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So let's review here now the anatomy of the visual system. We recall that we have the retina here, the eyeball in front. And passing from the eyeball, we have the optic nerve which, as we recall, is not actually a cranial nerve, but a part of the brain. And then we have the optic chiasma here, where some of the fibers cross. And then the optic tract then carries this visual information up to the thalamus and then on to the cortex.
And the distribution of fibers from the retina is very interesting. Fibers from the lateral, or sometimes called the temporal, retina pass up. They stay on the same side. But fibers from the nasal retina cross over, and they send to the opposite side. And because of the way the eyeball is arranged, the temporal retina is seeing things in the midline, and the nasal retina is seeing things laterally. So if we think now about the things which stay on the same side, things which cross-- and remember this sort of counterintuitive business that the temporal retina is actually seeing, if you will, the nasal visual field, and the nasal retina is seeing the temporal visual field. |
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You are examining a patient who has been complaining of head aches and visual “problems”. On the basis of the examination you conclude that there is midline pressure on the optic chiasm. • What kind of visual field defect will lead you to conclude this? • What might becausing this kind of deficit and what kind of lab tests might be helpful in this regard? |
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It means we have pressure on the optic chiasm, which as we said-- now what that means then is that the crossing fibers from the nasal part of the retina are damaged. So our individual is only seeing things towards the midline. So they have tremendous problem with peripheral vision, because they have to move their head from side to side to see what's happening.
So another rhetorical question I asked you was what else is located there that might cause that? Well, as you recall, the pituitary gland sits right here. And a tumor on the pituitary gland can press on the optic chiasm and cause this deficit. So I asked earlier on what other kind of tests might be useful. An array of hormone assays might tell you whether there was a hypersecreting mass in the pituitary. |
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Following an injury to the neck involving the superior cervical ganglion, a patient has a constricted pupil on one side. Why? What is the pathway for normal dilation? What other deficits might be found in the head in this patient? |
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You remembered that we were talking about pupillary constriction. We're talking about the oculomotor motor nerve-- its parasympathetic component working its action through and through the ciliary ganglion.
And we think now about autonomic innervation. We must have a preganglionic axon synapsing on a postganglionic cell. And that postganglionic cell happens to be in the superior cervical ganglion which is in the sympathetic chain right below the skull.
So information from the retina is passed through the brain with the conveying information that there is not as much light as the retina would like. And in order to get the pupil dilated, it needs to send that information via descending pathway. So they're descending sympathetic pathways that pass down to the upper thoracic spinal cord.
There that information passes out, ascends the sympathetic chain, and then returns to the eye through the blood vessels associated with the internal carotid artery. So you can see this is a very long reflex pathway. And you can imagine then that anything from injury in the brain stem to the spinal cord to the sympathetic chain to the internal carotid might produce these symptoms.
And I also asked you what other symptoms might you expect. So I think you may recall from earlier on we talked about a Horner syndrome. So you'd expect-- might well suspect a dry face on that side because of loss of sweat function from the sympathetic nerve as well as a red face, vasodilation, because of the absent sympathetic tone, and then, of course, a droopy eyelid because of paralysis of the smooth muscles. So all of these together help us make sense of how that injury could have such a widespread effect. |
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Pupillary dilation is Parasympathetic or Sympathetic? |
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The superior cervical ganglion receives its preganglionic input from A. The vagus B. C1 spinal nerve through the sympathetic chain C. T1 spinal nerve through the sympathetic chain |
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T1 spinal nerve through the sympathetic chain |
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The reflex pathway for pupillary dilation involves a descending pathway from the brain to the spinal cord and an ascending pathway involving the sympathetic chain and the internal carotid artery. A. True B. False |
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• Ayoungpatientappearsatyourclinicwithan unusual complaint. • Suddenonsetlossoftasteonhalfhistongue. • Yourneurologicexaminationdetectsamild facial palsy on the same side. Over the next 24 hours this palsy becomes increasingly evident. • What are your thoughts?
What cranial nerve is likely involved? A. III B. V C. VII D. X E. XII |
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CN VII
You recalled the most obvious thing about the facial nerve is, as its name implies, the facial nerve supplies the muscles of facial expression. But you also recall that it has this unusual function. It supplies taste on the anterior 2/3 of the tongue. So this is the anterior 2/3 of the tongue are kind of funny.
If you bite your tongue, the pain from that is sensed by the lingual branch of the mandibular nerve, which is the trigeminal. So general sensation is the trigeminal nerve. Special sensation, taste, is the facial nerve. And the muscles of the tongue are supplied by the hypoglossal nerve. So it's quite a complicated story.
the most urgent problem with respect to take care of the patient is the loss of lacrimation, tear production. Tear production is run by the facial nerve. So not only is your patient unable to produce tears satisfactorily, but they're unable to blink their eye because their orbicular soculli is damaged. So your patient may need to have artificial tears dropped into the eye, and also to wear protective eye wear to protect the cornea.
