95 posts · 78,469 views

News and views on the neural organization of language

Greg Hickok
94 posts

Sort by: Latest Post, Most Popular

View by: Condensed, Full

August 18, 2011
02:00 PM
562 views

Mirror Neuron Forum - some additional discussion - Part II

by Greg Hickok in Talking Brains

In my answer to Question 1 I suggested that mirror neurons can be viewed analogously to canonical neurons, that is, as a sensory-motor association system involved in action selection, not action understanding. Here is Gallese's response to this suggestion:

According to GH, both classes of neurons instantiate the action-oriented coding typical of the dorsal stream, whereas object and action semantics would be exclusively provided by the ventral stream. However, an exclu- sive action-oriented characterization of the dorsal stream falls short of explaining the functional role exerted by the ventral part of the dorsal stream (the ventro-dorsal stream) that reci- procally connects cortical areas of the inferior parietal lobe to ventral premotor areas (see Gallese, 2000, 2007a, 2007b; see also Rizzolatti & Gallese, 2006; Rizzolatti & Matelli, 2003). The meaning we attribute to objects is not exclusively the out- come of their visual description as instantiated by extra-striate visual areas within the ventral stream. That is, objects are not merely identified and recognized by virtue of their physical ‘‘appearance’’ but also in relation to the effects of the potential interaction with an agent...

Here is the problem with Gallese's counter-argument: it's not an argument at all. He states that my idea "falls short of explaining the functional role exerted by the ventral part of the dorsal stream" which I take to be spelled out in his next statement that "The meaning we attribute to objects is not exclusively the outcome of their visual description..." Gallese is describing his hypothesis, not an observation that needs explanation. Basically what Gallese is saying is that my view falls short of matching what he thinks is going on. The "argument" structure is: GH proposes Function A for the system. VG proposes Function B. Function A does not include Function B. Therefore Function A is wrong. Obviously, this is not an argument and should be disregarded.

What we need instead is to discuss how well the two hypotheses account for the available data. Is there any evidence that suggests that monkeys (remember this question is about MNs in monkeys) fail to understand objects or actions when the dorsal stream is damaged? No. All we have is evidence that cells in the dorsal stream fire both during movements directed at objects and during observation of actions or objects. Correlation does not imply causation as we all know so there is no direct evidence for Gallese's claim. Do we have direct evidence for my claim? Well, object recognition deficits can be induced by disruption of ventral visual areas (e.g., see the classic work by Ungerleider and Mishkin) and while not direct, the fact that the response properties of cells in the ventral stream have the right features for object and action recognition (specificity, invariant to size, etc.) is consistent with my proposal. In other words, there are empirical reasons why the "standard view" of dorsal and ventral stream function in the monkey visual system is what it is.

The predictable response from Gallese et al. will be that yes, the ventral stream is good at recognition but this recognition is devoid of true meaning. Again, this is a non-argument in that all it is, is a counter-hypothesis that is not supported empirically in the macaque. This is where the argument slips into human data as we'll see in Gallese's next point. (But I thought there was no reason to assume human and macaque systems would be doing the same thing Vittorio?)

Gallese, V., Gernsbacher, M., Heyes, C., Hickok, G., & Iacoboni, M. (2011). Mirror Neuron Forum Perspectives on Psychological Science, 6 (4), 369-407 DOI: 10.1177/1745691611413392... Read more »

Gallese, V., Gernsbacher, M., Heyes, C., Hickok, G., & Iacoboni, M. (2011) Mirror Neuron Forum. Perspectives on Psychological Science, 6(4), 369-407. DOI: 10.1177/1745691611413392

August 16, 2011
07:27 PM
622 views

Mirror Neuron Forum - Some additional discussion - Part I

by Greg Hickok in Talking Brains

Now that people have had a chance to digest the recently published "Mirror Neuron Forum" (Perspectives on Psychological Science 6(4) 369–407) I think it would be useful to revisit some of the claims and counter-claims. I will start working through some of the points in a series of posts. Of course, my focus will be on the parts of the forum that I participated in, but if you have some comments and thoughts on any part of it, feel free to email me and I'll post it as "guest post".

I would like to get the forum participants involved in this less formal discuss. I hope they will join in and of course, I will happy post anything from my co-forum participants.

Question 1: Do Mirror Neurons in Macaques or Humans Make an Important Contribution to Action Understanding?

I suggested in my answer to this question that if we have reason to question the role of macaque mirror neurons (MNs) in action understanding then we have reason to question the role of the mirror system in humans in action understanding and the various functions to which the system has been generalized.

Here is Gallese's response to my point:

VG. I will respond to some of the points raised by GH. First, the major premise of his initial argument is debatable. Accord- ing to GH, if one can question the relevance of MNs to action understanding in monkeys, then this would automatically jeopardize any conclusion about the role of MNs in human social cognition. Why? Do we assume that a given trait or neural mechanism found in different species must necessarily preserve identical characteristics? Evolutionary theory patently contradicts this assumption.

Gallese is right, of course. There is no reason to assume that a given system's function will be preserved evolutionarily. It is perfectly legitimate to assess the empirical merits of theories of MN function in macaque separately from the empirical merits of theories of the so-called mirror system function in humans; they may have very different functions, a point I made in my Eight Problems paper (it was problem #4). However, this is not how many people, including Gallese's group, have approached the two systems. Rather, theories of the function of the human mirror system has been built on the foundation of the MN theory of action understanding in macaques. Consider the abstract from one of Gallese's highly influential papers:

How do we understand other people's behavior? How can we assign goals, intentions, or beliefs to the inhabitants of our social world? A possible way to answer these challenging questions is to adopt an evolutionary frame of reference, both in phylogenetical and ontogenetical terms, envisaging these ‘mind-reading' capacities as rooted in antecedent, more ‘ancient' and simple mechanisms. This approach can capitalize on the results of different fields of investigation: neurophysiology can investigate the neural correlates of precursors of these mechanisms in lower species of social primates such as macaque monkeys. Developmental psychology can study how the capacity to attribute propositional attitudes to others develops.
In the present article we will propose that humans' mind-reading abilities rely on the capacity to adopt a simulation routine. This capacity might have evolved from an action execution/observation matching system whose neural correlate is represented by a class of neurons recently discovered in the macaque monkey premotor cortex: mirror neurons (MNs). Gallese and Goldman, 1998

So the logic is:
-MNs in macaques perform motor simulation/action recognition during observation
-humans posses a parallel motor simulation system (an assumption not mentioned in the abstract but on that gets its own section in the paper)
-therefore, mind-reading is evolutionarily built on this motor simulation function of MNs.

The point in my response to the MN Forum question was that if macaque MNs are not doing motor simulation/action recognition then the standard argument put forward by Gallese and others needs to be re-evaluated. Why? Because the logic of the argument in Gallese and Goldman, for example, would become this:

-MNs in macaques are NOT performing motor simulation/action understanding during observation
-humans posses a parallel system that may or may not be performing motor simulation/action understanding during observation
*therefore, mind-reading is evolutionarily built on this motor simulation function of macaque MNs -- Oops, doesn't follow! (neither did it follow logically above either, but here it is a larger stretch to even attempt the linkage).

Practical point: Gallese and others have used the claimed function of macaque mirror neurons to develop theories of the neural basis of everything from speech perception to mind-reading in humans. This is a reasonable approach. But if we learn that macaque mirror neurons are doing something else, then by the same approach -- i.e., to "adopt an evolutionary frame of reference, both in phylogenetical and ontogenetical terms" and to "capitalize on the results of different fields of investigation" -- we need to reconsidered our theories of the human mirror system.

References

Gallese, V., Gernsbacher, M.A., Heyes, C., Hickok, G., & Iacoboni, M. (2011). Mirror neuron forum. Perspectives on Psychological Science, 6, 369–407.

Gallese V, & Goldman A (1998). Mirror neurons and the simulation theory of mind-reading. Trends in cognitive sciences, 2 (12), 493-501 PMID: 21227300
... Read more »

Gallese V, & Goldman A. (1998) Mirror neurons and the simulation theory of mind-reading. Trends in cognitive sciences, 2(12), 493-501. PMID: 21227300

June 10, 2011
09:54 PM
377 views

Movement goals and feedback control in speech production

by Greg Hickok in Talking Brains

I just finished reading an excellent review article by Joseph Perkell, titled Movement goals and feedback and feedforward control mechanisms in speech production. If you want a nice survey of behavioral speech production research from the motor control perspective (as opposed to the psycholinguistic perspective), this should definitely be on your reading list. In the review, Perkell argues a few different points. One is that the goals, or targets, of speech production are sensory. I agree completely. Another is that there are two kinds of sensory targets, auditory and somatosensory. Again, I agree completely. He makes some interesting observations regarding differences between vowels and consonants, suggesting that the targets for vowels are predominantly auditory whereas the targets for most consonants are largely somatosensory. I kind of agree with this one. An alternative way of stating this generalization might be that the auditory system is more interested in syllables, vowels being syllabic units all on their own, and the somato system is more interested in sub-syllabic units, i.e., consonants, particularly stops. I'm working on a version of this general idea in a forthcoming pub. Stay tuned...Related to the auditory goal point, Perkell reviews an interesting body of data suggesting that one's auditory acuity for a particular phonemic contrast is correlated with the sharpness of one's own articulation for that contrast. Cool stuff. Here's the one thing I disagree with in the whole paper. Perkell writes, "it is widely believed that once speech is acquired and has matured, it operates almost entirely under feedforward control". This is an assumption of the DIVA model promoted by the Guenther/Perkell group. I like the DIVA model, but I think it is wrong in this (and a couple other) respects. The idea of feedforward control is that the system learns, via overt feedback and correction mechanisms, the motor routines necessary for hitting sensory targets. Once learned, speech production involves activating these motor programs. If something goes wrong, the only way to catch it is via overt feedback. In other words, there is no internal forward prediction/correction mechanism.There is a simple argument against this position: conduction aphasia. Conduction aphasics have nothing wrong with their auditory targets. They have normal speech perception and can readily detect errors in their own speech. They do not have a motor articulatory problem either. Much of their speech is fluent and accurate. However, they make phonemic errors more often than control subjects do. A natural explanation of this is that conduction aphasics have a damaged internal correction mechanism (Hickok et al. 2011). They can activate the learned motor programs, they can activate the auditory targets, but if something goes wrong in the motor programming, they can't generate an internal forward prediction and correct the error before it is spoken, thus their speech error rate goes up relative to individuals with an intact system. This is one aspect of the DIVA model that needs to be updated. Perkell, J. (2010). Movement goals and feedback and feedforward control mechanisms in speech production Journal of Neurolinguistics DOI: 10.1016/j.jneuroling.2010.02.011Hickok G, Houde J, & Rong F (2011). Sensorimotor integration in speech processing: computational basis and neural organization. Neuron, 69 (3), 407-22 PMID: 21315253... Read more »

