elder of two children of healthy parents. During pregnancy his mother suffered from mild toxemia. Delivery occurred spontaneously at the expected date, following prolongued labor. The newborn--according to the birth record--had transient respiratory problems. His motor development was unremarkable but speech was definitely delayed and remained poor. An attempt to enter kindergarten at 4 years of age failed within weeks due to destructive play behavior and inability to adjust to the peer group. School was equally difficult from the very beginning. Performance was average but he engaged frequently in fights for minor reasons, was known for his overreactions to teasing and soon became the social outcast in and outside school.
THE neural substrate of aggression is organized at different levels of the nervous system. Due to this complexity the studying of single clinical cases is probably of limited value to the understanding of the anatomical basis for such emotional states, but may, nevertheless, contribute some. It is the amygdaloid subdivision of the limbic system which is mostly related to aggression and defense. Focal lesions, f.i. in this subdivision, may have serious effects upon the entire system without explaining its complex functions. Therefore, attempts to relate one particular focal brain lesion to violent behavior in man have been of little success. This is the more understandable since experiments in animals have shown that the effects of hypothalamic or amygdaloid stimulation are influenced by additional factors such as the immediate situation and previous experience, i.e., learning [6,7]. Brain stimulation does not appear to produce pure drive states. Instead, the resultant behavior is determined by the interplay of central processes including memory and relevant situational cues. Keeping these cautionary notes in mind one would remain on safe grounds in looking at focal lesions of the limbic system in their proper perspective. On the other hand, it is well known that certain clinical states in man are not infrequently associated with aggressive behavior, namely temporal lobe epilepsy. Blumer et al. [I] found in their study a striking preponderance of left temporal lobe defects in a group of abnormally aggressive patients. Kligman and Goldberg [5] in reviewing the problem of temporal lobe epilepsy and aggression again cautioned against the supposition of one single causative parameter such as temporal lobe pathology while Flor-Henry [3] left no doubt that lateralization of cerebral pathology to either of the two
JPaper presented at the International Workshop on the Limbic System, Innsbruck-Igls, May 15-16, 1981.
419
420
MARTIN 1U S
FIG. 1. CT-scan of lesion found in right temporal lobe of R.N.
R.N. was feared and the object of aggression by others as well. When he reached puberty he became offensive towards females and on two occasions exhibited in public. At the age o f 13 he suffered one nocturnal grand mal seizure which was attributed to the then discovered Pseudohypohyperparathyreoidism, a rare metabolic condition causing a low serum calcium and osteitis fibrosa. R.N. was started on Mysoline, received, however, no further professional attention although his parents, his teachers and a social worker felt that he needed special education and, perhaps, psychotherapy. After the killing R.N. was admitted to a psychiatric unit for observation. There his behavior was similar to what had been reported previously. He was superficially adjusted but easily irritated. On minor demands he engaged in arguments and at times displayed a hostile attitude toward staff members. His psychic development was obviously below age, i.e., infantile. Feelings and thoughts were undifferentiated, unreflected and oriented towards immediate needs only. His personality structure was suggestive o f early acquired brain damage. Speech was poor in articulation and sentence production. Overall intellectual capacities were slightly below average.
Neurologically there were problems in fine motor coordination. Perimetry revealed a homonymous diminution of sensitivity and of Critical Flicker Fusion in the left upper quadrants of the visual fields. Repeated electroencephalographic recordings showed occasional sharp waves predominately over the right posterior temporal area. Axial computer tomography of the brain disclosed a distinctly localized lesion. There was a cystic defect in the right hippocampal gyrus, 1.5 by 2 cm in size, extending onto the posterior limits of the inner capsule. Over the course of 1 year the size of the lesion has remained unchanged. It was concluded that this defect which could not have been discovered pneumoencephalography interrupted most of the fibre connections between the right nucleus amygdalae and the right middle and posterior temporal cortex. The finding was felt to be relevant neuropsychologically and to causally correlate with specific functional disturbances such as facilitation of aggressive drives. The notion found support by the striking similarity in localization of the glioma, found at autopsy in the right hemisphere of Charles Whitman who in 1966 in Austin, Texas killed 16 people and wounded 32 others.
HOMICIDE OF AN AGGRESSIVE A D O L E S C E N T BOY
421
FIG. 2. Sections of the brain of Charles Whitman [8] showing tumor in the right temporo-occipital.
Neither did the report on the Whitman case nor do we attribute the violent behavior observed solely to the right temporal lesion. The case reported here is afflicted with dysfunction elsewhere in the brain. R. N. suffered at the time of the slaying from metabolic disease independently affecting emotion and had a long history of painful social experiences. Situational factors added to the outburst of violence. A number of developmental studies on aggressiveness [2,4] have shown that in some children a continuity exists
from th.e age of 3 onwards into adolescence. Given this persistence, at least in some individuals, a "constitutional" factor for aggressiveness has been hypothesized. Such factor could well be a brain lesion of the type described here. I therefore felt that it may have been worthwhile to draw your attention to this type of pathology. With the new diagnostic techniques in wide use perhaps more cases will be seen.
