Aggressive Behavior and the Brain: A DifferentPerspective for the Mental Health Nurse Sandy Harper-Jaques
and Marlene Reimer
Mental health nurses often provide care to individuals who have the potential for aggressive behavior. The expression of such behavior is influenced by the functioning of the central nervous system (CNS). The authors present a framework to assist the reader to understand the interrelationships among the limbic system, and frontal and temporal lobes as they relate to the expression of aggressive behavior. The implications for mental health nursing practice include detecting contributing factors such as head injury, temporal lobe epilepsy, alcoholism, and dietary imbalances, and interpreting patient behaviors to colleagues. Suggestions for proactive interventions are also included.
Copyright
A
0 1992 by W.B. Saunders
BEHAVIOR has been a dominant force in human interaction since the beginning of recorded history. Despite this longstanding familiarity with the phenomenon, knowledge about the origins of human aggression is incomplete. A perspective, often overlooked by nurses practicing in mental health, is the influence of neurological dysfunction on the expression of aggression. From time to time, individuals will experience conflict that arises from a desire by one person to convince the other that a particular point of view is correct (Maturana & Varela, 1987). Conflicts may erupt into disagreements, quarrels, and the use of physical force (Brinkerhoff & Lupri, 1988). Personal definitions of aggression vary and are influenced by past experience, beliefs, social group, and gender. For the purpose of this discussion, “aggression” is defined as a physical act of force intended to cause harm to a person or object to convey the message that the perpetrators point GGRESSIVE
From the Out Patient Program, Holy Cross Hospital, Cafgary; and the Faculty of Nursing, University of Calgary, Alberta, Canada. Address reprint requests to Sandy Harper-Jaques. M.N., 2719 Lionel Crescent SW., Calgary, Alberta T3E 661, Canada. Copyright 0 1992 by W.B. Saunders Company 06839417l92D605-0009$3.00l0
312
Company
of view is more correct (adapted from Gayford, 1983; Maturana, 1988). In considering the relationship between the nervous system and aggression, two questions can be asked. First, “does the aggressive individual behave in a forceful manner in response to his/her perceptions of the situation?” The answer would seem to be yes. Second, “are the perceptions of the situation influenced by a dysfunction in the nervous system?” This second question, the more puzzling of the two, will be explored here. NEUROLOGICAL BASIS
The authors search for answers to questions about the role of neurological activity during aggressive behavior has centered on three specific areas: the limbic system, the frontal lobe, and the temporal lobe. Three neurotransmitters in particular, serotonin, gamma-amniobutyric acid (GABA), and dopamine, have also been postulated to influence the expression or suppression of aggressive behaviors. The Limbic System
The limbic system is a circuit of neural pathways formed by structures in the cortical and subcortical portions of the brain. If the brain is visualized as a sphere, the limbic system forms a helix
Archives of Psychiatric Nursing, Vol. VI, No. 5 (October), 1992: pp 312-320
AGGRESSIVE
313
BEHAVIOR AND THE BRAIN
Frontal Lobe Motor Cortex Premotor Area Sensory Cortex Corpus Callosum Cingulate Gyrus
Cerebellum Brainstem
Fig 1.
Limbic system identified in boldface type; other brain structures labeled for reference.
of interconnected structures near the core (Fig 1). This ball encompasses the most primitive portions of the cerebral cortex, as well as the interconnected subcortical structures (deGroot & Chusid, 1988). The structures within the limbic system act to mediate primitive emotion and basic drives to produce behaviors necessary for the survival of the individual and the species. The functions include behaviors associated with eating, aggression, expression of emotion, and sexual response (deGroot & Chusid, 1988). The influence of the limbic system is exerted through the regulation of motor, autonomic, and endocrine activity. interconnections with neural pathways outside the boundaries
of the limbic system influence all areas of the central nervous system (CNS) (Damasio & Van Hoesen, 1983; Gilman & Winans Newman, 1987; Heilman, Bowers, & Valenstein, 1985). Structures commonly included in discussions of the limbic system are the hippocampus, amygdala, cingulate gyrus, and hypothalamus (Table 1; Breathnach. 1980; de Groot & Chusid, 1988). The interconnection of the various structures facilitates the ability of the limbic system to process. integrate and mediate information from the cortex. reticular formation, brain stem, and spinal cord (deGroot & Chusid, 1988). Synthesis of this information influences the emotions of the individual.
Table 1. The Limbic System structure Hippocampus
Function
Memory storage and information processing
Dysfuncmn
Confabulation
and aggressive behavior often
associated with Korsakoff’s Amygdala
Receives and interprets sensory information
Pica; hypersexuality
as seen in Kluver-Bucy
syndrome Cingulate gyrus
Receives input from other limbic structures
Disturbed affect, marked loss of ability to
Hypothalmus
Synthesizes input from all areas of nervous
Many aspects of emotional behavior such as
experience system; vital role in balance of hormones,
and express emotion
anger, placidity, and sexual activity
electrolytes, and body temperature; mediates activity of autonomic nervous system Data from Breathnach (1980), Byers and Guthrie 11984), Mesulam (19851, deGroot and Chusid (1988), Damasio and Van Hoesen 119831, and Gilman and Winans Newman.
314
Alterations in functioning of the structures of this system influence both the emotional experience and behavior of the individual, and may increase or decrease the potential for aggressive behavior. Limbic system dysfunction may be responsible for a range of psychiatric disorders such as panic attacks, depression, and schizophreniform conditions (Mesulam, 198.5). Damage to the amygdala and hippocampus may prevent the individual from processing cues necessary to match present stimuli with past experience. One example would be the catastrophic reactions sometimes displayed by dementia patients (LeNavenec, 1988). Hence, a situation may be perceived by the individual to be threatening when it is not (Mesulam, 1985). Conversely, lesions in the hypothalamus and septal regions may reduce episodes of fear or rage (Byers & Guthrie, 1984). Snyder (1988) proposes that aggression, in some instances, arises from abnormally increased behavioral arousal. Such hyperarousal can be the result of inaccurate interpretation of information from the environment leading to an aggressive response. Snyder suggests that this state may be due to defects in the sensory system or an inability to blend new and old information related to memory problems . The Frontal Lobe The frontal lobes, the second major area, mediate purposeful behavior, elaborate thought, and exert an initiatory influence over the limbic system (Boss & Coghlan Stowe, 1986). In essence, it is the frontal lobe where reason and emotion interact (Strub & Black, 1985). These lobes include the motor cortex, premotor area, and prefrontal area in each hemisphere. Detachment of cortical and subcortical regions of the brain has been demonstrated to lead to a separation of emotional expression from emotional experience (Heilman et al., 1985). Portions of the prefrontal area are thought to act as staging areas for information received from the limbic system (Eslinger & Damasio, 1985). Reciprocity between the staging areas of the prefrontal area and the limbic system permits regulation by the cortex of hypothalamic processes and activation of the cortex by basic drives thought to originate in the limbic system (Eslinger & Damasio, 1985). Without this two-way communication link, the areas involved have little means of influencing the other.
HARPER-JAQUES
AND REIMER
Damage to the frontal cortex impairs judgement. Changes in social behavior include inadequate decision-making and inappropriate conduct (Eslinger & Damasio, 1985; Tranel, Damasio, & Damasio, 1989). Bifrontal damage, as frequently seen in head injury, may result in personality changes, poor judgement, and occasional aggressive outbursts (Snyder, 1988). These outbursts are characteristically brief and unexplained, often set off by minor environmental stimuli (Silver, 1987). The Temporal Lobe The temporal lobes are intimately connected with the limbic system, actually sharing some structures such as the hippocampus. Besides interpretation of auditory stimuli, the temporal lobes play a major role in memory. Impairments and distortions in memory may also interfere with perceptual processing and integration of new stimuli (Beck, Rawlins, & Williams, 1988; Snyder, 1988). The temporal lobe dysfunction most frequently linked with aggressive behavior is epilepsy, particularly in those individuals with partial complex seizures (Cassidy, 1990). Discussions with mental health nurses have revealed a belief that individuals with temporal lobe epilepsy are more likely to be aggressive. This idea is debated in the literature. There is consensus that aggressive behavior during the ictal period is a defensive, nondirected response to attempts at restraint (Browne & Feldman, 1983; Devinsky & Bear, 1984). Postictal violence may occur while the individual is recovering from a seizure. At that point, the individual is confused and agitated. Attempts to provide assistance may be met with a defensive response (Burrowes, Hale, & Arrington, 1988). However, the relationship of electrophysiologic abnormality and assaultive behaviors during the interictal period is subject to debate. One source suggests that patient and family attitudes and beliefs about the seizure disorder can result in increased frustration for all family members. This may lead to assaultive behavior (Thompson, 1988). Browne and Feldman (1983) propose that violent behavior is more common in individuals with seizures than the general population. However, they emphasize that temporal lobe epilepsy may be a contributing factor in aggression, but it should not be considered a “cause” of violence. Cassidy (1990a) comments that “even
AGGRESSIVE
315
BEHAVIOR AND THE BRAIN
discharges that are sub-convulsive can produce behavior that mimics human dyscontrol syndromes, presumably due to a phenomenon known as kindling” (p. 85). Another viewpoint, which supports the notion of interictal aggression, is that the behavior is the result of forced normalization of electrical activity of the brain (Benson, 1986; Fedio, 1986). This normalization occurs due to the use of anticonvulsants. Increasing irritability can lead to episodes of aggression. Benson has gone so far as to recommend the use of drug holidays or electroconvulsive therapy (ECT) to allow occasional seizures .