And in this young patient, the disease, he tested soon positive for Lyme disease. At least in many parts of the country, while in Connecticut where I'm from, the most common cause of Bell's palsy, which is this constellation of symptoms produced by compression of the facial nerve is caused by Lyme disease. And the immediate treatment is of course to give antibiotics. And if it's caught early on, to give steroids to reduce swelling of the nerve as it passes through its long, bony course. |
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What other functions does the facial nerve serve? A. Lacrimation B. Salivation C. Taste D. All of the above |
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A patient has unilateral loss of the corneal blink reflex (light touch to cornea elicits closing of the eye). • What is the pathway for this reflex? |
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So I'd like you to think about the pathway for this reflex and recall the elements of a reflex require that you have a sensory component, something that senses the stimulus. You need a central nervous system pathway that passes that sensation to the appropriate motor response. And then finally, you need a motor response generated. So you need a sensory component, a central nervous system component, and a motor component. So think about the potential pathway for this reflex for a minute.
And you say, OK, well [? let's-- ?] we recall that the cornea is on the face and therefore it's supplied by the trigeminal nerve. And you recall the trigeminal nerve has three main branches, a ophthalmic, a maxillary, and a mandibular. And it seems pretty clear that with the name ophthalmic that it's going to be-- that the ophthalmic nerve is going to be the nerve that supplies sensation to the cornea. But it also supplies sensation to the forehead.
So we recall our quick and dirty neurologic exam for the trigeminal nerve was forehead ophthalmic, cheek maxillary, chin mandibular. So you do that and, although it's not particularly sophisticated, the person can feel sensation in all those regions. So given that, what are you thinking now?
OK. So then if sensation appears to be intact, what cranial nerve would you like to examine next?- VII
And we recall that the obicularis oculi, the muscle that closes the eye, is supplied by the facial nerve. So you've got to think now about examining the facial nerve. And you might look to see whether the patient's face was droopy on one side. You might do a more thorough examination. But your interest now, since sensation is intact, is thinking about whether this is a facial nerve problem. |
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A patient with a variety of neurological problems is referred to you. The exam reveals that the IX, X, and XI cranial nerves are involved. Imaging reveals a clot in the jugular bulb that is compressing the nerves in the jugular foramen. • What kinds of problems will this patient have? |
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So you start thinking now, well, you remember that the ninth, 10th, and 11th nerves are involved. So how are you going to test the function of the glossopharyngeal nerve? -test gag reflex -OK. If you said gag reflex, that's right, because you remembered that sensation on the oral pharynx is supplied by the glossopharyngeal nerve. I can say sort of parenthetically that there are also taste clinics scattered around the country where one can actually, with careful testing procedures, actually examine taste on both the anterior and posterior third of the tongue. So it is possible, with proper technique, to test taste. You recall that the glossopharyngeal nerve also supplies taste on the posterior third of the tongue.
OK, well, again, we recall we're talking about reflexes. That reflex has to have a sensory component, which we've just discussed is the glossopharyngeal nerve. So it's got a CNS component. And then it needs to have a motor component. So what do we recall of the gag reflex and the motor nerve involved in that?- CN X is also involved |
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How will you test for function of the glossopharyngeal nerve? |
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What other nerve is involved in the gag reflex? |
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What other deficits might you note from damage to the vagus? A. Difficulty swallowing B. Hoarse voice C. Droopy palate D. All of the above |
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How will you test the accessory nerve? |
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Have the patient shrug up against resistance and turn head each way against resistance |
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Another patient comes in with a visual field defect. Your examination of the visual field defect leads you to believe that there is lateral pressure on the optic tract just posterior to the chiasm. • What is the visual field defect? [image] |
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So here, we're talking now about pressure here in the-- we call the optic tract here, posterior to the chiasma. And we see that it's receiving fibers from the left eye, from the temporal part of the retina. But recall, the temporal part of the retina is looking to the right. And then on the opposite side, the nasal part of the retina crosses over. It is also looking to the right. So given that, what kind of visual field deficit would you expect? Right visual field in both eyes (right homonymous hemianopsia) And if you said right visual field defect in both eyes, that would be correct. It has an elaborate and somewhat amusing name of right homonymous hemianopsia, meaning it's a visual field-- a half of a visual field, and "homonymous" meaning the same visual field in both eyes.
Kind of the take-home message from this is that the visual cortex receives the visual field from the opposite. So the left optic tract sees the right visual field from both eyes. And the right optic tract sees the left visual field from both eyes. |
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Visual field defect from left optic tract compression causes: A. Left eye blindness B. Bitemporal hemianopsia C. Right visual field in both eyes (right homonymous hemianopsia) D. Left visual field in both eyes (left homonymous hemianopsia) |
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Right visual field in both eyes (right homonymous hemianopsia) |
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