Dowork123 - My friend is a doctor that studied medicine at Cambridge and works in anaesthetics. He said centralised pain is poorly understood. Some people diagnose centralised as present if anaesthetic does not work - but it doesn't work on me and sclerals take away my pain which would then suggest I don't have centralised pain otherwise why would they work? Here is the info he gave me on pain if it helps.
Pain is an essential special sense, required for animal/human survival. It is defined as the physiological response to actual or perceived tissue damage. Classically, though arbitrarily divided into acute (<6 weeks) or chronic (>6 weeks, and persisting beyond the period of tissue damage).
Acute pain is typically nocieptive, I.e. you get poked with a needle, or touch boiling water, or acid - it activates receptors which signal to the brain => it hurts. It can alternatively be neuropathic - if I squash a nerve (eg sciatica) this causes a distinct, but significant pain.
Pain, as opposed to any other sense, tends to sensitize over time. This is unique to pain. That is prolonged stimuli results in 1) non painful stimuli hurting (allodynia) - e.g airflow across the face hurts or combing hair causing pain, and 2) painful stimuli causing more pain than it ‘should’ (hyperalgesia) - eg people with fibromyalgia experience exquisite pain to ‘normally’ minimally painful stimuli.
How this sensitisation happens is complex. There are peripheral and central theories. There are definitely genetic, environmental and psychological aspects to centralisation.
At its most basic:
Peripheral sensitisation occurs due to:
1. Mg block release at NMDA receptors in the dorsal horn ganglia meaning that instead of getting brief AMPA mediated depolarisations, you get a prolonged NMDA action potential. More signal —> more pain.
2. Sprouting of neurones. More peripheral neurones mean non painful stimuli can activate postsynaptic pain pathways.
Central sensitisation is poorly understood.
1. LTP strengthens synapses which fire frequently
2. Reduced firing of desensitising descending pathways (e.g the endogenous opioid pathways suppress pain less)
3. Cortical remodelling
This is influenced by many factors, many not understood, but genetics, gender, drugs, psychological distress amongst others play important roles.
There will alwaya be a central component in people with chronic pain. However, regarding peripheral sensitisation... We know local anaesthesia preferentially blocks c-fibres (smallest nerves). Allodynia often Ad mediated (larger fibres) which LA does little for. The excessive dendritic sprouting is a big cause of allodynia.
Drugs for chronic pain are widespread and variably effective: tricyclics, gabapentinoids, duloxetine, antiepileptics, ketamine all have uses and are effective for some, and not for others. Almost all patients can find a drug regime which is opiate sparing, which has a positive effect for them, though finding this is a frustratingly slow process and requires patience to find what works for the individual.
Psychological strategies with chronic/severe pain based on a cognitive behaviour therapy model are showing very promising results, and we must not forget the complex psychological component of pain, and the way this effects mood/stress/daily functioning. Addressing this is some groups, though not all, has excellent benefits.
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Cornea neuralgia as a result of refractive surgery or corneal trauma.
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Guest repliedOriginally posted by Lena11 View PostDowork123 I've basically come to the same conclusions as you regarding neuropathy.
Also I think with confocals it's still early days in interpretating them. I've talked to a lot of people and 'damage' on the confocals doesn't always match how people feel. After lasik the nerves never look the same. I've also talked to someone with a twin and they both had a confocal. One had extreme pain and dry eye the other had nothing wrong but they both had nerve damage on the scan (neither had any eye surgery).
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Guest repliedDowork123 I've basically come to the same conclusions as you regarding neuropathy.
Also I think with confocals it's still early days in interpretating them. I've talked to a lot of people and 'damage' on the confocals doesn't always match how people feel. After lasik the nerves never look the same. I've also talked to someone with a twin and they both had a confocal. One had extreme pain and dry eye the other had nothing wrong but they both had nerve damage on the scan (neither had any eye surgery).
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Guest repliedOriginally posted by edmunder View PostThere is a corneal neuropathy facebook group. Many of the people go to Dr Hamrah and there are many prople who improved. Its the Lotemax gel every other day or twice a week plus blood serum 8+ times a day over a year.
