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Posted

I read somewhere that kids with Pandas may have dialated pupils. I have noticed the last few days that when Harley first gets up in the morning his eyes are dialated for a couple of hours. Anyone else heard of this? Has anyone else experienced this with their children? Whats going on when this is happening?

I wanted to let the doctor see this morning, but by the time he finally got to see Harley, they were no longer dialated. I told the doctor about it, and he acted like it was no big deal. He said this sometimes happens after long periods of rest when kids wake up of the morning and their eyes are adjusting to the lights. BOLOGNA!

This has been lasting for like a couple hours or so, when I notice it. I don't see that with my other son or anyone else. And when I say dialated, His pupils are huge, you can barely see a thin circle of color around the black pupil. So, I was just curious if anyone out there knows why this might be happening.

Posted

I can't say why it happens...but it does seem to be common in PANDAS and most doctors (I told many for years about this symptom) just don't seem to know what to do with that information.

Posted

There was a previous thread (someone posted pictures of their kids and another parent jokingly remarked what lovely, SMALL pupils they had! :) ), that this issue was taking up. One school of thought, I guess, is that the "fight or flight" anxiety that accompanies PANDAS in many cases contributes to these enlarged pupils.

 

My son's pupils, unfortunately, can take your son's pupils in a current contest! ;) Ever since that previous thread a week or so ago, I've made it a point of taking a look into my son's eyes, not just when he gets up but at various points throughout the day. His pupils are ALWAYS dialated, and I mean ALWAYS! Some times they are larger than others, but they're never the nice, beady eye centers that we generally expect them to be! :blink:

Posted

Yes, this is a classic symptom of PANDAS. Whenever our son was in exacerbation, his pupils would dilate widely and almost constantly. Not surprisingly, this was accompanied by extreme sensitivity to light.

 

As others have said, we believed this was related to the attack on the basal ganglia and the exaggerated "fight or flight" response.

Posted

Yes, watch to see if they get bigger during an episode or a period of intense symptoms. I could literally see my dd's eyes get large and then small as her episode would begin and end.

 

Susan

Posted

For us too, our dd9 had huge dilated pupils during the worst of the exacerbation. The first time, we thought it was activation/akathesia from an SSRI (Lexapro) -- and that may have been a contributing factor. However, we later found that the pupil dilation occurred during other exacerbations when not on Lexapro.

 

Buster

Posted

This is something I'm kinda working on right now. My oldest son was recently prescribed a drug similar to atrophine. Atrophine is a drug that is derived from belladona. Belladona used to be used by women to dialate their pupils as a beauty enhancing treatment. It's an anticholergenic drug which is sometimes used to treat parkinson's.

A gastro Dr. prescribed it to control stomach spasms for my oldest son. After he was scoped (upper) she said that she felt he had had a virus that affected his digestion (Gastroparesis). She said that he was young and she expected him to recover well :) He also had moderate acid reflux (no surprise there).

 

Okey dokey then. A parkinson's drug for a tic kid. I think maybe we'll just try to find a little something else (he did take one pill, it did help, no increase in any neuro problems). After I had her undivided attention for all of about 33 seconds, I took what I got out of the appt and hit the computer. I won't get off on our situation too much(looking at B vits B12 for nerve health and the use of l carnitine). What others might be more interested in is the cycling of the cholergenic pathways. There is some interesting stuff, even if you just read wiki. Makes you wonder about bladder spasms or frequency, etc.

 

On another note, nicotine has been shown to help some with tics. Antibodies have been found to affect these receptors (ex. Guillain-Barré and acetylcholine receptors). From what I remember of GBS, the antibody causes an initial burst of of acetylcholine, which is followd by paralysis due to the excessive amt (?).

 

Sorry, to randomly throw a bunch of info out here, but I've been trying to finish this post for a 1/2 hour now. Walk away and keep coming back as there's a lot of activity around here right now. I'm just going to leave a few notes here. I'm sorting all of this myself right now too. :(

 

http://en.wikipedia.org/wiki/Acetylcholine#cite_note-1

 

In the central nervous system, ACh has a variety of effects as a neuromodulator upon plasticity, arousal and reward. ACh has an important role in the enhancement of sensory perceptions when we wake up[1] and in sustaining attention.[2]

 

 

http://en.wikipedia.org/wiki/Atropine

Atropine is a tropane alkaloid extracted from deadly nightshade (Atropa belladonna)

 

It is a competitive antagonist for the muscarinic acetylcholine receptor. It is classified as an anticholinergic drug. Being potentially deadly, it derives its name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.