Devinsky and Bear (1984) studied five individuals in which aggressive behaviors were reported to occur following the onset of an epileptic focus in the temporal lobes. Assaults were observed during the interictal period. Another cluster of behaviors were increased interest in spirituality; changes in sexual intensity or orientation; and anxiety, phobias, or paranoia. These individuals were able to recall the violent episode. They took responsibility for the behavior and frequently experienced remorse or guilt. In concluding, Devinsky and Bear ( 1984) suggest that there is evidence for the development of a secondary foci following the onset of
seizures. The second foci could account for the aggressiveness. The Neurotransmitters
Most of the neurotransmitters can be classified into one of four categories: acetylcholine, monoamines, peptides, and amino acids. Changes in the balance of these compounds can aggravate or inhibit aggression. To function effectively as a neurotransmitter, a substance must be synthesized in the presynaptic neuron, released from the neuron into the synaptic cleft, bound to a receptor on the postsynaptic neuron, and then destroyed or removed from the receptor (Gilman & Winans Newman, 1987). Disruptions at any of these points will influence neurotransmitters concentrations. The neurotransmitters most frequently implicated as affecting behavior are the monoamines serotonin (5HT) and dopamine, and the amino acid GABA (Table 2). A surplus or deficit of one neurotransmitter can only be interpreted in the context of differing effects of neurotransmitters at differing synapses and the neural circuits involved in any behavior (PiacentC, 1986). Communication between neurons is accomplished via neurotransmitters crossing the synaptic cleft. Hence, commu-
Table 2. Neurotransmittars Postulated Neurotransmitter Serotonin
PMGUrSOr
[5-HT]
Tryptophan;
Normally found in high concentrations
in
limbic system
found in milk, beef, eggs,
With
Relationship
Aggressive
Behaviors
Modulates violence, sleep, sensory responses,
wheat, flour, & corn; production
mood, and performance;
impaired in thiamine deficient diets,
improved behavior in aggressive patients
e.g., alcoholism
treated with supplemental
case reports of tryptophan;
dietary restriction of tryptophan
shown to
increase aggression GABA
Glutamic acid
Inhibits impulsivity and aggression similar to
Dopamine
Tyrosine
Increases aggressive behavior and sexual
serotonin activity, vigilance heightens; elevated levels associated with idiopathic schizophrenia and organic delusional disorders; L-dopa in treatment
of Parkinsonism linked to
paranoid psychosis Norepinephrine
Tyrosine
Primarily released from
Increases aggressive behavior, heightens vigilance
the locus ceruleus Acetylcholine
Lecithin; Choline salt
Deficiency (as in Alzheimer’s
disease) may
directly increase aggressive tendencies through lowered threshold for confusion and loss of recent memory Data from Spring (1986). Piacentb (1986). Cassidy (1990), Burrowes et al. (1988). Cummings (1986). Gilman and Winans Newman 11987). and Gottfries (1990).
316
HARPER-JAQUES
nication between structures is affected by neurotransmitter concentrations. THE EMOTIONAL CIRCUIT
The interconnections of the limbic system and prefrontal area of the frontal lobe provide a communication link between the cognitive processes of the frontal lobes and the emotional processes of the limbic lobe. Disconnection of the circuit has been shown to result in a variety of problems, including aggression (Damasio, 1985). The phrase “the emotional circuit” has been chosen to describe the relationship between these two regions of the brain. This circuit can be thought of as an open system, in which the overall functioning is greater than the functioning of the individual structures. The interaction of the emotional circuit is hypothesized to determine the meaning given to a particular situation. Such meaning will be influenced by the individual’s current physiological capability to analyze incoming messages with stored memories and beliefs. With aggressive individuals, meaning given to a particular circumstance may be altered from that person’s usual perceptions or from the norm accepted by the social context. This alteration may contribute to assaultive behavior. One example of pervasive disruption of the emotional circuit is Alzheimer’s disease, in which there is widespread degeneration and atrophy of cortical neurons. The associated cognitive impairment, loss of memory and emotional control, and impairment of judgement contribute to sudden impulsive acts of aggression. These individuals are often seen to strike out in unfamiliar situations that they perceive as threatening. Loss of emotional control with explosive outbursts may be even more pronounced in patients with dementia secondary to multiple infarcts depending on the location of the infarcts. Multiinfarct dementia arises from many small emboli or strokes, often secondary to hypertension. The onset may be more abrupt and the effects on behavior more variable than those seen in Alzheimer’s disease (Petrie, 1984). NURSING IMPLICATIONS
The human response of aggression is multidimensional. Having considered the interrelationships of the structures of the brain, the mental health nurse can incorporate research findings and theory to expand the repertoire of approaches. Areas of importance for mental health nursing prac-
AND REIMER
tice are comprehensive history taking, proactive interventions, and the interpretation of patient behavior. HISTORY TAKING
Nurses can play an important role in identifying factors that may contribute to aggressive behavior. Those that are most relevant to the mental health nurse are head injury, alcohol and drug use, nutritional status, and temporal lobe epilepsy. Head injury
Irritability and aggressive outbursts are common sequelae of traumatic head injuries, particularly when the frontal lobe has been involved (Silver, 1987). Juvenile delinquents have been found to have more frequent history of head injury than the general population (Otnow Lewis, 1983). Even minor injuries such as concussion or perinatal insults may lead to minimal brain dysfunction (MBD). Episodic dyscontrol syndrome is often seen in those with MBD, especially when the lesion is in the dominant hemisphere of the frontal lobe (Burrowes et al., 1988; Flor-Henry, 1983). These individuals demonstrate recurrent episodes of rage and violence. When assessing the patient, the nurse can seek specific information regarding history of head injury, repeated falls, or other circumstances suggestive of minor head trauma such as being “knocked out” in fights or contact sports. Alcohol and Drug Use
The astute mental health nurse will watch for indications of alcohol and drug use and abuse, which increase the potential for aggressive behavior. Aggressive behavior associated with substance abuse tends to be linked with three stages: during intoxicated, during withdrawal, and later from accumulative residual effects (Piercy, 1984). The drugs most often implicated are (1) sedative effect of depressant agents, such as alcohol and diazepam; (2) stimulants such as cocaine, amphetamines, caffeine, and nicotine, (3) hallucinogens such as PCP, LSD, and marijuana; and (4) narcotits .
