Ventral premotor cortex¶

https://www.ncbi.nlm.nih.gov/pubmed?term=ventral%20premotor%20cortex

Introduction¶

{Vigneau et al., 2006, #88117}

Three frontal areas involved in phonological processing seem to be concerned with sensory–motor control, including an upper motor area for mouth motion control, a lower premotor area in the precentral gyrus that is dedicated to pharynx and tongue fine-movement coordination, and a sensory–motor integration region in the Rolandic operculum (Table 4, Fig. 2, bottom).

The area that encompasses the Rolandic operculum and the postcentral gyrus of the insula (RolOp) is activated by overt or covert syllable articulation (Heim et al., 2002), pseudo-word articulation (Herbster et al., 1997 and Warburton et al., 1996), or word repetition (Price et al., 1996a). A role in sensory–motor adjustments during speech articulation must be evoked for this area as it includes regions that are related to sensory integration. However, in contrast to the mouth area, activity asymmetry in this region depends on the nature of the material: leftward asymmetry is observed during silent recitation of the month of the year, and rightward asymmetry during silent singing (Wildgruber et al., 1996).

Hearing speech activates motor cortex¶

{Hickok, 2012, #81906}

Here, I only add the point that activation of an auditory speech form, whether internally or externally, seems to automatically define a potential target for action and consequently excites a corresponding motor program, regardless of whether there is an intention to speak. This assertion is based on the observation that the perception of others’ speech activates motor speech systems53, 54 and that the speech of others, even if it is ambient, can be unintentionally imitated by a listener or speaker55, 56, 57. The existence of echolalia, the tendency of individuals with certain acquired or developmental speech disorders to repeat heard speech58, 59, provides additional evidence for this assertion in that it suggests that an underlying, almost reflexive sensory-to-motor activation loop exists. In the normal brain, listening to speech and the consequent activation of the sensory-to-motor circuit does not normally result in motor execution (and hence repetition of heard speech), presumably because motor selection mechanisms inhibit this behaviour at some level. Echolalia seems to be induced by an abnormal release from inhibition of this motor selection system.

The ventral premotor cortex and motor vocabularies. The ventral premotor cortex has been implicated in motor vocabularies in both speech and manual gestures13, 40, 42, 67, 68. As noted above, Levelt et al.’s notion of a mental syllabary — a repository of gestural scores for the most highly used syllables in a language3 — has been linked to the ventral premotor cortex in a large-scale meta-analysis of functional imaging studies65. A recent prospective functional MRI (fMRI) study that was designed to distinguish phonemic and syllable representations in motor codes provided further evidence for this view by demonstrating adaptation effects in the ventral premotor cortex to repeating syllables69.

Apraxia of speech (AOS) is a motor speech disorder that seems to affect the planning or coordination of speech at the level that has been argued to correspond to syllable-sized units70, 71. Although this conclusion should be regarded as tentative, it is clear that AOS is not a low-level motor disorder such as dysarthria, which manifests as a consistent and predictable error (misarticulation) pattern in speech that is attributable to factors such as muscle weakness or tone. Rather, AOS is a higher-level disorder with a variable error pattern72. The ventral premotor cortex has been implicated in the aetiology of AOS73, as has the nearby anterior insula74, 75. It is worth noting that speech errors in AOS and conduction aphasia (Box 1) are often difficult to distinguish, the difference being most notable in speech fluency, with AOS resulting in more halting, effortful speech72. The similarity in error type and the distinction in fluency between AOS and conduction aphasia is consistent with the present model if one assumes that the two disorders affect the same level of hierarchical motor control (errors occur at the same level of analysis) but in different components of the circuit (AOS affects access to motor phonological codes and conduction aphasia affects internal SFC).

In the visual–manual domain, physiological evidence from monkeys has suggested the existence of grasping-related motor vocabularies in the ventral premotor cortex67, 68. Grafton has emphasized that such a motor vocabulary codes relatively higher motor programs — for example, correspondences between object geometry and grasp shape — that are then implemented by interactions with the primary motor cortex13. This conceptualization is similar to the present hierarchical model for speech actions.

{Murakami et al., 2015, #51819}

Speech processing models proposed parallel processing in two speech processing streams that connect temporal speech regions to frontal cortices (Hickok and Poeppel, 2007; Rauschecker and Scott, 2009): A ventral stream that originates in auditory cortex and connects anterior temporal lobe regions to anterior parts of Broca’s area is thought to mediate transformations between phonology and semantics. A dorsal stream is thought to map sensory speech representations in the posterior superior temporal lobe to articulatory motor cortices in ventral premotor cortex/posterior Broca’s area via a sensorimotor interface in area SPT. In our study, articulatory M1 involvement during passive listening to speech was dependent on integrity of the posterior input regions of the dorsal stream, namely, the pSTS and SPT (Hickok and Poeppel, 2007; Murakami et al., 2012), but not the aSTG in the ventral stream. Thus, facilitation of left articulatory M1 excitability during passive listening to speech was not mediated via the ventral stream or the right hemisphere, at least not to an extent to compensate for virtual lesions of the left dorsal stream. We cannot exclude that ventral stream output could also modulate M1 excitability under different conditions, such as linguistic or speech production tasks (see, e.g., Rauschecker, 2011; Hickok, 2012). Although we investigated dorsal stream components separately in this study, there is sufficient empirical evidence from effective connectivity studies (e.g., see Murakami et al., 2012) that they form a task-dependent functional network and thus a “speech processing stream.” Our double-knock-out versus individual lesioning data support dorsal stream models in which the dorsal stream is divided into a dorsodorsal stream that connects the SPT to the dPMC and a dorsoventral stream that connects the SPT to the pIFG (Hickok and Poeppel, 2007; Giraud and Poeppel, 2012). Such parallel branches within the dorsal stream could also explain why the dPMC usually is a “negative” language site (Sanai et al., 2008) that often can be safely removed during neurosurgery without gross adverse effects on language performance. Nevertheless, lesions of dPMC could affect subtler functions, such as synchronizing motor routines to external sensory cues (Neef et al., 2011), a function that relies upon efficient sensorimotor integration. Thus, the dPMC may be more important in feedback-controlled conditions that require highly precise sensorimotor timing, such as learning how to speak during development or how to utter unknown speech in adulthood (Hartwigsen et al., 2013).