Law Review Articles on Criminal Defense and Morality

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A Review of the Role of Chronic Traumatic Encephalopathy in Criminal Court

Journal of the American Academy of Psychiatry and the Police Online March 2021, 49 (1) 60-65; DOI: https://doi.org/x.29158/JAAPL.200054-twenty

Abstract

Chronic traumatic encephalopathy (CTE) is believed to be a degenerative brain disease characterized by repetitive encephalon trauma resulting in a specific pattern of neuropathological changes, which some take linked to functional disturbance and assailment. The diagnosis has gained greater public attention later on these same neuropathological changes were discovered in multiple deceased National Football game League (NFL) players, many of whom had exhibited signs of assailment, impulsivity, and poor executive performance, according to a widely publicized study. When an NFL player convicted of murder was found to have the neuropathological changes associated with CTE following his suicide, the New York Times editorial section asked whether CTE was a defense for murder. This idea raises an interesting legal and philosophical question about whether an individual's criminal actions can be adamant by something outside their control, such as by caput trauma. To begin to try an answer, this article reviews what is currently known nearly the neurobiology of traumatic brain injury, CTE, and morality. By looking at how U.Southward. criminal law courts have handled cases of dementia and traumatic encephalon injury in the past, we can ameliorate understand how to consider this postmortem diagnosis in its forensic context.

• chronic traumatic encephalopathy
• encephalon injury
• criminal law
• forensic psychiatry
• football injuries

In 2017, Aaron Hernandez, a star player for the National Football League, died by suicide in prison where he was serving a life sentence for first-degree murder.¹ On autopsy, Mr. Hernandez's brain exhibited neuropathological changes consistent with the proposed criteria for a diagnosis of chronic traumatic encephalopathy (CTE), a neurodegenerative disease thought to be associated with repetitive brain trauma and behavioral changes such as aggression, dementia, impulsivity, and poor executive functioning.² Similar weather condition have been described over the past century. Initially termed "dementia pugilistica," and described as "punch drunk," the diagnostic predecessor to CTE was thought to be unique to boxers sustaining forceful blows to the head and repeated episodes of loss of consciousness.^3,4 Renewed interest in the disease emerged in the 2000s, following the publication of several widely publicized studies by the laboratories of Ann McKee and Bennet Omalu, who linked consistent neuropathological changes to behavioral phenotypes in U.South. athletes, specially football players.^2,5,vi More than newspaper headlines came in July 2017 when McKee's grouping studied the donated brains of 202 deceased football game players with neurocognitive, emotional, and behavioral problems prior to death and reported that 177 met the recently established neuropathological criteria for the relatively new diagnosis of CTE.⁷

Such findings led the New York Times editorial page to ask, "Is CTE a Defense for Murder?"⁸ The authors, who are too law professors, answered apparently, "Mr. Hernandez should not have been convicted of first-caste murder. Given the conclusive diagnosis of Phase 3 CTE, it is probable that a lifetime of playing footbal —not Mr. Hernandez'south will—was to blame."^eight A greater understanding of the scientific discipline behind this diagnosis and the legal literature, however, suggests that the reply is not nearly and then unproblematic.

Defining CTE

CTE is a diagnosis that has been in the literature for the better office of a century. Originally recognized in boxers, case report data led early physicians to believe the clinical features of this illness, idea to be a result of numerous blows to the head, were primarily gait disturbance, dysarthria, tremor, and cognitive damage.^ix Over time, the name of the disorder, de-finitions, and clinical findings take changed, as further case reports and small observational studies were added to the literature. The consensus has been that CTE is due to the cumulative affect of numerous subconcussions and concussions, or balmy traumatic brain injuries.^x As defined past the Department of Veterans Affairs and the Department of Defence, mild traumatic encephalon injuries are head injuries with a loss of consciousness of less than 30 minutes, altered mental status of less than 24 hours, and no findings on neuroimaging.^ten Individuals with concussions do tend to have some symptoms (including headache and confusion) though they tend to be brief and self-limited.^x Subconcussions occur when a blow to the head occurs with no observable postinjury symptomatology. The vast bulk of traumatic brain injuries sustained by all individuals are subconcussions or mild traumatic brain injuries, but athletes, peculiarly football game players, sustain exponentially more than subconcussions and mild traumatic brain injuries than the average individual.¹² Effects from such cumulative brain traumas are idea to cause a pattern of neuropathological changes called CTE.¹³ CTE can just be diagnosed postmortem via a constellation of neuropathological changes. Several CTE researchers, including Omalu, have published case reports of individuals with CTE, diagnosed postmortem. He believes that CTE findings correlate with collateral reported history of retentivity loss, headache, executive dysfunction, language difficulties, aggression, apathy, motor disturbance, and dementia (Table i).¹¹