The use or withdrawal from combinations of such drugs exacerbate the risk of aggressive behavior (Piercy, 1984). Recent discontinuation or noncompliance with certain prescribed medications should also be explored because of their potential effects on aggressive behavior. For ex-
AGGRESSIVE
317
BEHAVIOR AND THE BRAIN
ample, antidepressants, cx,-agonists such as clonidine, and B-blockers such as propranolol (Inderal; Ayerst) are known to suppress the activity of the excitatory catecholamines such as norepinephrine and dopamine (Cassidy, 1990b). In contrast, fluoxetine (Prozac; Lilly) and lithium enhance the availability of serotonin by inhibiting the reuptake of the neurotransmitter (Cassidy, 1990b). Some anticonvulsants, particularly the ones affecting the limbic system, such as carbamazepine (Tegretol; Geigy), have been shown to reduce aggressive behavior. This is particularly apparent in patients with neurological dysfunction, even when frank seizure activity has not occurred (Cassidy, 1990b). Given the high risk of seizure activity among most patients with a cerebral insult through trauma, stroke, or tumor, many such patients are on prophylactic anticonvulsant therapy for up to 1 year postinsult. The nurse may predict a greater potential for aggressive behavior when there is a history of abrupt discontinuation or erratic compliance in individuals who are already vulnerable with impaired information processing. Alcohol is still the most frequently implicated when discussing aggressive behavior (Piercy, 1984). The effect that alcohol has on behavior and mood depends on the concentration of the alcohol in the body, the diet of the individual, the pattern of drinking, the previous experience of drinking, and the environment in which the drinking takes place (Burrowes et al., 1988; O’Sullivan, 1984). As a contributing factor to aggressive behavior, alcohol impacts the nervous system by three mechanisms: intoxication, withdrawal, and alcoholic dementia (Korsakoff’s syndrome) (Petrie, 1984). Piercy (1984) cites a typical scene in Western movies “where the bad guys drink in the saloon before leaving to kill the good rancher and ravish his beautiful daughter” (p. 130) as an example of the conscious use of alcohol as an intoxicant for its disinhibiting effect on cortical control. Less common and less well understood is alcohol idiosyncratic intoxication in which a dramatic change of behavior, usually involving violence, is seen following ingestion of a moderate amount of alcohol. The discomfort associated with withdrawal may contribute to consciously mediated aggressive acts associated with demands for alcohol. In those patients who experience alcohol withdrawal delirium, aggressive behavior may be seen in response to distorted perceptions associated with hallucina-
tions and paranoid delusions. Permanent cortical damage resulting from prolonged alcohol abuse, as seen in Korsakoff’s syndrome, is a contributing factor to aggressive behavior through the effects of memory disturbance, dementia, and agitation on the ability to interpret and cope with incoming stimuli (Petrie, 1984). Nutrition During the process of the initial assessment, the nurse can note aspects of physical appearance and behavior that may indicate poor nutrition. Research reports (Spring, 1986; Strain, 1981) point to an interrelationship between nutrition, brain function, and behavior. In particular, there is evidence to suggest that dietary deficiencies will influence the production of neurotransmitters which, in turn. influence CNS functioning (Conlay, 1988). Deficiencies may occur as the result of metabolic error, malabsorption, or dietary deficiency. Alcohol is one factor in the deficient use of available nutrients because of gut irritation, poor digestion, malabsorption, or metabolic inefficiencies. Excessive alcohol consumption can contribute to protein malnutrition, multiple vitamin deficiencies, and mineral depletion (Burton & Foster. 1988). Although single vitamin deficiencies are rare, deficiencies of two particular vitamins influence the production of the neurotransmitters previously discussed. Niacin deficiency may be seen in individuals who are indigent or have long-standing poor dietary habits, are afflicted by diseases that interfere with appetite, or are chronic alcohol abusers, as well as in some forms of drug therapy (Burton & Foster, 1988). Effects on the CNS can include disorientation, confusion, anxiety, fear, and paranoia. Sources of niacin include meat, fish, poultry, whole grain bread, and enriched cereals. Thiamine is the second vitamin that is most often deficient due to inadequate diet. Early manifestations of deficiency include neurasthenia, characterized by irritability, poor memory, and an inability to concentrate (Burton & Foster, 1988). Prolonged use of alcohol can block up to 70% of the uptake of thiamine. Some features of the patient’s presentation may appear to be symptoms of Korsakoff’s syndrome, but will be quickly corrected by administration of thiamine (Iber, 1988). It too is found in whole grain breads and enriched cereals, as well as in pork, liver, and legumes.
HARPER-JAQUES
318
AND REIMER
may also assist the patient to maintain a balanced diet within a limited budget.
One of the amino acids that acts as neurotransmitter precursor, tryptophan, is vulnerable to dietary changes. Tryptophan competes with other diet derived amino acids to cross the blood-brain barrier. It is found in the brain in higher concentrations following the ingestion of a highcarbohydrate meal than it is after a high-protein meal. The presence of proteins increases the competition for the movement of amino acids across the blood brain-barrier (Fernstrom, Wurtman, & Hammarstrom-Wikland, 1979). The production of the neurotransmitter serotonin is dependent on the concentrations of tryptophan in the plasma. Increased levels of tryptophan have been correlated with reduced insomnia and improved moods in depressed patients. Alterations to the diets of patients may help to increase the availability of necessary neurotransmitter precursors. However, the population cared for by the mental health nurse is often disadvantaged in many ways, not the least of which is possessing the knowledge and financial resources to maintain adequate nutrition. The nurse is presented with the challenge to help patients to consider the role of nutrition in reducing symptoms. The nurse
Temporal Lobe Epilepsy
Individuals who present with a history of violent episodes may also have a history of temporal lobe epilepsy (TLE). By adding questions about TLE to the nursing assessment, this factor may be discovered. An example is an adolescent who was placed in a residential treatment setting as a means of helping him control his aggressive behaviors. A review of past records revealed an electroencephalogram (EEG) report diagnosing a temporal lobe lesion. Some of the young man’s behavior was corrected with medication. In persons presenting with a history of seizure activity, the nurse should be alert to epileptogenic factors in the recent history such as sleep deprivation, excessive ingestion of alcohol or caffeine, and intense emotional stress (Grant, 1985; Santilli & Sierzant, 1987). Individuals with identified lesions or dysfunctions in the limbic system, temporal lobe, or frontal lobes may exhibit behaviors or report experiences that may be labeled “a psychiatric problem.” The nurse who understands the
Table 3. Proactive interventions Characteristics
Patient Profile
Belligerent
Example Male (22 years) admitted threatening fights,
behavior,
several
heavy alcohol
past, he played hospitalized
limited
with recent
use; and in the
hockey,
was
for a head injury
at
Interventions
and impulsive, appreciation
consequences
of
of behavior;
slow in complex
tasks;
agitated
depression;
diagnosis
epilepsy;
observe for triggering plan for positive
solving.
Valproic
shifts;
believes
as
epileptic
parital
on valproic
drugs cause weight
disturbed
Prior to had been “up”
depression;
effects include
insomnia
increased
serum levels to determine
(no unsupervised
Untidy,
poor hygiene;
dry
Some symptoms
skin and hair, skin lesions
deficiencies,
nights in the hostel;
on areas exposed
to
administration
diagnosis:
schizophrenia,
sunlight;
mucous
she is fearful
food or medications.
spends when of injesting
swollen
membranes increased
and tongue; salivation;
disorientation,
confusion
and anxiety;
hallucinations
and paranoia.
niacinamide
baths);
obtain
therapeutic
acid; establish
sleep/wake
occasional symptomatic
and
activity
dose of valproic
side untoward
risk for seizure
seizures
3 homeless,
GABA levels, she
effects include
consistent
and assess
deficiencies.
acid; gain so
provide
behavior
reinforcement;
acid elevates
aggression;
36 hours.
skips doses. Female (35 years),
events;
select target
and
circuit;
has used the drug erratically;
by frequent
admission
to decreased
for alcohol
of the emotional
problem
wakenings;
employed
aide, works controlled
diagnosis
secondary
since age 14, complex
Example
disruption
for thiamine
Female (27 years), primary
poorly
tolerance
structure;
Obese; sleep pattern
2
kitchen
may contribute
self-control,
poor ability to generalize,
age 19. Example
Head injury
cycle.
may be due to dietary particularly
niacin;
of oral or subcutaneous may be necessary;
provide
a well-balanced
diet that contains
150 g of protein
and 3,500 calories.
