Starting about a month ago, when I wake up in the morning the middle fingers on both hands (not a joke) are curled in towards my palms and I must pry them straight. Throughout the day my hands are weak and its hard to make tight fists. I've been lifting weights seriously for more than 30 years and thought I knew from personal experience or reports from others about all of the injuries and symptoms of overuse. This is new to me, and hopefully somone has some guidance. I don't think its arthritis or "trigger finger." I'm assuming that it probably has something to do with pressure on the tendons in my hands from the weights(?) I'm an American living in Aruba and not yet covered by the local healthcare program, so I will be out-of-pocket if I go to a local doctor here. Anyone know abut this?
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Hand Cramps - Curled Fingers
- Thread starter wineman
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This is a new one for me. Never heard of this problem in normally ambulatory individuals. In bedridden individuals, especially the elderly, its common.
I think this may be one for the medical books.
http://jnnp.bmjjournals.com/cgi/content/full/69/1/110
focal neuromyotonia
Now, in reading thru this paper, we note that these women had COPD (chronic obstructive pulmonary disease). Both were on corticosteroid treatment.
"A combination of factors such as local nerve root damage, chronic hypoxia, and salbutamol use may be contributing"
Local nerve root damage fits (from extensive gripping)?
Hypoxia..hmmm. I did a quick check on the pharmacology of the COPD drug mentioned. Salbutamol is a type of medicine known as a short-acting beta 2 agonist used for the treatment of asthma. Do you have asthma? If so, seasonal or nonseasonal? Treatment?
There *must* be a combination of factors present for this condition.
The biomechanics of the condition itself: (from the paper)
The selective flexion of just the middle and ring fingers is curious because the neuromyotonic discharges affect the whole of flexor digitorum superficialis muscle. There are two possible anatomical explanations.
Firstly, the additional extensor muscles (extensor digiti minimi and extensor indices) of the little and index finger may prevent their involuntary flexion.
Secondly the flexor digitorum superficialis muscle fibres are divided into superficial and deep layers ending in the tendons of ring and middle, and index and little fingers, respectively. There is a similar arrangement for their tendons behind the flexor retinaculum.
It is tempting to speculate that this superficial location of the flexor muscle fibres and tendons may make them more susceptible to irritation, enhancing the clinical manifestation of neuromyotonia in the middle and ring fingers.
Note that a localized nerve block treatment maybe attempted only by highly experienced physicans:
An awareness of this anatomical division during botulinum toxin injection in the flexor digitorum superficialis muscles is important because if the neuromuscular blockade involves the whole muscle, although the flexion deformity improves, the resulting weakness of the index flexor causes weakness of pinch grip and increased functional disability. This may be avoidable if the injection is given, in small dosage, in the superficial layer of the flexor digitorum superficialis muscles sparing the index and little finger flexors.
Ion imbalance is the heart of this condition:
Hyperventilation leading to decreased serum ionised calcium and alkalosis enhances neuromyotonia. In healthy subjects hypocalcaemia and ischaemia produce spasms with repetitive firing of motor units. The mechanism of ischaemia induced spasm is probably different from neuromyotonia although they both could be present in the same patient.
Salbutamol activates sodium-potassium transport in skeletal muscle producing hyperpolarisation and hypokalaemia but it is not clear if a similar effect is seen in the nerve membrane and if this leads to hyperexcitability at a later stage.
There are other drugs that induce this same dysfunctional sodium/potassium channel issue in skeletal muscle.
Print and take this article and post with you, when you visit a physican, preferrably one who readily refers you to a neuologist for examination.
If you read the article carefully and note the additional symptoms of the these patients (including excessive sweating)...
I would suspect that a shortage of taurine and magnesium are culprits.
http://www.austinchronicle.com/gyrobase/Issue/column?oid=oid:380830
This biomechanical problem and its underlying nerve and muscle ion channel conductance causes are far beyond the scope of my abilities to assess over the internet. What I provide you here is the beginning of a potential diagnosis that must be made by a neurologist, preferably in consult with a nephrologist and sports medicine physican.
Why? You have mechanical damage issues. There are exercises that, once the underlying conductance problems causing spasm are addressed, may address localized inflammation/tendonistis that I suspect is also present.
A sports medicine physican should be consulted regarding the causative nerve root damage. I have no idea if this condition has been reported among other long-term power lifters. Restorative training may be needed following nerve depolarization resolution (if possible). As I said, this appears to be a unique condition.
