Noncompliant Insanity: Does It Fit with Insanity?

George Maliha, Note, Noncompliant Insanity: Does It Fit Within Insanity?, 41 J.L. & Pub. Pol’y 647 (2018).

Abstract: In 1973, Herb Mullin was convicted of murdering thirteen people in Santa Cruz County, California. Before that fateful moment, Mullin had drifted between involuntary commitment, clinical improvement, noncompliance with medications, and release. His vacillation between treatment compliance and noncompliance is sadly typical. Mullin–as far as we can tell-never realized that he was ill and often refused treatment. One author described Mullin as “refus[ing] to take medication because prophets of God did not need it. Even today he continues to refuse [medication], convinced nothing is wrong with him. He even wonders whether it was the [medication] he took during his initial hospitalization that caused his homicidal behavior.” Indeed, around half of people suffering from schizophrenia do not realize that they are suffering from an illness and accordingly resist treatment.

The question is what to do about that other half if they commit a crime–that is, those who realize that they have an illness yet still refuse treatment. A classic problem in nearly every introductory criminal law course is what to do with an epileptic defendant who fails to take his medication or a defendant who consumes a substance that predisposes him to commit a crime. The case of a schizophrenic defendant is slightly different. On the one hand, when defendants have insight into their disease and “voluntarily” choose not to take medication, allowing them to plead the insanity defense seems counterintuitive. Indeed, “there is no explicit fault category in the law that we could call something like ‘self-induced insanity’ or ‘voluntary insanity.”’ On the other hand, that same defendant is suffering from a psychosis at the time of the crime. In essence, the question is how far back judicial inquiry should extend. Complicating this analysis is a growing body of research that suggests that psychiatric disease can affect many cognitive functions–even those not associated with delusions or psychoses.

This Note seeks to explore the question of insanity caused by an omission, namely failure to take medication. Part I will briefly describe the problem of noncompliance and lack of insight in psychiatric illness, focusing on schizophrenia. Part II will look at the limited judicial interaction with this problem, starting with the recent case of Commonwealth v. Shin. Although there are few cases that attempt to grapple with the problem head-on, the rising awareness of mental illness and its potential effects on blameworthiness may soon change that. In any event, the issue lies under the surface in many cases. Part III will consider how far back the inquiry into insanity should extend. This Part will conclude that the mental processes surrounding noncompliance require further elucidation. Part IV, however, will try to solve–or at least re-channel–this empirical question by exploring potential analogies from other areas of criminal law. A conclusion will follow that argues that courts should maintain the status quo for now–and confine the insanity inquiry to the events directly surrounding the  crime. But, as the neuroscience around treatment compliance develops, courts may need to reexamine their approach.

Andrea Yates: A Continuing Story About Insanity

Denno, Deborah W., Andrea Yates: A Continuing Story About Insanity (January 1, 2017). The Insanity Defense: Multidisciplinary Views on Its History, Trends, and Controversies 367- 416 (Mark D. White, ed. 2017) (Cal.: Praeger); Fordham Law Legal Studies Research Paper No. 2909041. Available at SSRN:

Abstract: In 2001, Andrea Yates did the unthinkable: she drowned her five children one by one in a bathtub within the course of minutes. She immediately confessed and explained that she killed them because she under the influence of Satan did not want them to be “tortured by Satan” as she was. Despite the defense uncovering evidence of Yates’ history of postpartum depression and psychosis, the jury did not accept her insanity defense and convicted her of capital murder with a sentence of life in prison. Influential in this decision was the testimony of prosecution expert Dr. Park Dietz, who pushed the view that Yates had rationally planned the murders. Dietz’s testimony was troubling, not only because there was little, if any, empirical basis for his conclusions, but because the defense discovered that he had introduced false testimony during the trial. During cross-examination, Dietz explained that he was a consultant for Law & Order and that one episode aired prior to Yates’ crime involving a woman with postpartum depression who drowned her children in a bathtub and was found insane. Yet the defense discovered no such show existed. Even though a grand jury found Dietz innocent of perjury, the defense appealed Yates’ sentence. Given the degree of Dietz’s impact on the jury, the Texas Court of Appeals reversed the judgment and remanded the case. In this second trial in 2006, Yates was no longer eligible for the death penalty and much more information had been uncovered regarding Yates’ mental condition. The jury unanimously found Yates not guilty by reason of insanity. While the Yates case helped to inform the world of the pervasiveness of postpartum depression and psychosis, no substantive changes have been made in Texas insanity law. This chapter explains how the state’s definition of insanity influenced the first trial and both constrained and confused how the jury could view Yates’ actions.


