DiMaio and DiMaio take on the issue of causation involving deaths from excited delirium syndrome following interventions by law enforcement personnel or mental health professionals. To the authors' dismay, this topic continues to receive sensationalistic attention from an uninformed entertainmentfocused media who participate in uneducated blame directed at these professionals with each new case.
In addition, many in the medical community have ignored the seminal research, already available in this area for review. However, the cocaine epidemic of the 's lead to a series of case reports describing sudden death in cocaine abusers with an extreme behavioral malady similar to what had been reported by Bell and others years earlier. The agitated cocaine delirium deaths were associated with cocaine abuse and their appearance coincided with the introduction of cocaine into the United States Fishbain and Wetli, ; Wetli, The trans-shipment of cocaine to South Florida through the Bahamian corridor and the increased incidence of cocaine-related medical emergency room admissions and drug related deaths placed Medical Examiners in Miami-Dade at the forefront of a new wave of cocaine-related excited delirium deaths.
The deaths occurred mostly in young cocaine intoxicated males, who exhibited extreme hyperactivity and violent behavior, hyperthermia and sudden cardiorespiratory collapse. Because these patients always presented with agitated and bizarre behavior, law enforcement was often called to the scene.
Medical examiner review of these cases did not reveal a definite anatomic cause of death, although drug overdose, trauma, and underlying cardiac disease were excluded Wetli, ; Ruttenber et al. Historical descriptions and terminology of excited delirium syndrome. Neuroleptic malignant syndrome NMS is a rare, life-threatening idiosyncratic reaction to antipsychotic drugs characterized by fever, altered mental status, muscle rigidity, and autonomic dysfunction Levenson, ; Weinberger and Kelly, ; Berman, The hallmark symptoms of NMS include hyperpyrexia and muscular rigidity, while the cocaine-associated syndrome is atypical in having minimal rigidity.
Based on these similarities, Kosten and Kleber proposed that cocaine-induced excited delirium should be considered a dopamine agonist variant of NMS. These observations lead him to hypothesize that there may be three related syndromes: Delirious mania and malignant catatonia both have non-malignant and malignant clinical features with early, non-malignant symptoms responding to neuroleptics, while patients who pass over into the malignant phase require sedation by benzodiazepines Mann et al. Although NMS is a rare, life-threatening idiosyncratic reaction associated with virtually all neuroleptics, including the newer atypical antipsychotics e.
The abrupt cessation or reduction in dose of dopaminergic agonists, such as levodopa, pergolide, and amantadine in Parkinson's disease may precipitate NMS in vulnerable patients Ito et al. Interestingly, the akinetic crisis of Parkinson's disease is associated with a severe loss of striatal dopamine transporter function Kasssinen et al.
This rare condition is a life-threatening complication of Parkinson's disease, with an estimated annual incidence of 0. The clinical picture is similar to that of NMS and has been termed as the malignant syndrome of parkinsonism-hyperpyrexia. The condition is not related to disease stage or medication dosage, but one of the main features is that, the akinetic crisis appears to be long lasting on average 11 days and the dopamine system is transiently blocked from treatments, which would usually give patients rapid motor benefit.
To date, none of the theories put forth as the underlying cause of the NMS related syndrome in Parkinson's disease have been able to explain why only a small fraction of patients exposed to dopaminergic agonists develop the condition, although state dopaminergic drugs and trait genetic vulnerabilities are likely risk factors. Hypothalamic dopamine antagonism leads to the elevated set point for thermoregulation and the myotoxicity associated with malignant hyperthermia.
Sympathoadrenal hyperactivity and the loss of hierarchical integration and homeostatic control may constitute important risk factors for NMS and its associated variants. Gurrera advanced this hypothesis, suggesting that sympathetic nervous system hyperactivity should be viewed as primary in the etiology of NMS. The sympathetic nervous system mediates the hypothalamic coordination of thermoregulatory activity and is a regulator of muscle tone and thermogenesis.
