Proposition: A Personality Disorder May Nullify Responsibility for a Criminal Act

The model test for legal insanity crafted by the American Law Institute for its 1962 Model Penal Code (or variants of it such as dropping the “volitional” prong) is the most common test used in American jurisdictions. The test holds that: “A person is not responsible for criminal conduct if at the time of such conduct as a result of mental disease or defect he lacks substantial capacity either to appreciate the criminality [wrongfulness] of his conduct or to conform his conduct to the requirements of law.”

The “cognitive” prong refers to awareness by the defendant that the misconduct is wrong or criminal in nature, or at least that the misconduct would be perceived that way by others. Different nuances have been applied to the cognitive prong such as whether it is sufficient that the defendant simply “know” that the misconduct is wrong or criminal, or must the defendant more broadly “appreciate” the wrongfulness or criminality of the act. Complex questions arise when the defendant may “know” or “appreciate” that an act is “wrong” or “criminal” or would be seen that way by others but is also operating under the influence of delusions. For example, a defendant may “know” that harming a family member is “wrong” but believe it to be necessary to save his own life out of the paranoid delusion that the family member is now a bodily host to alien beings that intend to kill him.

The “volitional” prong refers to the ability of the defendant to engage in a behavior other than the misconduct leading to prosecution. How much impairment in the exercise of a free will is sufficient to nullify criminal responsibility implicates complex arguments about the nature of free will and limits on the exercise of free will in a particular situation or under the influence of mental disorders. For example, is the question whether the defendant would have been capable of refraining from the criminal act if a policeman had been standing at his elbow? Capable of refraining from the criminal act if he had been compliant with psychiatric medication? Capable of refraining from the criminal act under the specific circumstances of the crime? The Durham test, once more widely used but now used only in New Hampshire, holds that a defendant is “not criminally responsible if his unlawful act is the product of a mental disease or defect” without further clarifying what it means to have an action be a “product” of a mental disease or defect.

None of the current tests for criminal responsibility require identification of a specific DSM-TR diagnosis. Diagnosis is often used as a means of establishing the prerequisite “mental disease or defect” commonly required in a test for legal insanity, but there is no legal reason why a functional description could not be used instead of a diagnosis. Indeed, once providing a diagnosis a skilled forensic mental health examiner will describe what specific impairments arise from that diagnosis that are linked to the cognitive and/or volitional prongs of the most commonly used versions of tests for legal insanity.

The American Law Institute test for legal insanity has both a cognitive and a volitional prong, but also included language stating that “the terms mental disease or defect do not include an abnormality manifested only by repeated criminal or otherwise antisocial conduct.” See American Law Institute, Model Penal Code, section 4.01(2).

The personality construct of psychopathy is primarily described by two dimensions, personality traits of “aggressive narcissism” and a behavioral history of chronic antisocial behavior. Core traits include lack of capacities for guilt or remorse, and persons who score highly on measures of psychopathy tend to have elevated rates of criminal recidivism. Psychopathy is considered a particularly virulent form of antisocial orientation with developmental antecedents in childhood; recent research has demonstrated that there is both genetic heritability for associated personality traits and neurobiological correlates on brain imaging. See Hare R. , “Psychopathy: A Clinical Construct Whose Time Has Come,” Criminal Justice and Behavior 23, no. 1 (1996): 25–54; Hare R. Clark D. Grann M. Thornton D. , “Psychopathy and the Predictive Validity of the PCL-R: An International Perspective,” Behavioral Sciences and the Law 18, no. 5 (2000): 623–645.

Following the acquittal as “not guilty by reason of insanity” of John Hinkley, public furor prompted Congress to enact a statute in 1984 that read: “No expert witness testifying with respect to the mental state or condition of a defendant in a criminal case may state an opinion or inference as to whether the defendant did or did not have the mental state or condition constituting an element of the crime charged or a defense thereto. Such ultimate issues are for the trier of fact alone.” Congress also removed the “volitional” prong from the test for legal insanity so that the test in federal cases now reads that a defendant is not criminally responsible if “at the time of the commission of the acts constituting the offense, the defendant, as a result of a severe mental disease or defect, was unable to appreciate the nature and quality or the wrongfulness of his acts. Mental disease or defect does not otherwise constitute a defense.” Federal Insanity Defense Reform Act, codified at 18 U.S.C. s. 17 (1984).