Forensic Practitioners’ Expectations and Moral Views Regarding Neurobiological Interventions in Offenders with Mental Disorders

Specker, J., Focquaert, F., Sterckx, S. et al., Forensic Practitioners’ Expectations and Moral Views Regarding Neurobiological Interventions in Offenders with Mental Disorders, BioSocieties (2017).

Cortical Thinning, Functional Connectivity, and Mood-Related Impulsivity in Schizophrenia: Relationship to Aggressive Attitudes and Behavior by Matthew J. Hoptman, Daniel Antonius, Cristina J. Mauro, Emily M. Parker, and Daniel C. Javitt, The American Journal of Psychiatry (2014)


A robust association was found in patients with schizophrenia between cortical thinning in ventral prefrontal regions and increased impulsivity, which likely reflects an impaired interaction with regions affecting cognitive control regions. As urgency plays a key role in aggression in people with schizophrenia, behavioral and neural targets may be found for interventions for remediation.

Aggression in schizophrenia is a major societal issue, leading to physical harm, stigmatization, patient distress, and higher health care costs. Impulsivity is associated with aggression in schizophrenia, but it is multidetermined. The subconstruct of urgency is likely to play an important role in this aggression, with positive urgency referring to rash action in the context of positive emotion, and negative urgency referring to rash action in the context of negative emotion.

The authors examined urgency and its neural correlates in 33 patients with schizophrenia or schizoaffective disorder and 31 healthy comparison subjects. Urgency was measured using the Urgency, Premeditation, Perseverance, and Sensation-Seeking scale. Aggressive attitudes were measured using the Buss-Perry Aggression Questionnaire.

Positive urgency, negative urgency, and aggressive attitudes were significantly and selectively elevated in schizophrenia patients (Cohen’s d values, 1.21–1.50). Positive and negative urgency significantly correlated with the Aggression Questionnaire total score (r>0.48 in all cases) and each uniquely accounted for a significant portion of the variance in aggression over and above the effect of group. Urgency scores correlated with reduced cortical thickness in ventral prefrontal regions including the right frontal pole, the medial and lateral orbitofrontal gyrus and inferior frontal gyri, and the rostral anterior cingulate cortex. In patients, reduced resting-state functional connectivity in some of these regions was associated with higher urgency.

These findings highlight the key role of urgency in aggressive attitudes in people with schizophrenia and suggest neural substrates of these behaviors. The results also suggest behavioral and neural targets for interventions to remediate urgency and aggression. Read the full article.

“Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies” by Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Molecular Genetics of Schizophrenia Consortium, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin, C. Robert Cloninger, and Igor Zwir, The American Journal of Psychiatry (2014)


The authors sought to demonstrate that schizophrenia is a heterogeneous group of heritable disorders caused by different genotypic networks that cause distinct clinical syndromes.

In a large genome-wide association study of cases with schizophrenia and controls, the authors first identified sets of interacting single-nucleotide polymorphisms (SNPs) that cluster within particular individuals (SNP sets) regardless of clinical status. Second, they examined the risk of schizophrenia for each SNP set and tested replicability in two independent samples. Third, they identified genotypic networks composed of SNP sets sharing SNPs or subjects. Fourth, they identified sets of distinct clinical features that cluster in particular cases (phenotypic sets or clinical syndromes) without regard for their genetic background. Fifth, they tested whether SNP sets were associated with distinct phenotypic sets in a replicable manner across the three studies.

The authors identified 42 SNP sets associated with a 70% or greater risk of schizophrenia, and confirmed 34 (81%) or more with similar high risk of schizophrenia in two independent samples. Seventeen networks of SNP sets did not share any SNP or subject. These disjoint genotypic networks were associated with distinct gene products and clinical syndromes (i.e., the schizophrenias) varying in symptoms and severity. Associations between genotypic networks and clinical syndromes were complex, showing multifinality and equifinality. The interactive networks explained the risk of schizophrenia more than the average effects of all SNPs (24%).

Schizophrenia is a group of heritable disorders caused by a moderate number of separate genotypic networks associated with several distinct clinical syndromes. Read the full article.