Table i

Symptoms Associated With Chronic Traumatic Encephalopathy

At that place are several neuropathological changes that are described as characteristic of CTE. These include depositions of hyperphosphorylated tau (p-tau) protein aggregates in neuronal and astrocytic cells in the brain.¹⁴ Distinguishing it from other tauopathies like Alzheimer disease, CTE p-tau aggregates are uniquely distributed in perivascular spaces, at the depths of the cortical sulci, in an irregular pattern.^5,fourteen Similar to other tauopathies, CTE is also associated with the accumulation of amyloid plaques, and p-tau aggregates in cortical layers II and III of hippocampal regions CA2 and CA4.¹⁶ Macroscopically, researchers report seeing frontotemporal atrophy, an overall reduction in brain mass, and increased ventricle size, likewise equally a cavum septum pellucidum.⁵ These macroscopic changes are associated with disinhibited behavior and cognitive impairment in other neurodegenerative illnesses as well, such every bit Alzheimer'due south disease and frontotemporal dementia.

McKee'south group has postulated that CTE is progressive based on a variance of severity of cases seen postmortem.² Omalu's group, nonetheless, has opined that differences in severity may be due to CTE consisting of several different disease groups. In each case, the illness itself is relatively stable, just the severity may differ by the subtype of CTE based on neurofibrillary tangle distributions.¹⁶ These distributions change based on the number and type of caput injuries endured. In that location are further differences among studies. For instance, Omalu states at that place is no atrophy in CTE,⁶ whereas McKee says widespread atrophy is common.² McKee'southward group feels that p-tau astrocytic tangles are pathognomonic for the illness,² whereas Omalu believes these are not present in all cases.¹⁶ The National Institutes of Wellness has adult a clinical consensus as to what pathological features must be present for a diagnosis to be reached. Primarily, perivascular tau accumulations in astrocytes and neurons in an irregular pattern deep in the sulci are considered diagnostic; other abnormal findings could be supportive or exclusionary.¹⁴

The neurocognitive and behavioral changes that some researchers have proposed as being associated with CTE are quite broad and embrace a big spectrum of severity. Researchers have differing opinions as to what must be present for diagnosis. McKee and her group have argued that there is a range of CTE symptoms, from no clinical manifestations² to severe CTE consisting of ataxia and mood dysregulation, impulsivity, and cerebral impairments similar to those with advanced dementia.¹⁷ Omalu, on the other manus, believes symptoms must exist present for diagnosis.¹¹

What is truly known about CTE and its symptomatology is still quite express because sample sizes have been minor and heterogeneous, and research has been conducted largely on postmortem brains. Thus, the majority of behavioral and cognitive correlations to neuropathology must exist inferred.¹⁵ Postmortem studies are inherently biased, with samples coming from relatives who might exist inclined, a priori, to aspect problematic personality traits and behaviors to neuropsychiatric conditions. Prospective studies following patients with head injuries and various exposures to encephalon trauma and other potentially modifying variables are even so needed to plant definitively the causation between repeated encephalon trauma and CTE.¹⁸ At that place does appear to be a pattern of p-tau deposition unique to athletes exposed to multiple mild head injuries, but whether this finding has clinical implications, specially implications that are distinctive from other established forms of dementia and neuroinjury, is still open for debate. Symptoms such as aggression, memory loss, and impulsivity are ultimately nonspecific and are seen in a variety of pathologies and personality types. Given that behavioral correlations are made postmortem, establishing the chronology of symptoms is very hard. For example, a football game player may accept been impulsive prior to many of his neuroinjuries and may have had earlier depressive tendencies. Thus, to aspect these characteristics solely to neurotrauma would exist inaccurate.

The Putative Neurobiology of Morality

Regardless of whether CTE is a validated diagnosis in and of itself, a larger question looms. If nosotros are to consider CTE as a defense for wrongdoing, we must assume that morality and behavior are at least partially neurobiologically mediated. In that location is some evidence that this may exist the instance. One of the most commonly injured areas of the brain in traumatic brain injury (TBI) is the ventromedial prefrontal cortex (VMPFC).^nineteen The VMPFC serves as an inhibitory command center for the limbic system, the seat of the fight-or-flight response. Thus, its damage results in anxiety, impulsivity, and aggression, representing unmitigated fight-or-flight responses.^19,20 Studies of what are thought to be more advanced cases of CTE have revealed avant-garde grey and white matter atrophy in multiple areas of the brain, typically nearly severe in the frontal lobe, specifically in the VMPFC.^xiii McKee et al. ² agree that harm to this area may underlie the lack of insight and aggressive tendencies seen in this population.

