Procedural Learning and Neostyrial Dysfunction in Man

Saint‐Cyr, Jean A.; Taylor, Ann E.; Lang, Anthony E.

doi:10.1093/brain/111.4.941

Cited by 508 publications

(260 citation statements)

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“…Although some lesion and recording studies in the rabbit have suggested striatal involvement in eyeblink conditioning (14,15), the nature of that involvement has not been clarified and may be a fruitful area for investigation in rabbits and humans. However, the striatum has been implicated as critical for other procedural learning tasks in humans and other animals (42)(43)(44)(45). Spatial resolution was insufficient to determine whether the areas of significant correlation included the basal forebrain region as well as the ventral striatum.…”

Section: Resultsmentioning

confidence: 99%

Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography.

Logan

Grafton

1995

Proc. Natl. Acad. Sci. U.S.A.

244

125

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Relative cerebral glucose metabolism was examined with positron-emission tomography (PET) as a measure of neuronal activation during performance of the classically conditioned eyeblink response in 12 young adult subjects. Each subject received three sessions: (i) a control session with PET scan in which unpaired presentations of the tone conditioned stimulus and corneal airpuff unconditioned stimulus were administered, (ii) a paired training session to allow associative learning to occur, and (iii) a paired test session with PET scan. Brain regions exhibiting learningrelated activation were identified as those areas that showed significant differences in glucose metabolism between the unpaired control condition and well-trained state in the 9 subjects who met the learning criterion. Areas showing significant activation included bilateral sites in the inferior cerebellar cortex/deep nuclei, anterior cerebellar vermis, contralateral cerebellar cortex and pontine tegmentum, ipsilateral inferior thalamus/red nucleus, ipsilateral hippocampal formation, ipsilateral lateral temporal cortex, and bilateral ventral striatum. Among all subjects, including those who did not meet the learning criterion, metabolic changes in ipsilateral cerebellar nuclei, bilateral cerebellar cortex, anterior vermis, contralateral pontine tegmentum, ipsilateral hippocampal formation, and bilateral striatum correlated with degree of learning. The localization to cerebellum and its associated brainstem circuitry is consistent with neurobiological studies in the rabbit model of eyeblink classical conditioning and neuropsychological studies in braindamaged humans. In addition, these data support a role for the hippocampus in conditioning and suggest that the ventral striatum may also be involved.Eyeblink conditioning is a basic form of associative learning that has been studied extensively in humans since the 1930s. Animal models of this form of conditioning have demonstrated close behavioral parallels with human conditioning, lending support to the hypothesis that the learning shares common neurobiological substrates in humans and other mammals (1). Eyeblink conditioning is well-suited for neurobiological analyses because the use of appropriate unpaired control procedures can help distinguish between areas of the brain that are responding to the sensory stimuli or the motor response and those that are selectively activated under paired learning conditions. This feature makes the paradigm an ideal candidate for neurobiological analysis in humans using positron-emission tomography (PET) to identify regions of the brain that are specifically activated under paired training conditions relative to unpaired control procedures.Although eyeblink conditioning is a seemingly simple form of learning, under normal conditions it appears to involve the interaction of diverse brain systems. Neurobiological studies (conducted primarily in rabbits) have identified the cerebellum and its brainstem connections as essential components of the eyeblink condit...

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Section: Resultsmentioning

confidence: 99%

Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography.

Logan

Grafton

1995

Proc. Natl. Acad. Sci. U.S.A.

244

125

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“…(For the sake of simplicity, below we also refer to the system as the "procedural system".) The system underlies aspects of rule-learning (Knowlton et al, 1996;Poldrack et al, 1999), and is particularly important for acquiring and performing skills involving sequences -whether the sequences are serial or abstract, or sensori-motor or cognitive (Aldridge and Berridge, 1998;Boecker et al, 2002;Graybiel, 1995;Jenkins et al, 1994;Saint-Cyr et al, 1988;Willingham, 1998). Acquisition of the procedures is gradual, in that learning occurs on an ongoing basis during multiple trials.…”

