bhuvi

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Can u describe the following types of pupils[or where they are seen]?
A- Marcus Gunn Pupil
B-Aedes Pupil
C-Pupils in pontine lesions
D-Pupil in Uncal herniation
E-Argyll Robertson Pupil
Any others? Thanks and GL!
 

BlackNDecker

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bhuvi said:
Can u describe the following types of pupils[or where they are seen]?
A- Marcus Gunn Pupil
B-Aedes Pupil
C-Pupils in pontine lesions
D-Pupil in Uncal herniation
E-Argyll Robertson Pupil
Any others? Thanks and GL!
Why don't you create a single thread for all your questions? That way you can add new questions at the bottom of the same thread without having to fill up the main page.
 

Rendar5

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bhuvi said:
Can u describe the following types of pupils[or where they are seen]?
A- Marcus Gunn Pupil
B-Aedes Pupil
C-Pupils in pontine lesions
D-Pupil in Uncal herniation
E-Argyll Robertson Pupil
Any others? Thanks and GL!
real tired now, so all I can tell you now is uncal herniations press on ipsi and contralateral oculomotor nerves. outer nerve fibers in CNIII are parasymps, so pupils widen w/ this problem. uncal herniations are a supratentorial mass effect.

pontine lesions? i'm assuming they mean PICA infarction? that'll hit descending sympathetic neurons before they ascend as the sympathetic cervical ganglion chain. so ipsilaterl horner's syndrome. pupilsare now small.
 
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bhuvi

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OK BlackNDecker will post my qns in a single thread....

Thanks Rendar5 for ur input..... Heres what i learnt...


.Adie's Pupil
Dilated pupil which may react better to near than to light. It is probably due to disease
affecting the ciliary ganglion. Is hyper-sensitive to any weak Pilocarpine (eg. 0.1%) with
constriction of the pupil, in contrast to the pharmacologically dilated pupil (eg. by atropine)
which will not constrict.
There may be an associated loss of tendon reflexes, particularly the ankle jerks, but there is
almost never any associated systemic disease. Over a period of years, the condition is likely
to become bilateral and the initially dilated pupil will gradually reduce in size. However, its
poor reaction to light will continue.

2.- Marcus Gunn Pupil-paradoxical dilatation of pupils in swinging flash-light test,seen in retinal detachment,optic neuritis etc.

3.Pupils in pontine lesions-; pontine lesions cause miosis but normal light response. pin-point pupils following pontine haemorrhage;

4.central diencephalic herniation causes fixed dilated pupils:

5.Argyll Robertson Pupil- Accomodation Reflex Present(ARP-mnemonic).

6.Pupil in Uncal herniation- findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III.
 

DOCTORSAIB

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bhuvi said:
OK BlackNDecker will post my qns in a single thread....

Thanks Rendar5 for ur input..... Heres what i learnt...


.Adie's Pupil
Dilated pupil which may react better to near than to light. It is probably due to disease
affecting the ciliary ganglion. Is hyper-sensitive to any weak Pilocarpine (eg. 0.1%) with
constriction of the pupil, in contrast to the pharmacologically dilated pupil (eg. by atropine)
which will not constrict.
There may be an associated loss of tendon reflexes, particularly the ankle jerks, but there is
almost never any associated systemic disease. Over a period of years, the condition is likely
to become bilateral and the initially dilated pupil will gradually reduce in size. However, its
poor reaction to light will continue.

2.- Marcus Gunn Pupil-paradoxical dilatation of pupils in swinging flash-light test,seen in retinal detachment,optic neuritis etc.

3.Pupils in pontine lesions-; pontine lesions cause miosis but normal light response. pin-point pupils following pontine haemorrhage;

4.central diencephalic herniation causes fixed dilated pupils:

5.Argyll Robertson Pupil- Accomodation Reflex Present(ARP-mnemonic).

6.Pupil in Uncal herniation- findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III.
Argyll Robertson Pupils react to accomodation but not to direct light. It's seen in tertiary syphillis ("neurosyphillis").
 

Rendar5

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bhuvi said:
OK BlackNDecker will post my qns in a single thread....

Thanks Rendar5 for ur input..... Heres what i learnt...