100 to
AGGRESSIVE
319
BEHAVIOR AND THE BRAIN
potential effects of these lesions will be better able to plan interventions that will assist the patient and family to adapt to his/her changed state. PROACTIVE INTERVENTIONS
Taking this information into account, the nurse has a greater range of proactive interventions to reduce potential for aggression. The nurse now has the option to intervene at several points (Table 3). INTERPRETATION OF PATIENT BEHAVIOR
Of equal importance is the interpretation of the patient’s behavior to colleagues and family members. In both authors’ experience, the patient who is rude, interpersonally unsophisticated, and who does not “learn” more acceptable behavior, is often labeled as “noncompliant” or “difficult” by the treatment team. Staff feelings of frustration with these patients may be manifest in brief interactions and/or simply ignoring the patient. This withdrawal by staff may increase the patient’s clumsy, often aggressive attempts to be acknowledged. In the end, staff may provide intense interest only when aggressive behaviors reach crisis proportions. CONCLUSION To this point, most of what is known about the neurological basis of aggression has been drawn from other disciplines. There is a paucity of nursing research or anecdotal literature regarding neurological functioning and aggressive behavior in the population cared for by mental health nurses. This mirrors the paucity of interventions available to respond to the needs of this population. However, greater understanding of the influence of the emotional circuit on assaultive behavior will enhance clinical practice by giving the nurse an alternate perspective when relating to the client with a history of aggressive behavior. REFERENCES Beck, C.M., Rawlins, R.P., &Williams. S.R. (1984). Mental health-psychiatric nursing: A holistic life cycle approach. St. Louis: C.V. Mosby Company. Benson, D.F. (1986). Interictal behavior in epilepsy disorders. Psychiatric Clinics of North America, 9(2), 283-291. Boss. B.J., & Coghlan Stowe, A. (1986). The neuroanatomical and neurophysiological basis of learning. Journal of Neuroscience Nursing, 18(S), 256-264. Breathnach, C.S. (1980). The limbic system, 1980. Journal of the Irish Medical Association. 73(9), 331-339.
Brinkerhoff. M.B., & Lupri, E. (1988). Interpersonal violence. Canadian Journal of Sociology, 13(4), 407-43 1. Browne, T.R., & Feldman, R.G. (1983). Epilepsy: Diagnosis and management. Boston: Little, Brown and Company. Burrowes, K.L.. Hales, R.E., & Arrington. E. (1988). Research on the biologic aspects of violence. Psychiatric Clinics of North America. 11(4), 409-509. Burton, B.T., & Foster, W.R. (1988). Human nutrition. Toronto: McGraw-Hill Book Company. Byers. V.L.. & Guthrie, M.D. (1984). The limbic system and behavior. Journal of Neurosurgical Nursing. l/5(2). 80. 83. Cassidy. J. W. (1990a). Neurochemical substrates of aggression: Toward a model for improved intervention. [part I]. Journal ofHead Trauma Rehabilitation. 5(2), 83-86. Cassidy. J.W. (1990b). Neurochemical substrates of aggression: Toward a model for improved intervention. [part II]. Journal of Head Trauma Rehabilitation. S(3). 7013. Conlay. L.A. (1988). Nutrients and brain function. in J.M. Kinney. K.N. Jeejeebhoy. G.L. Gill. & 0. Owen (Eds. I. Nurrition and metabolism in parient care (pp. 727-736). Philadelphia: W.B. Saunders Co. Cummings, J.L. (1986). Organic psychoses: Delusional disorders and secondary mania. Ps;chiatric Clinics qfhrorrh America. Y(2). 293-311. Damasio. A.R. (1985). The frontal lobes. In K.M. Heilman & E. Valenstein (Eds. ). Clinical Neurops,vcholo,qy (2nd ed.: pp. 339-376). New York: University Press. Damasio. A.R.. & Van Hoesen, G.W. (1983). Emotional disturbances associated with focal lesion of the limbic frontal lobe. In K.M. Heilman & P. Satz (Eds.). Neuropsychology of human emotion (pp. 85-t IO). New York: Guilford Press. deGroot, J., & Chusid, J.G. (1988). Correlative neuroanatomy. East Norwalk, CT: Appleton-Lange. Devinsky. 0.. & Bear, D. (1984). Varieties of aggression in temporal lobe epilepsy. American Journal of Pswhiafry, 141(5). 651-656. Eslinger. P.J.. & Damasio. A.R. (1985). Severe disturbance of higher cognition after bilateral frontal lobe ablation. Neurology. 35. 1731-1741. Fedio. P. (1986). Behavioral characteristics of patients with temporal lobe epilepsy. Psychiatric Clinics of Norrh America. 9(2), 267-281. Femstrom, J.D.. Wurtman. R.J.. & Hammarstrom-Wikland. B. ( 1979). Diurnal variations in plasma concentrations of tryptophan, tyrosine and their neutral amino acids: Effect of dietary protein intake. American Journal of Clinical Nutrition, 32. 1912. Flor-Henry. P. (1983). Neuropsychological studies in patients with psychiatric disorders. In K.M. Heilman & P. Satz (Eds.). Neuropsychology of human emorion (pp. 193. 220). New York: The Guilford Press. Gayford.
J.J. (1983). Battered wives. In R.J. Gelles & C. Pedrick Cornell (Eds.). Interpersonal perspectives on farnil? violence. Toronto: Lexington Books.
Gilman,
S.. & Winans Newman, S. (1987). Essenrials of clinical neuroanatomy and neurophwiologqv. Philadelphia: F.A. Davis Company.
Gottfries.
C.G. 11990). Neurochemical
changes
in the human
320
HARPER-JAQUES
brain and their importance for behavior Triungte, 29(2 13). 127-131.
in the senium.
Grant, I. (1985). The social environment and neurological disease. Advances in Psychosomatic Medicine, 13, 26-47. Heilman. K.M., Bowers, D., & Valenstein, E. (1985). Emotional disorders associated with neurological disorders. In K.M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology (2nd ed.; pp. 377-402). New York: Oxford University Press. Iber, F.L. (1988). Alcohol associated diseases. In J.M. Kinney, K.N. Jeejeebhoy, G.L. Gill, & 0. Owen (Eds.), Nutririon and metabolism in patienr care (pp. 429-444). Philadelphia: W.B. Saunders Co. LeNavenec, C.L. (1988). The care process with demenria patients: A practical handbook for nursing home staff and family care givers. Calgary, Alberta: The University of Calgary. Luria,
A.R. (1973). The working brain: An introduction to neuropsychology. (B. Haigh, Translator) New York: Basic Books, Inc.
Maturana, H.R. (1988, October). [Telephone conversation with Humberto Maturana and N651 class: The Calgary/ Chile coupling.] Unpublished manuscript. Maturana, H.R., & Varela, F.J. (1987). The tree of knowledge. Boston: New Science Library. Mesulam, M. (1985). Principles of behavioral neurology. Philadelphia: F.A. Davis Co. O’Sullivan, K. (1984). Depression and its treatment in alcoholics: A review. Canadian Journal of Psychiatry, 29, 379-384. Otnow Lewis, D. (1983). Neuropsychiatric vulnerabilities and violent juvenile delinquency. Psychiatric Clinics of North America, 6(4), 707-714. Petrie, W. (1984). Violence: The geriatric patient. In J. Turner (Ed.). Violence in the medical care setting: A survival guide (pp. 107-121). Rockville, MD: Aspen Publications.
AND REIMER
Piacente, G.J. (1986). Aggression. Psychiatric Clinics ofNorrh America, 9(2), 329-339. Piercy, D. (1984). Violence: The drug/alcohol patient. In J. Turner (Ed.), Violence in the medical care setting: A survival guide (pp. 123-151). Rockville, MD: Aspen Publications. Santilli, N., & Sierzant, T. (1987). Advances in the treatment of epilepsy. Journal of Neuroscience Nursing, 19(3), 141-155. Silver, J. (1987). Aggressive behavior in patients with neuropsychiatric disorders. Neurotrauma Medical Report, 3(2), l-3. Snyder, M. (1988). Abnormally increased behavioral arousal. In P.H. Mitchell, L.C. Hodges, M. Muswaswes, & C.A. Walleck @Is.). AANN’ Neuroscience nursing: Phenomena and practice (pp. 85-97). Norwalk, CT: Appleton-Lange. Spring, B. (1986). Effects of foods and nutrients on the behavior of normal individuals. In R.J. Wurtman & J. Wurtman (Eds.), Nutrition and the brain: Food constituenrs affecting normal and abnormal behaviors (pp. 1-48). New York: Raven Press. Strain, G.W. (1981). Nutrition, brain function and behavior. Psychiatric Clinics of North America, 4(2), 253-268. Strub, R.L., & Black, F.W. (1985). The menral status examination in neurology (2nd ed.). Philadelphia: F.A. Davis, Thompson, P.J. (1988). Methods and problems in the assessment of behavior disorders in epileptic patients. In M.R. Trimble & E.H. Reynolds (Eds.), Epilepsy, behavior and cognitive funcfion. Chichester, England: John Wiley and Sons. Tranel, D., Damasio, A.R., & Damasio, H. (1989, February). Acquired sociopathy as a domain-specific memory disorder: Impaired autonomic responses to social/ emotional stimuli following frontal damage. Paper presented at the meeting of the International Conference of Neuropsychology, Vancouver, B.C.
and Marlene Reimer
Mental health nurses often provide care to individuals who have the potential for aggressive behavior. The expression of such behavior is influenced by the functioning of the central nervous system (CNS). The authors present a framework to assist the reader to understand the interrelationships among the limbic system, and frontal and temporal lobes as they relate to the expression of aggressive behavior. The implications for mental health nursing practice include detecting contributing factors such as head injury, temporal lobe epilepsy, alcoholism, and dietary imbalances, and interpreting patient behaviors to colleagues. Suggestions for proactive interventions are also included.