The sympathetic nervous system's latent capacity for autonomous activity is expressed when tonic inhibitory inputs from higher central nervous system dopaminergic centers are disrupted. The predominant sources of spinal dopamine are the descending fibers projecting from the dopaminergic A10 and A11 cell groups of the posterior hypothalamus Skagerberg and Lindvall, ; Qu et al. These tonic inhibitory inputs relay to preganglionic sympathetic neurons by way of the dopaminergic hypothalamospinal tracts. State variables like the acute psychic stress reported originally in Bell's mania when coupled with a loss of presynaptic dopaminergic transporter function may lead to extremely elevated concentrations of synaptic dopamine, and the emergence of related clinical syndromes.
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A syndrome is the association of several clinically recognizable features, signs, symptoms, or characteristics that often occur together, so that the presence of one feature alerts to the presence of the others. Most recognize that the condition of excited delirium represents a syndromal disorder rather than a specific disease. What has not been emphasized in the literature is that various organic brain disorders, as well as functional psychiatric conditions and psychostimulant abuse, contribute to the expression of a CNS disorder with high fatality rates that share a common underlying neurochemical dysregulation of central dopamine homeostasis.
Persons at risk for excited delirium are most likely at the extreme end of the neuropsychiatric continuum of several DSM-IV recognized disorders, including delirium induced by a drug, manic excitement, and psychomotor agitation Vilke et al.
Those at risk for excited delirium and sudden death include people who are withdrawing from or non-compliant with psychotropic drugs, substance abusers suffering from reward deficiency syndrome or alcoholics in withdrawal, and persons suffering from acute manic episodes that may be triggered or worsened by sleep deprivation. The clinical description of excited delirium includes reports of increasing excitement with wild agitation and violent, often destructive behavior that can last for hours to days.
The forensic pathology descriptions suggest that the disorder can wax and wane in severity over time with rigidity or stupor alternating with excitement Wetli, ; DiMaio and DiMaio, These progress to increasing and possible fluctuations of fever and persistent autonomic instability with rapid and weak pulse and hypotension.
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Cocaine delirium shares clinical similarity to the acute onset of excitement, grandiosity, emotional lability, delusions, and insomnia associated with emergence of mania, and the disorientation and altered consciousness characteristic of delirium. Psychostimulant intoxication, drug withdrawal states, and undiagnosed mania and bipolar affective disorder are the most commonly reported antecedents Wetli, ; Mash et al. Transmission of reward signals is a function of dopamine, a neurotransmitter known to be involved in the mechanism of psychosis.
The symptoms of psychosis and mania are both related to dopaminergic hyperactivity in brain circuits implicated in neuropsychiatric disorders Cipriani et al. In psychosis, post-synaptic receptor sensitization causes dysfunctional neural processing, leading to the development of delusional symptoms. This understanding fits well with the traditional hyperdopaminergic hypothesis of psychosis and schizophrenia.botorganic.in/63.php
Excited Delirium Syndrome: Cause of Death and Prevention
The hyperdopaminergia and disordered signaling in dopamine target regions of the brain also serves as a model for mania, since dopaminergic blocking drugs are effective in alleviating mania and psychosis. Mania is the cardinal feature and a core symptom of bipolar disorder. PET scans in medicated, manic patients show abnormal brain activation in dorsal anterior cingulate, frontal polar, and right inferior frontal cortical regions Rubinsztein et al.
The increase in task-related anterior cingulate activation was positively correlated in this study with the severity of manic symptoms.
Anterior cingulate cortex activation may be related to increased nucleus accumbens dopamine signaling, which leads to cortical and subcortical hyperactivity in mania Perry et al. Genetic linkage studies have suggested an association of the dopamine transporter gene Kelsoe et al. Cocaine and methamphetamine increase extracellular dopamine and produce behavioral effects similar to mania Silverstone et al.
