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OPINION
Year : 2021  |  Volume : 19  |  Issue : 4  |  Page : 282-283

Paradox of the cranial nerves: Does the description of the facial nerve need a reinterpretation?


Department of Medicine, M.O.S.C Medical College and Hospital, Ernakulam, Kerala, India

Date of Submission28-Mar-2021
Date of Decision01-May-2021
Date of Acceptance29-May-2021
Date of Web Publication07-Dec-2021

Correspondence Address:
Prof. Abraham M Ittyachen
Department of Medicine, M.O.S.C Medical College and Hospital, Kolenchery, Ernakulam - 682 311, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_26_21

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  Abstract 


For years, generations of medical students were taught that in stroke, “;In a upper motor neuron (UMN) lesion, the upper part of the face is spared because this part of the face has bilateral representation while in a lower motor neuron (LMN) lesion, both parts of the face are involved.” Is this explanation apt ? Most of the fibers of the corticospinal tract decussate to the opposite side. But only 50% of the corticobulbar fibers decussate, meaning the muscles they supply receive fibers from both motor cortex (bilateral representation). Bilateral representation in the cortex is a perfect example of symmetry in the human body. An exception to this rule would be the lower part of the face which receives fibers from the contralateral cortex alone (unilateral representation). This goes against the general rule and so this represents the first paradox of the cranial nerves. The second paradox is entirely man made and is reversible. Should it not be, “;In a UMN lesion of the facial nerve, only the contralateral lower half of the face is affected, because this part of the face has unilateral representation only” and not “;In a UMN lesion of the facial nerve, the contralateral upper part of the face is spared because this part of the face has bilateral representation.” After all, is not bilateral representation the rule and unilateral representation the exception ?.

Keywords: Cranial nerves, facial nerve, decussation of cranial nerves


How to cite this article:
Ittyachen AM. Paradox of the cranial nerves: Does the description of the facial nerve need a reinterpretation?. Curr Med Issues 2021;19:282-3

How to cite this URL:
Ittyachen AM. Paradox of the cranial nerves: Does the description of the facial nerve need a reinterpretation?. Curr Med Issues [serial online] 2021 [cited 2022 Jan 27];19:282-3. Available from: https://www.cmijournal.org/text.asp?2021/19/4/282/331824



For years, generations of medical students were taught (and continue to be taught) that in stroke, “;In a upper motor neuron (UMN) lesion, the upper part of the face is spared because this part of the face has bilateral representation while in a lower motor neuron (LMN) lesion, both parts of the face are involved.” Is this explanation apt?

Any student of clinical medicine knows that knowledge of neuroanatomy is the key to localization of a nerve lesion. The cranial nerve nuclei in the brainstem along with the corresponding nerve comprise the LMN. The LMN in turn receives fibers from the contralateral motor cortex through the descending corticobulbar tracts (also called corticonuclear tracts). The neurons from which corticobulbar tracts arise are known as UMN, and their cell bodies lie in the primary motor cortex (Brodmann area 4) in the frontal lobe.

From the time of Hippocrates, in ancient Greece, it was known that injury to the left part of the brain resulted in weakness of the right side of the body. As science progressed, so did our knowledge about neuroanatomy. Most of the fibers of the corticospinal tract decussate (cross over) to the opposite side. This explains the weakness on the opposite side. But why decussation occurs in the nervous system has always been a mystery.[1] The first person to develop a conceptual framework to explain contralateral representation and decussation in a functional manner was Cajal.[2] Although Cajal's theory is still popular, it has got several problems. Hence, other theories have been put forward.[3],[4] A currently accepted theory is that decussation evolved as a byproduct of a genetically determined partial inversion of the body plan, which resulted in a 180° rotation posterior to the brain and oropharynx.[5]

But what about the corticobulbar tracts? Unlike the corticospinal tract, only 50% of the corticobulbar fibers decussate, meaning the muscles they supply receive fibers from both motor cortexes (bilateral representation). This includes corticobulbar fibers to the motor nuclei of the trigeminal (Cranial nerve V), part of facial (Cranial nerve VII), glossopharyngeal (Cranial nerve IX), vagus (Cranial nerve X), accessory (Cranial nerve XI), and hypoglossal (Cranial nerve XII) nerves.[6],[7] Hence, in a one-sided lesion involving the corticobulbar tract, there would be relative sparing of the orofacial and neck musculature (with the exception of muscles of the lower half of the face supplied by the facial nerve) because of bilateral innervation.

