Professor Murphy's research focuses on the intersection of neuroscience, behavioral science, and law. She writes about the use of neuroscience as evidence and how neuroscience and behavioral science shape public policy and legal systems. Prior to joining UC Hastings, Professor Murphy spent a year as a fellow in the Program in Understanding Law, Science, and Evidence at UCLA Law School. Before that, she practiced law at Munger, Tolles & Olson LLP, handling all aspects of complex commercial litigation, with an emphasis on professional liability and internal investigations. She represented clients in higher education, financial services, and professional services. Her pro bono practice focuses on housing issues and civil rights work addressing homelessness.
Professor Murphy earned her A.B. magna cum laude in Psychology from Harvard University, her Ph.D. in Behavioral Neuroscience and Psychopharmacology from University of Cambridge, Trinity College, as a Gates Cambridge Scholar, and her J.D. from Stanford Law School where she received the Gerald Gunther Prizes in Constitutional Litigation and Professional Responsibility. Prior to law school she was a postdoc with Stanford Law School's Center for Law and the Biosciences as well as the MacArthur Foundation's Law and Neuroscience Project. Following law school, she clerked for the Honorable Richard A. Paez of the U.S. Court of Appeals for the Ninth Circuit. Her recent work has been published in Stanford Law Review, Law & Psychology Review, and Psychology Public Policy & Law.
Areas of Expertise (7)
Stanford Law School: J.D. 2012
University of Cambridge, Trinity College: Ph.D., Behavioral Neuroscience / Psychopharmacology 2007
Harvard University: A.B., Psychology / Mind, Brain, Behavior 2003
Event Appearances (8)
The Enduring Importance of In re Gault: Neuroscience, the Juvenile Brain, and the Law
Youth, Rights & Justice Portland, Oregon
A Question of Fit: Translating Neuroscience for Law, Clinical Care, and Policy.
UCSF / UC Hastings Consortium on Law, Science & Health Policy San Francisco, CA.
Disentitlement as Discrimination, Flash Lecture (Competitive Selection)
International Neuroethics Society Annual Meeting
Experimental Methods in Legal Scholarship Workshop,
UCLA School of Law Los Angeles, CA.
Neuroscience & Evidence: The Science, The Scholarship, The Courtroom, and the Classroom.
AALS Evidence Section
Through a Scanner Darkly: Functional MRI as Evidence of Mental State at Stanford Law School Technology and Law Review Symposium
Cleveland-Marshall College of Law
Neuroscience and Alternative Sentencing Options at California Correctional Crisis Conference
UC Hastings School of Law San Francisco, CA.
Neurolaw: Revolution – and Retreat[?]
UC Irvine Irvine, CA.
Selected Articles (10)
Advances in basic and clinical neuroscience will soon present novel options for prediction, treatment, and prevention of antisocial behavior, particularly drug addiction. These hard-won advances have significant potential to improve public health and safety and increase efficiency in delivery of treatment and rehabilitation. Moreover, such therapies will undoubtedly find a large portion of their target population in the criminal justice system as long as drug possession remains criminalized. Improvements, however, are not without risks. The risks stem not only from the safety and side-effect profile of such treatments, but also from their insertion into a criminal justice and sentencing system that may be overburdened, overpoliticized, undertheorized, and lacking sufficient checks and balances on institutional competency and legitimacy.
Furthermore, as neurological and biological therapies become more targeted and effective, they may threaten to override multi-faceted rehabilitation measures designed to address the social, cultural, economic, and psychological aspects of drug use and involvement with the criminal justice system. While offering substantial therapeutic benefits, such advances might also short-circuit a critical policy discussion about the nature of drug use and its criminalization.
New neuroscience treatments for addiction and antisocial behavior should force a deep examination of the legal, social, political, and ethical roots of drug and problem-solving courts, and particularly the mixed criminal justice/public health model on which they rest. As technologies to control behavior become more direct, targeted, and powerful, so do the risks of their misuse and potential harms to constitutional rights, individual autonomy, institutional competency, and institutional legitimacy.