Drug sensitization occurs in drug addiction, and is defined as an increased effect of a drug following repeated doses the opposite of drug tolerance. Such sensitization involves increased brain mesolimbic dopamine transmission, as well as altered protein expression within mesolimbic dopamine neurons. Repeated treatment with psychostimulants leads to sensitization or reverse tolerance in animal models Post and Rose, ; Hooks et al. Paranoia in the context of cocaine abuse is common and potentially dangerous and several lines of evidence suggest that this phenomenon may be related to loss of function of the dopamine transporter protein Gelernter et al.
These observations suggest that certain dopamine transporter genotypes might predispose to paranoia with chronic psychostimulant abuse. The dopamine transporter undergoes neurobiological adaptations with chronic abuse of cocaine, depending on the duration, amount and pattern of use e.
Intermittent cocaine self-administration in rodents produces sensitization of the stimulant effects of cocaine at the dopamine transporter Calipari et al. This phenomenon is not unique to cocaine; other psychomotor stimulants, some other classes of drugs, and mental stress induce the phenomenon of behavioral sensitization. Since cocaine directly inhibits dopamine reuptake by binding to the transporter, repeated cocaine administration may lead to a reduced potency of cocaine, which leads to an elevation in synaptic dopamine and the expression of behavioral sensitization Zahniser et al.
The dopamine transporter expressed in presynaptic terminals of dopamine neurons regulates reuptake of dopamine from the synaptic cleft and keeps extracellular dopamine concentrations low Amara and Kuhar, ; Giros and Caron, ; Mortensen and Amara, The dopamine transporter is critical in regulating the concentration of extracellular dopamine and overall dopaminergic tone Mash and Staley, ; Drevits et al.
A decrease in dopamine transporter numbers or function in response to cocaine leads to reduced dopamine reuptake, elevated synaptic dopamine, and increased dopamine signaling at postsynaptic receptors. Dysregulated dopamine transporter function in ExDS. Located on presynaptic dopamine nerve terminals, the dopamine transporter functions to regulate the duration and intensity of synaptic dopamine signaling left. Cocaine red inhibits the reuptake of dopamine by blocking the transporter protein center. With chronic cocaine abuse, the dopamine transporter is trafficked to the plasma membrane as a compensatory adaptation to increases in synaptic dopamine.
In ExDS victims, there is a loss of dopamine transporter regulation, which causes dopamine overflow in the synapse right. The elevated synaptic dopamine leads to a state of hyperdopaminergia, that is associated with the intense motor excitement, paranoia, bizarre, and often violent behavior. The syndrome of excited delirium in drug abusers demonstrates that cocaine is the most frequent reported illicit drug Ruttenber et al.
Inhibition of dopamine transporter function is thought to be the primary mechanism underlying cocaine's addictive effects Ritz et al. Although excited delirium is most frequently reported in cocaine abusers, psychostimulants including, methamphetamine, MDMA, alpha-PVP, methylome, and ephedrine have been associated with the syndrome Mash et al. These psychostimulants directly interact with the dopamine transporter to cause a marked increase in the levels of synaptic dopamine. Postmortem neurochemical studies of the human brain at autopsy demonstrate that chronic cocaine abuse leads to a compensatory upregulation of dopamine transporter number and function Staley et al.
In contrast, there was no compensatory upregulation in dopamine transporter numbers in a case series of 90 cocaine-related excited delirium and exhaustive mania victims Mash et al. The cocaine-related excited delirium cases occurred in persons who had reported histories of chronic cocaine abuse, consistent with the quantification of benzoylecgonine in blood and cocaine and benzoylecgonine measured in brain at autopsy Mash et al.
Mean core body temperature among the 90 victims was Although the majority tested positive for cocaine, four had no licit or illicit drugs or alcohol measured in blood at autopsy. Forensic review of these four cases reported the cause of death as acute exhaustive mania, similar to the original description reported by Bell Dopamine can enhance both approach and avoidance behaviors and trigger extreme fear Faure et al.
