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I want to get my head round this once and for all so if you guys could help me would really appreciate it! I understand lesions to the optic nerve. It is the other nerves that I find difficult.

So far this is my understanding, please correct me if I'm wrong. The cranial nerves do not decussate generally with exceptions being CN2, CN4, CN7 and CN12. That means if a lesion affects Cranial Nerve 1, 5, 8, 9 and 11 or the respective nucleus there is either sensation loss or atrophy of the muscle (dependent on what the nerve does) of the ipsilateral side. For example in a lesion affecting CN6, the eye cannot look out in the side of the lesion.

In the case of CN4, I'm not too sure what happens but I imagine if there is damage to the nucleus the opposite side is affected (meaning superior oblique in the contralateral side will not work). If the nerve is affected, it is typically the ipsilateral side. The same I imagine is true for CN12.

In CN7, the forehead is bilaterally innervated so if the upper motor neurone is affected eyebrows can be raised but the lower side of the face is affected ipsilaterally. In a lower motor neurone lesion, there is complete loss of one side of the face ipsilaterally.

Am I correct?

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2 Answers 2

As you mentioned, the resulting impairment depends on the level of the injury: nuclear, fascicular, central / peripheral. So, you should differentiate lesions inside the brain tissue (which can be at nucleus, at any location of a tract, before crossing or after, and outside. From this, the first thing we should explain is the normal anatomy. From normal anatomy we can understand the pathology.

One interesting fact you probably wanted to know is that Optic Nerve it not a real nerve in a classic definition, because it begins outside the brain as grouping axons of RGCs (retinal ganglion cells) and after leaving the eye becomes a “nerve”. From this, you can understand its damage better, because the damage to the visual fields depends on the level of insult.

IV nerve is the only cranial nerve that completely crossed (decussated). Thus, the lesion before the crossing/decussation (you were right mentioning the nucleus, but we extend the “region” until the decussation) will cause palsy and consequent atrophy contralaterally to the lesion. After the decussation the palsy and atrophy will be ipsilateral.

Considering cranial nerve XII we should speak about nuclear-infranuclear and supranuclear damage and with this notion supranuclear damage will cause contralateral transient tongue paresis. Nuclear-infranuclear damage will cause more permanent palsy, which is mostly bilateral because the nuclei are close to each other.

Considering VII pair, nuclear-intranuclear damage (“peripheral”) will cause ipsilateral hemifacial palsy including the brow and eyelid, while supranuclear (“central”) lesion will cause contralateral facial palsy with brow/eyelid sparing.

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I just wanted to add, regarding CN VII.

CN VII receives stimulation via the facial nucleus from both the ipsilateral and the contralateral corticobulbar tracts. The upper muscles of facial expression (particularly around the eyes) receive stimulation from both the ipsilateral and the contralateral corticobulbar tracts. The lower portion of the face is innervated only from the contralateral corticobulbar tract. So in case of a stroke which wipes out an entire track (either left or right), there will be total loss of the lower muscles of facial expression, however there will be some sparing of the upper muscles because of the ipsilateral pathway redundancy.

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