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The primary motor cortex did not demonstrate any ramping of activity in these trials (Figure 6c).

Sham stimuli to motor cortex did not evoke MEPs even at 100% stimulator output.

Likewise, poly(GP) levels in the motor cortex did not associate with frontal cortical or hippocampal pTDP-43 pathology.

Importantly, the control experiment demonstrated that the excitability of the hand motor cortex did not differ during observation of known speech, unknown speech and gurns.

Moreover, the extent of DPR pathology in frontal cortex and motor cortex did not correlate with neurodegeneration in FTLD or MND cases.

Noteworthy is also that theta phase in the left primary motor cortex did not predict MEP size at all, nor did slow beta phase immediately before or at TMS onset.

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Similar(52)

Motor cortex does not contain articulatory representations of perceived actions in speech, but rather, represents auditory vocal information.

This means that the motor cortex does not control the details of limb movement directly but instead controls the abstract parameters of movement, regardless of the connected apparatus that is actually moving.

Thus, the absence of a representation of the missing limb in the motor cortex does not exclude the possibility that amelics possess a body schema that includes some form of sensorimotor representation of all four limbs.

Given this, we asked whether the absence of a phantom limb in the majority of amelics means that the motor cortex does not contain a cortical representation of the missing limb, or whether it is present but has been deactivated by the lack of sensorimotor experience.

We interpret this as evidence that their motor cortex does not contain a representation of the missing limb, or that if such a representation exists it receives extremely strong inhibitory inputs and cannot be accessed either voluntarily or following intense external stimulation.

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