neuro question

[jaeida8]

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I know the answer to this question, but don't have an explanation. I've never seen it in one of my books. Can someone please help?

A 52 year old male who has smoked three packs of cigarettes a day since he was in high school develops a persistent cough. Imaging of his chest shows that he has a tumor that has invaded the posterior mediastinum on the left. Physical examination reveals a partial ptosis of the left eyelid. What other physical sign would you look for?

A: Vasodilation on the left side of the face

 

[docuw]

This is a Pancoasts tumor. Pancoast tumors are neoplasms of pulmonary origin located at the apical pleuropulmonary groove (superior sulcus). By direct extension, they typically involve the lower trunks of the brachial plexus, intercostal nerves, stellate ganglion, adjacent ribs, and vertebrae. The stellate ganglia is part of the sympathetic chain ganglia. If you cut off the sympathetic innervation that follows up the carotids, you get Horners syndrome including ptosis, miosis, and anhydrosis.

The sympathetic (pupillodilator) pathway leaves the spinal column at the eighth cervical level (C8) through the second thoracic level (T2) via the ventral roots to the paravertebral sympathetic chain. These fibers then pass through the stellate ganglion near the apex of the lung; then, via the ansa subclavia, inferior and middle cervical ganglia synapse in the superior cervical ganglion. The postganglionic fibers then travel via the carotid artery to innervate the dilator pupillae along with the vasomotor apparatus of the face and the smooth muscle of the upper eyelid. Therefore, full disruption of the sympathetic chain produces the classic triad of Horner syndrome (ie, ptosis, miosis, anhydrosis).

 

[sdnsdn]

Just thought I?d throw in some junk to make the memory stick?.
I was just reading about a surgery (thoracic sympathectomy) to snip some of these innervations in the book "complications." This surgery is done combat persistent blushing or palmer hyperhydrosis. The goal, however, is to spare the nerves involving the eye while obliterating the hyperhydrosis and facial vasodilatation (blushing). The major risk in this procedure is development of Horner?s.

And yes, I am a bored premed just passing the time at a boring job while waiting for the fall. (Don't worry, I will not pick up a textbook!)

 

[Mossjoh]

Okay docuw...

How would a lesion in the stellate ganglion cause ptosis? For those who don't know, ptosis is the drooping of the eyelid. From my understanding, ptosis is caused by a lesion of the superior division of the occulomotor nerve. True, the occulomotor nerve carries with it in its course sympathetic fibers originating from the superior cervical ganglion and parasympathatic fibers from the EW Nucleus in the midbrain, but the levator palpebrae muscle that is responsible for lifting the eyelid is somatic, coming from the occulomotor nucleus of the midbrain.
The levator palpebrae muscle is skeletal, and not innervated by anything sympathetic.

So...how does this sympathetic lesion affect ptosis? I believe that is incorrect.

Mossjoh

 

[Malftap]

The levator muscle and Mueller's muscle elevates the eyelid. Postganglionic sympathetic fibers innervate Mueller's muscle, which is responsible for initiating eyelid retraction. So this is how disrupting the sympathetic fibers can lead to ptosis.

 

[PACtoDOC]

Mal is correct. There are autonomic fibers that innervate eyelid. It is not purely somatic efferent that causes the eyelid to raise.

This is actually a really cool thread guys. So, to keep things moving along in the interest of education, here is a good question related to the above question.

Why is it that if intracranial pressure increases, the pupil will be affected first before the eyelid in terms of presenting symptoms?

 

[monster2]

You forgot about the superior tarsal muscle, a smooth muscle innervated by sympathetics which is part of the levator palpebral aponeurosis and attaches to the tarsal plate. Hence partial ptosis.

 

[docuw]

Originally posted by PACtoDOC
Mal is correct. There are autonomic fibers that innervate eyelid. It is not purely somatic efferent that causes the eyelid to raise.

This is actually a really cool thread guys. So, to keep things moving along in the interest of education, here is a good question related to the above question.

Why is it that if intracranial pressure increases, the pupil will be affected first before the eyelid in terms of presenting symptoms?

The answer is myelination. When comparing neurons and their conduction speeds, myelination is proportional to speed. Parasympathetics conduct at slower rates than motor neurons and thus have less myelination. The Preganglionic Parasympathetic fibers from the EW (Edinger-Westfall) Nucleus and the motor (GSE) fibers travel in the oculomotor nerve (III). With uncal herniation, CNIII is compressed. Because the parasympathetic fibers that innervate the constrictor pupilae have less myelenation, they might be more susceptible to injury. Thus, mydriasis occurs first, followed by ptosis (levator palpebrae) and down and out (exotropia/external strabismus due to Superior Rectus, Inferior Rectus, Medial Rectus, Inferior Oblique which are all innervated by CNIII).

 

[BellKicker]

Originally posted by monster2
You forgot about the superior tarsal muscle, a smooth muscle innervated by sympathetics which is part of the levator palpebral aponeurosis and attaches to the tarsal plate. Hence partial ptosis.

Yes, it's M?ller's muscle, which was mentioned above. There's a similar one in the lower eyelid.

Regarding Horner's, one should always check for a possible reason. CXR for Pancoast tumor as in this one, although a quicker test would be to check for atrophy of the ipsilateral hand (as Pancoast tumor affects the brachial plexus, also). Neck scars for surgery (or even scars below the clavicle after a sympathotectomy for Raynoud's disease in an old patient). Difference in eye color would suggest congenital Horner's because the melanocytes need sympathetic innervation to migrate onto the iris.

 

[BellKicker]

Originally posted by PACtoDOC

Why is it that if intracranial pressure increases, the pupil will be affected first before the eyelid in terms of presenting symptoms?

docuw said it.

I'll just add a few things.

In this case, we're talking CNIII palsy. CNIII arises mainly from 2 things: pressure and infarction.

Pressure palsy involves the pupil.

Infarction palsy does not involve the pupil.

The reason is this: The autonomic fibers travel on the outside of CNIII. Therefore they die first with pressure. Conversely, they die last or not at all, if the cause is lack of blood.

The point here is that if the pupil is involved and there are other signs to suggest raised ICP, we gotta get off our med student @sses and call neurosurg (or in my case, probably a resident that could tell me I wasn't all wrong). Sometimes the pressure rises more slowly. In that case, we have time for a donut and to read up on this ptosis thing. Slowly rising pressure may involve CNIII aberrants, ie nerves that grow out where they shouldn't. If the eye acts all funny, like raising the upper eyelid when looking down, this is a sign of aberrants.