Perkell, J. (2010) Movement goals and feedback and feedforward control mechanisms in speech production. Journal of Neurolinguistics. DOI: 10.1016/j.jneuroling.2010.02.011

Hickok G, Houde J, & Rong F. (2011) Sensorimotor integration in speech processing: computational basis and neural organization. Neuron, 69(3), 407-22. PMID: 21315253

May 18, 2011
06:17 PM
714 views

Two new ways the mirror system claim is losing steam

by Greg Hickok in Talking Brains

Next week Giacomo Rizzolatti will give the Keynote Address at the 23rd annual meeting of the Association for Psychological Science. According to the published abstract of the talk... he will discuss the limits of the mirror mechanism in understanding other people. He will stress that the parieto-frontal mirror mechanism is, however, the only mechanism that allows a person to understand others’ actions from the inside, giving the observing individual a first-person grasp of other individuals’ motor goals and intentions.As is clear from this quote and from recent publications by Rizzolatti and colleagues (e.g., Rizzolatti & Sinigaglia, 2010), the Parma group is reining in their original claim that mirror neurons are the basis of action understanding, period. Now the mirror system has a much more restricted role in which the system allows understanding "from the inside". It's still not at all clear to me that this concept actually does any work, but even granting this point, it is worth noting that mirror neurons are only responsible for understanding actions that the observer knows how to perform. This is a highly restricted domain of function when considering the range of actions that one needs to understand yet has no experience executing. For example, I've never actually punched someone in the face, but I need to be able to recognize and understand such an action should I see it (and I believe that I can do so). Similarly, I've never coiled, but I can understand the intensions of a coiled snake. I've never reached for a holstered gun, but if saw such an action, I'd know what it meant. So what does understanding from the inside buy us? Not much in addition to what the regular action recognition system can already do, I would argue. Or put differently, not much that one couldn't pick up via pure sensory learning. (Side note relevant to this last point: motor knowledge and sensory learning are rather confounded. The more experience we have performing an action, the more opportunities we have to learn the sensory consequences.)I think there is a more serious theoretical concern with the direction that mirror neuron theory is going, however. There is a shift away from the idea that mirror neurons code particular movements and toward the idea that they code motor goals or intentions. So mirror neurons don't do their magic via motor simulation, but by activating the goal or intention directly. This sounds like a profound insight, but in fact it pushes mirror neurons right out of the motor system and into the dreaded cognitive system that Rizzolatti and colleagues so wish to avoid: "Because the observers are aware of the outcome of their motor acts, they also understand what the others are doing without the necessity of an intermediate cognitive mediation" (another quote from the APS abstract). Why is this the case? Because the high level goals or intentions, the things we are trying to understand, are inherently non-motoric. Now, movements can have goals, to bring my hand in proximity to a raisin, but being able to predict the trajectory of another's reaching movement is not the kind of understanding that Rizzolatti is talking about. He's arguing that mirror neurons code intentions, i.e., to possess the raisin, to eat the raisin. These are not motor goals. I can just as easily achieve this goal by grasping the raisin and putting it on my tongue, bending over and slurping it directly with my mouth, or asking someone to put it in my mouth for me. The goal is sensory (taste the raisin, satiate hunger) or cognitive (possess the raisin). The motor system is just a set of options for achieving the sensory/cognitive goal. Think of any action you like and you end up with same conclusion regarding the nature of the goal. The goal or intention is not the movement itself, it is the consequences of the movement. It's no wonder one doesn't need a motor system to understand the goals or intentions of actions: the goals and intentions are not motor! The progression of mirror neuron theory was predictable from what happened to the motor theory of speech perception. It started out quite strong and therefore interesting, but when it was discovered that strict motor simulation did not disrupt speech perception, the "motor representations" that were used for speech perception became more abstract. It was no longer the actual motor gestures, but the intended motor gestures that were critical. This pushed the critical representations right out of the motor system and into the "cognitive" system, or as I and others would argue, straight back into the sensory system.The mirror system is part of a larger system designed to for action control, not action understanding (Hickok & Hauser, 2010). As Rizzolatti has pointed out himself, the actions of others are clearly relevant to selecting and controlling one's own actions, just as the shape of objects are relevant to selecting and controlling actions. The idea that mirror neurons support action understanding is an interesting hypothesis, but one that has been thoroughly vetted. It's time to move on. Hickok G, & Hauser M (2010). (Mis)understanding mirror neurons. Current biology : CB, 20 (14) PMID: 20656198Rizzolatti, G., & Sinigaglia, C. (2010). The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations Nature Reviews Neuroscience, 11 (4), 264-274 DOI: 10.1038/nrn2805... Read more »

Hickok G, & Hauser M. (2010) (Mis)understanding mirror neurons. Current biology : CB, 20(14). PMID: 20656198

Rizzolatti, G., & Sinigaglia, C. (2010) The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations. Nature Reviews Neuroscience, 11(4), 264-274. DOI: 10.1038/nrn2805

April 26, 2011
08:39 PM
873 views

Relation between production and perception of voice onset time in aphasia

by Greg Hickok in Talking Brains

I'm constantly amazed at how much good information is available in the literature going back decades. It is unfortunate that much of this information is effectively lost to the current generation of researchers leaving us to re-invent the wheel in many cases. Even papers that we may be familiar with can contain tidbits of information that were overlooked. This is the case with a classic 1970s paper by Sheila Blumstein and colleagues -- including my former PhD advisor, Edgar Zurif, who I mention because he will enjoy the attention ;-). The paper is titled, The perception and production of Voice-Onset Time in aphasia and was published in Neuropsychology, 1977, Vol. 15, 371-383.This is a paper that I've been citing and talking about for sometime. I was interested in it originally because it clearly showed a dissociation between the ability to comprehend speech and perform syllable discrimination, the task effect that David and I have been talking about for a decade. I recently re-read the paper because Gabriele Miceli, another major player in aphasia research in the 1970s and 1980s (and still very active!), pointed out to me that the article is also quite relevant to the issue of the relation between perception and production of speech, as the title previews. What the authors did was measure VOT in aphasics' own speech utterances (they read a set of words aloud) and compared it their ability to discriminate syllables that differ in terms of the same VOT dimension. You can see the implication for motor theories: If a patient cannot reliable produce correct VOTs, then this should affect their ability to perceive (discriminate) VOT. So what did they find? I'll let Blumstein et al. summarize:It is quite clear, at least for the anterior aphasics (Broca and Mixed Anterior), that the ability to perceive the VOT continuum relates in no way to the ability to produce voiced and voiceless stops. Thus, the anterior aphasics maintain the ability to perceive this distinction, but make both phonemic as well as phonetic substitutions.This is a cool result because is zooms in on one feature, VOT, and shows a direct non-correspondence between perception and production of this speech dimension. Blumstein, S., Cooper, W.E., Zurif, E.B., & Carmazza, A. (1977). The perception and production of Voice-Onset Time in aphasia Neuropsychologia, 15 (3), 371-372 DOI: 10.1016/0028-3932(77)90089-6... Read more »

Blumstein, S., Cooper, W.E., Zurif, E.B., & Carmazza, A. (1977) The perception and production of Voice-Onset Time in aphasia. Neuropsychologia, 15(3), 371-372. DOI: 10.1016/0028-3932(77)90089-6

