Major Clinical Syndromes Of Aggression

A. General Considerations

The recognition that specific neurological lesions may lead to violent behavior in human beings, and that abnormalities at different levels of the neuraxis result in distinctive types of aggressive behavior, provides a guiding schema for the evaluation and treatment of inappropriately aggressive (and inappropriately hypoaggressive) individuals (Tables III-V). In addition to emphasizing the need for careful neuropsychiatrie evaluation of every violent patient, the hierarchical model for the regulation of aggression suggests important parameters that may help to characterize any aggressive act. Integrating information regarding the clinical manifestations of aggressive behavior, additional aspects of the history (particularly related to other drive-related behaviors), the neurological and psychiatric examinations, and structural and functional laboratory studies allows classification of individual patients among major syndromes of impulse dysregulation and aggression.

1. Hypothalamic/Brain Stem Syndromes

In patients with brain stem-mediated sleep-related disorders of violence, aggressive actions are generally nocturnal, associated with incomplete maintenance of REM or non-REM sleep states. The REM sleep behavior disorder predominantly occurs in middle-aged men. Violence most commonly occurs during a vivid and frightening dream, is often directed at a bed partner mistaken for a dream figure, and is unplanned, without the use of weapons. Affected patients are difficult to arouse from their dreaming state. Afterwards, they generally recall the dream material that provoked aggression but report believing they were attacking animal or human oneiric figures rather than their furniture or spouse. They exhibit remorse about their actions and, before a diagnosis is made, may self-treat their disorder by tying themselves in restraining devices at night.

Table III

Distinguishing Features of Focal Lesion Syndromes of Aggression in Humans

Table III

Distinguishing Features of Focal Lesion Syndromes of Aggression in Humans

Syndrome

Provocation

Eliciting stimulus

Outbursts

Complex plans

Amnesia for acts

Remorse

Hypothalamic

Basic drive (e.g. hunger); unprovoked

Individuals who happen to be present

Yes

No

No

Yes

Ictal

None

Any near individual or inanimate object

Yes

No

Yes

Yes

Postictal

Attempts to restrain/protect patient

Caretakers

Yes

No

Yes

Yes

Interictal

Perception of moral injustice; threat, including misinterpretation of trivial stimulus

Individuals

Occasional

Yes

No

Yes, may be intense

Orbitofrontal

Minor provocation

Individuals

Yes

No

No

No

The REM sleep disorder must be distinguished from other parasomnias that may be injurious to patient and spouse, such as somnambulism, sleep drunkenness,

Table IV

Selected Causes of Syndromes of Hyperaggressivity and Hypoaggressivity (Passivity)

Site/syndrome Common etiologies

Hyperaggressivity Hamartoma

Craniopharyngioma, astrocytoma Mesial temporal sclerosis Vascular malformation Glioma

Traumatic brain injury Traumatic brain injury Anterior communicating artery aneurysm Orbital meningioma Huntington's disease Frontotemporal dementias Herpes simplex encephalitis Combined frontotemporal Traumatic brain injury

Frontotemporal dementias Herpes simplex encephalitis Multifocal or poorly localized Attention deficit disorder

Toxic-metabolic encephalopathies Vitamin B12 deficiency Alcohol, cocaine Multiple sclerosis Vascular dementia Delusional cognition Paranoid schizophrenia

Late-life paraphrenia Endogenous depression Mania

Alzheimer's disease Vascular dementia Hypoaggressivity Bilateral amygalotemporal Herpes simplex encephalitis Frontotemporal dementias Posterior cerebral artery infarctions Traumatic brain injury Urbach-Wiethe disease Temporal lobectomies Dorsolateral frontal systems Subdural hematomas Glioma

Progressive supranuclear palsy Anterior cerebral artery infarctions and sleep terrors, which arise out of non-REM sleep. Nocturnal seizures must also be excluded. The evaluation in suspected cases includes a thorough history of sleep complaints from patient and bed partner, neurological and psychiatric examination, overnight polysomnographic study, and MRI. REM sleep behavior disorder has been associated with a variety of neurological conditions, including Parkinsonism, dementia, stroke, multiple sclerosis, and alcohol withdrawal. However, more than 50% of cases are idiopathic. Pontine tegmental lesions, which might be expected from animal studies, are rare, possibly because pontine injury frequently produces devastating motor and arousal deficits that preclude expression of the disorder. Approximately 90% of patients exhibit sustained improvement when treated with clonazopam.