 

Muscarinic receptors, or mAChRs, are G protein-coupled acetylcholine receptors found in the plasma membranes of certain neurons[1] and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous system.

 

Muscarinic receptors, or mAChRs, are G protein-coupled acetylcholine receptors found in the plasma membranes of certain neurons[1] and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous system.

 

 

http://en.wikipedia.org/wiki/Muscarinic_ac...holine_receptor

 

 

http://www3.interscience.wiley.com/journal...020636/abstract

 

Research Articles

IgG from patients with Guillain-Barré syndrome interact with nicotinic acetylcholine receptor channels

 

 

Muscarinic receptors were named as such because they are more sensitive to muscarine than to nicotine.[2] Their counterparts are nicotinic acetylcholine receptors (nAChRs), receptor ion channels that are also important in the autonomic nervous system. Many drugs and other substances (for example pilocarpine and scopolamine) manipulate these two distinct receptors by acting as selective agonists or antagonists.[3]

 

 

 

PANDAS gets a mention

 

Dysautonomia Disorders

Disorders of dysautonomia can result from both impaired and excessive functioning of the autonomic nervous system. Disorders in this family include Guillain-Barre syndrome, which is associated with vaccines, chronic inflammatory demyelinating polyneuropathy (CIDP), mitral vein prolapse dysautonomia, pure autonomic failure, postural orthostatic tachycardia syndrome (POTS), panic disorder, irritable bowel syndrome (IBS), neurocardiogenic syncope, multiple system atrophy (Shy-Drager Syndrome), chronic fatigue syndrome (CFS), fibromyalgia, and PANDA syndrome.

Posted

Kim,

You may be interested as well, in this paper by Mary Megson:

http://www.megson.com/readings/MedicalHypothesis.pdf

 

My daughter has been on Bethanechol (urecholine) for a couple of years now. Its a muscarinic cholinergic agonist- mimics mAch.

There are a few studies on its use to ameliorate the anticholinergic side effects of antipsychotic meds.

 

What I have found is that when my daughter 1st goes on it (she's been off and back on 2x), we see immediate improvements in calmness, fine motor control and communication. These don't seem to be sustained though (and higher or more frequent dosing do not change that). I don't know if that's because of PANDAS exacerbations intervening or not. Last spring, I decided to try pulsing-1 week on, one week off. What we saw was problems with elevated blood sugar (not diabetic range, but possibly prediabetes-ruled out by endo) on the off weeks. What I was trying to do is replicate the effects we saw when we began the medication, but the BS rises scared me, so I have her back on it full time.

 

Anyway, thought you might be interested. Also, the newer alzheimer meds are cholinesterase inhibiters-they reduce the enzyme that breaks synaptic Ach down into choline & acetic acid, in order to increase the time and amount of Ach in the synapse (the cholinergic version of inhibiting re-uptake). I did try a cholinesterase inhibiter with Allie-long ago- it made things worse instead of better. So, I think its the muscarinic side that we need to enhance-not the nicotinic side.

Posted

Just wanted to add the other immediate, but not sustained improvements we saw when starting bethanechol treatment were increased appetite and normal sleep patterns.

Posted
Anyway, thought you might be interested. Also, the newer alzheimer meds are cholinesterase inhibiters-they reduce the enzyme that breaks synaptic Ach down into choline & acetic acid, in order to increase the time and amount of Ach in the synapse (the cholinergic version of inhibiting re-uptake). I did try a cholinesterase inhibiter with Allie-long ago- it made things worse instead of better. So, I think its the muscarinic side that we need to enhance-not the nicotinic side.

 

Someone a week or so ago made a post asking about Namenda . . . I can't recall if it was for tics or OCD. Interestingly, when I looked that up, Namenda appears to be an Alzheimer med, also.

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