Section: The Procedural Memory Systemmentioning

confidence: 99%

Specific Language Impairment is not Specific to Language: the Procedural Deficit Hypothesis

Ullman

Pierpont

2005

Cortex

677

751

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Specific Language Impairment (SLI) has been explained by two broad classes of hypotheses, which posit either a deficit specific to grammar, or a non-linguistic processing impairment. Here we advance an alternative perspective. According to the Procedural Deficit Hypothesis (PDH), SLI can be largely explained by the abnormal development of brain structures that constitute the procedural memory system. This system, which is composed of a network of inter-connected structures rooted in frontal/basal-ganglia circuits, subserves the learning and execution of motor and cognitive skills.Crucially, recent evidence also implicates this system in important aspects of grammar. The PDH posits that a significant proportion of individuals with SLI suffer from abnormalities of this brain network, leading to impairments of the linguistic and non-linguistic functions that depend on it. In contrast, functions such as lexical and declarative memory, which depend on other brain structures, are expected to remain largely spared. Evidence from an in-depth retrospective examination of the literature is presented. It is argued that the data support the predictions of the PDH, and particularly implicate Broca's area within frontal cortex, and the caudate nucleus within the basal ganglia. Finally, broader implications are discussed, and predictions for future research are presented. It is argued that the PDH forms the basis of a novel and potentially productive perspective on SLI. INTRODUCTIONSpecific Language Impairment (SLI) is generally defined as a developmental disorder of language in the absence of frank neurological damage, hearing deficits, severe environmental deprivation, or mental retardation (for diagnostic definitions and prevalence of SLI, see Bishop, 1992;Leonard, 1998;Tomblin et al., 1997). Other terms have also been used to label such children, including developmental dysphasia, language impairment, language learning disability, developmental language disorder, delayed speech and deviant language (Leonard, 1998;Ahmed et al., 2001). Several factors have complicated attempts to provide a unified theory of SLI, or even of subgroups of SLI. First, despite the standard use of exclusionary criteria to diagnose SLI, the disorder is clearly not limited to language.Rather the linguistic impairments co-occur with a number of non-linguistic deficits, including impairments of motor skills and working memory, and with other disorders, such as Attention Deficit Hyperactivity Disorder (Hill, 2001;Leonard, 1998;Tirosh and Cohen, 1998). Second, even though SLI must be a consequence of some sort of neural dysfunction, the neural correlates of the disorder have been largely ignored. This potentially valuable information could provide important constraints on explanatory accounts of the disorder. Third, SLI is a classification that is quite heterogeneous (Leonard, 1998;Stromswold, 2000). Surveys document variation within and across subgroups in the particular aspects of language that are affected and in the types of co-occurring no...

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“…Neurological evidence, such as data from fMRI imaging studies, suggests that the basal ganglia implement procedural learning (Ashby & Waldron, 2000;Saint-Cyr, Taylor, & Lang, 1988) and theorists have proposed that these learning processes can be mapped onto the operations of the procedural module in ACT-R (Anderson, Qin, Sohn, Stenger, & Carter, 2003).…”

Section: Procedural Modulementioning

confidence: 99%

ACT-R/E: An Embodied Cognitive Architecture for Human-Robot Interaction

Trafton

Hiatt

Harrison

et al. 2013

JHRI

147

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We present ACT-R/E (Adaptive Character of Thought-Rational / Embodied), a cognitive architecture for human-robot interaction. Our reason for using ACT-R/E is two-fold. First, ACT-R/E enables researchers to build good embodied models of people to understand how and why people think the way they do. Then, we leverage that knowledge of people by using it to predict what a person will do in different situations; e.g., that a person may forget something and may need to be reminded or that a person cannot see everything the robot sees. We also discuss methods of how to evaluate a cognitive architecture and show numerous, empirically validated examples of ACT-R/E models.

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Procedural Learning and Neostyrial Dysfunction in Man

Cited by 508 publications

References 0 publications

Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography.

Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography.

Specific Language Impairment is not Specific to Language: the Procedural Deficit Hypothesis

ACT-R/E: An Embodied Cognitive Architecture for Human-Robot Interaction

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