Copyright
A
0 1992 by W.B. Saunders
BEHAVIOR has been a dominant force in human interaction since the beginning of recorded history. Despite this longstanding familiarity with the phenomenon, knowledge about the origins of human aggression is incomplete. A perspective, often overlooked by nurses practicing in mental health, is the influence of neurological dysfunction on the expression of aggression. From time to time, individuals will experience conflict that arises from a desire by one person to convince the other that a particular point of view is correct (Maturana & Varela, 1987). Conflicts may erupt into disagreements, quarrels, and the use of physical force (Brinkerhoff & Lupri, 1988). Personal definitions of aggression vary and are influenced by past experience, beliefs, social group, and gender. For the purpose of this discussion, “aggression” is defined as a physical act of force intended to cause harm to a person or object to convey the message that the perpetrators point GGRESSIVE
From the Out Patient Program, Holy Cross Hospital, Cafgary; and the Faculty of Nursing, University of Calgary, Alberta, Canada. Address reprint requests to Sandy Harper-Jaques. M.N., 2719 Lionel Crescent SW., Calgary, Alberta T3E 661, Canada. Copyright 0 1992 by W.B. Saunders Company 06839417l92D605-0009$3.00l0
312
Company
of view is more correct (adapted from Gayford, 1983; Maturana, 1988). In considering the relationship between the nervous system and aggression, two questions can be asked. First, “does the aggressive individual behave in a forceful manner in response to his/her perceptions of the situation?” The answer would seem to be yes. Second, “are the perceptions of the situation influenced by a dysfunction in the nervous system?” This second question, the more puzzling of the two, will be explored here. NEUROLOGICAL BASIS
The authors search for answers to questions about the role of neurological activity during aggressive behavior has centered on three specific areas: the limbic system, the frontal lobe, and the temporal lobe. Three neurotransmitters in particular, serotonin, gamma-amniobutyric acid (GABA), and dopamine, have also been postulated to influence the expression or suppression of aggressive behaviors. The Limbic System
The limbic system is a circuit of neural pathways formed by structures in the cortical and subcortical portions of the brain. If the brain is visualized as a sphere, the limbic system forms a helix
Archives of Psychiatric Nursing, Vol. VI, No. 5 (October), 1992: pp 312-320
AGGRESSIVE
313
BEHAVIOR AND THE BRAIN
Frontal Lobe Motor Cortex Premotor Area Sensory Cortex Corpus Callosum Cingulate Gyrus
Cerebellum Brainstem
Fig 1.
Limbic system identified in boldface type; other brain structures labeled for reference.
of interconnected structures near the core (Fig 1). This ball encompasses the most primitive portions of the cerebral cortex, as well as the interconnected subcortical structures (deGroot & Chusid, 1988). The structures within the limbic system act to mediate primitive emotion and basic drives to produce behaviors necessary for the survival of the individual and the species. The functions include behaviors associated with eating, aggression, expression of emotion, and sexual response (deGroot & Chusid, 1988). The influence of the limbic system is exerted through the regulation of motor, autonomic, and endocrine activity. interconnections with neural pathways outside the boundaries
of the limbic system influence all areas of the central nervous system (CNS) (Damasio & Van Hoesen, 1983; Gilman & Winans Newman, 1987; Heilman, Bowers, & Valenstein, 1985). Structures commonly included in discussions of the limbic system are the hippocampus, amygdala, cingulate gyrus, and hypothalamus (Table 1; Breathnach. 1980; de Groot & Chusid, 1988). The interconnection of the various structures facilitates the ability of the limbic system to process. integrate and mediate information from the cortex. reticular formation, brain stem, and spinal cord (deGroot & Chusid, 1988). Synthesis of this information influences the emotions of the individual.
Table 1. The Limbic System structure Hippocampus
Function
Memory storage and information processing
Dysfuncmn
Confabulation
and aggressive behavior often
associated with Korsakoff’s Amygdala
Receives and interprets sensory information
Pica; hypersexuality
as seen in Kluver-Bucy
syndrome Cingulate gyrus
Receives input from other limbic structures
Disturbed affect, marked loss of ability to
Hypothalmus
Synthesizes input from all areas of nervous
Many aspects of emotional behavior such as
experience system; vital role in balance of hormones,
and express emotion
anger, placidity, and sexual activity
electrolytes, and body temperature; mediates activity of autonomic nervous system Data from Breathnach (1980), Byers and Guthrie 11984), Mesulam (19851, deGroot and Chusid (1988), Damasio and Van Hoesen 119831, and Gilman and Winans Newman.
314
Alterations in functioning of the structures of this system influence both the emotional experience and behavior of the individual, and may increase or decrease the potential for aggressive behavior. Limbic system dysfunction may be responsible for a range of psychiatric disorders such as panic attacks, depression, and schizophreniform conditions (Mesulam, 198.5). Damage to the amygdala and hippocampus may prevent the individual from processing cues necessary to match present stimuli with past experience. One example would be the catastrophic reactions sometimes displayed by dementia patients (LeNavenec, 1988). Hence, a situation may be perceived by the individual to be threatening when it is not (Mesulam, 1985). Conversely, lesions in the hypothalamus and septal regions may reduce episodes of fear or rage (Byers & Guthrie, 1984). Snyder (1988) proposes that aggression, in some instances, arises from abnormally increased behavioral arousal. Such hyperarousal can be the result of inaccurate interpretation of information from the environment leading to an aggressive response. Snyder suggests that this state may be due to defects in the sensory system or an inability to blend new and old information related to memory problems . The Frontal Lobe The frontal lobes, the second major area, mediate purposeful behavior, elaborate thought, and exert an initiatory influence over the limbic system (Boss & Coghlan Stowe, 1986). In essence, it is the frontal lobe where reason and emotion interact (Strub & Black, 1985). These lobes include the motor cortex, premotor area, and prefrontal area in each hemisphere. Detachment of cortical and subcortical regions of the brain has been demonstrated to lead to a separation of emotional expression from emotional experience (Heilman et al., 1985). Portions of the prefrontal area are thought to act as staging areas for information received from the limbic system (Eslinger & Damasio, 1985). Reciprocity between the staging areas of the prefrontal area and the limbic system permits regulation by the cortex of hypothalamic processes and activation of the cortex by basic drives thought to originate in the limbic system (Eslinger & Damasio, 1985). Without this two-way communication link, the areas involved have little means of influencing the other.
HARPER-JAQUES
AND REIMER
Damage to the frontal cortex impairs judgement. Changes in social behavior include inadequate decision-making and inappropriate conduct (Eslinger & Damasio, 1985; Tranel, Damasio, & Damasio, 1989). Bifrontal damage, as frequently seen in head injury, may result in personality changes, poor judgement, and occasional aggressive outbursts (Snyder, 1988). These outbursts are characteristically brief and unexplained, often set off by minor environmental stimuli (Silver, 1987). The Temporal Lobe The temporal lobes are intimately connected with the limbic system, actually sharing some structures such as the hippocampus. Besides interpretation of auditory stimuli, the temporal lobes play a major role in memory. Impairments and distortions in memory may also interfere with perceptual processing and integration of new stimuli (Beck, Rawlins, & Williams, 1988; Snyder, 1988). The temporal lobe dysfunction most frequently linked with aggressive behavior is epilepsy, particularly in those individuals with partial complex seizures (Cassidy, 1990). Discussions with mental health nurses have revealed a belief that individuals with temporal lobe epilepsy are more likely to be aggressive. This idea is debated in the literature. There is consensus that aggressive behavior during the ictal period is a defensive, nondirected response to attempts at restraint (Browne & Feldman, 1983; Devinsky & Bear, 1984). Postictal violence may occur while the individual is recovering from a seizure. At that point, the individual is confused and agitated. Attempts to provide assistance may be met with a defensive response (Burrowes, Hale, & Arrington, 1988). However, the relationship of electrophysiologic abnormality and assaultive behaviors during the interictal period is subject to debate. One source suggests that patient and family attitudes and beliefs about the seizure disorder can result in increased frustration for all family members. This may lead to assaultive behavior (Thompson, 1988). Browne and Feldman (1983) propose that violent behavior is more common in individuals with seizures than the general population. However, they emphasize that temporal lobe epilepsy may be a contributing factor in aggression, but it should not be considered a “cause” of violence. Cassidy (1990a) comments that “even
AGGRESSIVE
315
BEHAVIOR AND THE BRAIN
discharges that are sub-convulsive can produce behavior that mimics human dyscontrol syndromes, presumably due to a phenomenon known as kindling” (p. 85). Another viewpoint, which supports the notion of interictal aggression, is that the behavior is the result of forced normalization of electrical activity of the brain (Benson, 1986; Fedio, 1986). This normalization occurs due to the use of anticonvulsants. Increasing irritability can lead to episodes of aggression. Benson has gone so far as to recommend the use of drug holidays or electroconvulsive therapy (ECT) to allow occasional seizures .