April 7, 2011
06:23 PM
782 views

The new semantic hub: the posterior middle temporal gyrus

by Greg Hickok in Talking Brains

Most of us agree that conceptual information is represented in a broadly distributed network throughout cortex, but there is disagreement about what the organizational principles of this knowledge might be (see debates between Alfonso Caramazza and Alex Martin or Friedemann Pulvermuller), as well as a debate about the system, or "hub", that binds all of this information together. Here I'm going to focus on the latter question.One hypothesis is that the anterior temporal lobe serves as the brain's semantic hub (Patterson, et al. 2007). The evidence for this claim comes primarily from semantic dementia, a degenerative condition in which patients have debilitating semantic deficits that seems to cut across language, visual objects, and hearing; i.e., it looks like an amodal conceptual semantic deficit. The neural degeneration is particularly evident in the anterior temporal lobes (among other regions). If you were at the Neurobiology of Language Conference last year in San Diego, you heard a very lively debate over this issue by Carolyn Patterson and Alex Martin, which raised several questions for the ATL=semantic hub position. An alternative position has been suggested previously on the basis of stroke data, namely, that the posterior middle temporal region is critical for some form of lexical semantic integration. For example, we argued that this region serves as a sound-to-meaning interface (Hickok & Poeppel, 2004) or in other terminology, as a "lexical interface" (Hickok & Poeppel, 2007). Why? Because damage to that part of the brain is associated with (primarily) semantic comprehension deficits (Dronkers, et al. 2004; Bates, et al. 2003).A new paper by Turken and Dronkers (2011) adds important new information to this debate and goes so far as to elevate the MTG to the status of a "semantic hub". They used publicly available DTI and resting state fMRI datasets to map the fiber tracts and functional connectivity of several ROIs define on the basis of Dronkers et al. (2004) lesion study. The basic result was that the MTG ROI was found to be wired up, tract wise, to a broad network including STS/AG, STG, and frontal area BA 47 (the functional connectivity map shows similar areas, see below, bottom portion). This same set of regions have been independently identified by Jeff Binder's group as being involved in semantic processes on the basis of a recent meta-analysis of functional imaging studies (see below, top portion) (Binder et al. 2009).px; height: 400px;" src="http://www.frontiersin.org/files/TempImages/imagecache/8794_fnsys-05-00001-HTML/images/image_m/fnsys-05-00001-g016.jpg" border="0" alt="" /What's interesting to me about these images is that the "semantic" areas seem to form a ring around the lower-level auditory-motor areas (STG PT pIFG), suggesting a hierarchical organization associated with phonological (lower-level) and semantic processes (higher level). It is worth mentioning as well that the connectivity pattern of the MTG was bilateral, both in the fiber tracing and functional connectivity analyses. The ATL ROI was more sparsely connected both in terms of fiber tracts and functional connectivity. An analysis of the connectivity of the STS region showed that it was largely connected to "dorsal stream" structures, but also, importantly, connected with the MTG. In general, this strikes me as a fairly nice confirmation of the broad organization laid out in the dual stream model (HP, 2004, 2007), but I might be biased. I'm interested in your thoughts!ReferencesBates, E., Wilson, S. M., Saygin, A. P., Dick, F., Sereno, M. I., Knight, R. T., et al. (2003). Voxel-based lesion-symptom mapping. Nat Neurosci, 6(5), 448-450.Binder, J. R., Desai, R. H., Graves, W. W., & Conant, L. L. (2009). Where is the semantic system? A critical review and meta-analysis of 120 functional neuroimaging studies. Cereb Cortex, 19(12), 2767-2796.Dronkers, N. F., Wilkins, D. P., Van Valin, R. D., Jr., Redfern, B. B., & Jaeger, J. J. (2004). Lesion analysis of the brain areas involved in language comprehension. Cognition, 92(1-2), 145-177.Hickok, G., & Poeppel, D. (2004). Dorsal and ventral streams: a framework for understanding aspects of the functional anatomy of language Cognition, 92 (1-2), 67-99 DOI: 10.1016/j.cognition.2003.10.011Hickok, G., & Poeppel, D. (2007). The cortical organization of speech processing Nature Reviews Neuroscience, 8 (5), 393-402 DOI: 10.1038/nrn2113Patterson, K., Nestor, P., & Rogers, T. (2007). Where do you know what you know? The representation of semantic knowledge in the human brain Nature Reviews Neuroscience, 8 (12), 976-987 DOI: 10.1038/nrn2277 Turken AU, & Dronkers NF (2011). The neural architecture of the language comprehension network: converging evidence from lesion and connectivity analyses. Frontiers in systems neuroscience, 5 PMID: 21347218... Read more »

Hickok, G., & Poeppel, D. (2004) Dorsal and ventral streams: a framework for understanding aspects of the functional anatomy of language. Cognition, 92(1-2), 67-99. DOI: 10.1016/j.cognition.2003.10.011

Hickok, G., & Poeppel, D. (2007) The cortical organization of speech processing. Nature Reviews Neuroscience, 8(5), 393-402. DOI: 10.1038/nrn2113

Patterson, K., Nestor, P., & Rogers, T. (2007) Where do you know what you know? The representation of semantic knowledge in the human brain. Nature Reviews Neuroscience, 8(12), 976-987. DOI: 10.1038/nrn2277

Turken AU, & Dronkers NF. (2011) The neural architecture of the language comprehension network: converging evidence from lesion and connectivity analyses. Frontiers in systems neuroscience, 1. PMID: 21347218

March 10, 2011
04:54 PM
759 views

On the relation between language and music

by Greg Hickok in Talking Brains

Much has been said on the relation between music and language. Most of it arguing for common computational foundations:...syntax in language and music share a common set of processes (instantiated in frontal brain area) - Patel, 2003...some aspects of structural integration in language and music appear to be shared -Fedorenko, et al., 2009All formal differences between language and music are a consequence of differences in their fundamental building blocks (arbitrary pairings of sound and meaning in the case of language; pitch-classes and pitch-class combinations in the case of music).† In all other respects, language and music are identical. -Katz & Pesetsky, 2011 http://ling.auf.net/lingBuzz/000959This claim predicts that there should be overlap in the brain regions involved in processing both language and music. Surprisingly, no one has assessed this directly in the same subjects. Until now. A new paper in the Journal of Neuroscience reports a study in which participants listened to either sentences or melodic stimuli during fMRI scanning (Rogalsky et al., 2011). Overlap between the two conditions was, in fact, observed, but only in relatively early auditory areas (not surprisingly, given that both stimuli are acoustic). No overlap was found in regions thought to be involved in structural processing, i.e., Broca's area and the anterior temporal lobe. Language activated a more lateral temporal lobe network, while music activated a dorsomedial pattern in the temporal lobes. Broca's area, a prime candidate for structural processing according to many, was not reliably activated by either stimulus class, once acoustic envelope information was controlled. Even within the region of overlap in upstream auditory areas, pattern classification analysis revealed that music and language activated a different pattern of activity. What does this mean? Despite the recent hype, I don't think structural processing music and language have all that much in common, at least in terms of neural resources. I think previous behavioral and electrophysiological evidence for shared resources has more to do the tasks employed (typically violation studies) than normal structural processing itself. Fedorenko E, Patel A, Casasanto D, Winawer J, & Gibson E (2009). Structural integration in language and music: evidence for a shared system. Memory & cognition, 37 (1), 1-9 PMID: 19103970Patel, A. (2003). Language, music, syntax and the brain Nature Neuroscience, 6 (7), 674-681 DOI: 10.1038/nn1082Rogalsky, C., Rong, F., Saberi, K., & Hickok, G. (2011). Functional anatomy of language and music perception: Temporal and structural factors investigated using fMRI. Journal of Neuroscience, 31(10): 3843-3852... Read more »

Fedorenko E, Patel A, Casasanto D, Winawer J, & Gibson E. (2009) Structural integration in language and music: evidence for a shared system. Memory , 37(1), 1-9. PMID: 19103970

Patel, A. (2003) Language, music, syntax and the brain. Nature Neuroscience, 6(7), 674-681. DOI: 10.1038/nn1082

March 9, 2011
01:51 PM
783 views

Action understanding "from the inside"? Or is it just sensory learning?

by Greg Hickok in Talking Brains

As I noted previously, Rizzolatti and colleagues have backed off the claim that mirror neurons enable action understanding via strict motor simulation. Instead they emphasize that the really important mirror neurons code the "goals of the action":By matching individual movements, mirror processing provides a representation of body part movements that might serve various functions (for example, imitation), but is devoid of any specific cognitive importance per se. By contrast, through matching the goal of the observed motor act with a motor act that has the same goal, the observer is able to understand what the agent is doing. – Rizzolatti & Sinigaglia, 2010, Nature Rev. Neurosci., p. 269(The shift in emphasis from movements to goals is actually problematic for the theory because one could argue that the goals of an action are sensory, e.g., in the case of speech the goal is to produce a sound. Therefore understanding is a sensory phenomenon. But that is not what I want to talk about here.) They are also careful to point out that action recognition can be achieved using non-motoric means. ...the recognition of the motor behaviour of others can rely on the mere processing of its visual aspects. This processing is similar to that performed by the ‘ventral stream’ areas for the recognition of inanimate objects. It allows the labelling of the observed behaviour, but does not provide the observer with cues that are necessary for a real understanding of the conveyed message. – Rizzolatti & Sinigaglia, 2010, Nature Rev. Neurosci., p. 270This "real understanding" comes "from the inside" as they say. But what does this mean? One interpretation, is that knowing how to perform an action allows one to predict the outcome of an observed action ahead of time, i.e., "I know what you are doing". As Marco Iacoboni writes in the context of watching sports, We understand the players’ actions because we have a template in our brains for that action, a template based on our own movements. -Iacoboni, 2008, Mirroring People, p. 5I think this is true to some extent. Experience performing an action can allow us to predict the consequences of that action when we observe someone else performing it. It is important to recognize, however, that this predictive coding isn't unique to the motor system. We can learn to predict the consequences of actions that we have never performed just by observing the action performed repeatedly. For example, my dog is really good at this. He loves to play fetch, and after many exposures to viewing my throwing action, he can predict the direction of the ball's flight. Below is a video demonstrating this. There are 6 successive trials. Each starts with me holding the ball and my dog watching me intently. I then turn in some direction and make a throwing action in that direction. I don't actually release the ball to ensure that he is cueing off my actions and isn't just following the trajectory of the ball. As is clear from the video, he recognizes that I am making a throwing action and immediately responds by turning to run after it. Further, the direction in which he runs shows that he is correctly predicting where I planned to throw the ball. (Once he's on his way, I throw the ball so his chasing response isn't extinguished.) I should say that I don't normally throw the ball for him in random directions. It is usually in one general direction, yet he had not trouble with this task, even without any practice.You can see in the last trial that he takes off running even before the forward motion of my arm. Similar experiments have been carried out in monkeys observing overhand throwing actions by a human. It was argued that the monkeys understood the action even though they can't make overhand throwing actions themselves. The dog example is even stronger though because they can't grasp or throw at all yet seem to understand throwing actions quite well. This behavior is no surprise to owners of dogs who like to fetch, but it does illustrate the simple fact that predictive knowledge of "intention" does not have to come from the motor system. In fact, given that there is survival value in predicting the actions of prey or predators, some of which differ in terms of their motor repertoire compared to the observing animal, one could argue that prediction based on sensory learning is even more important than motor-based predictions when it comes to others' behaviors.Rizzolatti, G., & Sinigaglia, C. (2010). The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations Nature Reviews Neuroscience, 11 (4), 264-274 DOI: 10.1038/nrn2805... Read more »