Three states had abolished the use of the insanity defense by 1995. These states (Montana, Idaho, Utah, Kansas) do permit evidence of impairments arising from mental disorders for the limited purpose of showing that a defendant could not form the intent required for conviction of crimes requiring a showing “specific intent” such as first degree premeditated murder.

Mental health courts attempt to divert defendants with significant mental disorders from criminal justice systems (including forensic mental health systems) to community mental health systems, in recognition of the disproportionate numbers of severely mentally ill persons who are found in the criminal justice system. The Center for Court Innovation maintains a website with information on mental health courts, available at <http://mentalhealthcourts.org> (last visited September 16, 2010).

Melton G. B. Petrila J. Poythress N. G. Slobogin C. , Psychological Evaluations for the Courts: A Handbook for Mental Health Professionals and Lawyers , 3rd ed. (New York: Guilford Press, 2007): At 203 (finding upon review of research upon use of the insanity defense that research results “appear to counter the belief that the plea is an everyday occurrence,” that “the absolute number of individuals found not guilty by reason of insanity (NGRI) is very low” and less than 1% of criminal cases, and that some 70% of insanity acquittals were from plea agreements with prosecutors because prosecutors “agreed that the defendants were so ‘crazy’ that they should be hospitalized rather than convicted and imprisoned.” See also Reid W. H. , “The Insanity Defense: Bad or Mad or Both?” Journal of Psychiatric Practice (May 2000): 169–172.

American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 4th ed., Text Revision (DSM-IV TR) (Washington, D.C.: American Psychiatric Association, 2000) [hereinafter cited as DSM].

The DSM diagnostic system has five dimensions. Axis I is defined as “Clinical Disorders” or “Other Conditions that May Be A Focus of Clinical Attention.” These are typically mental disorders identified as primary targets of clinical attention and intervention. Axis II is defined as “Personality Disorders” or “Mental Retardation” in an effort to identify conditions with clinically significant impairments that that are stable and persistent.

Perhaps the most public example of a shift in psychiatric diagnosis was the reconsideration by the American Psychiatric Association of homosexuality as a mental disorder. Less well-known examples reflecting social forces and/or advances in clinical science also include the inclusion in more recent editions of the DSM diagnostic scheme of cultural specific syndromes, factitious disorders by proxy, and inclusion of codes for “Relational Problems” among intimate partners or family members, or “Problems Related to Abuse or Neglect” of children or adults. See DSM, supra note 10, at 896.

The currently recognized personality disorders in the DSM-IV-TR diagnostic scheme are: Paranoid Personality Disorder; Schizoid Personality Disorder; Schizotypal Personality Disorder; Antisocial Personality Disorder; Borderline Personality Disorder; Histrionic Personality Disorder; Narcissistic Personality Disorder; Avoidant Personality Disorder; Dependent Personality Disorder; Obsessive-Compulsive Personality Disorder; and, Personality Disorder Not Otherwise Specified. See DSM, supra note 10, at 685.

See DSM, supra note 10, at xxvi. The DSM-IV-TR acknowledges that the diagnostic scheme “attempted to be neutral with respect to theories of etiology.”

One laudable goal of the DSM system has been to create a common vocabulary and set of clinical descriptions for diagnostic entities so that mental health professionals can more effectively and accurately communicate among themselves about how persons present clinically to them. However, the criteria which constitute the descriptive diagnoses are themselves evolved by consensus through committees within the American Psychiatric Association that advise on the development of the DSM diagnostic scheme.

See DSM, supra note 10, at xxxiii. The DSM-IV-TR cautions that “a diagnosis does not carry any necessary implications regarding the causes of the individual's mental disorder or its associated impairments” and that a diagnosis “does not carry any necessary implications regarding the individual's degree of control over one's behavior….”