People also tske other psin relievers during this time such as gabapentin ( im on this, very small dose but it works well) or others.
I have read that many people on Accutane get corneal neuropathy because the eye gets bad slowly over a long period where the nerves get damaged badly over that period. Especially at the end. This is what happened to me.
Moisture chambe/goggles + lotemax gel + blood serum all day + gabapentin has given me back my life in many ways, though ive inly been on blood serum plus steroids a month its helped a lot. I will continue for a long time. My pressure actually decreased on steroids plus blood serum.
im in the same boat as you pretty much exactly. Moisture chambers, methylpred, serum at least every two hours, oxycodone. I’m thinking about a trycyclic antidepressent if the pain doesn’t get where I need it to be. So glad your pressures good...you can use steroids, they’re so strong, that’s great. Have you run an antibiotic yet like moxafloxacin or an ointment like erythromycin? I want to add this soon to the right eye and see if I can get some more comfort. This right ones on fire right now, moisture chambers on and everything.
let me also add..what you said about accutane, I think the same goes for lasik. You get a reduced blink rate and damage accumulates over time. You don’t realize it then one day, everything just falls apart. There may be a defining incident, there may not.
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There is a corneal neuropathy facebook group. Many of the people go to Dr Hamrah and there are many prople who improved. Its the Lotemax gel every other day or twice a week plus blood serum 8+ times a day over a year.
People also tske other psin relievers during this time such as gabapentin ( im on this, very small dose but it works well) or others.
I have read that many people on Accutane get corneal neuropathy because the eye gets bad slowly over a long period where the nerves get damaged badly over that period. Especially at the end. This is what happened to me.
Moisture chambe/goggles + lotemax gel + blood serum all day + gabapentin has given me back my life in many ways, though ive inly been on blood serum plus steroids a month its helped a lot. I will continue for a long time. My pressure actually decreased on steroids plus blood serum.
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Guest repliedOriginally posted by hopeful_hiker View PostI am glad you are taking corneal neuralgia seriously. I was not able to get confocal microscopy, and even recognized dry eye specialists failed to see nerve malfunction as an issue. This is still very much a novel concept to them.
I have had shitty days with TBUT of 11-15s and low osmolarity and no staining. My journey is still unfolding with ups and downs.
I started listening to a book recommended by another user during my recent flare up. “You are not your pain”, I really really recommend it. Both authors suffered trauma and subsequent severe pain requiring opioids.
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Guest repliedOriginally posted by deep_dry_eye View Post
As in you linked two patients? That is not statistically significant. Additionally, the ophthalmologytimes.com article you linked is not peer-reviewed.
I'm not doubting this protocol, but I'm doubting whether you can draw (strong) conclusions based on these anecdotal evidence. As you probably know, things that work for 1-patient may not work for another patient (you); restasis is a classical example.
This protocol may or may not work for you, but what I am suggesting is that Prokera is an (additional) option for treatment. You should consider it. It is minimal risk, definitely much better than taking steroids long term, and may help you.
I have to cosider if a treatment will will be negative for me also. Because any irritation will set me back. I know myself, I can’t wear soft contacts without inflammation. The prokera ring will irritate my eye im certain. So I’ve decided the benefits don’t outweigh the risk. I believe there are better treatments for me personally.
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Originally posted by Dowork123 View Post
I linked two here, but I’ll link more for you. His sample size is his patient population, however large that is. He came up with this protocol and has proven its benefits by tracking nerve growth. I have a couple good examples that it works...I’ll provide more though...text wall to follow in the next day or so.
I'm not doubting this protocol, but I'm doubting whether you can draw (strong) conclusions based on these anecdotal evidence. As you probably know, things that work for 1-patient may not work for another patient (you); restasis is a classical example.
This protocol may or may not work for you, but what I am suggesting is that Prokera is an (additional) option for treatment. You should consider it. It is minimal risk, definitely much better than taking steroids long term, and may help you.