Rizzolatti, G., & Sinigaglia, C. (2010) The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations. Nature Reviews Neuroscience, 11(4), 264-274. DOI: 10.1038/nrn2805

February 10, 2011
12:13 PM
677 views

On the nature of sensorimotor integration for speech processes

by Greg Hickok in Talking Brains

For the last few years I have been thinking a lot about a few different things: What specifically is our proposed dorsal stream doing? How does the motor system contribute to speech perception? What is the relation between sensorimotor processes used during speech production (e.g., feedback-based motor control models) and purported sensorimotor processes in speech perception? How do computational models of speech production (e.g., feedback control models, psycholinguistic models, neurolinguistic models) relate to neural models of speech processing? A new "Perspective" article which just appeared today in Neuron and is currently free to download, summarizes the outcome of my thoughts on these questions, mixed with a heavy dose of input from my co-authors John Houde (UCSF) and Feng Rong (Talking Brains West post doc). Yes, I'm very proud that the piece has been labeled a "perspective" rather than a "review" -- that means it is theoretically novel rather than a summary statement ;-) The starting point for the article is the observation that there are two main lines of research on sensorimotor integration, which paradoxically do not interact. Namely the idea that the auditory system is critically involved in speech production (exemplified by the motor control folks like Frank Guenther and John Houde) and the idea that the motor system is critically involved in speech perception (exemplified by folks like Stephen Wilson, Pulvermuller, and many others). We wondered whether these two lines of work could be integrated into one model. The answer, we propose, is yes. The basic idea is the dorsal stream sensorimotor integration circuit is built to support speech production via a state feedback control architecture of the sort that is common in the visual-manual motor control literature. But the computational properties of the system, particularly the generation of forward sensory predictions of motor consequences provides a ready made mechanism for the motor system to modulate (not drive) the perception of others' speech under some circumstances (e.g., when the acoustic signal is weak or ambiguous). In addition, we attempted to show how psycholinguistic models of speech production (e.g., Levelt, Dell) as well as neurolinguistic models (e.g., the concept of input and output phonological lexicons) relate to the proposed state feedback control model. I never liked the idea of there being two phonological "lexicons" but it actually makes a lot of sense in the framework of state feedback control architectures. The model also does a decent job of explaining some of the key symptoms of conduction aphasia and stuttering which are explained as different types of disruption of the same feedback control mechanism. The graphic depiction of the model is below. I'm looking forward to your feedback on this!Hickok, G., Houde, J., & Rong, F. (2011). Sensorimotor Integration in Speech Processing: Computational Basis and Neural Organization Neuron, 69 (3), 407-422 DOI: 10.1016/j.neuron.2011.01.019... Read more »

Hickok, G., Houde, J., & Rong, F. (2011) Sensorimotor Integration in Speech Processing: Computational Basis and Neural Organization. Neuron, 69(3), 407-422. DOI: 10.1016/j.neuron.2011.01.019

February 9, 2011
05:15 PM
711 views

Why is Broca's aphasia/area the focus of research on "syntactic comprehension"? Was it a historical accident?

by Greg Hickok in Talking Brains

Arguably it was the classic paper by Caramazza and Zurif, published in 1976, that kicked off what turned into decades of research on the role of Broca's area in syntactic computation. We all know from our grade school lessons that Caramazza and Zurif found that Broca's aphasics exhibit not only agrammatic production, but also a profound deficit in using syntactic knowledge in sentence comprehension. The critical bit of evidence was that Broca's aphasics seemed perfectly fine in using semantic information (lexical and real-world knowledge) to derive the meaning of an utterance: they could correctly understand a so-called semantically non-reversible sentence like, The apple that the boy is eating is red. But they failed when interpretation required the use of syntactic information, i.e., when the sentence was semantically reversible like, The boy that the girl is chasing is tall. This finding suggested that Broca's aphasics had a deficit in syntax, one that affected both production AND comprehension. Broca's area, via its association with Broca's aphasia (a dubious association, but a topic for another post) then became the major anatomical focus for the localization of syntax, including its role in comprehension of sentences. This obsession with Broca's area and syntax (comprehension in particular) persists today. But is it all a historical accident? I happened to re-read Caramazza and Zurif today (I'm working on a chapter on Broca's aphasia and it is always a good idea to go back to original sources). C&Z tested not only Broca's aphasics, but also conduction aphasics, a little-remembered fact. Conduction aphasics have posterior lesions and don't have agrammatic speech output. But guess what? C&Z report that the conduction aphasics performed exactly like the Broca's aphasics. Check out the graph below which I recreated by eye-balling the relevant values from their Figure 3 which shows percent correct on the sentence-to-picture matching task for object-gap semantically reversible vs. nonreversible sentences like the examples above. The failure of conduction aphasics to use syntactic knowledge was, of course, noted by the authors. ...the conclusion is inescapable- Broca’s and Conduction aphasics do not seem at all capable of using algorithmic [syntactic] processes. Thus, for those sentences that were semantically constrained, performance was approximately at the 90% level, but it dropped to chance level when these semantic constraints were not available. p. 580Why then did all subsequent work focus on Broca's aphasics and Broca's area? Why was conduction aphasia and more posterior lesion sites not considered as a possible test case/source for the neural substrate for syntax? The answer derives from the common interpretation of conduction aphasia at the time, which is that of a disconnection syndrome. Conduction aphasia was caused, the story went, not by damage to any computational system, but by a disconnection of computational systems, namely Wernicke's and Broca's area. C&Z argued that the conduction aphasics comprehension problems derived from a disconnection of syntactic systems, which lived in Broca's area. Conduction aphasics also were incapable of using syntactic algorithmic processes [see also Saffran & Matin (in press) and Scholes (in press)]. The question arises, therefore, as to whether syntactic operations also rely on cortical regions posterior to Broca’s area or whether the conduction deficit should be considered within a disconnection framework, that is, as the severing of a connection to Broca’s area (Geschwind, 1970). Given the impressive arguments offered by Geshwind, we are presently satisfied in treating it as a problem of disconnection, but a disconnection from an area that subserves sytactic processes. p. 581But the interpretation of conduction aphasia has evolved since in the 1970s. It is no longer considered a disconnection syndrome but rather a deficit caused by cortical dysfunction. We can, and should, argue about what conduction aphasia is, functionally. Maybe our final conclusion will be the same as C&Z's (I don't believe it will), but the point is that based on an assumption about the nature of conduction aphasia, research emphasis shifted entirely to Broca's aphasia and Broca's area, ignoring conduction aphasia and more posterior cortices. I believe this was an unfortunate and ultimately misleading turn.Maybe historical accident isn't the right word for what happened in the 1976 publication. It wasn't an accident that C&Z assumed the popular account, articulated so eloquently by Geschwind. It was a reasonable conclusion. But it did dramatically shape the focus of subsequent research and we are still living with the consequences of this theoretical argument. There are still heated debates both in print and in conference forums regarding the role of Broca's area in syntactic comprehension (Grodzinsky & Santi, 2008; Rogalsky & Hickok, 2011; Willems & Hagoort, 2009). Conversely, there is no concerted effort aimed at determining the role of the temporal-parietal junction (the location of lesions associated with conduction aphasia) in syntactic comprehension. This is a shame because I believe we are missing a big part of the puzzle. This is a good lesson though. Sometimes ideas become entrenched in the scientific literature by "accidents" of the current theoretical milieu, and sometimes the resulting scientific path that a field takes can be the wrong one. It is important to occasionally re-visit the reasons why choices were made and to evaluate whether a new direction is worth exploring. ReferencesCaramazza A, & Zurif EB (1976). Dissociation of algorithmic and heuristic processes in language comprehension: evidence from aphasia. Brain and language, 3 (4), 572-82 PMID: 974731Grodzinsky Y, & Santi A (2008). The battle for Broca's region. Trends in cognitive sciences, 12 (12), 474-80 PMID: 18930695Rogalsky C, & Hickok G (2010). The Role of Broca's Area in Sentence Comprehension. Journal of cognitive neuroscience PMID: 20617890Willems RM, & Hagoort P (2009). Broca's region: battles are not won by ignoring half of the facts. Trends in cognitive sciences, 13 (3) PMID: 19223227... Read more »

Caramazza A, & Zurif EB. (1976) Dissociation of algorithmic and heuristic processes in language comprehension: evidence from aphasia. Brain and language, 3(4), 572-82. PMID: 974731

Grodzinsky Y, & Santi A. (2008) The battle for Broca's region. Trends in cognitive sciences, 12(12), 474-80. PMID: 18930695

Rogalsky C, & Hickok G. (2010) The Role of Broca's Area in Sentence Comprehension. Journal of cognitive neuroscience. PMID: 20617890

Willems RM, & Hagoort P. (2009) Broca's region: battles are not won by ignoring half of the facts. Trends in cognitive sciences, 13(3). PMID: 19223227

February 2, 2011
04:48 PM
628 views

Why is Broca's area active during speech perception?