Recent developments in the neuropsychology of criminal behavior have given rise to concerns that neuroimaging evidence (such as MRI and functional MRI [fMRI] images) could unduly influence jurors. Across four experiments, a nationally representative sample of 1,476 jury-eligible participants evaluated written summaries of criminal cases in which expert testimony was presented in support of a mental disorder as exculpatory. The evidence varied in the extent to which it presented neuroscientific explanations and neuroimages in support of the expert's conclusion. Despite suggestive findings from previous research, we found no evidence that neuroimagery affected jurors' judgments (verdicts, sentence recommendations, judgments of the defendant's culpability) over and above verbal neuroscience-based testimony. A meta-analysis of our four experiments confirmed these findings. In addition, we found that neuroscientific evidence was more effective than clinical psychological evidence in persuading jurors that the defendant's disorder reduced his capacity to control his actions, although this effect did not translate into differences in verdicts.
Previous work has demonstrated a profound effect of N-methyl-D: -aspartic acid receptor (NMDAR) antagonism in the infralimbic cortex (IL) to selectively elevate impulsive responding in a rodent reaction time paradigm. However, the mechanism underlying this effect is unclear.
As with phrenology and the polygraph, society is again confronted with a device that the media claims is capable of reading our minds. Functional magnetic resonance imaging ("fMRI"), along with other types of functional brain imaging technologies, is currently being introduced at various stages of a criminal trial as evidence of a defendant's past mental state. This Article demonstrates that functional brain images should not currently be admitted as evidence into courts for this purpose. Using the analytical framework provided by Federal Rule of Evidence 403 as a threshold to a Daubert/Frye analysis, we demonstrate that, when fMRI methodology is properly understood, brain images are only minimally probative of a defendant's past mental states and are almost certainly more unfairly prejudicial than probative on balance. Careful and detailed explanation of the underlying science separates this Article from others, which have tended to paint fMRI with a gloss of credibility and certainty for all courtroom-relevant applications. Instead, we argue that this technology may present a particularly strong form of unfair prejudice in addition to its potential to mislead jurors and waste the court's resources. Finally, since fMRI methodology may one day improve such that its probative value is no longer eclipsed by its extreme potential for unfair prejudice, we offer a nonexhaustive checklist that judges and counsel can use to authenticate functional brain images and assess the weight these images are to be accorded by fact finders.
This paper explores whether brain images may be admitted as evidence in criminal trials under Federal Rule of Evidence 403, which weighs probative value against the danger of being prejudicial, confusing, or misleading to fact finders. The paper summarizes and evaluates recent empirical research relevant to these issues. We argue that currently the probative value of neuroimages for criminal responsibility is minimal, and there is some evidence of their potential to be prejudicial or misleading. We also propose experiments that will directly assess how jurors are influenced by brain images.
Impulsivity is a core deficit of a number of neuropsychiatric disorders including attention-deficit hyperactivity disorder (ADHD), anti-social conduct disorder and drug addiction. Recent research has highlighted the multifaceted nature of impulsivity and the myriad of putative neural and psychological mechanisms thought to underpin behavioural syndromes of impaired self-control. Here we report a novel conceptualisation of impulsivity based on 'waiting' and 'stopping' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction. Rats selected for high levels of impulsivity on a reaction time task analogous to the continuous performance test in humans exhibited correspondingly high levels of impulsive decision-making on a delay-of-reward task. The same rats, however, were unimpaired on a stop-signal task requiring inhibition of an already initiated motor response. The specific nature of this deficit in 'waiting impulsivity' was confirmed by unimpaired acquisition of appetitive Pavlovian conditioning, a putative ancillary measure of impulsive behaviour. These findings are significant in light of recent evidence linking impulsivity in rats to high levels of cocaine self-administration and development of compulsive cocaine seeking behaviour. We thus suggest that an inability to bridge delays to future rewards and reward-related stimuli is a candidate behavioural endophenotype that pre-disposes to clinical psychopathology.