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Originally posted by Dowork123 View Post
Did you read the methods on this study? Because the participants wore prokera for max 3-5 days and were told to then continue with maximum treatments....which included serum tears among other drugs. So this study didn’t isolate prokera as the causitive agent. Probably grew the nerves because of the constant application of serum and anti inflammatories. If anything, I’d say this proves my point. But I won’t say that, because I can’t account for what prokera did either. Garbage lol.
so people can see it easily....
excerpt...For the study group, PKS was inserted in the office under topical anesthesia with 0.5% proparacaine hydrochloride eye drops. After placement, the subjects were asked to continue topical medications as needed and return 3–5 days later to remove the PKS. Subjects in the control group were asked to continue their conventional maximum treatment throughout the duration of the study including artificial tears, cyclosporine A, serum tears, antibiotics, steroids, and nonsteroidal anti-inflammatory medications. All subjects returned at 1 and 3 months for clinical evaluation.
However, if you read the details, yes, Prokera patients continue w/ existing treatment, but so does the control group as you pasted. And hence, it's still a valid study protocol. More importantly, you need to look at the p-values, which is p=0.015 in Section 3.4, which is statistically significant, but not super convincing either.
For example, see Fig 4, it is promising. It's obviously not a complete study as there is only 20 patients, and the control does not have a placeblo and not double-blind (and hence published in not a top tier journal).
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I am glad you are taking corneal neuralgia seriously. I was not able to get confocal microscopy, and even recognized dry eye specialists failed to see nerve malfunction as an issue. This is still very much a novel concept to them.
I have had shitty days with TBUT of 11-15s and low osmolarity and no staining. My journey is still unfolding with ups and downs.
I started listening to a book recommended by another user during my recent flare up. “You are not your pain”, I really really recommend it. Both authors suffered trauma and subsequent severe pain requiring opioids.
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Guest repliedOriginally posted by deep_dry_eye View Post
What's the sample size? p-values? 1 guy is not statistically significant.
Prokera on nerve improvements:
https://www.hindawi.com/journals/joph/2017/6404918/
However, this is not a reputable journal and 1 of the authors is from TissueTech (maker of Prokera).
so people can see it easily....
excerpt...For the study group, PKS was inserted in the office under topical anesthesia with 0.5% proparacaine hydrochloride eye drops. After placement, the subjects were asked to continue topical medications as needed and return 3–5 days later to remove the PKS. Subjects in the control group were asked to continue their conventional maximum treatment throughout the duration of the study including artificial tears, cyclosporine A, serum tears, antibiotics, steroids, and nonsteroidal anti-inflammatory medications. All subjects returned at 1 and 3 months for clinical evaluation.
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Guest repliedOriginally posted by deep_dry_eye View Post
What's the sample size? p-values? 1 guy is not statistically significant.
Prokera on nerve improvements:
https://www.hindawi.com/journals/joph/2017/6404918/
However, this is not a reputable journal and 1 of the authors is from TissueTech (maker of Prokera).
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Originally posted by Dowork123 View Post
I posted above I use 20% 50% and I make 100% at home.
The 20% is what’s recommended, every two hours by Pedram Hamrah. He has shown nerve regeneration with this protocol. The link at the bottom labeled, tommyboy shows a guy that improved with his protocol.
Prokera on nerve improvements:
https://www.hindawi.com/journals/joph/2017/6404918/
However, this is not a reputable journal and 1 of the authors is from TissueTech (maker of Prokera).
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Guest repliedOriginally posted by deep_dry_eye View Post
Prokera is usually done once, maybe twice. It's inserted and your eye will absorb the amniotic tissue (usually 2-7 days as mentioned). 20% serum is also a pretty low concentration, you might want to up it. Also, some folks I've talked w/ claim plasma rich platelets to be much better than serum.
The 20% is what’s recommended, every two hours by Pedram Hamrah. He has shown nerve regeneration with this protocol. The link at the bottom labeled, tommyboy shows a guy that improved with his protocol.
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Guest replieddeep_dry_eye
Can you link me to a reputable source showing improvement in nerve regeneration from prokera shown by in Vivo confocal microscopy?
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