Causes

There are two ways to describe the causes of agitation and aggression: by the underlying disease state (see Table 1), or the exact pathophysiology that causes the aggression. The DSM-IV-TR has several diagnostic categories describing the relationship between a medical condition or substance and the specific psychiatric symptoms or syndrome they cause. Examples of medical conditions that more commonly cause aggression and agitation symptoms include central nervous system disorders such as head trauma, stroke, tumor, and epilepsy; metabolic disorders such as fluid and electrolyte abnormalities, acid-base abnormalities, thiamine deficiency, hyper- and hypothyroidism, and hypoglycemia; infections such as sepsis, HIV, encephalitis, and urinary tract infections; and others such as systemic lupus erythematosus, postoperative states, especially in transplant or hip replacement procedures, terminal illnesses, and dialysis. Table 2 identifies medications and drugs that may be associated with inducing symptoms of agitation or aggression.

Four characteristics contribute to aggression and violence among people with serious mental illness: acute, poorly controlled mental illness, medication noncompliance, substance abuse, and previous violent behavior. Each is an independent risk factor, and the risk is heightened when factors are combined. People with and without mental illness who use drugs and alcohol have an increased risk for agitation and aggression.

There is no single unifying theory for the underlying pathophysiology of aggression. Brain lesions and changes in neurotransmitter function are two widely accepted theories. As the frontal lobes are responsible for higher order thinking, censoring, disciplining, planning and decision-making, damage to the frontal cortex produces a variety of disinhibited behaviors (patient becomes more agitated or aggressive than prior to receiving medication). Lesions or injury to the basal ganglia, limbic system, thalamus, hypo-thalamus, hippocampus and temporal lobes may also result in abnormal behavior. In a simplistic approach, agents that reduce dopaminergic or noradrenergic tone or increase serotonergic or GABAergic tone decrease aggression (such as any benzodiazepine or antipsychotic agent), no matter what the cause.

There is specific evidence demonstrating an inverse correlation between 5-HIAA, the major meta-bolite of serotonin, and aggressive behaviors.Other theories propose that the mechanism of agitated depression is increased serotonergic responsiveness and decreased GABAergic tone, whereas acute psychosis results from increased dopamine.The pathophysiology is generally more important when planning a long-term strategy to treat the underlying disease rather than when managing an acutely agitated patient who needs immediate attention.

Related posts:

1. Acute Agitation and Aggression in Psychiatric Illnesses. Part 5. Treatment Treatment Goals The first goal is to ensure safety of the patient and those around him. Secondly, symptoms need to be reduced to such a degree that safety is no longer a problem and further medical and psychiatric assessments can be completed in order...