by Greg Hickok in Talking Brains

A now-common finding in the functional imaging literature on speech perception is that Broca's area is active during the perception of speech. The activation magnitude is sometimes not as strong or consistent as one finds in auditory cortex, but it is there and so requires some explanation. There are a few possibilities. (I'm talking about Broca's area as if it were one functional region, which it isn't, but we'll gloss over that for now.)1. Broca's area drives the analysis of speech sounds (i.e., the motor theory of speech perception is correct).2. Broca's area supports/modulates the analysis of speech sounds via some predictive coding process (articulation driven forward model or analysis by synthesis).3. Broca's area activation is epiphenomenal -- it simply reflects spreading activation in association networks and serves no function in speech perception.4. Broca's area activity reflects a higher-order process (e.g., cognitive control) that is involved in say, response selection.We can quickly rule out #1 for reasons that have been articulated previously, e.g., here.Regarding the other possibilities, I think the question is still open for debate. As additional fuel for this debate, consider the following recently published (epub-online) finding reported by Vaden et al. In an fMRI study, listeners heard sets of words that varied in terms of phonotactic probability, which is a measure argued to reflect sublexical properties of words (density was also manipulated but didn't show a robust effect). The task was to monitor for occasional non-words embedded in the word sets -- these trials were excluded from analysis. The goal was to try to identify neural regions that are sensitive to sublexical properties of words. One might have expected to find such effects in relatively early stages of processing in auditory cortex, based on the standard hierarchical assumption that word recognition first analyses segmental-level information which it then uses to access the appropriate lexical-phonological codes, generally acknowledged to be coded/processed in the STS. However, Vaden et al. found no effects in auditory cortex, indeed in the entire temporal lobe. Instead, activation in Broca's area (~pars opercularis) was modulated as a function of phonotactic frequency: word sets comprised of higher phonotactic frequency words yielded greater activity in Broca's area. What's interesting about this is subjects have no conscious idea that the words vary according to frequency of the sounds sequences that comprise them, yet Broca's area sure does.So what's up? Does this mean that the motor theory is right? Is Broca's area critically involved in the early analysis of speech information? Nope. (Refer again to the reasons why #1 above can't be right.) It must be something else. Cognitive control? Subjects were trying to find occasional non-words. Maybe phonotactic modulations vary cognitive decision load... This is possible but not likely: no effect in Broca's area was found for neighborhood density, which is argued specifically to induce competition and therefore should affect decision processes. Further, cognitive control effects tend to involve more anterior regions. Forward prediction? Yes, possibly. High phonotactic frequency items are associated with more predictability. Maybe Broca's area gets excited when it encounters a predictable pattern. Epiphenominal? Yes, possibly. High phonotactic frequency items likely have stronger associations between auditory and motor representations of speech; the stronger the association, the more spreading activation one sees. Here's what I really think is going on. Basically, the strength of the association between auditory and motor representations of a phonemic sequence is what's driving the correlation, as in the epiphenominal account. Why do these associations exist? Because the goal of speech production is to reproduce a particular *sound*. To achieve this production task we need to relate sound and movement. Those auditory-motor codes that are more frequent are more strongly associated leading to more activation. HOWEVER, even though the underlying explanation for this effect has more to do with speech production than speech perception, it may be possible for the speech system to take advantage of the situation and use this information to augment perception, in a forward predictive manner. Returning to the question of hierarchical models of word recognition, it is interesting that no such effects of phonotactic probability showed up in auditory regions. This is consistent with the view that speech recognition does not necessarily involve access to segmental level units. But it could also be that phonotactic probability isn't a good metric of segmental level processing. ReferencesVaden, K., Piquado, T., & Hickok, G. (2011). Sublexical Properties of Spoken Words Modulate Activity in Broca's Area but Not Superior Temporal Cortex: Implications for Models of Speech Recognition Journal of Cognitive Neuroscience, 1-10 DOI: 10.1162/jocn.2011.21620... Read more »

Vaden, K., Piquado, T., & Hickok, G. (2011) Sublexical Properties of Spoken Words Modulate Activity in Broca's Area but Not Superior Temporal Cortex: Implications for Models of Speech Recognition. Journal of Cognitive Neuroscience, 1-10. DOI: 10.1162/jocn.2011.21620

January 26, 2011
08:36 PM
577 views

On the relation between auditory-motor area Spt and conduction aphasia

by Greg Hickok in Talking Brains

Conduction aphasia is characterized by relatively frequent phonemic speech errors with self-correction attempts and difficulty repeating speech verbatim; comprehension is relatively well-preserved. The classical account holds that conduction aphasia is caused by damage to the arcuate fasciculus. However, we have been arguing for some time that conduction aphasia is caused by damage to area Spt -- a functionally defined region in the vicinity of the left planum temporale that exhibits auditory-motor response properties, and which we claim computes a mapping between auditory and motor speech representations, critical for aspects of speech production. Our hypothesized link between conduction aphasia and area Spt just got stronger. In a forthcoming paper in Brain and Language Buchsbaum et al. show that the region of maximal overlap in lesion distribution of a group of 14 conduction aphasics includes area Spt (based on fMRI data from over 100 participants). We argue that the auditory-motor transformation function carried out by Spt is necessary for verbatim repetition but also plays a critical role in internal monitoring during speech production, thus explaining the increased speech error rate when the system is damaged. This explanation does a better job of explaining the co-occurrence of phonemic paraphasias and repetition deficits than does the current dominant model of the deficit in conduction aphasia, namely, that it is a working memory deficit. ReferencesBuchsbaum BR, Baldo J, Okada K, Berman KF, Dronkers N, D'Esposito M, & Hickok G (2011). Conduction aphasia, sensory-motor integration, and phonological short-term memory - An aggregate analysis of lesion and fMRI data. Brain and language PMID: 21256582Baldo, J.V., Klostermann, E.C., and Dronkers, N.F. (2008). It's either a cook or a baker: patients with conduction aphasia get the gist but lose the trace. Brain Lang 105, 134-140.Hickok, G., Buchsbaum, B., Humphries, C., and Muftuler, T. (2003). Auditory-motor interaction revealed by fMRI: Speech, music, and working memory in area Spt. Journal of Cognitive Neuroscience 15, 673-682.Hickok, G., Erhard, P., Kassubek, J., Helms-Tillery, A.K., Naeve-Velguth, S., Strupp, J.P., Strick, P.L., and Ugurbil, K. (2000). A functional magnetic resonance imaging study of the role of left posterior superior temporal gyrus in speech production: implications for the explanation of conduction aphasia. Neuroscience Letters 287, 156-160.Hickok, G., Okada, K., and Serences, J.T. (2009). Area Spt in the human planum temporale supports sensory-motor integration for speech processing. J Neurophysiol 101, 2725-2732.... Read more »

Buchsbaum BR, Baldo J, Okada K, Berman KF, Dronkers N, D'Esposito M, & Hickok G. (2011) Conduction aphasia, sensory-motor integration, and phonological short-term memory - An aggregate analysis of lesion and fMRI data. Brain and language. PMID: 21256582

December 1, 2010
02:43 PM
664 views

Why the obsession with intelligibility in speech processing studies?