Neuromarketing is upon us. Companies are springing up to offer their clients brain-based information about consumer preferences, purporting to bypass focus groups and other marketing research techniques on the premise that directly peering into a consumer's brain while viewing products or brands is a much better predictor of consumer behavior. These technologies raise a range of ethical issues, which fall into two major categories: (1) protection of various parties who may be harmed or exploited by the research, marketing, and deployment of neuromarketing and (2) protection of consumer autonomy if neuromarketing reaches a critical level of effectiveness. The former is straightforward. The latter may or may not be problematic depending upon whether the technology can be considered to so effectively manipulate consumer behavior such that consumers are not able to be aware of the subversion. We call this phenomenon stealth neuromarketing. Academics and companies using neuromarketing techniques should adopt a code of ethics, which we propose here, to ensure beneficent and non-harmful use of the technology in consideration of both categories of ethics concerns.
The core and shell subregions of the nucleus accumbens receive differential projections from areas of the medial prefrontal cortex that have dissociable effects on impulsive and perseverative responding. The contributions of these subregions to simple instrumental behaviour, inhibitory control and behavioural flexibility were investigated using a 'forced choice' task, various parameter manipulations and an omission schedule version of the task. Post-training, selective core lesions were achieved with microinjections of quinolinic acid and shell lesions with ibotenic acid. After a series of behavioural task manipulations, rats were re-stabilized on the standard version of the task and challenged with increasing doses of d-amphetamine (vehicle, 0.5 or 1.0 mg/kg i.p. 30 min prior to test). Neither core- nor shell-lesioned rats exhibited persistent deficits in simple instrumental behaviour or challenges to behavioural flexibility or inhibitory control. Significant differences between lesion groups were unmasked by d-amphetamine challenge in the standard version of the forced task. Core lesions potentiated and shell lesions attenuated the dose-dependent effect of d-amphetamine on increasing anticipatory responses seen in sham rats. These data imply that the accumbens core and shell subregions do not play major roles in highly-trained task performance or in challenges to behavioural control, but may have opposed effects following d-amphetamine treatment. Specifically, they suggest the shell subregion to be necessary for dopaminergic activation driving amphetamine-induced impulsive behaviour and the core subregion for the normal control of this behaviour via conditioned influences.
The application of neuroimaging technology to the study of the injured brain has transformed how neuroscientists understand disorders of consciousness, such as the vegetative and minimally conscious states, and deepened our understanding of mechanisms of recovery. This scientific progress, and its potential clinical translation, provides an opportunity for ethical reflection. It was against this scientific backdrop that we convened a conference of leading investigators in neuroimaging, disorders of consciousness and neuroethics. Our goal was to develop an ethical frame to move these investigative techniques into mature clinical tools. This paper presents the recommendations and analysis of a Working Meeting on Ethics, Neuroimaging and Limited States of Consciousness held at Stanford University during June 2007. It represents an interdisciplinary approach to the challenges posed by the emerging use of neuroimaging technologies to describe and characterize disorders of consciousness.
Stimulant addiction is often linked to excessive risk taking, sensation seeking, and impulsivity, but in ways that are poorly understood. We report here that a form of impulsivity in rats predicts high rates of intravenous cocaine self-administration and is associated with changes in dopamine (DA) function before drug exposure. Using positron emission tomography, we demonstrated that D2/3 receptor availability is significantly reduced in the nucleus accumbens of impulsive rats that were never exposed to cocaine and that such effects are independent of DA release. These data demonstrate that trait impulsivity predicts cocaine reinforcement and that D2 receptor dysfunction in abstinent cocaine addicts may, in part, be determined by premorbid influences.