The results of multiple other neuromodulatory and neuroimaging studies further suggest that the VMPFC may exist the structure responsible for one'due south innate moral sense.²¹ Fumagalli et al. targeted the VMPFC with transcranial directly current stimulation (tDCS) in control subjects. Responses to moral dilemmas changed significantly in female subjects after tDCS. Anodal tDCS appeared to decrease VMPFC activation, acting like a lesion. Afterwards anodal tDCS, female subjects responded with a colder, more than detached, and "utilitarian" pattern on moral dilemma.²² Other disorders associated with aggressive behavior take been reported to involve VMPFC pathology, as would be expected if the VMPFC were the essential structure responsible for moral behavior. For example, near half of individuals with frontotemporal dementia exhibit hating (amoral) behavior, and those who exhibit such behavior have clear VMPFC atrophy.²³ Yet some other study published past the Fumagalli et al. group reported that psychopathic individuals had significantly less VMPFC activation on functional magnetic resonance imaging when shown upsetting, emotionally charged images.²¹

Incarcerated individuals are some other candidate population for studying the connection between brain trauma and ambitious, criminal acts. A 2012 meta-assay estimated that threescore pct of inmates across many studies have a history of TBI, a significantly higher incidence than in the general population.²⁴ A 2016 cohort study of more than one million immature adults living in Ontario, Canada, used authorities health and incarceration records to analyze the potential association between TBI and later incarceration. The study reported that individuals with a history of TBI were approximately 2.5 times more than likely to be incarcerated than those without prior TBI (2.47 times for men, 2.76 times for women).²⁵ A 2011 study of 200 Australian prisoners with 200 controls matched past place of residence reported that TBI was associated with impulsivity, dissocial (hating) personality traits, alcohol apply, illicit drug use, and level of educational activity.²⁶ Though TBI was significantly more common in the prisoner group, TBI frequency was not significantly associated with incarcerated condition, whereas the post-obit factors were: lower education, drug apply, alcohol corruption, impulsivity, and dissocial traits. Moreover, when TBI was removed from the logistic model, the odds ratio for incarcerated status was relatively unchanged for impulsivity and dissocial traits. In contrast, when impulsivity and dissocial traits were excluded from the model, a weak association was noted between TBI frequency and incarcerated status.

A Hypothetical CTE Defense

The literature suggests an argument could be made that individuals with CTE might be predisposed to impulsive, ambitious, and hating beliefs due to harm to putative morality-associated neurobiological circuits, which, if intact, would serve to inhibit such beliefs. To address whether CTE could be a defence force for murder, equally the New York Times asked,⁸ we must also review how mental wellness and other medical experts piece of work with the legal organisation on matters of criminal accountability. The insanity defense and related criminal defenses (e.one thousand., diminished capacity or diminished responsibleness) focus on 2 main elements: the defendant's mental land at the fourth dimension of the criminal offence and how exactly that state incapacitated the defendant at the time. The incapacities to be investigated vary with jurisdiction and with the asserted defense, simply they may include the ability to capeesh the legal or moral wrongfulness of the criminal act charged and the ability to refrain from committing that act. The expertise of mental health and other medical professionals is most relevant and helpful to the question of the defendant'south mental state at the fourth dimension of the offense. Capacity evidence presumes concepts fundamental to criminal law and justice, such equally free will and equality of choice, which are potentially at odds with neuroscience, given that the neurobiological bases for these concepts take not been established.

An Expert's Possible Office

A forensic psychiatrist asked to evaluate a living defendant claiming that CTE rendered him insane would face an firsthand and probable insurmountable bulwark: CTE cannot currently be diagnosed in a living defendant considering the diagnosis relies on postmortem studies. Therefore, testimony suggesting that a defendant had CTE that rendered him insane at the fourth dimension of the crime might well exist considered inadmissible from the showtime based on either a Frye test or a Daubert test of admissibility.²⁷

Setting this bated, an evaluator approaching such a case would first focus on the defendant'south medical and psychiatric history, noting other conditions that might mimic or derange the diagnosis. Particular attention would be given to the defendant'due south history of head injury, including TBI every bit well as subclinical injuries. A standardized instrument, such as the Ohio State University TBI Identification Method-Interview Course,²⁸ might be used to identify past head trauma, just more impartial data sources such as hospitalization, school, legal, or military machine records would be desirable to corroborate the defendant's claims for both the incidence of trauma every bit well equally tracing the onset and progression of behavioral changes. Temporal correlation between the onset of behavioral changes and head trauma, as well as correlation with other comorbid or potentially misreckoning atmospheric condition, would be crucial. The mental condition examination would focus on signs of behavioral disinhibition and cognitive deficits. Although at that place is no standardized clinical instrument for the diagnosis of CTE, neurocognitive testing with validity testing would exist recommended in such a case, every bit would a neurological exam. At the least, without strong correlation between repetitive brain trauma and later onset of behavioral and cognitive changes with consequent mental condition test and neurocognitive testing findings, a CTE diagnosis could not exist made, much less any proposition that it affected the defendant's mental state at the time of the offense.