by Greg Hickok in Talking Brains

There was a very interesting speech/language session at SfN this year organized by Jonathan Peelle. Talks included presentations Sophie Scott, Jonas Obleser, Sonia Kotz, Matt Davis and others spanning an impressive range of methods and perspectives on auditory language processing. Good stuff and a fun group of people. It felt kind of like a joint lab meeting with lots of discussion. I want to emphasize one of the issues that came up, namely, the brain's response to intelligible speech and what we can learn from it. Here's a brief history.2000 - Sophie Scott, Richard Wise and colleagues published a very influential paper which identified a left anterior temporal lobe region that responded more to intelligible speech (clear and noise vocoded sentences) than unintelligible speech (spectrally rotated versions of the intelligible speech stimuli). It was argued that this is the "pathway for intelligible speech".2000 - Hickok & Poeppel published a critical review of the speech perception literature arguing, on the basis of primarily lesion data, that speech perception is bilaterally organized and implicates posterior superior temporal regions in speech sound perception. 2000-2006 - Several more papers from Scott/Wise's group replicated this basic finding but additional areas started creeping into the picture including left posterior regions and right hemisphere regions. The example figure below is from Sptsyna et al. 20062007 - Hickok & Poeppel again reviewed the broader literature on speech perception including lesion work as well as studies that attempted to isolate phonological-level processes more specifically. It is concluded, yes you guessed it, that Hickok & Poeppel 2000 were pretty much correct their claim of a bilaterally organized posterior temporal speech perception system. 2009 - Rauschecker and Scott publish their "Maps and Streams" review paper arguing just as strongly that speech perception is left lateralized and is dependent on an anterior pathway. As far as I can tell, this claim is based on (i) analogy to the ventral stream pathway projection in monkeys (note: we might not yet fully understand the primate auditory system and given that monkeys don't have speech, the homologies may be less than perfect), and (ii) the fact that the peak activation in intelligible minus unintelligible sentences tends to be greatest in the left anterior temporal lobe. 2010 - Okada et al. publish a replication of Scott et al. 2000 using a much larger sample than any previous study (n=20 compared to n=8 in the Scott et al. 2000) and find robust bilateral anterior and posterior activations in the superior temporal lobe for intelligible compared to unintelligible speech. See figure below which shows the group activation (top) and peak activations in individual subjects (bottom). Note that even though it doesn't show up in the group analysis, activation extends to right posterior STG/STS in most subjects.So that's the history. As was revealed at the SfN session controversy still remains, despite the existence of what I thought was fairly compelling evidence against an exclusively anterior-going projection pathway. Here's what came out at the conference. I presented lesion evidence collected with my collaborators Corianne Rogalsky, Hanna Damasio, and Steven Anderson, which showed that destruction of the left anterior temporal lobe "intelligibility area" has zero effect on speech perception (see figure below). This example patient performed with 100% accuracy on a test of auditory word comprehension (4AFC, word to picture matching with all phonemic foils, including minimal pairs), and 98% accuracy on a minimal pair syllable discrimination test. Combine this with the fact that auditory comprehension deficits are most strongly associated with lesions in the posterior MTG (Bates et al. 2003) and this adds up to a major problem for the Scott et al. theory. The counter-argument from the Scott camp was addressed exclusively at the imaging data. I'll try to summarize their main points as accurately as possible. Someone correct me if I've got them wrong.1. Left ATL is the peak activation in intelligible vs. unintelligible contrasts2. Okada et al. did not use sparse sampling acquisition (true) which increased the intelligibility processing load (possible) thus recruiting posterior and right hemisphere involvement3. Okada et al. used an "active task" which affected the activation pattern (we asked subjects to press a button indicating whether the sentence was intelligible or not). First and most importantly, none of these counter-arguments provides an account of the lesion data. We have to look at all sources of data in building our theories. Regarding point #2: I will admit that it is possible that the extra noise taxed the system more than normal and this could have increased the signal throughout the network. However, these same regions are showing up in the reports of Scott and colleagues, even in the PET scans, and the regions that are showing up (bilateral pSTG/STS) are the same as those implicated in lesion work and in imaging studies that target phonological level processes. Regarding point #3: I'm all for paying close attention to the task in explaining (or explaining away) activation patterns. However, if the task directly assesses the behavior of interest (which is not the case in many studies), this argument doesn't hold. The goal of all this work is to map the network for processing intelligible speech. If we are asking subjects to tell us if the sentence is intelligible, this should drive the network of interest. Unless, I suppose, you think that the pSTG is involved decision processes which is highly dubious.This brings us to point #1: Yes, it does appear that the peak activation in the intell vs. unintell contrast is in the left anterior temporal lobe. This tendency is what drives the Scott et al. theory. But why the obsession with this contrast? There are two primary reasons why we shouldn't be obsessed with it. In fact, these points question whether there is any usefulness to the contrast at all. 1. It's confounded. Intelligible speech differs from unintelligible speech on a host of dimensions: phonemic, lexical, semantic, syntactic, prosodic, and compositional semantic content. Further, the various intelligibility conditions are acoustically different, just listen to them, or note that A1 can reliably classify each condition from the other (Okada et al. 2010). It is therefore extremely unclear what the contrast is isolating. 2. By performing this contrast, one is assuming that any region that fails to show a difference between the conditions is not part of the pathway for intelligible speech. This is clearly an incorrect assumption: in the extreme case, peripheral hearing loss impairs the ability understand speech even though the peripheral auditory system does not respond exclusively to intelligible speech. Closer to the point, even if it was the case that the left pSTG/STS did not show an activation difference between intelligible and unintelligible speech it could still be THE region responsible for speech perception. In fact, if the job of a speech perception network is to take spectrotemporal patterns as input and map these onto stored representations of speech sound categories, one would expect activation of this network across a range of spectrotemporal patterns, not only those that are "intelligible". I don't expect this debate to end soon. In fact, one suggestion for the next "debate" at the NLC conference is Scott vs. Poeppel. That would be fun.ReferencesBates, E., Wilson, S.M., Saygin, A.P., Dick, F., Sereno, M.I., Knight, R.T., and Dronkers, N.F. (2003). Voxel-based lesion-symptom mapping. Nat Neurosci 6, 448-450.Hickok, G., and Poeppel, D. (2000). Towards a functional neuroanatomy of speech perception. Trends in Cognitive Sciences 4, 131-138.Hickok, G., and Poeppel, D. (2007). The cortical organization of speech processing. Nat Rev Neurosci 8, 393-402.... Read more »

Okada K, Rong F, Venezia J, Matchin W, Hsieh IH, Saberi K, Serences JT, & Hickok G. (2010) Hierarchical organization of human auditory cortex: evidence from acoustic invariance in the response to intelligible speech. Cerebral cortex (New York, N.Y. : 1991), 20(10), 2486-95. PMID: 20100898

October 7, 2010
08:34 PM
662 views

Internal forward models -- New insight or just hype?

by Greg Hickok in Talking Brains

In case you haven't noticed, the concept of internal forward models -- an internal prediction about a future event or state -- are all the rage. The concept comes out of the motor control literature where one can find pretty solid evidence that motor control makes use of forward predictions of the sensory consequences of motor commands (e.g., check out the seminal paper by Wolpert, Ghahramani, & Jordan, 1995). These concepts have been extended to speech (e.g., Tourville et al. 2008; van Wassenhove et al., 2005) and there has been a ton of work trying to establish the neural correlates of these networks (e.g., see Golfinopoulos et al. 2009; Shadmehr & Krakauer, 2008), recent work suggesting an association with clinical conditions such as aspects of schizophrenia (Heinks-Maldonado, et al. 2007) and stuttering (Max et al. 2004), and even applications of the concept of high-level cognition such as "thought" (Ito, 2008), as well as applications to social cognition (Wolpert et al. 2003) with links to the mirror system (Miall, 2003).I'm a big fan of control theory in general and I think there is a lot to be gained by thinking about speech processes in these terms. At the same time, I'm a little uncomfortable with the widespread application of these models. It kind of reminds me of the mirror neuron situation in that a framework for thinking about one problem is generalized to all kinds of situations. I'm also a bit uncomfortable about the assumed tethering between forward models and the motor system. A forward model is just a prediction. In the context of motor control, it makes sense to make predictions (e.g., sensory predictions) based on the likely outcomes of motor commands. But more generally, predictions can come from lots of sources. Perceptual fill-in processes are a kind of forward model: the visual system for example makes predictions about the color and texture of a given portion of the visual scene based on the color and texture around that region. One can predict the consequences of an ocean wave hitting a rock based on past perceptual experiences. So forward models don't have to come from the motor system and there are probably lots of systems and mechanisms that generate predictions (forward models). It is worth having a look at Karniel's (2002) short comment, "Three creatures named 'forward model'" for some cautionary discussion.So is the internal forward model concept just hype? No, I don't think so. It has already demonstrated its utility in the motor control literature and there are systems in the brain that appear to support motor-related forward models (cerebellum is one, posterior parietal cortex is another). There are some real insights to be gained from this framework in the speech domain as well, but I think there is the danger of over-application of the concept and we need to proceed cautiously. ReferencesGolfinopoulos, E., Tourville, J.A., and Guenther, F.H. (2009). The integration of large-scale neural network modeling and functional brain imaging in speech motor control. Neuroimage 52, 862-874.Heinks-Maldonado, T.H., Mathalon, D.H., Houde, J.F., Gray, M., Faustman, W.O., and Ford, J.M. (2007). Relationship of imprecise corollary discharge in schizophrenia to auditory hallucinations. Arch Gen Psychiatry 64, 286-296.Ito, M. (2008). Control of mental activities by internal models in the cerebellum. Nat Rev Neurosci 9, 304-313.Karniel, A. (2002). Three creatures named 'forward model'. Neural Networks 15, 305-307.Max, L., Guenther, F.H., Gracco, V.L., Ghosh, S.S., and Wallace, M.E. (2004). Unstable or insufficiently activated internal models and feedback-biased motor control as sournces of dysfluency: A theoretical model of stuttering. Contemporary Issue in Communication Science and Disorders 31, 105-122.Miall, R.C. (2003). Connecting mirror neurons and forward models. Neuroreport 14, 2135-2137.Shadmehr, R., and Krakauer, J.W. (2008). A computational neuroanatomy for motor control. Exp Brain Res 185, 359-381.Tourville, J.A., Reilly, K.J., and Guenther, F.H. (2008). Neural mechanisms underlying auditory feedback control of speech. Neuroimage 39, 1429-1443.van Wassenhove, V., Grant, K.W., and Poeppel, D. (2005). Visual speech speeds up the neural processing of auditory speech. Proc Natl Acad Sci U S A 102, 1181-1186.Wolpert, D., Ghahramani, Z., & Jordan, M. (1995). An internal model for sensorimotor integration Science, 269 (5232), 1880-1882 DOI: 10.1126/science.7569931Wolpert, D.M., Doya, K., and Kawato, M. (2003). A unifying computational framework for motor control and social interaction. Philos Trans R Soc Lond B Biol Sci 358, 593-602.... Read more »

Wolpert, D., Ghahramani, Z., & Jordan, M. (1995) An internal model for sensorimotor integration. Science, 269(5232), 1880-1882. DOI: 10.1126/science.7569931