For a review of research on genetic heritability of personality disorder traits, see Lang K. L. , “The Behavioral Genetics of Psychopathology: A Clinical Guide,” in The Personality Disorders (Mahway, NJ: Lawrence Erlbaum Associates, Publishers, 2005): Chapter 5, at 87–110.

Id., at 166. (Noting that “virtually all disorders have a significant heritable basis” with schizophrenia and bipolar disorders with 70–80%, alcoholism and personality disorders at 45–55%, anxiety disorders at 20–40% and some forms of depression lower at approximately 30%.)

Adverse childhood experiences in an insured commercial HMO population (N = over 17,000) have been significantly correlated with adulthood depression, suicide attempts, hallucinations, alcohol and drug abuse, smoking, unintended pregnancy, intimate partner violence, sexually transmitted diseases, liver disease, obesity ischemic coronary disease, diabetes, hypertension, chronic obstructive pulmonary disease, and other health, behavioral health and mental health conditions. For a summary of this research, see the Adverse Childhood Experiences study results webpage at the Centers for Disease Control, available at <http://www.cdc.gov/NCCDPHP/ACE/index.htm> (last visited September 16, 2010). See also Felitti V. J. Anda R. F. Nordenberg D. , “Relationship of Childhood Abuse and Household Dysfunction to Many of the Leading Causes of Death in Adults: The Adverse Childhood Experiences (ACE) Study,” American Journal of Preventive Medicine 14, no. 4 (1998): 245–258.

Factors associated with emergence of personality disorders include: Dysfunctional family experiences (e.g., parenting impaired by substance abuse or mental illness, family breakdown resulting in parental conflict or loss); traumatic experiences (e.g., emotional, physical or sexual maltreatment); or social stressors (e.g., attachment disruptions, early elementary school maladjustment). While no variable accounts for substantial amount of the variance in development of a personality disorder, cumulative factors appear to contribute beyond the heritability of personality traits associated with personality disorder. For a review, see Livesley W. J. , ed., Handbook of Personality Disorders: Theory, Research and Treatment (New York: Guilford Press, 2001).

Anda R. F. Felitti V. J. Walker J. Whitfield C. L. Bremner J. D. Perry B. D. Dube S. R. Giles W. H. , “The Enduring Effects of Abuse and Related Adverse Experiences in Childhood: A Convergence of Evidence from Neurobiology and Epidemiology,” European Archives of Psychiatry and Clinical Neurosciences 56, no. 3 (2006): 174–186.

Teicher M. H. Anderson S. L. Polcari A. , “The Neurobiological Consequences of Early Stress and Childhood Maltreatment,” Neurosciences and Biobehavioral Review 27, nos. 1–2 (2003): 33–44. (neurodevelopmental impact of adverse life experiences and reflection in emotional and behavioral dysregulation); see also Cicchetti D. Toth S. L. , “Developmental Psychopathology and Disorders of Affect,” in Cicchetti D. Cohen D. J. , eds., Developmental Psychopathology, vol. 2: Risk, Disorder and Adaptation (New York: John Wiley and Sons, 1995): 369–420.

Zangarini M. C. , “Childhood Experiences Associated with the Development of Borderline Personality Disorder,” Psychiatric Clinics of North America 23, no. 1 (2000): At 89–101 (finding childhood maltreatment a common antecedent to BPD); National Institute of Mental Health. Borderline Personality Disorder (NIH Publication No. 01–4928) (reporting that “[r] esearchers believe that BPD results from a combination of individual vulnerability to environmental stress, neglect or abuse as young children, and a series of events that trigger the onset of the disorder as young adults).