Devinsky and Bear (1984) studied five individuals in which aggressive behaviors were reported to occur following the onset of an epileptic focus in the temporal lobes. Assaults were observed during the interictal period. Another cluster of behaviors were increased interest in spirituality; changes in sexual intensity or orientation; and anxiety, phobias, or paranoia. These individuals were able to recall the violent episode. They took responsibility for the behavior and frequently experienced remorse or guilt. In concluding, Devinsky and Bear ( 1984) suggest that there is evidence for the development of a secondary foci following the onset of
seizures. The second foci could account for the aggressiveness. The Neurotransmitters
Most of the neurotransmitters can be classified into one of four categories: acetylcholine, monoamines, peptides, and amino acids. Changes in the balance of these compounds can aggravate or inhibit aggression. To function effectively as a neurotransmitter, a substance must be synthesized in the presynaptic neuron, released from the neuron into the synaptic cleft, bound to a receptor on the postsynaptic neuron, and then destroyed or removed from the receptor (Gilman & Winans Newman, 1987). Disruptions at any of these points will influence neurotransmitters concentrations. The neurotransmitters most frequently implicated as affecting behavior are the monoamines serotonin (5HT) and dopamine, and the amino acid GABA (Table 2). A surplus or deficit of one neurotransmitter can only be interpreted in the context of differing effects of neurotransmitters at differing synapses and the neural circuits involved in any behavior (PiacentC, 1986). Communication between neurons is accomplished via neurotransmitters crossing the synaptic cleft. Hence, commu-
Table 2. Neurotransmittars Postulated Neurotransmitter Serotonin
PMGUrSOr
[5-HT]
Tryptophan;
Normally found in high concentrations
in
limbic system
found in milk, beef, eggs,
With
Relationship
Aggressive
Behaviors
Modulates violence, sleep, sensory responses,
wheat, flour, & corn; production
mood, and performance;
impaired in thiamine deficient diets,
improved behavior in aggressive patients
e.g., alcoholism
treated with supplemental
case reports of tryptophan;
dietary restriction of tryptophan
shown to
increase aggression GABA
Glutamic acid
Inhibits impulsivity and aggression similar to
Dopamine
Tyrosine
Increases aggressive behavior and sexual
serotonin activity, vigilance heightens; elevated levels associated with idiopathic schizophrenia and organic delusional disorders; L-dopa in treatment
of Parkinsonism linked to
paranoid psychosis Norepinephrine
Tyrosine
Primarily released from
Increases aggressive behavior, heightens vigilance
the locus ceruleus Acetylcholine
Lecithin; Choline salt
Deficiency (as in Alzheimer’s
disease) may
directly increase aggressive tendencies through lowered threshold for confusion and loss of recent memory Data from Spring (1986). Piacentb (1986). Cassidy (1990), Burrowes et al. (1988). Cummings (1986). Gilman and Winans Newman 11987). and Gottfries (1990).
316
HARPER-JAQUES
nication between structures is affected by neurotransmitter concentrations. THE EMOTIONAL CIRCUIT
The interconnections of the limbic system and prefrontal area of the frontal lobe provide a communication link between the cognitive processes of the frontal lobes and the emotional processes of the limbic lobe. Disconnection of the circuit has been shown to result in a variety of problems, including aggression (Damasio, 1985). The phrase “the emotional circuit” has been chosen to describe the relationship between these two regions of the brain. This circuit can be thought of as an open system, in which the overall functioning is greater than the functioning of the individual structures. The interaction of the emotional circuit is hypothesized to determine the meaning given to a particular situation. Such meaning will be influenced by the individual’s current physiological capability to analyze incoming messages with stored memories and beliefs. With aggressive individuals, meaning given to a particular circumstance may be altered from that person’s usual perceptions or from the norm accepted by the social context. This alteration may contribute to assaultive behavior. One example of pervasive disruption of the emotional circuit is Alzheimer’s disease, in which there is widespread degeneration and atrophy of cortical neurons. The associated cognitive impairment, loss of memory and emotional control, and impairment of judgement contribute to sudden impulsive acts of aggression. These individuals are often seen to strike out in unfamiliar situations that they perceive as threatening. Loss of emotional control with explosive outbursts may be even more pronounced in patients with dementia secondary to multiple infarcts depending on the location of the infarcts. Multiinfarct dementia arises from many small emboli or strokes, often secondary to hypertension. The onset may be more abrupt and the effects on behavior more variable than those seen in Alzheimer’s disease (Petrie, 1984). NURSING IMPLICATIONS
The human response of aggression is multidimensional. Having considered the interrelationships of the structures of the brain, the mental health nurse can incorporate research findings and theory to expand the repertoire of approaches. Areas of importance for mental health nursing prac-
AND REIMER
tice are comprehensive history taking, proactive interventions, and the interpretation of patient behavior. HISTORY TAKING
Nurses can play an important role in identifying factors that may contribute to aggressive behavior. Those that are most relevant to the mental health nurse are head injury, alcohol and drug use, nutritional status, and temporal lobe epilepsy. Head injury
Irritability and aggressive outbursts are common sequelae of traumatic head injuries, particularly when the frontal lobe has been involved (Silver, 1987). Juvenile delinquents have been found to have more frequent history of head injury than the general population (Otnow Lewis, 1983). Even minor injuries such as concussion or perinatal insults may lead to minimal brain dysfunction (MBD). Episodic dyscontrol syndrome is often seen in those with MBD, especially when the lesion is in the dominant hemisphere of the frontal lobe (Burrowes et al., 1988; Flor-Henry, 1983). These individuals demonstrate recurrent episodes of rage and violence. When assessing the patient, the nurse can seek specific information regarding history of head injury, repeated falls, or other circumstances suggestive of minor head trauma such as being “knocked out” in fights or contact sports. Alcohol and Drug Use
The astute mental health nurse will watch for indications of alcohol and drug use and abuse, which increase the potential for aggressive behavior. Aggressive behavior associated with substance abuse tends to be linked with three stages: during intoxicated, during withdrawal, and later from accumulative residual effects (Piercy, 1984). The drugs most often implicated are (1) sedative effect of depressant agents, such as alcohol and diazepam; (2) stimulants such as cocaine, amphetamines, caffeine, and nicotine, (3) hallucinogens such as PCP, LSD, and marijuana; and (4) narcotits .
