The nature and treatment of stuttering as revealed by fMRI A within- and between-group comparison

This article reviews some of our recent functional magnetic resonance imaging (fMRI) studies of stuttering. Using event-related fMRI experiments, we investigated brain activation during speech production. Results of three studies comparing persons who stutter (PWS) and persons who do not stutter (PWNS) are outlined. Their findings point to a region in the right frontal operculum (RFO) that was consistently implicated in stuttering. During overt reading and before fluency shaping therapy, PWS showed higher and more distributed neuronal activation than PWNS. Immediately after therapy differential activations were even more distributed and left sided. They extended to frontal, temporal, and parietal regions, anterior cingulate, insula, and putamen. These over-activations were slightly reduced and again more right sided two years after therapy. Left frontal deactivations remained stable over two years of observation, and therefore possibly indicate a dysfunction. After therapy, we noted higher activations in persons who stutter moderately than in those who stutter severely. These activations might reflect patterns of compensation. We discuss why these findings suggest that fluency-inducing techniques might synchronize a disturbed signal transmission between auditory, speech motor planning, and motor areas.

Educational objectives: The reader will learn about and be able to: (1) identify regions of brain activations and deactivations specific for PWS; (2) describe brain activation changes induced by fluency shaping therapy; and (3) discuss the correlation between stuttering severity and brain activation.     

Cortical localisation of the visual and auditory word form areas: a reconsideration of the evidence

In this paper we examine the evidence for human brain areas dedicated to visual or auditory word form processing by comparing cortical activation for auditory word repetition, reading, picture naming, and environmental sound naming. Both reading and auditory word repetition activated left lateralised regions in the frontal operculum (Broca's area), posterior superior temporal gyrus (Wernicke's area), posterior inferior temporal cortex, and a region in the mid superior temporal sulcus relative to baseline conditions that controlled for sensory input and motor output processing. In addition, auditory word repetition increased activation in a lateral region of the left mid superior temporal gyrus but critically, this area is not specific to auditory word processing, it is also activated in response to environmental sounds. There were no reading specific activations, even in the areas previously claimed as visual word form areas: activations were either common to reading and auditory word repetition or common to reading and picture naming. We conclude that there is no current evidence for cortical sites dedicated to visual or auditory word form processing.     

Anterograde Episodic Memory in Korsakoff Syndrome

A profound anterograde memory deficit for information, regardless of the nature of the material, is the hallmark of Korsakoff syndrome, an amnesic condition resulting from severe thiamine (vitamin B1) deficiency. Since the late nineteenth century when the Russian physician, S. S. Korsakoff, initially described this syndrome associated with "polyneuropathy," the observed global amnesia has been a primary focus of neuroscience and neuropsychology. In this review we highlight the historical studies that examined anterograde episodic memory processes in KS, present a timeline and evidence supporting the myriad theories proffered to account for this memory dysfunction, and summarize what is known about the neuroanatomical correlates and neural systems presumed affected in KS. Rigorous study of KS amnesia and associated memory disorders of other etiologies provide evidence for distinct mnemonic component processes and neural networks imperative for normal declarative and nondeclarative memory abilities and for mnemonic processes spared in KS, from whence emerged the appreciation that memory is not a unitary function. Debate continues regarding the qualitative and quantitative differences between KS and other amnesias and what brain regions and neural pathways are necessary and sufficient to produce KS amnesia.     

Severity of dysfluency correlates with basal ganglia activity in persistent developmental stuttering

Previous studies suggest that anatomical anomalies [Foundas, A. L., Bollich, A. M., Corey, D. M., Hurley, M., & Heilman, K. M. (2001). Anomalous anatomy of speech-language areas in adults with persistent developmental stuttering. Neurology, 57, 207-215; Foundas, A. L., Corey, D. M., Angeles, V., Bollich, A. M., Crabtree-Hartman, E., & Heilman, K. M. (2003). Atypical cerebral laterality in adults with persistent developmental stuttering. Neurology, 61, 1378-1385; Foundas, A. L., Bollich, A. M., Feldman, J., Corey, D. M., Hurley, M., & Lemen, L. C. et al., (2004). Aberrant auditory processing and atypical planum temporale in developmental stuttering. Neurology, 63, 1640-1646; Jancke, L., Hanggi, J., & Steinmetz, H. (2004). Morphological brain differences between adult stutterers and non-stutterers. BMC Neurology, 4, 23], in particular a reduction of the white matter anisotropy underlying the left sensorimotor cortex [Sommer, M., Koch, M. A., Paulus, W., Weiller, C., & Buchel, C. (2002). Disconnection of speech-relevant brain areas in persistent developmental stuttering. Lancet, 360, 380-383] could be at the origin of persistent developmental stuttering (PDS). Because neural connections between the motor cortex and basal ganglia are implicated in speech motor functions, PDS could also be associated with a dysfunction in basal ganglia activity [Alm, P. (2004). Stuttering and the basal ganglia circuits: a critical review of possible relations. Journal of Communication Disorders, 37, 325-369]. This fMRI study reports a correlation between severity of stuttering and activity in the basal ganglia and shows that this activity is modified by fluency shaping therapy through long-term therapy effects that reflect speech production improvement. A model of dysfunction in stuttering and possible repair modes is proposed that accommodates the data presented here and observations previously made by us and by others.     

