Facial droop

In working with stroke patients one of the most obvious symptoms is facial droop on one side. Often swallowing is also affected.  If there is a common drive for this musculature and it was the only drive that mattered then facial droop or swallowing problems should not be seen if the vascular accident is in the non dominant hemisphere.  However I don't think that is the case.

In my own older movements of the left face, throat, sublingual musculature and tongue I do think that they are and were left hemisphere dominant (right side of face). My newer movements that feel strange and left sided are I think right hemisphere dominant. So back to the original point even if there is a common drive as referenced in the link below it can not be the only input that matters or there would not be seen the facial droop or swallowing problems expressed on the non dominant side.

How can I rectify the two ideas? It suggests to me that learned behaviors have a role and can be dominant over the left right wiring system. Does the common drive ladder itself over the input from the nondominant hemisphere?  There are weak at points in both that I do not have a good explanation for.

From my Disconnect post.

My gut feel is that my structures close to my midline are somehow more or less directed by the left hemisphere in my older more normal way of moving and still by far the usual if I am not paying attention.  In a study referred by the Doctor it suggests what I found in my own movement. (Evidence for bilateral innervation of certain homologous motoneurone pools in man L. J. Carr, Linda M. Harrison * and J. A. Stephens)

What it feels like is I have not learned to differentiate degrees of relaxation (inhibition) on my left facial, throat, sublingual musculature and the very recalcitrant left tongue. Sort of it's on or it's off in the case of a stroke, but the gradations of relaxation needed for coordination come the contralateral hemisphere.

common drive


1. Surface EMG recordings were made from left and right homologous muscle pairs in healthy adults. During each recording session subjects were requested to maintain a weak isometric contraction of both the left and right muscle. 2. Cross-correlation analysis of the two multiunit EMG recordings from each pair of muscles was performed. Central peaks of short duration (mean durations, 11.3-13.0 ms) were seen in correlograms constructed from multiunit EMG recordings obtained from left and right diaphragm, rectus abdominis and masseter muscles. No central peaks were seen in correlograms constructed from the multiunit EMG recordings from left and right upper limb muscles. 3. To investigate descending pathways to the homologous muscle pairs, the dominant motor cortex was stimulated using a focal magnetic brain stimulator whilst recording from homologous muscle pairs. 4. Following magnetic stimulation of the dominant motor cortex, a response was recorded from both right and left diaphragm, rectus abdominis and masseter muscles. In contrast, when recording from homologous upper limb muscles, a response was only seen contralateral to the side of stimulation. 5. The finding of short duration central peaks in the cross-correlograms constructed from multiunit recordings from left and right diaphragm, rectus abdominis and masseter, suggests that muscles such as these, that are normally co-activated, share a common drive. The mechanism is discussed and it is argued that the time course of the central correlogram peaks is consistent with the hypothesis that they could be produced by a common drive that arises from activity in last-order branched presynaptic fibres although presynaptic synchronization of last-order inputs is also likely to be involved. 6. The results of the magnetic stimulation experiments suggest that this common drive may involve the corticospinal tract. 7. We saw no evidence for a common drive to left and right homologous muscle pairs that may be voluntarily co-activated but often act independently.