In patients with hypothalamic lesions, outbursts of violent behavior in the awake period may be precipitated by internal or visceroceptive states, such as hunger, fatigue, light deprivation, or hormonal stimulation. Alternatively, patients may exhibit a heightened general level of aggressivity. Frequently, attacks are on individuals who happen to be near the patient, without the formation of complex plans. Patients often have diminished insight into the reasons for their actions, although they recall and may demonstrate remorse for their behaviors. Subjects with hypothala-mic lesions may demonstrate altered patterns of sleeping or eating, polydipsia, and polyuria or deficient regulation of sex hormones, thyroid, or adrenocortical function. Heteronymous visual field impairments may be evident if lesions extend to involve the optic nerves, chiasm, or tracts. The workup of patients with suspected hypothalamic lesions should include MRI or other structural imaging of the region of the third ventricle, endocrine studies, and formal visual fields. The differential diagnosis includes benign and malignant tumors such as craniopharyngiomas and astro-cytomas, which present with subacute alterations in behavior. Another etiology is hypothalamic hamarto-ma, which usually presents with a distinctive clinical profile of childhood onset of gelastic epilepsy (ictal laughter), sometimes accompanied by precocious puberty, along with interictal bouts of uncontrolled rage (Fig. 4).

2. Temporolimbic Epilepsy Syndromes

Few topics in behavioral neuroscience are more controversial than the relationship of aggression to

Hypothalamic Temporal lobe epilepsy

Orbitofrontal systems

Setting of aggression

Impulsive aggressive acts in setting of congenital or acquired intellectual impairment or hypothalamic injury

Aggression related to deepened affect or ideation in the interctal syndrome of temporolimbic epilepsy (moralistic conviction)

Disinhibited aggression in response to transient environmental stimuli, + frontal systems dysexecutive signs

Aggressions precipitated by delusions, hallucinations

Irritability related to manic or hypomanic states Acute agitation

Table V

Strategies for Treating Aggressive Behavior

Initial therapeutic approaches

Control of appetite, sleep, diurnal cues b-Adrenergic blocker Selective serotonin reuptake inhibitors Cholinergic (muscarinic) antagonists (?) Valproic acid

Avoid barbituates, benzodiazepines, sedatives Antiepileptic medications Selective serotonin reuptake inhibitors Reality-oriented psychotherapy Avoid lithium carbonate (may worsen seizures) Explicit, concrete social structure Selective serotonin reuptake inhibitors b-Adrenergic blocker

Avoid barbituates, benzodiazepines, sedatives

Atypical antipsychotics

Neuroleptics

Mood stabilizers

Neuroleptics

Benzodiazepines epilepsy. Failure to adequately distinguish between aggressive actions in the ictal, postictal, and interictal periods has contributed greatly to the confusion regarding the relationship between temporolimbic epileptic foci and violent behavior.

Ictal aggression does occur, but with extreme rarity. An international consensus panel found that only 7 of 5400 patients studied on video EEG monitoring exhibited aggressive behavior during recorded seizures. Hostile behaviors ranged from physical violence directed toward inanimate objects to mild verbal or physical aggression directed toward a person. When aggressive acts during complex seizures occur, they may appear without provocation or in response to an environmental stimulus and are characterized by spontaneous, undirected aggression toward nearby objects or individuals. The patient is amnestic for actions and often expresses remorse.

A much more common form of aggressive behavior in epilepsy is resistive violence during the postictal period. Following a complex partial seizure or, more frequently, a generalized convulsion, patients may be disoriented and confused. During this epoch, well-

intended attempts at physical restraint can provoke aggression, which almost always ceases when restraint is withdrawn. The attacks generally involve striking out without the use of a weapon or sometimes with objects that happen to be close at hand. Patients have no memory for their actions upon clearing of consciousness and will express dismay if they have injured others.