Neugebauer R. Hoek H. Susser E. , “Prenatal Exposure to Wartime Famine and Development of Antisocial Personality Disorder in Early Adulthood,” JAMA 282, no. 5 (1999): 455–462 (noting association of intrauterine malnutrition and risk of development of antisocial orientation in early adulthood); Steiner H. Garcia I. G. Matthews Z. , “Posttraumatic Stress Disorder in Incarcerated Juvenile Delinquents,” Journal of American Academy of Child and Adolescent Psychiatry 36, no. 3 (1997): 357–365 (high prevalence of PTSD in incarcerated delinquent population); Farrington D. , “Family Background and Psychopathy,” in Patrick C. , ed., Handbook of Psychopathy (New York: Guildford Press, 2006) (noting family pattern contributing to emergence of psychopathy in adulthood); Frick P. Marsee M. , “Psychopathy and Developmental Pathways to Antisocial Behavior in Youth,” in Patrick C. , ed., Handbook of Psychopathy (New York: Guilford Press, 2006) (describing developmental antecedents and trajectories towards antisocial behavior); Johansson P. Kerr M. Andershed H. , “Linking Adult Psychopathy with Childhood Hyperactivity-Impulsivity-Attention Problems and Conduct Problems through Retrospective Self-Reports,” Journal of Personality Disorders 19, no. 1 (2005): At 94–101 (analysis of developmental trajectory through childhood mental disorders and behavior problems towards adult antisocial orientation and psychopathy).

Lis E. Greefield B. Henry M. Guile J. M. Dougherty G. , “Neuroimaging and Genetics of Borderline Personality Disorder: A Review,” Journal of Psychiatry and Neuroscience 32, no. 3 (2007): 162–173, quotation below at 170 (summarizing neuroscience studies of BPD and noting a consistency of findings that in BPD “areas of the brain that are used to regulate and control emotion are hypometabolic and that activation of limbic systems, when it occurs is excessive.…[and this] might reflect a failure of rational thought to control rational thought, leading to the emotional instability that is characteristic of BPD.”); Prado C. , “Functional Impairments in Patients with Borderline Personality Disorders Demonstrated by NeuroSPECT HMPAO Tc 99 m in Basal Conditions and Under Frontal Activation,” Alasbimn Journal 2, no. 7 (April 2000): Article No. AJ07–1 (finding frontal lobe dysfunction correlated at p<.005 with ahedonia, negative anticipation and emotion, diminished working memory, emotional disturbance); Davidson R. J. Jackson D. C. Kalin N. H. , “Emotion, Plasticity, Context and Regulation: Perspectives from Affective Neuroscience,” Psychological Bulletin 126, no. 6 (2000): At 873–879 (finding impairments of neural circuitry underlying impulsive aggression such as is found in BLPD); Davidson R. J. Putnam K. M. Larson C. L. , “Dysfunction in the Neural Circuitry of Emotional Regulation: A Possible Prelude to Violence,” Science 289, no. 5479 (2000): At 591–594 (finding impairments in prefrontal activation of inhibitory circuitry predicts the ability to suppress negative emotion); National Institute of Mental Health. Borderline Personality Disorder (NIH Publication No. 01–4928) (reporting that NIMH funded neuroscience research “is revealing brain mechanisms underlying the impulsivity, mood instability, aggression, anger, and negative emotion seen in BPD); New A. S. Hazlett E. A. Buchsbaum M. S. Goodman M. , “Amygdala-Prefrontal Disconnection in Borderline Personality Disorder,” Neuropsychopharmacology 32, no. 32 (2007): 1629–1640 (noting dysfunction of neural connections between prefrontal areas and the amygdala among BPD subjects with impulsive aggression compared with health normal subjects).

