The fallacy beneath the base rate fallacy is that we know what a base rate is. We talk as if base rates and individuating information were two different kinds of information. From a Bayesian perspective, however, the only difference between base rate and individuating information is – which comes first.

Any instance (i.e., event, behavior, trait) belongs to infinitely many reference classes, hence there are infinitely many base rates from which to choose. People clearly do not entertain all possible reference classes, however, so something must be limiting the search space. We suggest some possible mechanisms that determine which reference class is evoked for the purpose of judgment and decision.

Koehler is right that base rate information is used, to various degrees, both in laboratory tasks and in everyday life. However, it is not time to turn our backs on laboratory tasks and focus solely on ecologically valid decision making. Tightly controlled experimental data are still needed to understand how base rate information is used, and how this varies among groups.

Consistent with Koehler's position, we propose a generalization of the base rate fallacy and earlier conservatism literatures. In studies using both traditional tasks and new tasks based on ecologically valid base rates, our subjects typically underweight individuating information at least as much as they underweight base rates. The implications of cue consistency for averaging heuristics are discussed.

Base rates are vital in predicting violent criminal recidivism. However, both lay people given simulated prediction tasks and professionals milking real life predictions appear insensitive to variations in the base rate of violent recidivism. Although there are techniques to help decision makers attend to base rates, increased decision accuracy is better sought in improved actuarial models as opposed to improved clinicians.

When base rates are learned and used in an experiential manner subjects show better base rate use, perhaps because the implicit learning system is engaged. A causal framework in which base rates are relevant might also be necessary. Humans might thus perform better on more ecologically valid tasks, which are likely to contain those three components.

This commentary presents a self-assessment inventory that will allow readers to determine their own attitude toward the base rate fallacy and its literature. The inventory is scientifically valid but not Medicare/Medicaid reimbursable.

Koehler's summary and critique of research on the base rate fallacy is cogent and persuasive. However, he may have overstated the case, and his suggestions for future research may be too restrictive. We agree that methodological approaches to this topic should be broadened, but we argue that experimental laboratory research and the Bayesian normative standard are useful and should not be abandoned.

(1) The miscitations of seminal experiments in the base rate literature adds to the existing database of systematic miscitations of wellknown psychological experiments. These miscitations may be caused by a process of reconstructive remembering. (2) Representative design should be the methodological core of Koehler's call for ecologically valid research. This approach can benefit both basic and applied research.

Base rates have no necessary relation to judgments that are not themselves probabilities. There is no logical imperative, for instance, that behavioral base rates must affect causal attributions or that base rate information should affect judgments of legal liability. Decision theorists should be cautious in arguing that base rates place normative constraints on judgments of anything other than posterior probabilities.

Commentators agree that simple conclusions about a general base rate fallacy are not appropriate. It is more constructive to identify conditions under which base rates are differentially weighted. Commentators also agree that improving the ecological validity of the research is desirable, although this is less important to those interested exclusively in psychological processes. The philosophers and ecologists among the commentators offer a kinder perspective on base rate reasoning than the psychologists. My own perspective is that the interesting questions (both psychological and normative/prescriptive) are best answered through empirical studies that use real-world performance standards.

Redundancy of the motor control system is an important feature that gives the central control structures options for solving everyday motor problems. The choice of particular control patterns is based on priorities (coordinative rules) that are presently unknown. Motor patterns observed in unimpaired young adults reflect these priorities. We hypothesize that under certain atypical conditions, which may include disorders in perception of the environment and in decision making, structural or biochemical changes within the central nervous system (CNS), and/or structural changes of the effectors, the central nervous system may reconsider its priorities. A new set of priorities will reflect the current state of the system and may lead to different patterns of voluntary movement. Under such conditions, changed motor patterns should be considered not pathological but rather adaptive to a primary disorder and may even be viewed as optimal for a given state of the system of movement production. Therapeutic approaches should not be directed toward restoring the motor patterns to as close to “normal” as possible but rather toward resolving the original underlying problem. We illustrate this approach using, as examples, movements in amputees, in patients with Parkinson's disease, in patients with dystonia, and in persons with Down syndrome.

Changes in anticipatory postural adjustment following below-the-knee amputation may be considered as adaptive for reacquiring balance control.

Latash & Anson's explanation of bradykinesia in patients with Parkinson's disease and cocontraction in dystonic patients is intriguing. However, the proposed adaptive changes in the central nervous system do not fit well with both clinical and experimental evidence of motor impairment in these patients. In particular, we question the explanation of: (1) the role of postural reactions and spatial accuracy in bradykinesia, (2) certain abnormalities during the execution of sequential and simultaneous movements, (3) the sudden changes in mobility (ON and OFF) of Parkinsonian patients, and (4) the meaning of reflex circuitry changes in dystonia.

The commentary focuses on the need for motor control modeling as a rationale for rehabilitation. We give examples in a bimanual unloading task and examine the potential consequences for recovery in patients with cerebral lesions. Hierarchical models of motor control lead to a distinction between “task optimization” and “motor optimization” and to a qualifier on Latash & Anson's “hands-off” position.

“Normal movements” in atypical populations address the question of postural control: Voluntary movement is a perturbation of body balance and cannot be executed without a convenient counterperturbation. Despite a change in the postural program in relation to the impairment (Parkinson's disease, paraplegia), the performance level is decreased. Movements are not “normal,” owing to a reduction in posturokinetic capacity.

Latash & Anson's contention that movement patterns that are different from those typically observed in persons without impairments should not be considered abnormal and usually should not be corrected is consistent with Davis & Burton's Ecological Task Analysis (ETA). Extending from the ETA concept of performer-scaled performance measures, the use of Froude numbers may offer insight into the global dynamics of a person's action system.

Adaptive motor patterns that emerge after a neuromusculoskeletal lesion reflect not only the primary lesion, but also the dynamic characteristics of the musculoskeletal linkage and environment in which the action is performed. Although these patterns may be optimal, they may also be ineffective as goal-directed actions; effectiveness may only be regained if training addresses primary deficits and ensures practice without gross biomechanical adaptations.

Latash & Anson argue that changed motor patterns should not be viewed as pathological. Instead, they should be viewed as adaptations to a primary deficit. We argue that the evidence shows: (1) bradykinesia is not an adaptation to a different primary deficit, and (2) bradykinetic movements are not “normal” slowed movements but, to the contrary, bradykinesia is part of the pathophysiology of Parkinson's disease.

We agree with Latash & Anson that therapeutic approaches should be directed toward solving the underlying problem, not toward adapting the abnormal to normal behaviour. The fundamental obstacle, however, is that doing so requires a solution of the “equivalence problem” in movement control.