Aggression in the subacute period following the end of a seizure activity can also occur. Often, the aggression appears in the context ofpostictal psychosis and mania, especially in patients with paranoid delusions and threatening hallucinations. However, recently a syndrome of subacute postictal aggression was described in four patients, occurring hours to days after a seizure, without postictal psychosis or mania. Subacute postictal aggression appears to be a rare phenomenon. The attack behaviors are intentionally directed after minor provocations, and patients retain full recall of the episodes.

Overt aggression related to the interictal behavior syndrome of temporolimbic epilepsy is unusual because the heightened moral and religious values that

Figure 4 Aggression due to hypothalamic lesion. A 19-year-old man presented with several years of aggressive behavior, poor social adjustment, and seizures of multiple types, including ictal laughter. Coronal proton density-weighted MRI scan demonstrates a hypothalamic hamartoma, evident as a 1-cm-high signal intensity mass in the substance of the hypothalamus (reproduced with permission from S. F. Berkovic, F. Andermann, and D. Melanson, et al., 1988, Ann. Neurol. 435).

Figure 4 Aggression due to hypothalamic lesion. A 19-year-old man presented with several years of aggressive behavior, poor social adjustment, and seizures of multiple types, including ictal laughter. Coronal proton density-weighted MRI scan demonstrates a hypothalamic hamartoma, evident as a 1-cm-high signal intensity mass in the substance of the hypothalamus (reproduced with permission from S. F. Berkovic, F. Andermann, and D. Melanson, et al., 1988, Ann. Neurol. 435).

are features of the syndrome preclude violent actions. However, in rare circumstances, intense emotional reactions to perceived injustice or threat can lead subjects to formulate and carry out complex plans of violent response. Attacks may be directed against a specific individual and could involve the use of a weapon. Not all hostile actions by these patients involve long-term planning—rarely, the intensity of feelings evoked in a particular situation might lead to an immediate response. Patients fully recall their actions and often exhibit extreme remorse. Some individuals continue to believe their acts had ample moral justification.

In individuals with epilepsy, sedative antiepileptic medications such as barbiturates may contribute to hostile behaviors by impairing impulse control. Irritability, a common complaint among patients with poorly controlled partial and primary generalized seizures, may result from environmental factors, medications, or in relation to the underlying cerebral pathology or epileptogenic process.

The laboratory evaluation for epilepsy in violent individuals includes routine scalp EEG and more sensitive sleep recordings and the use of nasopharyo-geal or spheroidal leads. In select cases, ambulatory EEG, long-term inpatient video EEG monitoring with scalp and sphenoidal electrodes, or invasive subdural grids or depth electrodes may be necessary to establish the seizure focus.

CT and especially MRI are utilized to exclude slowly growing gliomas and other mass lesions. Volumetric

MRI or careful visual analysis of the hippocampus and amygdala (seen best on T1-weighted coronal cuts) may aid in the diagnosis of mesial temporal sclerosis by demonstrating unilateral or bilateral atrophy. Metabolic imaging with PET or SPECT may show increased blood flow and hypermetabolism in mesial temporal structures during ictal discharges and decreased blood flow and hypometabolism interictally. PET is the more sensitive technique interictally; SPECT is more practical for capturing ictal events. Common etiologies of temporolimbic epilepsy include mesial temporal sclerosis, hamartomas, dysplasia, low-grade astrocy-tomas, oligodendrogliomas, vascular malformations, and traumatic brain injury.

3. Orbitofrontal Systems Syndromes

Patients with lesions in orbitofrontal cortices or associated subcortical structures such as the caudate nucleus may engage in directed acts of aggression. However, they are often incapable of planning or executing a complex response that requires an extended sequence of actions. Failure to consider long-term and especially social consequences of violent outbursts is a salient feature. Frequently, the patient engages in impulsive, unreflective responses to identifiable but trivial environmental provocations. In some patients, extended but inefficient rational analysis of social situations without guidance from somatic-emotional systems is observed. Patients remember their actions but often lack remorse, and they fail to link aggressive actions with punishment or other long-term adverse outcomes, contributing to repeated offenses.

