Four main developments have stirred discussion and debate in neuroethics this past year: commercialization of lie detection, proposals to use deep brain stimulation for treating depression, advances in the genetic understanding of addiction, and improvements in brain imaging for diagnostic purposes.
Commercialization of Lie Detection
In recent years, advances in the ability to use functional magnetic resonance imaging (fMRI) to map activity in different brain regions fueled research into using the technology for detecting lies. And though the research is still preliminary and the results problematic, two companies have rushed to develop fMRI-based lie-detection products and services: Cephos Corporation and No Lie MRI. The companies say potential uses include crime investigations, parole and child-custody hearings, counterintelligence, and insurance and government security interrogations.
In 2007, the American Journal of Law and Medicine published a paper, coauthored by Henry Greely of Stanford and Judy Illes, now of the University of British Columbia, that analyzed existing research on fMRI-based lie detection and made an urgent call for regulation.1 The authors argue that while the technology is promising, the existing studies do not prove it to be reliable with any accuracy in the real world, particularly given the artificial and trivial nature of the lies tested in these experiments.
What’s more, none of these small-scale studies have been replicated by outside investigators, nor did the studies look at the possibility of subjects’ using countermeasures to outwit the lie detectors. The authors’ proposed regulatory scheme, modeled after the way the FDA controls the use of drugs, would require marketers of lie-detection technology to prove that it is accurate and effective based on large-scale trials. Under this system, marketing the technology without regulatory approval would be illegal.
Illes also coauthored (with Margaret Eaton of Stanford) a commentary in the April 2007 Nature Biotechnology discussing some of the ethical, social, and policy issues associated with the commercialization of cognitive neurotechnology in general.2 These concerns include accuracy, brain privacy and confidentiality, and potential conflicts of interest for the people bringing these technologies to market.
One danger of an unregulated lie-detection industry is the exploitation of the most vulnerable members of the population, such as those suffering from neurologic or psychiatric disorders. Yet our society seems so eager for lie-detection devices that many people are quick to accept claims that they work, the authors stress.
Deep Brain Stimulation for Severe Depression
Following the success of using deep brain stimulation (DBS) to treat physical symptoms of Parkinson’s, and following imaging research that identified a specific brain region involved in depression that might be treated with deep brain stimulation, researchers began clinical trials of this technique in a small number of patients with intractable depression. Findings of remarkable symptomatic relief in many of these surgical patients were published in 2005, but in 2007 the treatment began to receive ethical scrutiny.
Given the relative newness of using deep brain stimulation, even for treating Parkinson’s disease, researchers are learning more about unanticipated risks. In June 2007, Acta Neuropsychiatrica published a case report documenting how slight adjustments in the electrode contact or voltage in two Parkinson’s patients induced life-threatening (suicidal) depression.3
Questions of safety are always important, but people tend to accept significant risk in treating debilitating and sometimes deadly diseases such as Parkinson’s, researchers say. Depression is far more controversial: some patient advocacy groups believe it is overdiagnosed; some say that even if it is real sufferers should learn to cope with it, and still others cite the existence of many antidepressant drugs.
However, deep brain stimulation is meant for intractable depression, the sort that doesn’t respond to drugs. And, lacking effective treatment, patients can be debilitated and are sometimes at risk for suicide. Deep brain stimulation for depression and other clinical uses currently lacks clinical-trial guidelines, and in 2007 a group of leading DBS researchers participated in a consensus development meeting to draft guidelines for experimental use of DBS in patients.
Another ethical concern is informed consent. The impaired cognition and desperation that can accompany severe depression may greatly compromise patients’ judgment. Hovering over the whole debate is the specter of electroconvulsive shock therapy, whose therapeutic benefits are not disputed, but whose use remains enormously controversial.
Genetic Underpinnings of Addiction
Several scholarly articles on genes that may underlie addiction were published in 2007. For example, Colin Haile and colleagues published an article titled “Genetics of Dopamine and Its Contribution to Cocaine Addiction” in Behavior Genetics.4 Joel Gelernter and colleagues published “Genomewide Linkage Scan for Nicotine Dependence: Identification of a Chromosome 5 Risk Locus,” which appeared in Biological Psychiatry.5
For alcoholism, according to a commentary by Charles O’Brien6 published in the November 2007 issue of Addiction, there is increasing evidence that a variant of the gene for the brain’s mu opiate receptor is associated with increased sensitivity to alcohol euphoria, increased risk of alcoholism, increased risk of opiate addiction, and good clinical response to the drug naltrexone for alcoholism in clinical trials.
Evidence suggesting that genes predispose some individuals to addictive behaviors raises ethical questions. One set of questions revolves around testing. If certain genes contribute to addiction but don’t determine it with certainty, should we test for them at all? How much predictive power, or value for selecting a treatment, must the genes have before we do decide to test for them? How early should testing begin? Learning that a child is prone to nicotine addiction, for example, might enable parents to take necessary precautions, such as extra education and protection from cigarette ads—or this knowledge might lead to overparenting and unnecessary parental anxiety. Knowing about one’s own propensity toward addiction also could become a self-fulfilling prophecy. Additionally, knowledge of predisposing genes, once addiction is diagnosed, would be valuable in selecting the most appropriate treatment.
