Facial palsy in stroke. Will there be upper facial involvement? 

You’re examining a patient presented with a stroke and you are expecting an upper motor neuron lesion. In your medical school training period you have been tought that opthalmic division of facial nerve has bilateral innervation and the lower facial group has singular contralateral innervation. Hence, supranuclear lesion of the VII nerve will result in contralateral facial palsy with sparing of the forehead (opthalmic division of facial nerve). This is the traditional knowlegde mentioned in all typical textbook.

However, sometimes you came across a number of patients for whom you confidently labelled having a upper motor neuron lesion; but on routine examination you noticed there is some forehead muscle weakness and eyelid closure is slightly weak compared to the contralateral side. Is there component of lower motor neuron lesion? Or is this a brainstem lesion? Neither both explained a simple hemiplegia  with ipsilateral facial weakness that included the opthalmic division.

A study by Morecraft et al. [ref 1], for which they studied the corticobulbar projection to musculotopically defined subsectors of the facial nucleus; from the face representation of the primary (M1), supplementary (M2), rostral cingulate (M3), caudal cingulate (M4) and ventral lateral pre- (LPMCv) motor cortices in the rhesus monkey.


Image 1 (image reproduced from ref 1). Schematic diagrams of the medial (top) and lateral (bottom) surfaces of the cerebral cortex of the rhesus monkey depicting the basic organization of the frontal lobe and adjacent cingulate cortex. A arm; as arcuate sulcus; cf calcarine fissure; cgs cingulate sulcus; cs central sulcus; Ea ear; F face; FEF frontal eye fields; Fr frontalis; ios inferior occipital sulcus; ips intraparietal sulcus; L leg; lf lateral fissure; LL lower lip; LPMCd dorsal lateral premotor cortex; LPMCv ventral lateral premotor cortex; ls lunate sulcus; M1 primary motor cortex; M2 supplementary motor cortex; M3 rostral cingulate motor cortex; M4 caudal cingulate motor cortex; OO orbicularis oculi; P platysma; pre-SMA pre- supplementary motor cortex; rs rhinal sulcus; SEF supplementary eye field; sts superior temporal sulcus; poms medial parieto- occipital sulcus; sts superior temporal sulcus; UL upper lip.

In summary from their research, the neuroanatomical pathway is as follow: M1, LPMCv, LPMCd (dorsal lateral premotor cortex) and M4 projected primarily to the contralateral lateral subnucleus, which innervated the perioral musculature. M2 projected bilaterally to the medial subnucleus, which supplied the auricular musculature. M3 projected bilaterally to the dorsal and intermediate subnuclei, which innervated the frontalis and orbicularis oculi muscles, respectively.

Hence, we can draw conclusion that damages area at M3 can result in upper facial weakness which is a upper motor neuron lesion. The next question in mind will be why ipsilateral since it is a bilateral innervation. The works that done by Morecraft et al. would suggest a symmetrical weakness in frontralis and orbicularis oculi muscles. It is also suggested by Morecraft et al. that laterality might exist in different in par with Damasio’s observation of weakness occurring in the contralateral orbicularis oculi in patients with unilateral anterior cingulate damage [ref1] [ref 2].

A clinical studies conducted by Cattaneo et al. [ref3] in 2010, where they investigate pattern of volitional facial motor deficits in acute stroke patients. They do so by assessing the strength of single facial movements and its correlation to the site of infarct classified on computed tomography scans. They showed that that central volitional facial palsy is not a uniform entity but rather there is a variability in the involvement of different voluntary facial movements.  There is a more complex pattern rather than a clear-cut distinction in upper and lower movements. In this study, they found that ACA territory significantly predicts eyelid weakness, but eyelid weakness is present at times also in MCA infarction. Correlation with the radiological features shows that eyelid closure movements are supported by a motor representation within the ACA territory, although present also in the Rolandic regions. Therefore there might be a  duplex representation of voluntary eyelid movements, one in the mesial frontal cortex and the other in the Rolandic region. The movements of forehead elevation and mouth closure were observed in both ACA and MCA infarction. They had no significant predictor in the different vascular territories, and were always mildly affected. If you read the result in table 1, there is some weakness in forehead though considered as non-significant in this study. In fact, it may be upper facial sparing is relative rather than absolute [ref 4, 5]. Below is the table showing the result of the study [ref 3 ]

Table 1 and 2 reproduced from [ref 3]

In summary, facial representation in corticofacial pathway is complex. Although upper facial innervation is bilateral as shown in animal studies, there might be laterality in difference species hence one side might be weaker than contralateral side (Cattaneo et al. 2010 paper done by comparing the contralateral side, hence we unable to jugde if both side is reduced with one side more significant). Therefore upper motor neuron lesion (central facial nerve lesion) can provide you the impairment of opthalmic division of the facial nerve.

References

1. Morecraft RJ, Louie JL, Herrick JL, Stilwell-Morecraft KS. Cortical innervation of the facial nucleus in the non-human primate: a new interpretation of the effects of stroke and related subtotal brain trauma on the muscles of facial expression. Brain 2001;124:176–208.

2. Damasio AR. Descartes’ error: emotion, reason, and the human brain. New York: Grosset/Putnam; 1994. p. 139–43.

3. Luigi Cattaneo, Elena Saccani, Piero De Giampaulis, Girolamo Crisi, and Giovanni Pavesi. Central Facial Palsy Revisited: A Clinical-Radiological Study. ANN NEUROL 2010;68:404–408.

4. Bradley WG, Daroff RB, Fenichel GM, Marsden CD. Neurology in clinical practice. Oxford, UK: Butterworth-Heinemann, 2000.

5. Campbell WW. DeJong’s The Neurologic Examination. Philadel- phia, PA: Lippincott Williams & Wilkins, 2005.

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