Futurity Possibilities for CTE Defenses

The possibility of diagnosing CTE without postmortem studies could soon be on the horizon. Researchers are showtime to apply positron emission tomography scans to attempt to diagnose CTE in living subjects, with some promising results.²⁹ If that science advances, courts could potentially allow a well-reasoned expert's opinion in favor of a CTE defense. In the context of the insanity defence force, the first question is whether an individual's aberrant behavior qualifies as a mental disease. So long as the question is accounted a matter of fact, the defence has the opportunity to prove to the finder of fact that the accused is properly diagnosed with the disorder. Next to prove would be whether a given illness sufficiently compromised the defendant's cognitive (whether moral or legal cognition) or volitional (whether limited to instantaneous impulses or broadened to longer-term command deficits) capacities. The definition and inclusion of such capacity dimensions are dependent on the police in the relevant jurisdiction. A review of like situations in cases involving frontotemporal dementia indicated that affected individuals may accept relatively intact cerebral faculties and are frequently aware of the wrongfulness of their actions but showroom deficits in their volitional capacities.^thirty

If a total insanity defense is unavailable at the guilt phase, a diminished chapters or macerated responsibility defence might exist some other avenue for the defense team. Testimony would be given on the accused's capacity to form intent, and experts could speak of the cognitive and behavioral shortcomings of the defendant and people like the defendant. In terms of outcome, a successful macerated chapters assertion typically leads to conviction on a bottom included charge. An insanity verdict typically results in compulsory mental wellness treatment until the accused is no longer accounted dangerous because of mental illness. Overcoming the dangerousness prognosis and stigma is a dubious prospect in cases of neurodegenerative diseases.

A potential complication for the defense squad seeking to employ a CTE defense force during the sentencing phase is that CTE could be taken as proof of dangerousness and thus could be more aggravating than mitigating. Courts have generally been receptive to admitting neuroimaging prove of alleged encephalon abnormalities, especially at the sentencing stage in majuscule cases where the judge or jury must consider all potentially mitigating testify presented. The testify may backlash from the defense's perspective, however, if the sentencer, whether articulated or not, counts it in bedevilment of the crime.

A famous case comes from Missouri, where in 1974 a sawmill accident left Cecil Clayton with significant encephalon trauma. It reportedly led to profound personality changes, culminating 22 years later (in 1996) in his killing a sheriffs' deputy during a domestic dispute. Despite his lawyers' raising both diminished capacity and sentence mitigation level defenses based on the history of injury, Mr. Clayton received the death penalisation. In the various appeals that followed, the insanity defense was as well raised, in addition to other defenses not previously described. In 2015, Mr. Clayton was executed at age 74, the oldest person on Missouri'southward death row.³¹

Conclusions

Although there is a growing body of prove that human moral behavior is partly inherited and partly embodied in the VMPFC, an area of the brain ofttimes injured in TBI, much stands in the way of using CTE as a defence for murder at this fourth dimension. First, there is the obvious obstacle of having expert testimony asserting a CTE diagnosis reach a general acceptance standard. The biological validity and reliability of CTE is untested. There is no consensus equally to whether CTE is a detached illness and whether it is distinguishable from other forms of dementia and neurotrauma. Furthermore, nosotros lack an empirical ways to determine if the symptoms blamed on the neuropathological findings of CTE are acquired by them.³² Fifty-fifty if CTE is determined to be the entire cause of an individual's problematic beliefs, there are examples of other forms of dementia not leading to successful defenses for individuals who accept committed crimes.

Equally of now, the but way to diagnose CTE is postmortem, and that diagnosis itself is still debated. Our current agreement of CTE is rapidly changing, however. Multiple researchers are working on better characterizing the pathological changes associated with the disease in beast models and at present in living individuals believed to have the condition. Labs are using positron emission tomography neuroimaging to find biomarkers that may, i day, prove to be pathognomonic for the disorder.²⁹ Existing studies are hampered past small samples and heterogeneity, but this may modify as neuroimaging abilities evolve. Whether neurobiological defenses tin can more reliably succeed in the future volition likely crave evolution in jurisprudence in add-on to, and hopefully tracking, advances in neuroscience.

Footnotes

• The views expressed in this article exercise not reflect the official policy or views of the U.Southward. Section of Veterans Affairs or Northwestern University.

• Disclosures of fiscal or other potential conflicts of involvement: None.

• © 2021 American University of Psychiatry and the Police force

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Source: http://jaapl.org/content/49/1/60

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