Counseling raises additional questions: What should a doctor say to a parent whose child has genes that make the child more likely to become a smoker, alcoholic, or heroin addict? The question becomes even thornier if genetic information is available in utero; some parents might reconsider whether they want the pregnancy.
Advance knowledge of propensity toward addiction also raises questions of whether anti-addictive drugs (such as naltrexone) should be given prophylactically, before addiction actually develops. Given the high costs of treating addiction, prospective employers and insurance companies might have a strong vested interest in testing—and could discriminate against carriers of the genes. (Laws currently do prevent unauthorized disclosure of genetic information to insurers and employers.)
Social stigma is another consideration, just as for any genetic abnormality. Mere carriers may have a harder time finding marriage and reproductive partners, and parents may feel guilty for passing on bad genes, even if the child shows no sign of actual addiction. Discussion around these questions is bound to heat up as we learn more about the genetic risk factors for addiction.
Brain Imaging for Diagnostic Purposes
While the use of brain imaging for diagnosing most psychiatric disorders is still a distant prospect, there were strides in 2007 in the experimental use of specific imaging compunds that may identify people with early Alzheimer’s and other forms of dementia. In August 2007, Agneta Nordberg published a review article in Current Opinion in Neurology7 discussing a new amyloid imaging technique using positron emission tomography that shows clear differences between the brains of Alzheimer’s patients and healthy controls. This study suggests that early diagnosis of Alzheimer’s disease may be possible. Similarly, a case study published in the March 2007 issue of the Archives of Neurology8 reported successful use of the imaging agent Pittsburgh Compound B to spot mild cognitive impairment.
Studies such as these give hope that imaging will help provide more precision for diagnosing anxiety disorders and autism spectrum disorders, once the biological bases of these disorders are better understood. But the hottest area in the search for better diagnosis is with limited states of consciousness, especially in accurately differentiating people who are in a permanent vegetative state from those who are in a minimally conscious state.
While no major technical strides were made in this area in 2007, the ethical framework continued to develop. In June, Judy Illes and Joseph Fins led a well-attended workshop at Stanford University, “Ethics, Neuroimaging, and Limited States of Consciousness,” at which scholars discussed these issues. They reached agreement on several aspects of them, including research and clinical goals for carrying out neuroimaging studies of patients in limited states of consciousness, concerns about obtaining informed consent or authorization for such studies, and experimental protocols such as ethically coherent approaches to selecting candidates and designing tests. A special issue of American Journal of Bioethics Neuroscience dedicated to this topic is forthcoming.
But even as neuroethicists reach consensus on these questions, and although imaging will undoubtedly continue to improve, researchers and clinicians continue to debate the much trickier questions of how to interpret the brain images and what their prognostic value is in patients with disorders of consciousness. In an April article in Neurology, Joseph Fins, Nicholas Schiff, and Kathleen Foley recommended trying to define the epidemiology of the minimally conscious state, clarify mechanisms of recovery, and identify clinically useful diagnostic and prognostic markers to aid decision making at the bedside.9
1. Greely HT, and Illes J. Neuroscience-based lie detection: The urgent need for regulation. American Journal of Law and Medicine 2007 33(2 and 3):377–431.
2. Eaton ML, and Illes J. Commercializing cognitive neurotechnology: The ethical terrain. Nature Biotechnology 2007 25(4):393–397.
3. Balash Y, Merims D, and Giladi N. Suicidal thoughts in patients with Parkinson's disease treated by deep brain stimulation of the subthalamic nuclei: Two case reports and review of the literature. Acta Neuropsychiatrica 2007 19(3):208–210.
4. Haile CN, Kosten TR, and Kosten TA. Genetics of dopamine and its contribution to cocaine addiction. Behavior Genetics 2007 37(1):119–145.
5. Gelernter J, Panhuysen C, Weiss R, Brady K, Poling J, Krauthammer M, Farrer L, and Kranzler HR. Genomewide linkage scan for nicotine dependence: Identification of a chromosome 5 risk locus. Biological Psychiatry 2007 61(1):119–126.
6. O'Brien C. Treatment of addiction in the era of genomic medicine. Addiction 2007 102(11):1697–1699.
7. Nordberg A. Amyloid imaging in Alzheimer's disease. Current Opinion in Neurology 2007 20(4):398–402.
8. Bacskai BJ, Frosch MP, Freeman SH, Raymond SB, Augustinack JC, Johnson KA, Irizarry MC, Klunk WE, Mathis CA, Dekosky ST, Greenberg SM, Hyman BT, and Growdon JH. Molecular imaging with Pittsburgh Compound B confirmed at autopsy: A case report. Archives of Neurology 2007 64(3):315–316.
9. Fins JJ, Schiff ND, and Foley KM. Late recovery from the minimally conscious state: Ethical and policy implications. Neurology 2007 68(4):304–307.
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