MudPhud20XX

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So Tabes dorsalis is a demyelination dz. Then why would you get hypersensitivity touch stimulus? How do you explain shooting pain you see from patients with Tabes dorsalis? Shouldn't it be the opposite less sensitive to the pain since demyelination will hinder the signal of the nerves?

Many thanks in advance.
 

Fatalis

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the shooting pain is just a feature of paresthesia; eventually yes the patient will stop feeling pain and that can account for Charcot's joints; loss of sensation= more prone to injuries.
as an aside, you really gotta start looking stuff up yourself. I am all for asking questions, etc but when I log on here and I see that you flood the forums with your questions [questions that can be easily google'd or in first aid that is really self explanatory] it makes me wonder.
 

sarah65

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Anyone reading this, please feel free to correct any mistakes. Here's my take on the issue:

Tabes dorsalis occurs in about 30% of untreated syphilis. Gummatous inflammatory lesions occur in the spinal cord, specifically in dorsal roots and meninges. It causes dystrophic changes of myelin and axons of thick sensitive fibers that pass through dorsal roots, specifically affecting fascicles gracilis (recall axon myelination proprioception > mechanoreceptors > sharp pain > dull pain). Clinics in Dermatology Volume 23, Issue 6, November–December 2005, Pages 555–564

Pain in tabes dorsalis has been described as lightning and lancinating, sometimes occurring in a traveling or 'pulling' distribution (lower leg -> upper leg -> buttocks -> back). Successful treatment of tabetic lightning pain and visceral crisis with gabapentin J Anesth. 2011 December; 25(6): 952.
I prefer to specify it as allodynia (pain produced by a stimulus that would not normally produce pain) rather than paresthesia (as paresthesia is 'alteration of sensation', not necessarily 'pain caused by a stimulus that would otherwise not cause pain'), although both terms are used. On a cellular level, allodynia is caused by inappropriate cross-communication between dermal mechanoreceptors (Meissner's corpuscles, specific for light touch) and Adelta/type III sensory fibers (specific for sharp pain), both of which go to dorsal roots. Here's where it gets a bit tricky: There are several theories as to how and why this cross-communcation happens, but the bottom line is that stimulation of mechanoreceptors in the skin either transmits pain sensation itself, or inappropriately activates nociceptors. (wiki: Allodynia)

In contrast to Fatalis' opinion, this wasn't as straightforward as he'd like to believe. Secondly, proprioceptive dysfunction occurs simultaneously with allodynia ("Charcot joints" is a neuropathic arthritis, a severe form of osteoarthritis. The arthritic knee joints result from the relative insensitivity of the joints, due to destruction of the dorsal root fibers, and the resultant repeated injury; remaining pain fibers however were still sufficient to permit pain to occur. Charcot joints occur in less than 10 percent of tabes patients http://isc.temple.edu/neuroanatomy/lab/lesions/8.htm). Thirdly, and I've said this in another post, I absolutely appreciate asking questions because someone with prior knowledge will clarify it for you, or other people will realize they don't know it either. I personally have learned a whole lot from the responses to your questions.
 
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MudPhud20XX

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Thank you very much sarah65 for the detailed and helpful explanation.
Best,
 

Anastomoses

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Actually, I don't mind. Even when I posted before that you could have easily looked that up, now that I think about it you're providing a nice option for another review to retain random ideas that we all need to know. I'm sure the above poster would agree. And hey, if you like interactive learning, you should hook up with some hardcore students who are into these things too. :) But I'm game, carry on.
 
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