The idea of machines overcoming humans can be intrinsically related to conscious machines. Surpassing humans would mean replicating, reaching and exceeding key distinctive properties of human beings, for example, high-level cognition associated with conscious perception. However, can computers be compared with humans? Can computers become conscious? Can computers outstrip human capabilities? These are paradoxical and controversial questions, particularly because there are many hidden assumptions and misconceptions about the understanding of the brain. In this sense, it is necessary to first explore these assumptions and then suggest how the specific information processing of brains would be replicated by machines. Therefore, this article will discuss a subset of human capabilities and the connection with conscious behavior, secondly, a prototype theory of consciousness will be explored and machines will be classified according to this framework. Finally, this analysis will show the paradoxical conclusion that trying to achieve conscious machines to beat humans implies that computers will never completely exceed human capabilities, or if the computer were to do it, the machine should not be considered a computer anymore.
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Glt 121 Theory Pdf Free
First we summarize the evidence for the transient fluctuations in task performance of individuals with ADHD, and the inadequacy of current explanations to account for the short time scales involved. Our hypothesis, introduced initially by Todd and Botteron [13], is then elaborated with evidence for important elements of the theory. Finally we outline strategies for testing the hypothesis and discuss its theoretical and clinical significance.
Reaction time variability is reduced with appropriate monetary reward [45], but such rewards are not differentially effective for children with ADHD. The reason for this may be that reinforcers may be less effective for tasks requiring continual responses to rapid, externally-paced stimuli than for subject-paced (free-operant) responding [68]. The reason for this is probably that reinforcers work on free-operant behaviour, but not on instructed behaviour typical in tasks requiring continual responses to rapid, externally-paced stimuli (cf., [68]). Methylphenidate medication improves accuracy, speeds reaction time, and reduces reaction time variability in individuals with ADHD [35, 58]. Moreover, methylphenidate has been shown to improve time on-task, with concomitant decreases in the number of shifts in attention as the task progressed [67]. Such treatment effects suggest that the increased availability of extra-neuronal catecholamines arising from the blockade of their uptake by methylphenidate could lead to increased activity of noradrenaline at β-adrenoceptors and possibly also dopamine acting at D1 receptors found on astrocytes [15, 69]. A key fact is that stimulation of α1- and β-adrenoceptors on astrocytes enhances glycolysis and lactate production [69]. Dopamine acting on D1 receptors may have similar effects, but these are not well documented.
The dynamic developmental theory of ADHD [8, 9, 20] explains intra-individual behavioural variability as deficient acquisition of stimulus control of long chains of behaviour. This deficiency is rooted in reduced efficacy of reinforcers ("rewards") combined with poorer extinction ("unlearning") of inefficient behaviour. The dynamic developmental theory addresses free-operant behaviour without time constraints. However, neither the dynamic developmental theory of ADHD, nor other theories and explanations account for the intra-individual performance variability of ADHD on tasks that require continual responses to rapid, externally-paced stimuli. The present paper addresses this aspect by postulating that reaction time variability and other manifestations of transient fluctuations in performance, which arise in the context of the need for continuous rapid neuronal firing, reflect the effects of transient depletion of neuronal energy on the efficiency of information processing.
PKU results from high concentrations of phenylalanine (Phe), that arise from an inability to convert it into tyrosine, and which inhibit transport across the blood brain barrier of neutral amino acids such as tyrosine and tryptophan necessary for the synthesis of the three principle monoamine transmitters. If children are placed on Phe-free diet early enough, microcephaly, mental retardation and motor problems can be avoided, although sub-clinical symptoms may remain, particularly in the cognitive domain [183, 184]. Children with PKU (off-diet) are rated by parents and teachers as more distractible, hyperactive, and impulsive than healthy controls [185], with many symptoms similar to ADHD (e.g. restlessness, fidgeting, concentration difficulty, short attention span, low frustration tolerance [186]). Realmuto et al. [187] noted that 9/13 of their subjects either manifested or had a history of comorbidity with ADHD. Prenatal exposure was associated with a higher likelihood of expressing hyperactive/impulsive symptoms and postnatal exposure was associated with a higher likelihood of expressing inattentive symptoms [188]. Indeed, a considerable proportion of people with treated PKU take psychostimulant medication for their attentional problems (e.g. 26% of a sample of 38 school-aged children with PKU [189]).
The hypothesis H1 implies that myelinated and unmyelinated axons will be affected differently. Non-myelinated axons are less efficient than myelinated axons and we predict that they may be more vulnerable to the lactate deficiency. Interestingly this would target non-myelinated nigrostriatal, mesocortical and mesolimbic dopamine projections, among others, which would affect the development of their target structures including striatum, prefrontal cortex and hippocampus. Compromised dopamine neuronal firing could account for decreased dopamine function in target areas as proposed by Sagvolden et al [20] in the dynamic developmental theory of ADHD. Drugs used to treat ADHD, such as methylphenidate, block the dopamine transporter and can thereby enhance the dopamine signal without requiring increased firing of dopamine neurons.
One proposal attributes many features of ADHD to problems with the regulation of 'state' that affects the allocation of 'energy' and 'effort' [274, 275]. Based on the "cognitive-energetic" model of Sanders [276] they define state regulation as the allocation of extra effort to defend performance in the presence of stressors such as high presentation rates of stimuli. Whereas CNS activation normally increases with event-rates, long inter-event intervals engender a sub-optimal hypoactivation in people with ADHD, who then are unable to recruit the necessary effort to adjust appropriately to the demands of the situation. Activation can be viewed as a state of readiness in selectively targeting possible outcomes of behaviour: The monitoring of input, endogenous interactions and feedback are involved. Effort is viewed as a process necessary for coupling and re-coupling input-information, neuronal modules and activational processes [277]. Our hypothesis is broadly consistent with this 'state-regulation' theory, but elaborates details of its potential physiological basis, and that in turn is specifically directed to account for intra-individual variability of performance on sustained demand. The distinction with our formulation lies with a) our emphasis on coping with high energy demands rather than a state of hypoactivation at low event-rates, and b) our prediction that the consequences of impaired lactate shuttle function lie with reduced rapid neuronal firing when that is required, and the delayed development of myelination. We do not predict a generalized 'state of activation' as described by Sergeant and van der Meere [274, 275].
Our hypothesis overlaps with the explanations offered by Sonuga-Barke [278] and Sagvolden et al. [20]. Sonuga-Barke's dual pathway theory invokes a role for the mesocortical dopamine system in modulating (deficient) dorsal fronto-striatal glutamatergic mediation of some executive functions. It also envisages a role for the mesolimbic dopamine system in the anomalously functioning reward and motivation-influencing circuits of the more ventral frontal-accumbens glutamatergic system [107]. The mesolimbic role is often associated with the preference of ADHD subjects for immediate rather than delayed rewards. This relates to the dynamic developmental theory of Sagvolden et al., which concentrates on the registration of reinforcement and related motivational consequences, in particular, a mesolimbic impairment of the "efficiency with which the contingency between present action and future rewards is signalled". In ADHD research there is widespread agreement that there is a reduction in the control by future rewards of current behaviour, and an increase in the extent to which they are discounted (i.e., a steeper delay of reward gradient). Sagvolden et al. also extend their theory to impaired function of the ascending nigrostriatal and mesocortical dopamine pathways.
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