The neurological exam may reveal anosmia due to damage to the olfactory nerves or tracts on the undersurface of the frontal lobes and release phenomena such as the grasp reflex. If the lesion is confined strictly to orbitofrontal cortices, subjects may show few deficits on conventional IQ tests or even on neuropsychological tests explicitly designed to probe frontal-executive function. When lesions trespass upon dorsolateral frontal territories, deficits in go-no-go testing, verbal and nonverbal fluency, and set shifting may be evident. CT and especially MRI studies are helpful in screening for structural lesions. Common etiologies indude traumatic brain injury, anterior communicating artery aneurysm rupture, anterior cerebral artery infarction, orbital meningio-ma, the frontotemporal dementias (Fig. 5), and Huntington's disease.

4. Syndromes of Diffuse or Multifocal Brain Injury

Several medical conditions that produce aggression have effects on the brain that are diffuse or multifocal. A large body of investigative literature has demonstrated an increased frequency of "minimal brain dysfunction" and poorly localized neurological "soft signs'' in violent patients. In one study, minor and irregularly distributed perceptual, motor, sensory, reflex, and cognitive defects were noted in 119 of 286 patients with a history of recurrent attacks of uncontrollable rage. Minor neurologic findings are common in violent individuals in juvenile reform school and on death row. Attention deficit disorder was significantly correlated with criminal and violent offenses in a prospective study. Not surprisingly, developmental or acute medical conditions producing scattered minor neurological impairments place an individual at higher risk of expressing aggressive impulses. Diffuse or multifocal brain insults are likely to affect one or several circuits within the multiregional, hierarchical aggression regulatory system. In addition, a history of being abused or reared in an unstable household is likely to interact synergistically with multifocal brain injuries. An individual who has learned a model of acting on impulse and possesses a limited repertoire of other response options is all the more likely to demonstrate diminished flexibility and inhibition of aggression after diffuse, especially frontal, injuries.

Figure 5 Aggression with bifrontal lesions. Over 3 years, a 56-year-old man developed frequent violent outbursts and persistent foul language, as well as ritualistic behaviors, disinhibition, and jocularity. MRI demonstrates focal frontal lobar atrophy, consistent with Pick's disease. [Reproduced with permission from Saver et al., 1996, Neuropsychiatry of aggression. In Neuropsychiatry: A Comprehensive Textbook. (Fogel, B. S., Schiffer, R. B., Rao, S. M., eds.) p. 540. Williams & Wilkins, Baltimore].

Figure 5 Aggression with bifrontal lesions. Over 3 years, a 56-year-old man developed frequent violent outbursts and persistent foul language, as well as ritualistic behaviors, disinhibition, and jocularity. MRI demonstrates focal frontal lobar atrophy, consistent with Pick's disease. [Reproduced with permission from Saver et al., 1996, Neuropsychiatry of aggression. In Neuropsychiatry: A Comprehensive Textbook. (Fogel, B. S., Schiffer, R. B., Rao, S. M., eds.) p. 540. Williams & Wilkins, Baltimore].

The clinical manifestations of aggression in these patients are heterogeneous. History of school difficulty, learning disability, hyperactivity, or head trauma associated with brief loss of consciousness or amnesia are often elicited. School records are helpful because patients may deny or minimize past academic or disciplinary problems. A clouded sensorium or subtle sensorimotor or visual impairments may be found on neurological examination. Etiologies of diffuse brain dysfunction with episodic violence include, in addition to attention deficit disorder, toxic-metabolic encephalopathies (such as hyper- and hy-poglycemia, B12 deficiency, and thiamine deficiency), multiple schlerosis, and subcortical vascular dementia.

5. Delusional Syndromes

Delusional individuals are prone to violent behavior. In these patients, aggression-related neural systems may, like the intellect, be placed in service of the psychosis. In a variety of neuropsychiatric disorders, including schizophrenia, endogenous depression, mania, Alzheimer's disease (AD), and other dementias, the presence of thought disorder and hallucinations, especially of the persecutory type, increases the risk of violent outbursts. In a series of 181 subjects with probable AD, physical aggression was observed in 30% of patients; delusions and misidentifications frequently preceded violent outbursts. Dementia patients with paranoia and aggressive behavior have an increased rate of early institutionalization. Delusions are more likely to lead to aggression if frontal systems are also impaired.

The clinical approach to these patients is focused on the diagnosis and treatment of the underlying psychotic disorder. Etiologies of delusional disorders include paranoid schizophrenia, affective illness, late-life paraphrenia, AD, multiinfarct dementia, and subcortical dementias.

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