“Prefrontal Cortical Dendritic Spine Pathology in Schizophrenia and Bipolar Disorder” by Glenn T. Konopaske, Nicholas Lange, Joseph T. Coyle, and Francine M. Benes, JAMA Psychiatry (2014)

Importance: Prior studies have demonstrated reduced dendritic spine density in the dorsolateral prefrontal cortex (DLPFC) in schizophrenia. However, it remains unclear how generalizable this finding is in schizophrenia and if it is seen in bipolar disorder, a historically distinct psychiatric condition.

Objective: To assess whether spine loss is present in the DLPFC of individuals with schizophrenia and individuals with bipolar disorder.

Design, Setting, and Participants: This study used postmortem human brain tissue from individuals with schizophrenia (n = 14), individuals with bipolar disorder (n = 9), and unaffected control participants (n = 19). Tissue samples containing the DLPFC (Brodmann area 46) were Golgi-stained, and basilar dendrites of pyramidal cells in the deep half of layer III were reconstructed.

Main Outcomes and Measures: The number of spines per dendrite, spine density, and dendrite length were compared across groups. We also assessed for the potential effects of clinical and demographic variables on dendritic parameters.

Results: The mean (SD) spine density was significantly reduced (ie, by 10.5%) in individuals with bipolar disorder (0.28 [0.04] spines/μm) compared with control participants (0.31 [0.05] spines/μm) (P = .02). In individuals with schizophrenia, the mean (SD) spine density was also reduced (by 6.5%; 0.29 [0.03] spines/μm) but just missed significance when compared with control participants (P = .06). There was a significant reduction in the mean (SD) number of spines per dendrite in both individuals with schizophrenia (72.8 [24.9] spines per dendrite) and individuals with bipolar disorder (68.9 [12.9] spines per dendrite) compared with controls (92.8 [31.1] spines per dendrite) (individuals with schizophrenia vs controls: 21.6% reduction [P = .003]; individuals with bipolar disorder vs controls: 25.8% reduction [P = .005]). In addition, both individuals with schizophrenia and individuals with bipolar disorder had a reduced mean (SD) dendrite length (246.5 [67.4] and 245.6 [29.8] μm, respectively) compared with controls (301.8 [75.1] μm) (individuals with schizophrenia vs controls: 18.3% reduction [P = .005]; individuals with bipolar disorder vs controls: 18.6% reduction [P = .005]).

Conclusions and Relevance: Dendritic spine loss in the DLPFC was seen in both individuals with schizophrenia and individuals with bipolar disorder, suggesting that the 2 disorders may share some common pathophysiological features. Read the full article.

“Biological Insights from 108 Schizophrenia-Associated Genetic Loci” by the Schizophrenia Working Group of the Psychiatric Genomics Consortium, Nature (2014)

Abstract: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia. Read the full article.


“A Practitioner’s Guide to Defending Capital Clients Who Have Mental Disorders and Impairments” by Anne James and Matthew Cross (2006)

Abstract: This manual focuses on the issues arising solely in the representation of persons with mental disorders and impairments in death penalty cases. It does not address the legal excuses for criminal responsibility, the various affirmative defenses such as not guilty by reason of insanity or diminished capacity, available in both capital and non-capital contexts. Clearly, the assertion of such defenses implicates myriad strategic considerations in death penalty cases—most notably, how to resolve the inherent conflict between offering mental health evidence as an excuse in the first phase of a trial and then, if it is rejected for that purpose, arguing that the same evidence is not an excuse, but a reason to spare an individual’s life. In most jurisdictions, insanity defenses may also expose the client to early discovery of defense work product and a wide-ranging evaluation by a prosecution expert. It is simply beyond the scope of this manual to discuss these complex legal and strategic questions. Instead, the manual focuses on the issues unique to capital cases (especially mitigation evidence). Competency questions are addressed because of the unusual ways in which they implicate every phase of capital litigation. Read the full guide.


“Recovery From ‘Schizophrenia’: One Man’s Journey From Patient to Therapist” by Allen Frances, The Huffington Post (2014)

This article describes the story of James Hickman, a licensed clinical social worker, psychotherapist, and mental health advocate who was able to overcome poverty, orphanhood, and schizophrenia. Excerpts from Hickman’s memoir, The Mindful Son: A Beacon of Hope Through the Storm of Mental Illness, are included. Read the full article.