In dorsal midbrain syndrome, the lesion is not caused by a vascular insult. Instead, the lesion is caused
by a pineal gland tumor. The pineal gland is shown here. If there is a tumor growth, an expansion of that
tumor will grow downward and then have an influence or a negative influence on the superior colliculi,
for example. Superior colliculi are involved. With further expansion of the pineal gland tumor, you can
narrow the cerebral aqueduct which is this communication between the third and fourth ventricles that contains
cerebrospinal fluid. With a lesion of the superior colliculi, you will see a classic triad of upward gaze palsy.
Pupils will respond to near stimuli but pupils do not react to light and you would have a form of nystagmus
known as convergence-retraction nystagmus. A finding associated with involvement of the cerebral
aqueduct is that you would have hydrocephalus. Youâ€™d have an increased accumulation of cerebrospinal
fluid in the third and fourth lateral ventricles. This specific form of this hydrocephalus would be a
non-communicating hydrocephalus. Medial midbrain or Weber syndrome is a vascular lesion. You can see the area
thatâ€™s damaged. This is a vascular lesion of the posterior cerebral artery. Structures involved in this
syndrome would include the corticospinal and corticobulbar tracts. You would also get involvement of
the oculomotor nerve. This is the oculomotor nerve here. The nucleus of this nerve is shown in here.
The nucleus of the opposite one is shown here. But we do not see the other oculomotor in this level section.
We see it here. What are the symptoms associated with involvement of each one of these structural elements?
First, letâ€™s take a look at the corticospinal tract symptoms. Again, this is a tract, so the findings will be contralateral.
This is a motor descending tract, so we have contralateral paresis of the upper and lower extremities.
Weâ€™re also involving the corticobulbar tract. So here, weâ€™re looking at innervation of the facial musculature.
This would demonstrate contralateral paresis. This would involve the lower facial muscles specifically.
A lesion of the oculomotor nerve would produce ipsilateral findings. This would be ipsilateral oculomotor palsy.
This will be characterized by a triad of symptoms. The first is lateral strabismus. The oculomotor nerve
innervates most of the extraocular muscles. One thatâ€™s still intact would be the lateral rectus. Since itâ€™s still
functional, that lateral rectus is going to cause a lateral movement of the eyeball. Thatâ€™s the lateral
strabismus component here. Oculomotor nerve also innervates the levator palpebrae superioris.
So, if this is paralyzed, the upper eyelid will droop. Thatâ€™s ptosis. The oculomotor nerve is essential in
constricting the pupil, activating the sphincter pupillae. So if thatâ€™s paralyzed, the pupil will be dilated.