September 29, 2010
01:05 PM
640 views

Disconnection between phonological input and output codes

by Greg Hickok in Talking Brains

Neuropsychology is not dead.I just read an interesting case study, in the traditional neuropsych style with a detailed behavioral work up of a single stroke patient and an extended discussion of what the findings mean for models of language processing. I like it. I think we can still learn a lot from this sort of investigation. The paper, by Jacquemot, Dupoux, and Bachoud-Levi (2007), reports on a patient, F.A., who suffered a left temporal-parietal stroke with a language profile typical of conduction aphasia: good comprehension, fluent production with occasional paraphasic errors and word-finding problems, and a significant deficit in repetition. F.A. was administered a battery of tests including:Syllable discrimination, minimal pair AX design. Performance = normal.Auditory word-to-picture matching with semantic, phonological, and unrelated foils. Performance = normal.Picture naming involving words of various length/frequency. Performance = "slightly impaired": 84% accuracy compared to 99.7% for controls; a marginal length effect for low frequency words, but not high frequency words.Word repetition involving words of various length/frequency. Performance = mild/moderately impaired: 82.3% correct (cf. 99.7% for controls), with significant length and freq effects.Non-word repetition with items of various length and high vs. low neighborhood density. Performance = SEVERELY impaired: 35.4% correct (cf., 99.6% correct for controls), with no length/density effect. Errors were predominantly phonemic.What does this mean? Speech recognition systems appear to be intact (normal syllable discrimination), speech production systems are at least partially intact (only moderate deficits on picture naming and word repetition), but the link between the two systems is severely damaged (very poor nonword repetition). Non-word repetition is a particularly sensitive metric of the link between perception and production system because you have to use the lower-level sensory ("input lexicon") to motor ("output lexicon") route to perform the task; you can't circumvent this route by using the higher-order sensory-concept-motor route, which is presumably the mechanism allowing for substantially better word repetition performance.As a further test, the authors assessed word and nonword reading. On this task F.A. showed no significant difference between words and nonwords and performed reasonably well on both (91.7% and 83.3% respectively). Maybe with more power a difference could be detected, but clearly the word/nonword performance difference is not nearly as dramatic as with the auditorily presented stimuli in the repetition task. In order to explain the good performance in reading nonwords, we must assume that written forms can access the "output lexicon" (motor speech systems) rather directly. This is reasonable: for example, think back to what you know about the phonological loop -- visual word forms seem to be able to gain access to this system via the articulatory mechanism. So again, this result suggests that the motor speech system is relatively intact with damage primarily to the connection between the sensory and motor systems.Here is the model proposed by Jacquemot et al. as an explanation for F.A.'s performance. (Note: they believe in bidirectional sensory-motor connections, but only show the direction of the damaged link; see below):For those of you schooled in traditional aphasiology, this should look really familiar as it is essentially the Wernicke-Lichtheim model (note: I use the model depiction that Lichtheim actually subscribed to rather than the more commonly used "house-model" depiction that he actually rejected based on the directional arrows. This depiction also accurately reflects W-L's belief in distributed conceptual representations):The A-M disconnection in the Wernicke-Lichtheim model resulted in conduction aphasia (good comprehension, errors in otherwise fluent speech production), and F.A. certainly fit this profile clinically. It's amazing how right Wernicke was about so many things -- more on this in a subsequent post. In terms of more modern models, I've argued previously that the "disconnection" is due to damage to area Spt, which we argue supports sensory-motor transformations. The one thing I disagree with in the Jacquemot et al. paper is the claim for an asymmetry in the connections between input and output systems. Jacquemot et al. claim that while the link between perception and production is impaired, the reverse link, from production to perceptual systems is not. They base this claim on tasks that they argue require phonological access first in the motor system and then transmission to the perception system. One task is written word rhyme judgment, the other is picture-auditory word rhyming. The assumption is that (i) decoding a word or picture into a phonological form can only be achieved on the motor side, and (ii) rhyme judgment is performed on the sensory side. I'm not convinced either of these assumptions are true. Jacquemot C, Dupoux E, & Bachoud-Lévi AC (2007). Breaking the mirror: Asymmetrical disconnection between the phonological input and output codes. Cognitive neuropsychology, 24 (1), 3-22 PMID: 18416481... Read more »

Jacquemot C, Dupoux E, & Bachoud-Lévi AC. (2007) Breaking the mirror: Asymmetrical disconnection between the phonological input and output codes. Cognitive neuropsychology, 24(1), 3-22. PMID: 18416481

September 21, 2010
05:35 PM
843 views

Neuroimaging of language: Why hasn't a clearer picture emerged?

by Greg Hickok in Talking Brains

This is the question raised in a paper by Evelina Fedorenko and Nancy Kanwisher published last year in Language and Linguistics Compass. The main point that they want to make is that language neuroimagers need to stop doing group studies and start doing functional localization in individual subjects, like the vision folks do. I don't disagree at all; e.g., see this post. In fact, we have used individual subject analyses in several of our papers (e.g., Okada & Hickok, 2006; Okada et al., in press).What I found a bit on the irritating side though was the extremely dim and distressingly myopic view of progress in the field of the neural basis of language. They start by stating that two questions have driven dozens of studies on the neural basis of language published in the last several decades: (i) Are distinct cortical regions engaged in different aspects of language? (ii) Are regions engaged in language processing specific to the domain of language? And they suggest that "Neuroimaging has not yet provided clear answers to either question". Regarding question one, there is strong evidence from functional imaging regarding the involvement of distinct cortical regions/circuits in phonemic (STS), lexical-semantic (MTG), prosodic (anterior dorsal STG), and higher-level combinatorial processes (anterior temporal/inferior frontal regions). Additional circuits have been delineated that support auditory-motor integration and auditory/phonological short-term memory. Here are some relevant reviews of this literature: Binder et al., 2000; Hickok and Poeppel, 2007; Indefrey and Levelt, 2004.Regarding question two, several studies have clearly identified voice-specific responses in the STG (Belin et al. 2000), higher-level speech specific responses in the STS (Scott et al. 2000; Okada et al. 2010), and even what we might as well call the anterior temporal lobe sentence area, given how selective it is to the perception of sentence-level stimulation (Humphries et al., 2006; Humphries et al., 2005; Humphries et al., 2001; Rogalsky and Hickok, 2009; Vandenberghe et al., 2002). But more importantly, some of us have moved beyond the specificity issue with the aim of trying to identify the circuits and computations involved in a given process whether or not it is special to speech.So F&K are a bit misinformed in regarding the contribution of neuroimaging to the questions they raise. Even worse, though, is their summary of "where things stand" concerning our understanding of the "neural basis of language" -- a rather sweeping domain, especially if they have in mind only the two questions they raise at the outset. Nonetheless, concerning the Neural Basis of Language they emphasize: 1. that the 19th century idea that Broca's area = speech production and Wernicke's area = speech comprehension doesn't hold up to modern data2. that left frontal regions activate to a variety of language tasks, and indeed even non-linguistic tasks3. that regions outside of the traditional peri-Sylvian cortex activate during language processing4. that meta analyses show lots of overlap between language tasksThis is frankly a pathetic summary of the state of the field and a pretentious starting point for the methodological schooling that F&K provide in the following sections of their paper. Completely ignored in this summary is (i) a body of work showing that much of the confusion (and overlapping activations) evaporates if one is careful about task selection (Hickok & Poeppel, 2007), (ii) convergence on the involvement of the STS in phonemic level processes in speech perception (Leibenthal et al., 2005; Scott & Johnsrude, 2003; Hickok & Poeppel, 2007), (iii) convergence on the idea of a dual stream architecture in language system (Hickok & Poeppel, 2007; Rauchecker & Scott, 2009), (iv) recent progress in mapping the circuit that supports sensory-motor integration in speech processing (Golfinopoulus et al. 2009; Hickok et al., 2009), (v) progress in understanding the basis of hemispheric asymmetries for acoustic and phonemic processing in auditory cortex (Boemio, et al. 2005); Zatorre, et al. 2002) , (vi) convergence on the idea that anterior temporal regions support some aspect of sentence-level processing (the linguistic equivalent of the FFA), (vii) convergence on the relation between sensory-motor circuits and phonological short-term memory (Buchsbaum et al. 2008; Postle, 2006)... I could go on.Yes, there is still plenty of murkiness, much of it surrounding the function of Broca's area, and yes, individual subject analyses would be helpful, but it is not a magic bullet (e.g., task selection is more important in my view) -- e.g., I'm willing to bet that the vision folks still have some work to do -- and the existence of murkiness doesn't justify the characterization of an entire field as failing to make progress due to methodological ineptness. This kind of argumentation was prominent in another of Fedorencko's papers that was featured prominently on this blog. It's a bit disturbing to see it showing up again.F&K's paper has generated a more formal (i.e., published) response by Grodzinsky (2010) who is critical of their take on the field as well but for different reasons. Definitely worth a look.The field of the neural basis of language has made significant progress in the last several years, despite what F&K assert. ReferencesFedorenko, E., & Kanwisher, N. (2009). Neuroimaging of Language: Why Hasn't a Clearer Picture Emerged? Language and Linguistics Compass, 3 (4), 839-865 DOI: 10.1111/j.1749-818X.2009.00143.xBinder, J.R., Frost, J.A., Hammeke, T.A., Bellgowan, P.S., Springer, J.A., Kaufman, J.N., and Possing, E.T. (2000). Human temporal lobe activation by speech and nonspeech sounds. Cerebral Cortex 10, 512-528.Belin, P., Zatorre, R.J., Lafaille, P., Ahad, P., and Pike, B. (2000). Voice-selective areas in human auditory cortex. Nature 403, 309-312.Buchsbaum, B.R., and D'Esposito, M. (2008). The search for the phonological store: from loop to convolution. J Cogn Neurosci 20, 762-778.Golfinopoulos, E., Tourville, J.A., and Guenther, F.H. (2009). The integration of large-scale neural network modeling and functional brain imaging in speech motor control. Neuroimage.Grodzinsky, Yosef. 2010. A clearer view of the linguistic brain: reply to Fedorenko and Kanwisher. Language and Linguistic Compass, 4, pp. 605-622.Hickok, G., and Poeppel, D. (2007). The cortical organization of speech processing. Nat Rev Neurosci 8, 393-402.Humphries, C., Binder, J.R., Medler, D.A., and Liebenthal, E. (2006). Syntactic and semantic modulation of neural activity during auditory sentence comprehension. J Cogn Neurosci 18, 665-679.Humphries, C., Love, T., Swinney, D., and Hickok, G. (2005). Response of anterior temporal cortex to syntactic and prosodic manipulations during sentence processing. Human Brain Mapping 26, 128-138.Humphries, C., Willard, K., Buchsbaum, B., and Hickok, G. (2001). Role of anterior temporal cortex in auditory sentence comprehension: An fMRI study. Neuroreport 12, 1749-1752.Indefrey, P., and Levelt, W.J. (2004). The spatial and temporal signatures of word production components. Cognition 92, 101-144.Liebenthal, E., Binder, J.R., Spitzer, S.M., Possing, E.T., and Medler, D.A. (2005). Neural substrates of phonemic perception. Cereb Cortex 15, 1621-1631.Okada, K., and Hickok, G. (2006). Identification of lexical-phonological networks in the superior temporal sulcus using fMRI. Neuroreport 17, 1293-1296.Okada, K., Rong, F., Venezia, J., Matchin, W., Hsieh, I.H., Saberi, K., Serences, J.T., and Hickok, G. (in press). Hierarchical Organization of Human Auditory Cortex: Evidence from Acoustic Invariance in the Response to Intelligible Speech. Cereb Cortex.Postle, B.R. (2006). Working memory as an emergent property of the mind and brain. Neuroscience 139, 23-38.Rauschecker, J.P., and Scott, S.K. (2009). Maps and streams in the auditory cortex: nonhuman primates illuminate human speech processing. Nat Neurosci 12, 718-724.Rogalsky, C., and Hickok, G. (2009). Selective Attention to Semantic and Syntactic Features Modulates Sentence Processing Networks in Anterior Temporal Cortex. Cereb Cortex 19, 786-796.Scott, S.K., and Johnsrude, I.S. (2003). The neuroanatomical and functional organization of speech perception. Trends Neurosci 26, 100-107.Scott, S.K., Blank, C.C., Rosen, S., and Wise, R.J.S. (2000). Identification of a pathway for intelligible speech in the left temporal lobe. Brain 123, 2400-2406.... Read more »