Cortical oscillations and sensory predictions

Many theories of perception are anchored in the central notion that the brain continuously updates an internal model of the world to infer the probable causes of sensory events. In this framework, the brain needs not only to predict the causes of sensory input, but also when they are most likely to happen. In this article, we review the neurophysiological bases of sensory predictions of "what' (predictive coding) and 'when' (predictive timing), with an emphasis on low-level oscillatory mechanisms. We argue that neural rhythms offer distinct and adapted computational solutions to predicting 'what' is going to happen in the sensory environment and 'when'.     

Constructing formal semantics from an ontological perspective. The case of second-order logics

In a first part, I defend that formal semantics can be used as a guide to ontological commitment. Thus, if one endorses an ontological view \(O\) and wants to interpret a formal language \(L\) , a thorough understanding of the relation between semantics and ontology will help us to construct a semantics for \(L\) in such a way that its ontological commitment will be in perfect accordance with \(O\) . Basically, that is what I call constructing formal semantics from an ontological perspective. In the rest of the paper, I develop rigorously and put into practice such a method, especially concerning the interpretation of second-order quantification. I will define the notion of ontological framework: it is a set-theoretical structure from which one can construct semantics whose ontological commitments correspond exactly to a given ontological view. I will define five ontological frameworks corresponding respectively to: (i) predicate nominalism, (ii) resemblance nominalism, (iii) armstrongian realism, (iv) platonic realism, and (v) tropism. From those different frameworks, I will construct different semantics for first-order and second-order languages. Notably I will present different kinds of nominalist semantics for second-order languages, showing thus that we can perfectly quantify over properties and relations while being ontologically committed only to individuals. I will show in what extent those semantics differ from each other; it will make clear how the disagreements between the ontological views extend from ontology to logic, and thus why endorsing an ontological view should have an impact on the kind of logic one should use.     

Which processes are involved in cognitive procedural learning?

Procedural memory is characterised by a relative resistance to pathology, making its assessment of the utmost importance. However, few studies have looked at the cognitive processes involved in cognitive procedural learning. In an initial experiment, we studied the role of different cognitive functions in massed cognitive procedural learning. Our results confirmed the existence of three separate learning phases and, for the first time, demonstrated the involvement of episodic memory and executive functions in the first learning phase. In a second experiment, we studied the effect of distributed learning conditions on the dynamics of procedural learning. This second study confirmed our results but showed that these conditions slow down the process of cognitive procedural learning. Our overall findings call into question the status of functionally autonomous memory system that is currently allotted to procedural memory, and suggest that the role of nonprocedural cognitive components should be taken into account in patient rehabilitation.     

Which processes are involved in cognitive procedural learning?

Procedural memory is characterised by a relative resistance to pathology, making its assessment of the utmost importance. However, few studies have looked at the cognitive processes involved in cognitive procedural learning. In an initial experiment, we studied the role of different cognitive functions in massed cognitive procedural learning. Our results confirmed the existence of three separate learning phases and, for the first time, demonstrated the involvement of episodic memory and executive functions in the first learning phase. In a second experiment, we studied the effect of distributed learning conditions on the dynamics of procedural learning. This second study confirmed our results but showed that these conditions slow down the process of cognitive procedural learning. Our overall findings call into question the status of functionally autonomous memory system that is currently allotted to procedural memory, and suggest that the role of nonprocedural cognitive components should be taken into account in patient rehabilitation.     

Cortical plasticity associated with stuttering therapy

Neuroimaging studies have indicated that persistent developmental stuttering (PDS) may be associated both with an abnormality in white matter of left-hemispheric speech areas and a right-hemispheric hyperactivity. The latter may compensate for the deficient structural connectivity in the left hemisphere. To investigate the effects of stuttering therapy on brain activity nine male adults with PDS underwent functional magnetic resonance imaging (fMRI) before and within 12 weeks after fluency shaping therapy. Brain response differences during overt sentence reading before and after therapy were assessed by utilizing random effects analyses. After therapy, a more widespread activation was observed in frontal speech and language regions and temporal areas of both hemispheres, particularly and more pronounced on the left side. Interestingly, distinct posttreatment left-sided activation increases were located directly adjacent to a recently detected area of white matter anomaly [M. Sommer, M.A. Koch, W. Paulus, C. Weiller, C. Buchel (2002). Disconnection of speech-relevant brain areas in persistent developmental stuttering. The Lancet, 360, 380-383] suggesting that fluency shaping techniques reorganize neuronal communication between left-sided speech motor planning, motor execution, and temporal areas. Hence, a therapeutic mechanism can be assumed to remodel brain circuitry close to the source of the dysfunction instead of reinforcing compensation via homologous contralateral brain networks. EDUCATIONAL OBJECTIVES: The reader will learn about and be able to: (1) describe brain activation changes detected shortly after fluency-shaping therapy; (2) identify left-hemispheric regions where a (re)functionalization after fluency-shaping therapy seems to occur adjacent to a recently described abnormal white matter region in PDS subjects; and (3) discuss how an effective cerebral compensation mechanism for stuttering could work.     

Contributions of Studies on Alcohol Use Disorders to Understanding Cerebellar Function

Neuropathological, neuropsychological, and neuroimaging studies of human alcoholism provide evidence for degradation of frontal, pontine, thalamic, and cerebellar brain sites and disturbed associated functions. Current studies using neuroimaging combined with examination of executive functions, traditionally considered the sole purview of the frontal lobes, have identified a role for the cerebellum serving as a compensatory processing adjunct to enable normal performance on challenging tasks tapping executive functions. This overview proposes that disruption of an executive frontocerebellar network is a major contributor to characteristic behaviors of alcoholism that, on the one hand, enable alcohol use disorders, and on the other hand, lead to compensation for dysfunctions in alcoholism traditionally considered frontally-based.