The use or withdrawal from combinations of such drugs exacerbate the risk of aggressive behavior (Piercy, 1984). Recent discontinuation or noncompliance with certain prescribed medications should also be explored because of their potential effects on aggressive behavior. For ex-
AGGRESSIVE
317
BEHAVIOR AND THE BRAIN
ample, antidepressants, cx,-agonists such as clonidine, and B-blockers such as propranolol (Inderal; Ayerst) are known to suppress the activity of the excitatory catecholamines such as norepinephrine and dopamine (Cassidy, 1990b). In contrast, fluoxetine (Prozac; Lilly) and lithium enhance the availability of serotonin by inhibiting the reuptake of the neurotransmitter (Cassidy, 1990b). Some anticonvulsants, particularly the ones affecting the limbic system, such as carbamazepine (Tegretol; Geigy), have been shown to reduce aggressive behavior. This is particularly apparent in patients with neurological dysfunction, even when frank seizure activity has not occurred (Cassidy, 1990b). Given the high risk of seizure activity among most patients with a cerebral insult through trauma, stroke, or tumor, many such patients are on prophylactic anticonvulsant therapy for up to 1 year postinsult. The nurse may predict a greater potential for aggressive behavior when there is a history of abrupt discontinuation or erratic compliance in individuals who are already vulnerable with impaired information processing. Alcohol is still the most frequently implicated when discussing aggressive behavior (Piercy, 1984). The effect that alcohol has on behavior and mood depends on the concentration of the alcohol in the body, the diet of the individual, the pattern of drinking, the previous experience of drinking, and the environment in which the drinking takes place (Burrowes et al., 1988; O’Sullivan, 1984). As a contributing factor to aggressive behavior, alcohol impacts the nervous system by three mechanisms: intoxication, withdrawal, and alcoholic dementia (Korsakoff’s syndrome) (Petrie, 1984). Piercy (1984) cites a typical scene in Western movies “where the bad guys drink in the saloon before leaving to kill the good rancher and ravish his beautiful daughter” (p. 130) as an example of the conscious use of alcohol as an intoxicant for its disinhibiting effect on cortical control. Less common and less well understood is alcohol idiosyncratic intoxication in which a dramatic change of behavior, usually involving violence, is seen following ingestion of a moderate amount of alcohol. The discomfort associated with withdrawal may contribute to consciously mediated aggressive acts associated with demands for alcohol. In those patients who experience alcohol withdrawal delirium, aggressive behavior may be seen in response to distorted perceptions associated with hallucina-
tions and paranoid delusions. Permanent cortical damage resulting from prolonged alcohol abuse, as seen in Korsakoff’s syndrome, is a contributing factor to aggressive behavior through the effects of memory disturbance, dementia, and agitation on the ability to interpret and cope with incoming stimuli (Petrie, 1984). Nutrition During the process of the initial assessment, the nurse can note aspects of physical appearance and behavior that may indicate poor nutrition. Research reports (Spring, 1986; Strain, 1981) point to an interrelationship between nutrition, brain function, and behavior. In particular, there is evidence to suggest that dietary deficiencies will influence the production of neurotransmitters which, in turn. influence CNS functioning (Conlay, 1988). Deficiencies may occur as the result of metabolic error, malabsorption, or dietary deficiency. Alcohol is one factor in the deficient use of available nutrients because of gut irritation, poor digestion, malabsorption, or metabolic inefficiencies. Excessive alcohol consumption can contribute to protein malnutrition, multiple vitamin deficiencies, and mineral depletion (Burton & Foster. 1988). Although single vitamin deficiencies are rare, deficiencies of two particular vitamins influence the production of the neurotransmitters previously discussed. Niacin deficiency may be seen in individuals who are indigent or have long-standing poor dietary habits, are afflicted by diseases that interfere with appetite, or are chronic alcohol abusers, as well as in some forms of drug therapy (Burton & Foster, 1988). Effects on the CNS can include disorientation, confusion, anxiety, fear, and paranoia. Sources of niacin include meat, fish, poultry, whole grain bread, and enriched cereals. Thiamine is the second vitamin that is most often deficient due to inadequate diet. Early manifestations of deficiency include neurasthenia, characterized by irritability, poor memory, and an inability to concentrate (Burton & Foster, 1988). Prolonged use of alcohol can block up to 70% of the uptake of thiamine. Some features of the patient’s presentation may appear to be symptoms of Korsakoff’s syndrome, but will be quickly corrected by administration of thiamine (Iber, 1988). It too is found in whole grain breads and enriched cereals, as well as in pork, liver, and legumes.
HARPER-JAQUES
318
AND REIMER
may also assist the patient to maintain a balanced diet within a limited budget.
One of the amino acids that acts as neurotransmitter precursor, tryptophan, is vulnerable to dietary changes. Tryptophan competes with other diet derived amino acids to cross the blood-brain barrier. It is found in the brain in higher concentrations following the ingestion of a highcarbohydrate meal than it is after a high-protein meal. The presence of proteins increases the competition for the movement of amino acids across the blood brain-barrier (Fernstrom, Wurtman, & Hammarstrom-Wikland, 1979). The production of the neurotransmitter serotonin is dependent on the concentrations of tryptophan in the plasma. Increased levels of tryptophan have been correlated with reduced insomnia and improved moods in depressed patients. Alterations to the diets of patients may help to increase the availability of necessary neurotransmitter precursors. However, the population cared for by the mental health nurse is often disadvantaged in many ways, not the least of which is possessing the knowledge and financial resources to maintain adequate nutrition. The nurse is presented with the challenge to help patients to consider the role of nutrition in reducing symptoms. The nurse
Temporal Lobe Epilepsy
Individuals who present with a history of violent episodes may also have a history of temporal lobe epilepsy (TLE). By adding questions about TLE to the nursing assessment, this factor may be discovered. An example is an adolescent who was placed in a residential treatment setting as a means of helping him control his aggressive behaviors. A review of past records revealed an electroencephalogram (EEG) report diagnosing a temporal lobe lesion. Some of the young man’s behavior was corrected with medication. In persons presenting with a history of seizure activity, the nurse should be alert to epileptogenic factors in the recent history such as sleep deprivation, excessive ingestion of alcohol or caffeine, and intense emotional stress (Grant, 1985; Santilli & Sierzant, 1987). Individuals with identified lesions or dysfunctions in the limbic system, temporal lobe, or frontal lobes may exhibit behaviors or report experiences that may be labeled “a psychiatric problem.” The nurse who understands the
Table 3. Proactive interventions Characteristics
Patient Profile
Belligerent
Example Male (22 years) admitted threatening fights,
behavior,
several
heavy alcohol
past, he played hospitalized
limited
with recent
use; and in the
hockey,
was
for a head injury
at
Interventions
and impulsive, appreciation
consequences
of
of behavior;
slow in complex
tasks;
agitated
depression;
diagnosis
epilepsy;
observe for triggering plan for positive
solving.
Valproic
shifts;
believes
as
epileptic
parital
on valproic
drugs cause weight
disturbed
Prior to had been “up”
depression;
effects include
insomnia
increased
serum levels to determine
(no unsupervised
Untidy,
poor hygiene;
dry
Some symptoms
skin and hair, skin lesions
deficiencies,
nights in the hostel;
on areas exposed
to
administration
diagnosis:
schizophrenia,
sunlight;
mucous
she is fearful
food or medications.
spends when of injesting
swollen
membranes increased
and tongue; salivation;
disorientation,
confusion
and anxiety;
hallucinations
and paranoia.
niacinamide
baths);
obtain
therapeutic
acid; establish
sleep/wake
occasional symptomatic
and
activity
dose of valproic
side untoward
risk for seizure
seizures
3 homeless,
GABA levels, she
effects include
consistent
and assess
deficiencies.
acid; gain so
provide
behavior
reinforcement;
acid elevates
aggression;
36 hours.
skips doses. Female (35 years),
events;
select target
and
circuit;
has used the drug erratically;
by frequent
admission
to decreased
for alcohol
of the emotional
problem
wakenings;
employed
aide, works controlled
diagnosis
secondary
since age 14, complex
Example
disruption
for thiamine
Female (27 years), primary
poorly
tolerance
structure;
Obese; sleep pattern
2
kitchen
may contribute
self-control,
poor ability to generalize,
age 19. Example
Head injury
cycle.
may be due to dietary particularly
niacin;
of oral or subcutaneous may be necessary;
provide
a well-balanced
diet that contains
150 g of protein
and 3,500 calories.