Kiehl K. Smith A. Hare R. Mendrek A. Forster B. Brink J. , “Limbic Abnormalities in Affective Processing by Criminal Psychopaths as Revealed by Functional Magnetic Resonance Imaging,” Biological Psychiatry 50 (2001): 677–684; Kiehl K. Bates A. Laurens K. Liddle P. , “Brain Potentials Implicate Temporal Lobe Abnormalities in Psychopathy,” Journal of Abnormal Psychology 115, no. 3 (2006): 443–453; LaPierre D. Braun C. Hodgins S. , “Ventral Frontal Deficits in Psychopathy: Neurological Test Findings,” Neuropsychologia 33, no. 2 (1995): 139–151; Blair J. Mitchell D. Blair K. , The Psychopath: Emotion and the Brain (Maiden, MA: Blackwell Publishing, 2005); Blair J. Jones L. Clark F. Smith M. , “The Psychopath: A Lack of Responsiveness to Distress Cues?” Psychophysiology 34, no. 2 (1997): 192–198; Raine A. Ishikawa S. Arce E. Lencz T. Knuth K. Bihrle S. , “Hippocampal Structural Asymmetry in Unsuccessful Psychopaths,” Biological Psychiatry 55 (2004): 185–191; Barratt E. S. Stanford M. S. Kent T. A. , “Neuropsychological and Cognitive Psychophysiological Substrates of Impulsive Aggression,” Biological Psychiatry 41, no. 10 (May 1977): 1045–1061; Pridmore S. Chambers A. McArthur M. , “Neuroimaging in Psychopathy,” Australian and New Zealand Journal of Psychiatry 39, no. 10 (2005): 856–865; Keihl K. A. , “Cognitive Neuroscience Perspective on Psychopathy: Evidence for Paralimbic System Dsyfunction,” Psychiatry Research 142, nos. 2–3 (2006): 107–128.

Generally, these studies document emerging research and controversies in neurobiologically mediated deficits associated with violent offending, Antisocial Personality Disorder, and Psychopathy, including: Impaired prefrontal lobe (executive) functioning and decreased prefrontal grey matter; dysfunction of the orbital frontal cortex; dysfunction in the medial temporal lobe; reduced activity during language process in the right anterior superior temporal gyrus, amygdala, and other areas; hippocampal abnormalities in functioning and decreased volume in the posterior hippocampus; and other areas. See Keil (2006), id., summarized these as reflecting, in part, significant dysfunction of the prefrontal lobes, the paralimbic cortex, and core limbic structures. Functionally, behavioral correlates associated with these brain abnormalities include impulsive aggression, inefficient processing of salient environmental stimuli, abnormalities in processing language and emotionally charged stimuli, hypo reactivity to fear stimuli, errors in attention and orientation, and social cuing such as facial expressions of fear.

See Jang K. L. , “The Behavioral Genetics of Psychopathology,” in Classification and Diagnosis (Five Limitations of Our Current Diagnostic System (Mahway, NJ: Lawrence Erlbaum Associates, 2005): Chapter 3, at 47 (contrasting the DSM categorical diagnostic scheme with a dimensional approach and noting that “a dimensional model of psychopathology states that disorder represents the extremes of the normal distribution of function. Illness is operationally defined by a threshold placed on the frequency distribution of severity. An important feature of dimensional models is that they are also multidimensional. This means that there is a frequency distribution for the severity of every symptom defining a disorder and each person is assumed to be able to display all of the symptoms to some degree.”)

Id., at 46 noting that the issue of functional “severity has been handled in a rather awkward fashion in recent editions of the DSM and ICD by providing new diagnostic categories for premorbid and less severe forms of the major disorders (e.g., dysthymia vs. depression). This approach can lead to misdiagnoses as the number of possible diagnoses increases.”

The DSM, supra note 10, at xxxi, acknowledges that in a categorical diagnostic system there is “no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries,” that there is “also no assumption that all individuals described as having the same mental disorder are alike in all important ways,” and that “boundary cases will be difficult to diagnose in any but a probabilistic fashion.”

See DSM, supra note 10, at 729. DSM-IV-TR describes Personality Disorder NOS (Not Otherwise Specified) as a personality disorder that “does not meet criteria for any specific Personality Disorder” but that causes “clinically significant distress or impairment in one or more important areas of functioning…”

See, for example, proposed modifications to the DSM scheme based upon findings from neuroimaging, behavioral genetics and other emerging sciences. One proposal would designate Axis I disorders as “Genotype” conditions with assignment of disorders by genetic links to disorders, symptoms, resiliencies and drug responses, and Axis II conditions as the “Neurobiological Phenotype” assigned by factors including cognitive capacities, emotional regulation, and neuroimaging profiles. See chart of proposed modification of DSM Axial system in Charney D. J. , “Neuroscience Research Agenda to Guide Development of a Pathophysiologically Based Classification,” in Kupfer D. J. First M. B. Reiger D. A. , eds., A Research Agenda for DSM-V (Washington, D.C: American Psychiatric Association, 2002): at 72.