Fedorenko, E., & Kanwisher, N. (2009) Neuroimaging of Language: Why Hasn't a Clearer Picture Emerged?. Language and Linguistics Compass, 3(4), 839-865. DOI: 10.1111/j.1749-818X.2009.00143.x

August 20, 2010
04:16 PM
756 views

Conduction aphasia, speech repetition, and the left parietal lobe

by Greg Hickok in Talking Brains

Julius Fridriksson has been featured on this blog before and now his team has just published another noteworthy paper in J. Neuroscience. This paper sought to identify the neural correlate of repetition disorder in aphasia. Repetition deficits are characteristic of conduction aphasia although they are not exclusive to conduction aphasia nor is repetition the only deficit in conduction aphasia. Some historical background is useful, if for no other reason than most people get it wrong in one way or another. Here are two myths/misunderstandings about conduction aphasia.1. It is a disorder of repetition. 2. It was first discovered/reported by Lichtheim.As Fridricksson is careful to point out, the repetition disorder is only one symptom of conduction aphasia, the others being impaired word-finding and phonemic paraphasias in production. In fact, the first characterization of the symptoms of conduction aphasia (by Wernicke not Lichtheim) did not make reference to a repetition deficit; rather the hallmarks were impaired word-finding and speech errors, typically with many self-corrective attempts, in the face of otherwise fluent and grammatical speech and good comprehension. Describing the predicted theoretical consequences of a lesion to the connecting pathway between the sensory and motor speech centers, Wernicke (1874) writes,In this case... the patient understands everything. He can always express himself, but his ability to choose the correct word is disturbed in a manner similar to that in the form just described [sensory, aka Wernicke's aphasia]. p. 54Repetition was a clinical assessment invented by Lichtheim which essentially was a means to highlight the paraphasic deficit. In my view, conduction aphasia is a disorder of speech production affecting phonological/phonetic levels of processing and which manifests in paraphasic output on a range of tasks including naming, connected speech and repetition. Regarding the second point, Wernicke was the first to describe a case of conduction aphasia. Most people get this wrong as the Fridriksson et al. paper demonstrates, "Although Wernicke had never seen such a patient, one was later described by Lichtheim" (p. 11057). Not that it matters that much to the science, but it is nice to get the history straight, so here is a quote from Wernicke 1874 (p. 73-74), 11 year before Lichtheim's monograph appeared:The following is a clear case of conduction aphasia... He understands everything correctly and always answers questions correctly. ... He shows no trace of motor aphasia .... He cannot, however, find words for many objects he wishes to designate [word finding deficit]. He makes an effort to find them, becoming agitated in the process, and if one names them for him he repeats the name without hesitation. ... He can say many things fluently, especially familiar expressions. He then comes to a word on which he stumbles, remains caught on it, exerts himself and becomes irritated. After that every word that he utters, haltingly, is nonsensical [phonemic paraphasias]; he corrects himself over and over again [self-corrective attempts], and the harder he tries the worse the situation becomes...Classically, conduction aphasia is thought to result from a disconnection between sensory and motor speech areas caused by damage to the arcuate fasciculus (the idea of AF involvement came after Wernicke's 1874 monograph, but he bought into it). Recent work has provided a pretty strong case against the AF being the critical structure. Here's a previous entry on this topic based on the work of Nina Dronkers and colleagues.Ok, enough with the history. Now on to the paper. Friderksson et al. studied a series of 45 acute stroke patients behaviorally, including a test of repetition, and neuroradiologically. For the latter they acquired by structural MRI and perfusion weighted MRI. The use of perfusion weighted imaging in acute stroke is a method championed by Argye Hills at Johns Hopkins, and is, in my view, an excellent tool. What's interesting about the study is that they didn't select patients on the basis of aphasia type or even the presence of a repetition disorder. Instead they included a range of patients, measured their repetition ability and looked to see what correlated with deficits. This is a useful approach. The only problem in this case is that, as noted in the paper, repetition deficits can result from disruption anywhere along the pathway between perception and production (e.g., peripheral hearing loss will cause a repetition deficit), so in this sense the study is kind of a shotgun approach that will only capture central tendencies. Nonetheless, here is what they found.Structural damage to the white matter beneath the left supramarginal gyrus, which includes the arcuate fasciculus, was the most strongly correlated region with repetition impairment. HOWEVER, perfusion imaging told a different story, implicating a cortical zone that included the parietal operculum (inferior SMG) (see their Figure 2, bottom row) and a temporal-parietal junction region (which unfortunately they don't picture). This is the same general region implicated in conduction aphasia (Baldo et al. 2008) and where sensory-motor area Spt lives (Hickok et al. 2003, 2009).Fridriksson et al. are appropriately cautious in concluding that it is the cortical involvement that causes the deficit, instead concluding that speech repetition is "strongly associated with damage to the left arcuate fasciculus, supramarginal gryus, and TPJ" (p. 11060). I wouldn't disagree that the AF, as a connecting pathway plays an important role, but I would argue strongly that the deficit results, computationally speaking, from damage to cortex, area Spt in particular. In addition, Fridriksson et al. suggest that their findings do not address the other symptoms of conduction aphasia. It is true that they didn't explicitly examine these symptoms, but I believe the symptoms are connected, particularly the repetition and phonemic paraphasias.ReferencesBaldo JV, Klostermann EC, & Dronkers NF (2008). It's either a cook or a baker: patients with conduction aphasia get the gist but lose the trace. Brain and language, 105 (2), 134-40 PMID: 18243294Fridriksson J, Kjartansson O, Morgan PS, Hjaltason H, Magnusdottir S, Bonilha L, & Rorden C (2010). Impaired speech repetition and left parietal lobe damage. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (33), 11057-61 PMID: 20720112Hickok, G., Buchsbaum, B., Humphries, C., & Muftuler, T. (2003). Auditory-Motor Interaction Revealed by fMRI: Speech, Music, and Working Memory in Area Spt Journal of Cognitive Neuroscience, 15 (5), 673-682 DOI: 10.1162/jocn.2003.15.5.673... Read more »

Baldo JV, Klostermann EC, & Dronkers NF. (2008) It's either a cook or a baker: patients with conduction aphasia get the gist but lose the trace. Brain and language, 105(2), 134-40. PMID: 18243294

Fridriksson J, Kjartansson O, Morgan PS, Hjaltason H, Magnusdottir S, Bonilha L, & Rorden C. (2010) Impaired speech repetition and left parietal lobe damage. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30(33), 11057-61. PMID: 20720112

Hickok, G., Buchsbaum, B., Humphries, C., & Muftuler, T. (2003) Auditory-Motor Interaction Revealed by fMRI: Speech, Music, and Working Memory in Area Spt. Journal of Cognitive Neuroscience, 15(5), 673-682. DOI: 10.1162/jocn.2003.15.5.673

Hickok G, Okada K, & Serences JT. (2009) Area Spt in the human planum temporale supports sensory-motor integration for speech processing. Journal of neurophysiology, 101(5), 2725-32. PMID: 19225172

August 11, 2010
01:30 PM
817 views

Importance of phonemes in speech production

by Greg Hickok in Talking Brains

In a previous post I have questioned whether we need to explicitly represent phonemes in speech perception. Massaro and others have raised this issue in the past. Phonemes, the line of thinking goes, are only really important for production. There are linguistic arguments for this that I won't detail here. There is also well-known speech error data which shows that phoneme size units can break off and dislocate themselves. Here I want to highlight some evidence from aphasia. A reviewer of one of my papers pointed me to this study by Lindsey Nickels and David Howard.A group of aphasics who exhibited speech production errors were asked to repeat words that varied in terms of the number of phonemes, number of syllables, or syllable complexity (defined in terms of consonant clusters). These variables are, of course, highly correlated, but the stimuli were carefully designed so that the contribution of each of these factors could be examined using logistic regression analyses. The main result was that only number of phonemes in a word predicted correct repetition (see graph below derived from their Table 4) and once this variable was taken into account, the number of syllables or syllable complexity did not explain any additional variance. Phonemes seem to matter in speech production. I have to say, though, that I'm not fully convinced that the others factors aren't also important.Nickels, L., & Howard, D. (2004). Dissociating Effects of Number of Phonemes, Number of Syllables, and Syllabic Complexity on Word Production in Aphasia: It's the Number of Phonemes that Counts Cognitive Neuropsychology, 21 (1), 57-78 DOI: 10.1080/02643290342000122... Read more »

Nickels, L., & Howard, D. (2004) Dissociating Effects of Number of Phonemes, Number of Syllables, and Syllabic Complexity on Word Production in Aphasia: It's the Number of Phonemes that Counts. Cognitive Neuropsychology, 21(1), 57-78. DOI: 10.1080/02643290342000122

login

Talking Brains

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

Why is this post inappropriate?

search

topics

dates

View

Language

Languages to Display

join us!

News