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Small Fiber Neuropathy associated to Posterior Cingulate Cortex atrophy in HIV

pattismith

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@ScottTriGuy

Evidence for a novel subcortical mechanism for posterior cingulate cortex atrophy in HIV peripheral neuropathy

Abstract

We previously reported that neuropathic pain was associated with smaller posterior cingulate cortical (PCC) volumes, suggesting that a smaller/dysfunctional PCC may contribute to development of pain via impaired mind wandering.

A gap in our previous report was lack of evidence for a mechanism for the genesis of PCC atrophy in HIV peripheral neuropathy.

Here we investigate if volumetric differences in the subcortex for those with neuropathic paresthesia may contribute to smaller PCC volumes, potentially through deafferentation of ascending white matter tracts resulting from peripheral nerve damage in HIV neuropathy.

Since neuropathic pain and paresthesia are highly correlated, statistical decomposition was used to separate pain and paresthesia symptoms to determine which regions of brain atrophy are associated with both pain and paresthesia and which are associated separately with pain or paresthesia.

HIV+ individuals (N = 233) with and without paresthesia in a multisite study underwent structural brain magnetic resonance imaging.

Voxel-based morphometry and a segmentation/registration tool were used to investigate regional brain volume changes associated with paresthesia.

Analysis of decomposed variables found that smaller midbrain and thalamus volumes were associated with paresthesia rather than pain.

However, atrophy in the PCC was related to both pain and paresthesia.

Peak thalamic atrophy (p = 0.004; MNI x = − 14, y = − 24, z = − 2) for more severe paresthesia was in a region with reciprocal connections with the PCC.

This provides initial evidence that smaller PCC volumes in HIV peripheral neuropathy are related to ascending white matter deafferentation caused by small fiber damage observed in HIV peripheral neuropathy.
 

Pyrrhus

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In case it's not clear, what they are talking about is how peripheral neuropathy might cause changes in the brain. They claim that the small fiber neuropathy produces insufficient stimulation to the midbrain, which means insufficient stimulation to the thalamus, which provides insufficient stimulation to the cingular cortex. As a result of the insufficient stimulation, all three areas shrink. It's an hypothesis.

In HIV, the main explanation for peripheral neuropathy is the fact that earlier HIV drugs were quite toxic to mitochondria. Newer drugs are much less toxic to mitochondria, which is why HIV peripheral neuropathy is becoming a thing of the past.

a smaller/dysfunctional PCC may contribute to development of pain via impaired mind wandering
?! I think something got lost in translation here...

Analysis of decomposed variables found that smaller midbrain and thalamus volumes were associated with paresthesia rather than pain.
Why are they differentiating paresthesia and pain? Paresthesia is felt in the early stages of peripheral neuropathy, while pain is felt in the later stages of peripheral neuropathy...

Just my 2 cents.
 

pattismith

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Why are they differentiating paresthesia and pain? Paresthesia is felt in the early stages of peripheral neuropathy, while pain is felt in the later stages of peripheral neuropathy...

Just my 2 cents.
Really, are you sure of that? My neuropathy started with pain and then paresthesia came long after (20 years later actually).

Not sure if their conclusion is right, but I found interesting to find correlation between PCC atrophy and peripheral neuropathy in HIV patients, whatever the pathogenesis involved.
 

Pyrrhus

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Really, are you sure of that? My neuropathy started with pain and then paresthesia came long after (20 years later actually).
If that's your experience, no one can tell you otherwise. Everybody's different.

My comment was based on the traditional model of peripheral nerve death, where paresthesia is the warning sign that the nerve is starting to fail, and pain is when the neurons start dying. (diabetes and HIV neuropathy are examples of this model)

But that is just one model of peripheral neuropathy, and it may not even be the most common model. There can be nerve pain that has nothing to do with cell death of neurons, such as nerve pain due to inflammation. (As you already know!)

So you're right, paresthesia doesn't always come before pain.

Not sure if their conclusion is right, but I found interesting to find correlation between PCC atrophy and peripheral neuropathy in HIV patients, whatever the pathogenesis involved.
It is an interesting and plausible hypothesis- thanks for sharing.
 
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pattismith

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In case it's not clear, what they are talking about is how peripheral neuropathy might cause changes in the brain. They claim that the small fiber neuropathy produces insufficient stimulation to the midbrain, which means insufficient stimulation to the thalamus, which provides insufficient stimulation to the cingular cortex. As a result of the insufficient stimulation, all three areas shrink. It's an hypothesis.
in Diabetes, some doctors found brain lesions associated to peripheral neuropathy as well, but they conclude the opposite:

"Overall, our study showed sensorimotor and pain‐related Gray Matter and White Matter alterations in patients with DPN, which might be involved in the development of Diabetes Peripheral Neuropathy. "

https://onlinelibrary.wiley.com/doi/full/10.1002/hbm.24834

It's interesting that doctors are divided into 2 categories, on one hand those who think the lesion/dysfunction is in the brain and that it causes peripheral neuropathy, and on the other hand the lesion is peripheral first which causes brain reorganization:atrophy....
(Needless to say that Psy docs are in the first, as they are those that believe the mental issue is the root of it all)
 

Pyrrhus

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It's interesting that doctors are divided into 2 categories, on one hand those who think the lesion/dysfunction is in the brain and that it causes peripheral neuropathy, and on the other hand the lesion is peripheral first which causes brain reorganization:atrophy....
Isn't that always the case... As much as people like to say "correlation does not imply causation", they also like to ignore that saying.

Both categories of doctors are ignoring what may be the most obvious explanation: that both peripheral and central nervous system observations are independent symptoms of the same neuro/inflammatory process...
 

ScottTriGuy

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Thanks for the heads up @pattismith -- interesting study, and your convo with @Pyrrhus -- fortunately I don't have HIV neuropathy (or ME pain) -- when I first started on ARVs, AZT was part of my cocktail, and it made me feel sick in a different way to pre-ARVs, and very often an easy run or bike ride would alleviate the nausea -- once I got off AZT, my functioning increased, returned to work -- fwiw, I've never experienced fatigue from ARVs.

I sometimes wonder if cannabis, with its neurogenesis effects, is what is sparing me from pain and brain fog.