See, for example, Livesley J. , “Toward a Genetically-Informed Model of Borderline Personality Disorder,” Journal of Personality Disorders 22, no. 1 (February 2008): 42–71 (holding that the diagnosis of BPD is built upon heritable personality traits reflecting the genetic contribution to the disorder, while individual expressions of these traits reflect maladaptive adaptive mechanisms arising from adverse developmental experiences and resulting dysregulation of the brain's threat management system).

Widiger T. A. , “Personality Disorder and Axis I Psychopathology: The Problematic Boundary of Axis I and Axis II,” Journal of Personality Disorders 17, no. 2 (2003): 90–108.

See DSM, supra note 10, at xxxii-xxxiii, noting that there are “significant risks that diagnostic information will be misused or misunderstood,” at least in part because forensic and legal decision-makers should be “cautioned that a diagnosis does not carry any necessary implications regarding the causes of the individual's mental disorder or its associated impairments” and, most importantly, that a DSM diagnosis “does not carry any necessary implications regarding the individual's degree of control over the behaviors that may be associated with the disorder.”

Gardner D. L. Cowdry R. W. , “Suicidal and Parasuicidal Behavior in Borderline Personality Disorder,” Psychiatric Clinics of North America 8, no. 2 (1985): 389–403 (noting high rates of self-harm in BPD); Grant B. F. Chou S. P. Goldstein R. B. Huang B. Stinson F. S. Saha T. D. Smith S. M. Dawson D. A. , “Prevalence, Correlates, Disability, and Co-Morbidity of DSM-IV Borderline Personality Disorder: Results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions,” Journal of Clinical Psychiatry 69, no. 4 (April 2008): 533–545 (reporting large sample study findings including that “BPD was associated with substantial mental and physical disability, especially among women.”)

Siever L. J. Koenigsberg H. W. , “The Frustrating No-Man's Land of Borderline Personality Disorder,” Cerebrum, The Dana Forum on Brain Science 2, no. 4 (2000) (noting the utility of antipsychotic medication in treatment of disturbances of thought in BPF); Zanarini M. C. Frankenburg F. R. DeLuca C. J. Hennen J. Khera G. S. Gunderson J. G. , “The Pain of Being Borderline: Dysphoric States Specific to Borderline Personality Disorder,” Harvard Review of Psychiatry 6, no. 4 (1998): 201–207 (noting intensity and impairment associated with dysphoric mood in BPD).

See DSM, supra note 10, at 343. Psychotic Disorder NOS (Not Otherwise Specified) is to include “psychotic symptomatology (i.e., delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior) about which there is inadequate information to make a specific diagnosis or about which there is contradictory information, or disorders with psychotic symptoms that do not meet the criteria for any specific Psychotic Disorder.” At p. 688 the DSM-IV-TR notes that for three Personality Disorders that “may be related to the Psychotic Disorders” (Paranoid, Schizoid, Schizotypal), there is “an exclusion criterion stating that the pattern of behavior must not have occurred exclusively during the course of Schizophrenia, a Mood Disorder with Psychotic Features, or another Psychotic Disorder.”

See DSM, supra note 10, at 688–687, advising that a clinician considering a personality disorder should be “cautious” giving a Personality Diagnosis “during an episode of a Mood Disorder or an Anxiety Disorder because these conditions may have cross-sectional symptom features that mimic personality traits,” advising that at Post-traumatic Stress Disorder diagnosis should be considered “after an individual has been exposed to extreme stress,” and that a Personality Disorder should not be awarded instead of a Substance-Related Disorder “based solely on behaviors that are consequences of Substance Intoxication or Withdrawal or that are associated with activities in the service of sustaining a dependency (e.g. antisocial behavior).”

National Institute of Mental Health, Borderline Personality Disorder (NIH Publication No. 01–4928) (reporting that Borderline Personality Disorder often co-occurs with Bipolar Disorder, depressive disorders, anxiety disorders, substance abuse, other personality disorders); see DSM, supra note 10, at 708 notes that persons with Borderline Personality Disorder may “develop psychotic-like symptoms (e.g., hallucinations, body image distortions, ideas of reference, and hypnagogic phenomena) during times of stress.”