422
MARTINIUS
z
:~'~-~= ~ i i',~
FIG. 3. White matter (drawn from an information supplied by Dr. C. de Chenar).
REFERENCES
1. Blumer, D. P., H. W. Williams and V. H. Mark. The study and treatment, on a neurological ward, of aggresive patients with focal brain disease. Confin Neurol 36: 125-176, 1974. 2. Farrington, D. The family background of aggressive youths. In: Aggression and Antisocial Behavior in Childhood and Adolescence, edited by L. Hersov, M. Berger and D. Shaffer. Oxford: Pergamon Press, 1978. 3. Flor-Henry, P. Lateralized temporallimbic dysfunction and psychopathology. Ann "NY Acad Sci 280: 777-797, 1976. 4. Kagan, J. and H. Moss. From Birth to Maturity. New York: John Wiley, 1962.
5. Kligman, D. and D. A. Goldberg. Temporal lobe epilepsy and aggression. J Nerve Ment Dis 100: 324-341, 1975. 6. Moyer, K. E. The Physiology o f Hostility. Chicago: Markham, 1971. 7. Valenstein, E. S. Modification of motivated behavior elicited by electrical stimulation of the hypothalamus. Science 159:11191121, 1968. 8. Report to the governor. Medical aspects Charles G. Whitman catastrophe, Austin TX, September 8, 1966.
Homicide of an Aggressive Adolescent Boy with Right Temporal Lesion: A Case Reporf JOEST MARTINIUS M a x - P l a n c k - I n s t i t u t f u r P s y c h i a t r i e , Kraepelinstr. 10, D-8000 M u n c h e n 40, F R G
MARTINIUS, J. Homicide of an aggressive adolescent boy with right temporal lesion: A case report. NEUROSCI BIOBEHAV REV 7(3)419-422, 1983.---Thecase is reported of a 14-year-oldmale who killed an 8-year-old child following an alleged insult. The subject had been known to be aggressive throughout his school career. He had suffered one nocturnal seizure at the age of 13, but he never was amnesic for any of his fights. There was a history of possible hypoxic birth trauma. Neuropsychiatric investigation revealed developmental lags in speech and other psychosocial skills and, on computer tomography, a circumscribed lesion (cystic defect) lateral to the right nucleus amygdalae. Homicide
Brain lesion
Case report
hemispheres correlates with distinct psychopathological manifestations, in the dominant left hemisphere with paranoid states and in the non-dominant right hemisphere with dysphoria, excitability and manic-depressive states. In brief, the argument about aggression and localized or lateralized brain dysfunction in man is not settled. The case reported here may add to the argument, particularly because it presented a topological similarity with another unusual case of violent behavior who probably is well remembered by many working in the field. Our patient is a male who at the age of 14 years killed an 8 year old boy by beating, strangling and stabbing, following an alleged verbal insult by the young boy. The two had consented to enter a deserted house to make fire in the basement--which they did. There an argument arose. After the killing R.N. went home and only on the following morning when it became known that the child was missing indicated and finally confessed what had happened. He was not amnesic. R.N. is the elder of two children of healthy parents. During pregnancy his mother suffered from mild toxemia. Delivery occurred spontaneously at the expected date, following prolongued labor. The newborn--according to the birth record--had transient respiratory problems. His motor development was unremarkable but speech was definitely delayed and remained poor. An attempt to enter kindergarten at 4 years of age failed within weeks due to destructive play behavior and inability to adjust to the peer group. School was equally difficult from the very beginning. Performance was average but he engaged frequently in fights for minor reasons, was known for his overreactions to teasing and soon became the social outcast in and outside school.
THE neural substrate of aggression is organized at different levels of the nervous system. Due to this complexity the studying of single clinical cases is probably of limited value to the understanding of the anatomical basis for such emotional states, but may, nevertheless, contribute some. It is the amygdaloid subdivision of the limbic system which is mostly related to aggression and defense. Focal lesions, f.i. in this subdivision, may have serious effects upon the entire system without explaining its complex functions. Therefore, attempts to relate one particular focal brain lesion to violent behavior in man have been of little success. This is the more understandable since experiments in animals have shown that the effects of hypothalamic or amygdaloid stimulation are influenced by additional factors such as the immediate situation and previous experience, i.e., learning [6,7]. Brain stimulation does not appear to produce pure drive states. Instead, the resultant behavior is determined by the interplay of central processes including memory and relevant situational cues. Keeping these cautionary notes in mind one would remain on safe grounds in looking at focal lesions of the limbic system in their proper perspective. On the other hand, it is well known that certain clinical states in man are not infrequently associated with aggressive behavior, namely temporal lobe epilepsy. Blumer et al. [I] found in their study a striking preponderance of left temporal lobe defects in a group of abnormally aggressive patients. Kligman and Goldberg [5] in reviewing the problem of temporal lobe epilepsy and aggression again cautioned against the supposition of one single causative parameter such as temporal lobe pathology while Flor-Henry [3] left no doubt that lateralization of cerebral pathology to either of the two
JPaper presented at the International Workshop on the Limbic System, Innsbruck-Igls, May 15-16, 1981.
