The medial region or area of the pons can be damaged due to vascular insult. If it’s the medial structures
of the pons, this would be medial pontine syndrome. This is going to be due to a lesion of the basilar
artery that travels over the pons and gives rise to numerous pontine vessels to help supply them.
Structures that are damaged in the medial pontine syndrome, there will be three. The corticospinal tract,
the descending pathway is damaged. The medial lemniscus pathway, ascending tract is damaged.
You’ll have damage to abducens nerve fibers, so you have a cranial nerve involvement as well.
So two pathways and one cranial nerve being involved. We can see a couple of this very readily.
At this level section, here’s your medial lemniscus here in blue. Then here you have your corticospinal
components here in red. The abducens fibers are not visible at this axial level. We would have to be
distal or inferior to this level. If injury to each one of these structures, what would we see or what would
you see? First, the corticospinal tract symptoms. This would result in contralateral hemiparesis of upper
and lower extremities. The medial lemniscus system is conveying vibration, conscious proprioception,
and fine touch. If this pathway is lesioned, then you’ll have a contralateral loss of those functions.
With abducens fiber injury, you will essentially inhibit or cause paralysis of the lateral rectus, the muscle
that moves the eyeball laterally or moves it so that it adducts. If you can’t do that any longer, the eye
will move medially and that is medial strabismus. You can also have injury or lesion of the lateral
structural components of the pons. This would result in lateral pontine syndrome. This is also due to
vascular insult, so it's a vascular lesion. A couple of vessels can produce this. The basilar artery is a culprit.
The anterior inferior cerebellar arteries can also produce this lesion. Several structures are damaged
or lesioned in this particular syndrome. One of which would be the spinothalamic tract components.
Communications or a tract connection with the cerebellum is lesioned. Vestibular and cochlear nuclei
are also damaged. The facial nucleus is an involved structure. It’s damaged. Descending hypothalamic
fibers are also injured in this syndrome. There’s a lesion of the trigeminal nucleus, so we do have some
cranial nerve components that are damaged or lesioned in this syndrome. We do have some tracts
that are damaged as well. Injury to the spinothalamic tract would result in a loss of pain and temperature
from the contralateral side of the body. This would be distal to the face. A lesion of the cerebellar tract
would cause ipsilateral ataxia. Vestibular and cochlear nuclei involvement would result in ipsilateral
hearing impairment. There’d be vertigo and nystagmus as well. Involvement of the facial nerve, a lesion
of this cranial nerve would result again in ipsilateral paralysis, ipsilateral loss of gustation from the
anterior two-thirds of the tongue. You would lose your excitatory or secretory excitation over lacrimal
and salivary gland secretions. So those are inhibited. There will be an impaired corneal reflex as a result
of injury to this cranial nerve nucleus. A lesion of the descending hypothalamic fibers, these are
sympathetic fibers, descending would cause ipsilateral Horner’s syndrome. Involvement of the trigeminal
nucleus would cause ipsilateral loss of pain and temperature from the face. Trigeminal nerve innervates
muscles of mastication. So a lesion of this nucleus would result in their weakness. The jaw, as a result,
will deviate toward the side of the lesion as a result of the weakness of the muscles of mastication.