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some disadvantages to this approach as well. The training and assessment of animals carrying out cognitive tasks is considerably more difficult than for similar studies in humans, and making deliberate lesions in the brains of healthy animals, particularly non-human primates, can raise ethical concerns. Nevertheless, the use of carefully controlled brain lesions in experimental animals has provided useful information complementing that derived from neuropsychological studies in humans. Lesion studies, whether in humans or in animals, also present problems of interpretation. The mammalian brain is a highly interconnected structure. If one area of the brain is lesioned, other areas of the brain innervated by the damaged area may, from the loss of input, also cease to function normally. Such effects, known as diaschisis, can lead to wrongly attributing the lost functionality to the lesioned area rather than to the downstream area. Another possible misinterpretation of lesion findings is that damage to a cortical area can also damage nearby fiber tracts, thereby disrupting the function of more distant areas. Nevertheless, clinical-pathological correlation studies remain highly informative in cognitive neuroscience. Their continued relevance has been greatly augmented by modern neuroimaging methods that allow brain lesions to be localized with considerable precision in living patients who are still available for detailed behavioral testing. Such knowledge of the exact site of a lesion can inform and guide the behavioral testing in a far more focused way than when the definitive localization of the lesion could be attained only postmortem. Such modern methods of imaging brain structure, particularly those using magnetic resonance imaging (MRI), are fundamental to cognitive neuroscience; they are described in Box 2A. Other sorts of imaging techniques, such as the MRI-based technique of diffusion tensor imaging (DTI), are being used to delineate the structural connections of the brain (Box 2B). Pharmacological perturbations Another way of perturbing cognitive function in the brain is via pharmacological manipulation. As described in the Appendix, signaling between neurons involves the release of and response to neurotransmitter molecules at synapses. Many drugs interfere with or augment these processes and can thereby change cognitive functions. Cognitive neuroscientists have taken advantage of psychoactive drugs such as caffeine, cocaine, antidepressants, and a host of others to gain insight into the neuropharmacology of these functions, both in humans and in experimental animals. Pharmacological studies in humans have taken two main forms. The first approach is to examine the influence of chronic drug use or abuse on cognitive processes, taking advantage of the unfortunate prevalence of these social problems and the disorders they cause. An example is the set of cognitive impairments apparent in cocaine addicts, which include changes in reward evaluation (i.e., a person’s ability to properly assess the positive or negative value of events and behaviors). Impaired reward evaluation in turn affects the ability to make self-protective decisions and to formulate and pursue successful life strategies. Cocaine and other drugs of abuse lead to specific changes in neurotransmission in the brain systems that underlie these functions. Cocaine specifically activates dopamine receptors, altering the physiology of the dopamine system, which is known to play a major role in reward evaluation (see Chapter 14). Although the dysfunction that leads to addiction is still not completely understood, the altered sense of reward associated both with the cocaine “high” and with cocaine addiction is clear. Chronic use leads to drug tolerance (i.e., the need for increasing amounts of the drug in order to achieve the same pharmacological effect), which results in further negative consequences. (On a less problematic level, this sort of pharmacological adaptation is familiar to habitual coffee