419
420
MARTIN 1U S
FIG. 1. CT-scan of lesion found in right temporal lobe of R.N.
R.N. was feared and the object of aggression by others as well. When he reached puberty he became offensive towards females and on two occasions exhibited in public. At the age o f 13 he suffered one nocturnal grand mal seizure which was attributed to the then discovered Pseudohypohyperparathyreoidism, a rare metabolic condition causing a low serum calcium and osteitis fibrosa. R.N. was started on Mysoline, received, however, no further professional attention although his parents, his teachers and a social worker felt that he needed special education and, perhaps, psychotherapy. After the killing R.N. was admitted to a psychiatric unit for observation. There his behavior was similar to what had been reported previously. He was superficially adjusted but easily irritated. On minor demands he engaged in arguments and at times displayed a hostile attitude toward staff members. His psychic development was obviously below age, i.e., infantile. Feelings and thoughts were undifferentiated, unreflected and oriented towards immediate needs only. His personality structure was suggestive o f early acquired brain damage. Speech was poor in articulation and sentence production. Overall intellectual capacities were slightly below average.
Neurologically there were problems in fine motor coordination. Perimetry revealed a homonymous diminution of sensitivity and of Critical Flicker Fusion in the left upper quadrants of the visual fields. Repeated electroencephalographic recordings showed occasional sharp waves predominately over the right posterior temporal area. Axial computer tomography of the brain disclosed a distinctly localized lesion. There was a cystic defect in the right hippocampal gyrus, 1.5 by 2 cm in size, extending onto the posterior limits of the inner capsule. Over the course of 1 year the size of the lesion has remained unchanged. It was concluded that this defect which could not have been discovered pneumoencephalography interrupted most of the fibre connections between the right nucleus amygdalae and the right middle and posterior temporal cortex. The finding was felt to be relevant neuropsychologically and to causally correlate with specific functional disturbances such as facilitation of aggressive drives. The notion found support by the striking similarity in localization of the glioma, found at autopsy in the right hemisphere of Charles Whitman who in 1966 in Austin, Texas killed 16 people and wounded 32 others.
HOMICIDE OF AN AGGRESSIVE A D O L E S C E N T BOY
421
FIG. 2. Sections of the brain of Charles Whitman [8] showing tumor in the right temporo-occipital.
Neither did the report on the Whitman case nor do we attribute the violent behavior observed solely to the right temporal lesion. The case reported here is afflicted with dysfunction elsewhere in the brain. R. N. suffered at the time of the slaying from metabolic disease independently affecting emotion and had a long history of painful social experiences. Situational factors added to the outburst of violence. A number of developmental studies on aggressiveness [2,4] have shown that in some children a continuity exists
from th.e age of 3 onwards into adolescence. Given this persistence, at least in some individuals, a "constitutional" factor for aggressiveness has been hypothesized. Such factor could well be a brain lesion of the type described here. I therefore felt that it may have been worthwhile to draw your attention to this type of pathology. With the new diagnostic techniques in wide use perhaps more cases will be seen.
422
MARTINIUS
z
:~'~-~= ~ i i',~
FIG. 3. White matter (drawn from an information supplied by Dr. C. de Chenar).
REFERENCES
1. Blumer, D. P., H. W. Williams and V. H. Mark. The study and treatment, on a neurological ward, of aggresive patients with focal brain disease. Confin Neurol 36: 125-176, 1974. 2. Farrington, D. The family background of aggressive youths. In: Aggression and Antisocial Behavior in Childhood and Adolescence, edited by L. Hersov, M. Berger and D. Shaffer. Oxford: Pergamon Press, 1978. 3. Flor-Henry, P. Lateralized temporallimbic dysfunction and psychopathology. Ann "NY Acad Sci 280: 777-797, 1976. 4. Kagan, J. and H. Moss. From Birth to Maturity. New York: John Wiley, 1962.
5. Kligman, D. and D. A. Goldberg. Temporal lobe epilepsy and aggression. J Nerve Ment Dis 100: 324-341, 1975. 6. Moyer, K. E. The Physiology o f Hostility. Chicago: Markham, 1971. 7. Valenstein, E. S. Modification of motivated behavior elicited by electrical stimulation of the hypothalamus. Science 159:11191121, 1968. 8. Report to the governor. Medical aspects Charles G. Whitman catastrophe, Austin TX, September 8, 1966.