Conduction aphasia, speech repetition, and the left parietal lobe

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. 54

Repetition 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.

References

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

Wernicke, C. (1874/1969). The symptom complex of aphasia: A psychological study on an anatomical basis. In Boston studies in the philosophy of science, R.S. Cohen, and M.W. Wartofsky, eds. (Dordrecht: D. Reidel Publishing Company), pp. 34-97.