There are also other lesser-known pathways in the central nervous system where the decussation is not symmetric and one such pathway is the dentatorubrothalamic tract.[8] Bilateral influence on limb movement by the individual cerebellar hemispheres is yet another example and has been shown in several functional magnetic resonance imaging studies under physiological conditions.[9] Then, there is the question of emotional movements which are considered involuntary and are clinically dissociated from voluntary facial movements. This can be explained only by a separate supranuclear pathway. The current thinking is that the cingulate motor area and/or supplementary motor areas are the areas considered vital for emotional facial movement.[10] However, it is not known with certain pathways which mediate the innervation of facial muscles for this movement.[11],[12]

Symmetry is well known in physics. The laws of physics are symmetric under translation in space and time; they do not change.[13] Bilateral representation in the cortex that was explained above is a perfect example of symmetry in the human body. One well-known exception to this rule as explained above would be the lower part of the face which receives fibers from the contralateral cortex alone (unilateral representation only). This goes against the general rule of distribution of motor fibers through the cranial nerves, and so, this represents the first paradox of the cranial nerves. This paradox is probably one of creation; apart from that we can only theorize. This paradox is permanent and cannot be changed.

Now, the second paradox is entirely man made and is reversible. Should it not be, “;In a UMN lesion of the facial nerve, only the contralateral lower half of the face is affected, because this part of the face has unilateral representation only” and not “;In a UMN lesion of the facial nerve, the contralateral upper part of the face is spared because this part of the face has bilateral representation.” After all, is not bilateral representation the rule and unilateral representation the exception?

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Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Vulliemoz S, Raineteau O, Jabaudon D. Reaching beyond the midline: Why are human brains cross wired? Lancet Neurol 2005;4:87-99.  Back to cited text no. 1
    
2.
Cajal RY, Santiago. Estructura del kiasma optico y teoria general de los entrecruzamientos de las vias nerviosas (Structure of the Chiasma opticum and general theory of the crossing of nerve tracks). Rev Trim Micrográfica 1898;3:15-65.  Back to cited text no. 2
    
3.
de Lussanet MH, Osse JW. An ancestral axial twist explains the contralateral forebrain and the optic chiasm in vertebrates. Animal Biol 2012; 62:193-216.  Back to cited text no. 3
    
4.
Kashalikar SJ. An explanation for the development of decussations in the central nervous system. Med Hypotheses 1988;26:1-8.  Back to cited text no. 4
    
5.
Kinsbourne M. Somatic twist: A model for the evolution of decussation. Neuropsychology 2013;27:511-5.  Back to cited text no. 5
    
6.
Benarroch EE, Westmoreland BF, Daube JR, Reagan TJ, Sandok BA. Medical neurosciences: An approach to anatomy, pathology, and physiology by systems and levels. The Motor System. 4th ed., Ch. 8. Philadelphia, PA: Lippincott Williams & Wilkins; 1999. p. 193-247.  Back to cited text no. 6
    
7.
Heimer L. The human brain and spinal cord. Functional neuroanatomy and dissection guide. Spinal cord and the Descending Supraspinal Pathways. 2nd ed., Ch. 15. New York, Berlin, Heidelberg, London, Paris, Tokyo, Hong Kong, Barcelona, Budapest: Springer-Verlag; 1995. p. 316-34.  Back to cited text no. 7
    
8.
Meola A, Comert A, Yeh FC, Sivakanthan S, Fernandez-Miranda JC. The nondecussating pathway of the dentatorubrothalamic tract in humans: Human connectome-based tractographic study and microdissection validation. J Neurosurg 2016;124:1406-12.  Back to cited text no. 8
    
9.
Ellerman JM, Flament D, Kim SG, Fu QG, Merkle H, Ebner TJ, et al. Spatial patterns of functional activation of the cerebellum investigated using high field (4 T) MRI. NMR Biomed 1994;7:63-8.  Back to cited text no. 9
    
10.
Jox R, Bruning R, Hamann G, Danek A. Volitional facial palsy after a vascular lesion of the supplemental motor area. Neurology 2004;63:756-7.  Back to cited text no. 10
    
11.
Gilden DH. Bell's palsy. N Engl J Med 2004;351:1323-31.  Back to cited text no. 11
    
12.
Hopf HC, Müller-Forell W, Hopf NJ. Localization of emotional and volitional facial paresis. Neurology 1992;42:1918-23.  Back to cited text no. 12
    
13.
Livio M. Physics: Why symmetry matters. Nature 2012;490:472-3.  Back to cited text no. 13
    




 

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