Stages of Excited Delirium
When this homeostatic control of synaptic dopamine fails, it leads to a functional hyperdopaminergia, which triggers the acute onset of delirium and marked agitation in ExDS victims Staley et al. Rhabdomyolysis secondary to mania and cocaine excited delirium is related to extreme physical exertion, although increased sympathetic tone during manic states and elevated epinephrine also play a role in its development Manchip and Hurel, ; Ruttenber et al.
Both hyperthermia and hyperactivity play important roles in the evolution of cocaine-associated rhabdomyolysis and excited delirium. Interestingly, in NMS, the elevated risk for hyperthermia results from disordered dopamine signaling precipitated by chronic administration of neuroleptic drugs Strawn et al. The hyperthermia of neuroleptic malignant syndrome is associated with psychomotor agitation, and both syndromes have been related to increases in dopamine concentrations involved in thermoregulation and neuromuscular homeostasis Keck et al.
Some undiagnosed psychiatric patients or those who are neuroleptic medication non-compliant may be at increased risk for excited delirium and sudden cardiac death. Dopamine transporter numbers fall below the normal homeostatic range for regulating dopamine in all cases of fatal excited delirium, including those with no known history of drug abuse and a negative toxicology screen at autopsy.
Excited Delirium Syndrome: Cause of Death and Prevention - CRC Press Book
These results suggest that the unabated conditions, which favor the development of excited delirium, are psychostimulant abuse, extreme mental stress or an underlying, or perhaps undiagnosed psychiatric condition. A final common pathway for excited delirium related to chronic stimulant drug abuse, extreme environmental stress or acute mania of bipolar disorder might be a failure of the dopamine transporter to dynamically regulate synaptic dopamine.
This failure of regulation leads to a hyperdopaminergic state, which triggers the violent behavior, delirium, agitation, and motor excitement. Dopamine systems in the brain also play a role in temperature regulation Mann and Boger, The rise in core body temperature is most likely induced by dopamine stimulation of D1 receptors in the human hypothalamus which occurs because of a downregulation in D2 mediated hypothermia Mash, A dopamine transporter murine model of hyperdopaminergia displays a distinctive cardiorespiratory and thermal phenotype, providing further support for altered dopamine transporter regulation in excited delirium Vincent et al.
Dopamine also regulates sleep and arousal, suggesting that there might be an inter-relationship between thermal behavior and circadian rhythms mediated by disrupted CNS dopamine signaling in excited delirium. Mental and emotional stress is expressed in the brain as fluctuations in the activity of a subset of brain regions, including the insula, cingulate cortex, and amygdala Critchley, These regions serve as an interface between emotional feeling states and visceral responses of the body.
Cause of Death and Prevention , however, propose a different explanation. In this groundbreaking book, they cite the reason being a condition called Excited Delirium Syndrome, in which the normal physiological changes produced by violent activity culminate in sudden cardiac death, often in conjunction with the effects of a drug. In addition, it illustrates the effects that stressors, legal medication, and drugs of abuse have on the cardiovascular system. The effects of underlying disease, including endogenous mental disease are also discussed. These topics, along with the many actual case studies that provide further insight, make Excited Delirium Syndrome: Cause of Death and Prevention an essential resource for anyone treating or interacting with those that may have this disorder.
It also provides a well-constructed discussion of the chronology of the mechanism resulting in sudden death during an episode of excited delirium with extensive references. It outlines the features used to identify patients susceptible to excited delirium and the actions to prevent sudden death.
The chapters are well organized and laid out, easy to read, and provide useful information and references. Again, this book is an excellent resource to all members of the law enforcement, forensic, investigation, treatment, and prosecuting teams. We provide complimentary e-inspection copies of primary textbooks to instructors considering our books for course adoption.
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