.Adie's Pupil
Dilated pupil which may react better to near than to light. It is probably due to disease
affecting the ciliary ganglion. Is hyper-sensitive to any weak Pilocarpine (eg. 0.1%) with
constriction of the pupil, in contrast to the pharmacologically dilated pupil (eg. by atropine)
which will not constrict.
There may be an associated loss of tendon reflexes, particularly the ankle jerks, but there is
almost never any associated systemic disease. Over a period of years, the condition is likely
to become bilateral and the initially dilated pupil will gradually reduce in size. However, its
poor reaction to light will continue.

2.- Marcus Gunn Pupil-paradoxical dilatation of pupils in swinging flash-light test,seen in retinal detachment,optic neuritis etc.

3.Pupils in pontine lesions-; pontine lesions cause miosis but normal light response. pin-point pupils following pontine haemorrhage;

4.central diencephalic herniation causes fixed dilated pupils:

5.Argyll Robertson Pupil- Accomodation Reflex Present(ARP-mnemonic).

6.Pupil in Uncal herniation- findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III.

thinking better now, so stuff to add. argyll robertson would be associated w/ syphilis, i believe. don't ask me why accomodation is spared while the standard light reflex is not.

isn't central diencephalic herniation same thing as an uncal herniation? (uncus of temporal lobe shoved downward. ipsilateral is first, but contralateral should also happen from the mass effect

pontine lesion u mentioned can be associated w/ Wallenberg Syndrome (PICA infarct). ipsilateral horner's syndrome, ipsilateral facial (spinal tract of V) and contralateral body (spinothalamic) pain/temp loss, vertigo (CNVII), ataxia (inferior cerebellar peduncle), and dysarthria/dysphagia (CNX)
 

NR117

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Rendar5 said:
don't ask me why accomodation is spared while the standard light reflex is not.

pontine lesion u mentioned can be associated w/ Wallenberg Syndrome (PICA infarct). ipsilateral horner's syndrome, ipsilateral facial (spinal tract of V) and contralateral body (spinothalamic) pain/temp loss, vertigo (CNVII), ataxia (inferior cerebellar peduncle), and dysarthria/dysphagia (CNX)
Actually Wallenberg syndrome is also known as the lateral medullary syndrome so it is different from a pontine syndrome.

The reason why accomodation is spared in Adie's and Argyl-Robertson pupil is a phenomenon called light-near dissociation. If anyone's interested to know more about this, I'll be happy to elaborate.
 

GuP

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NR117 said:
Actually Wallenberg syndrome is also known as the lateral medullary syndrome so it is different from a pontine syndrome.

The reason why accomodation is spared in Adie's and Argyl-Robertson pupil is a phenomenon called light-near dissociation. If anyone's interested to know more about this, I'll be happy to elaborate.

i do...i dont feel like looking it up ;)
 

NR117

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The pupillomotor fibers to the iris sphincter muscle make up only 3 % of the total number of postganglionic neurons that leave the parasympathetic ciliary ganglion; the rest(a whopping 97 %!) are involved in accommodation. So when the ciliary ganglion is injured, there is greater chance of survival for fibers that serve accommodation than those that serve the pupil (light reaction). That is the basis of light-near dissociation in Adie's pupil.
 

GuP

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thanks for the info...but i think u meant in Argyl-Robertson instead of Adie's :)
 

NR117

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No I didn't . That explanation was for Adie's pupil.

The problem in Argyl- Robertsson pupil is not in the ciliary ganglion, it is within the central nervous system (midbrain). That requires a lot more anatomy than anyone needs to know for USMLE Step 1 (or 2 or 3!). But I am guessing that you're not gonna feel like looking that up either ;) so here goes:

The near reflex (accommodation) has its supranuclear control via occipitomesencephalic pathways influencing the pupillary constrictor neurons in the visceral oculomotor complex by a different route than the retinomesencephalic afferents that control the light reflex. Therefore it may be unaffected by pretectal lesions that interrupt the pupillary light reflex. The site of lesion in Argyl-Robertson pupil is thought to be in the rostral midbrain.

I should probably point out that there are other examples of light-near dissociation, which is a non-specific entity meaning that the pupil does not constrict as well to light as it does in response to accommodative effort. The most common cause of light near dissociation is an lesion causing a Marcus-Gunn pupil. Because of the afferent defect you have a poor reaction to light but if the patient is asked to activate their near response, the pupil will constrict (you do not need vision to accommodate).
 
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GuP

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i guess i got 0wned! LOL

anyways, just wanted to say thanks for the detailed explanations...really appreciate it!

if you have any more random info about the eye or anything else for that matter, please do ;)
 
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