100 to
AGGRESSIVE
319
BEHAVIOR AND THE BRAIN
potential effects of these lesions will be better able to plan interventions that will assist the patient and family to adapt to his/her changed state. PROACTIVE INTERVENTIONS
Taking this information into account, the nurse has a greater range of proactive interventions to reduce potential for aggression. The nurse now has the option to intervene at several points (Table 3). INTERPRETATION OF PATIENT BEHAVIOR
Of equal importance is the interpretation of the patient’s behavior to colleagues and family members. In both authors’ experience, the patient who is rude, interpersonally unsophisticated, and who does not “learn” more acceptable behavior, is often labeled as “noncompliant” or “difficult” by the treatment team. Staff feelings of frustration with these patients may be manifest in brief interactions and/or simply ignoring the patient. This withdrawal by staff may increase the patient’s clumsy, often aggressive attempts to be acknowledged. In the end, staff may provide intense interest only when aggressive behaviors reach crisis proportions. CONCLUSION To this point, most of what is known about the neurological basis of aggression has been drawn from other disciplines. There is a paucity of nursing research or anecdotal literature regarding neurological functioning and aggressive behavior in the population cared for by mental health nurses. This mirrors the paucity of interventions available to respond to the needs of this population. However, greater understanding of the influence of the emotional circuit on assaultive behavior will enhance clinical practice by giving the nurse an alternate perspective when relating to the client with a history of aggressive behavior. REFERENCES Beck, C.M., Rawlins, R.P., &Williams. S.R. (1984). Mental health-psychiatric nursing: A holistic life cycle approach. St. Louis: C.V. Mosby Company. Benson, D.F. (1986). Interictal behavior in epilepsy disorders. Psychiatric Clinics of North America, 9(2), 283-291. Boss. B.J., & Coghlan Stowe, A. (1986). The neuroanatomical and neurophysiological basis of learning. Journal of Neuroscience Nursing, 18(S), 256-264. Breathnach, C.S. (1980). The limbic system, 1980. Journal of the Irish Medical Association. 73(9), 331-339.
Brinkerhoff. M.B., & Lupri, E. (1988). Interpersonal violence. Canadian Journal of Sociology, 13(4), 407-43 1. Browne, T.R., & Feldman, R.G. (1983). Epilepsy: Diagnosis and management. Boston: Little, Brown and Company. Burrowes, K.L.. Hales, R.E., & Arrington. E. (1988). Research on the biologic aspects of violence. Psychiatric Clinics of North America. 11(4), 409-509. Burton, B.T., & Foster, W.R. (1988). Human nutrition. Toronto: McGraw-Hill Book Company. Byers. V.L.. & Guthrie, M.D. (1984). The limbic system and behavior. Journal of Neurosurgical Nursing. l/5(2). 80. 83. Cassidy. J. W. (1990a). Neurochemical substrates of aggression: Toward a model for improved intervention. [part I]. Journal ofHead Trauma Rehabilitation. 5(2), 83-86. Cassidy. J.W. (1990b). Neurochemical substrates of aggression: Toward a model for improved intervention. [part II]. Journal of Head Trauma Rehabilitation. S(3). 7013. Conlay. L.A. (1988). Nutrients and brain function. in J.M. Kinney. K.N. Jeejeebhoy. G.L. Gill. & 0. Owen (Eds. I. Nurrition and metabolism in parient care (pp. 727-736). Philadelphia: W.B. Saunders Co. Cummings, J.L. (1986). Organic psychoses: Delusional disorders and secondary mania. Ps;chiatric Clinics qfhrorrh America. Y(2). 293-311. Damasio. A.R. (1985). The frontal lobes. In K.M. Heilman & E. Valenstein (Eds. ). Clinical Neurops,vcholo,qy (2nd ed.: pp. 339-376). New York: University Press. Damasio. A.R.. & Van Hoesen, G.W. (1983). Emotional disturbances associated with focal lesion of the limbic frontal lobe. In K.M. Heilman & P. Satz (Eds.). Neuropsychology of human emotion (pp. 85-t IO). New York: Guilford Press. deGroot, J., & Chusid, J.G. (1988). Correlative neuroanatomy. East Norwalk, CT: Appleton-Lange. Devinsky. 0.. & Bear, D. (1984). Varieties of aggression in temporal lobe epilepsy. American Journal of Pswhiafry, 141(5). 651-656. Eslinger. P.J.. & Damasio. A.R. (1985). Severe disturbance of higher cognition after bilateral frontal lobe ablation. Neurology. 35. 1731-1741. Fedio. P. (1986). Behavioral characteristics of patients with temporal lobe epilepsy. Psychiatric Clinics of Norrh America. 9(2), 267-281. Femstrom, J.D.. Wurtman. R.J.. & Hammarstrom-Wikland. B. ( 1979). Diurnal variations in plasma concentrations of tryptophan, tyrosine and their neutral amino acids: Effect of dietary protein intake. American Journal of Clinical Nutrition, 32. 1912. Flor-Henry. P. (1983). Neuropsychological studies in patients with psychiatric disorders. In K.M. Heilman & P. Satz (Eds.). Neuropsychology of human emorion (pp. 193. 220). New York: The Guilford Press. Gayford.
J.J. (1983). Battered wives. In R.J. Gelles & C. Pedrick Cornell (Eds.). Interpersonal perspectives on farnil? violence. Toronto: Lexington Books.
Gilman,
S.. & Winans Newman, S. (1987). Essenrials of clinical neuroanatomy and neurophwiologqv. Philadelphia: F.A. Davis Company.
Gottfries.
C.G. 11990). Neurochemical
changes
in the human
320
HARPER-JAQUES
brain and their importance for behavior Triungte, 29(2 13). 127-131.
in the senium.
Grant, I. (1985). The social environment and neurological disease. Advances in Psychosomatic Medicine, 13, 26-47. Heilman. K.M., Bowers, D., & Valenstein, E. (1985). Emotional disorders associated with neurological disorders. In K.M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology (2nd ed.; pp. 377-402). New York: Oxford University Press. Iber, F.L. (1988). Alcohol associated diseases. In J.M. Kinney, K.N. Jeejeebhoy, G.L. Gill, & 0. Owen (Eds.), Nutririon and metabolism in patienr care (pp. 429-444). Philadelphia: W.B. Saunders Co. LeNavenec, C.L. (1988). The care process with demenria patients: A practical handbook for nursing home staff and family care givers. Calgary, Alberta: The University of Calgary. Luria,
A.R. (1973). The working brain: An introduction to neuropsychology. (B. Haigh, Translator) New York: Basic Books, Inc.
Maturana, H.R. (1988, October). [Telephone conversation with Humberto Maturana and N651 class: The Calgary/ Chile coupling.] Unpublished manuscript. Maturana, H.R., & Varela, F.J. (1987). The tree of knowledge. Boston: New Science Library. Mesulam, M. (1985). Principles of behavioral neurology. Philadelphia: F.A. Davis Co. O’Sullivan, K. (1984). Depression and its treatment in alcoholics: A review. Canadian Journal of Psychiatry, 29, 379-384. Otnow Lewis, D. (1983). Neuropsychiatric vulnerabilities and violent juvenile delinquency. Psychiatric Clinics of North America, 6(4), 707-714. Petrie, W. (1984). Violence: The geriatric patient. In J. Turner (Ed.). Violence in the medical care setting: A survival guide (pp. 107-121). Rockville, MD: Aspen Publications.
AND REIMER
Piacente, G.J. (1986). Aggression. Psychiatric Clinics ofNorrh America, 9(2), 329-339. Piercy, D. (1984). Violence: The drug/alcohol patient. In J. Turner (Ed.), Violence in the medical care setting: A survival guide (pp. 123-151). Rockville, MD: Aspen Publications. Santilli, N., & Sierzant, T. (1987). Advances in the treatment of epilepsy. Journal of Neuroscience Nursing, 19(3), 141-155. Silver, J. (1987). Aggressive behavior in patients with neuropsychiatric disorders. Neurotrauma Medical Report, 3(2), l-3. Snyder, M. (1988). Abnormally increased behavioral arousal. In P.H. Mitchell, L.C. Hodges, M. Muswaswes, & C.A. Walleck @Is.). AANN’ Neuroscience nursing: Phenomena and practice (pp. 85-97). Norwalk, CT: Appleton-Lange. Spring, B. (1986). Effects of foods and nutrients on the behavior of normal individuals. In R.J. Wurtman & J. Wurtman (Eds.), Nutrition and the brain: Food constituenrs affecting normal and abnormal behaviors (pp. 1-48). New York: Raven Press. Strain, G.W. (1981). Nutrition, brain function and behavior. Psychiatric Clinics of North America, 4(2), 253-268. Strub, R.L., & Black, F.W. (1985). The menral status examination in neurology (2nd ed.). Philadelphia: F.A. Davis, Thompson, P.J. (1988). Methods and problems in the assessment of behavior disorders in epileptic patients. In M.R. Trimble & E.H. Reynolds (Eds.), Epilepsy, behavior and cognitive funcfion. Chichester, England: John Wiley and Sons. Tranel, D., Damasio, A.R., & Damasio, H. (1989, February). Acquired sociopathy as a domain-specific memory disorder: Impaired autonomic responses to social/ emotional stimuli following frontal damage. Paper presented at the meeting of the International Conference of Neuropsychology, Vancouver, B.C.