See DSM, supra note at 10, at 703–704 indicates that individuals with Antisocial Personality Disorder constitute about 3% in males and 1% in females “may have associated Anxiety Disorders, Depressive Disorders, Substance-Related Disorders, Somatization Disorder, Pathological Gambling, and other disorders of impulse control” as well as criteria for other Personality Disorders.

See Jang K. L. , “The Behavioral Genetics of Psychopathology,” in Classification and Diagnosis (The Phenotypic Structure of Common Mental Disorders) (Mahway, NJ: Lawrence Erlbaum Associates, 2005): Chapter 3, at 52 (noting that the confusion of Axis I and Axis II Disorders by both clinicians and researchers arises from “the failure of existing criterion sets to indicate how personality disorders are to be distinguished effectively from Axis I Disorders. For example, some of the behaviors used to diagnose personality disorders, such as wrist slashing and purging, might be better understood as expressions of a time-limited, circumscribed mood, eating, psychotic, or other disorder rather, rather than as maladaptive personality traits [citations omitted].”)

See DSM, supra note 10, at xxxiii, noting that forensic purposes “a diagnosis does not carry any necessary implications regarding the causes of the individual's mental disorder or its associated impairments” and that “[e]ven when diminished control over one's behavior is a feature of the disorder, having the diagnosis in itself does not demonstrate that a particular individual is (or was) unable to control his or her behavior at a particular time.”

Ordinarily the specific diagnostic origin of a legally relevant functional impairment to criminal responsibility is not crucial as long the impairment(s) it reflects rise to the level of a legally cognizable mental disease, disorder or defect. There are exceptions. For example, the ALI Model Penal Code insanity test has been amended to exclude impairments arising from “sociopathy” or antisocial personality. Whether or not a defendant's impairment arose specifically from acute alcohol or other substance intoxication, and if so, whether that intoxication was voluntary or involuntary may be relevant. Similarly, the “automatism” defense asks whether the defendant's actions arose from epilepsy or some other condition that eliminated the defendant's capacity to know or direct their behavior (e.g., striking somebody while having the automatic muscle movements of a grand mal seizure).

See supra note 37.

See supra note 36.

For example, the prosecutions of Hinkley John Jr. Dahmer Jeffrey White Daniel .

A similar situation arises when mental health expert witnesses offer ultimate opinions on whether a defendant is Competent to Stand Trial. Criminal defendants have a constitutional right to be competent to proceed so that the proceedings against them are fundamentally fair. Arguably, while mental health expertise may educate a court about the capacities and impairments manifested by a defendant that are relevant to an ability to participate in his own defense, “how fair is fair enough” is a social and moral decision and not a legal one. While Courts commonly ask for and then rely upon the opinions of forensic mental health professionals when they opine as to whether or not a defendant is competent to stand trial, arguably there is nothing in training as a mental health professional that grants special expertise in “how much fairness is fair enough” to proceed in a criminal prosecution. A parallel would be asking a nuclear plant design engineer if the calculated risks of a plant meltdown resulting in a range of civilian casualties is worth the amount of electricity the plant would generate: How much risk of mass death is worth how much estimated electricity output is a social and moral decision, not an engineering calculation.

See supra note 4.

See supra note 24.

See Kansas v. Hendricks, 521 U.S. 346 (1997).

See O'Connor v. Donaldson, 422 U.S. 563 (1975), where Chief Justice Burger wrote: “In short, the idea that States may not confine the mentally ill except for the purpose of providing them with treatment is of very recent origin, and there is no historical basis for imposing such a limitation on state power. Analysis of the sources of the civil commitment power likewise lends no support to that notion. There can be little doubt that in the exercise of its police power [422 U.S. 563, 583] a State may confine individuals solely to protect society from the dangers of significant antisocial acts or communicable disease. Cf. Minnesota ex rel. Pearson v. Probate Court, 309 U.S. 270 (1940); Jacobson v. Massachusetts, 197 U.S. 11, 25–29 (1905).”