The nephrologist should be consulted regarding kidney function for ion balance. Taurine depletion is typically observed in chronically stressed patients; I suspect that it is also a common condition in patients with gastrointestinal disorders. Given the prevalence of GERD in particular within the adult population (>50% by age 45), I suggest that you *might* have a magnesium, calcium absorption, and taurine deficiency associated with damaged (leaky) intestinal mucosa. Note that ion uptake and mucosal cell transport has reported to be a primary secondary deficiency, along with vitamin absorption shortage.
Simply taking a magnesium and calcium supplement may not be enough (as indicated in the last website). Note that diuretics and high blood pressure medication are known to cause hypokalemia as well.
This technical reply and its content is not meant to replace professional evaluation and treatment afford via a medical specialist. Is is provided for informational purposes only.
Good luck. We empathize with your present treatment dilemma (lack of medical coverage at present). I would visit the American Consulate and ask for assistance with this severe debiliating medical condition. It will worsen over time if left untreated.
I think this may be one for the medical books.
http://jnnp.bmjjournals.com/cgi/content/full/69/1/110
focal neuromyotonia
Now, in reading thru this paper, we note that these women had COPD (chronic obstructive pulmonary disease). Both were on corticosteroid treatment.
"A combination of factors such as local nerve root damage, chronic hypoxia, and salbutamol use may be contributing"
Local nerve root damage fits (from extensive gripping)?
Hypoxia..hmmm. I did a quick check on the pharmacology of the COPD drug mentioned. Salbutamol is a type of medicine known as a short-acting beta 2 agonist used for the treatment of asthma. Do you have asthma? If so, seasonal or nonseasonal? Treatment?
There *must* be a combination of factors present for this condition.
The biomechanics of the condition itself: (from the paper)
The selective flexion of just the middle and ring fingers is curious because the neuromyotonic discharges affect the whole of flexor digitorum superficialis muscle. There are two possible anatomical explanations.
Firstly, the additional extensor muscles (extensor digiti minimi and extensor indices) of the little and index finger may prevent their involuntary flexion.
Secondly the flexor digitorum superficialis muscle fibres are divided into superficial and deep layers ending in the tendons of ring and middle, and index and little fingers, respectively. There is a similar arrangement for their tendons behind the flexor retinaculum.
It is tempting to speculate that this superficial location of the flexor muscle fibres and tendons may make them more susceptible to irritation, enhancing the clinical manifestation of neuromyotonia in the middle and ring fingers.
Note that a localized nerve block treatment maybe attempted only by highly experienced physicans:
An awareness of this anatomical division during botulinum toxin injection in the flexor digitorum superficialis muscles is important because if the neuromuscular blockade involves the whole muscle, although the flexion deformity improves, the resulting weakness of the index flexor causes weakness of pinch grip and increased functional disability. This may be avoidable if the injection is given, in small dosage, in the superficial layer of the flexor digitorum superficialis muscles sparing the index and little finger flexors.
Ion imbalance is the heart of this condition:
Hyperventilation leading to decreased serum ionised calcium and alkalosis enhances neuromyotonia. In healthy subjects hypocalcaemia and ischaemia produce spasms with repetitive firing of motor units. The mechanism of ischaemia induced spasm is probably different from neuromyotonia although they both could be present in the same patient.
Salbutamol activates sodium-potassium transport in skeletal muscle producing hyperpolarisation and hypokalaemia but it is not clear if a similar effect is seen in the nerve membrane and if this leads to hyperexcitability at a later stage.
There are other drugs that induce this same dysfunctional sodium/potassium channel issue in skeletal muscle.
Print and take this article and post with you, when you visit a physican, preferrably one who readily refers you to a neuologist for examination.
If you read the article carefully and note the additional symptoms of the these patients (including excessive sweating)...
I would suspect that a shortage of taurine and magnesium are culprits.
http://www.austinchronicle.com/gyrobase/Issue/column?oid=oid:380830
This biomechanical problem and its underlying nerve and muscle ion channel conductance causes are far beyond the scope of my abilities to assess over the internet. What I provide you here is the beginning of a potential diagnosis that must be made by a neurologist, preferably in consult with a nephrologist and sports medicine physican.
Why? You have mechanical damage issues. There are exercises that, once the underlying conductance problems causing spasm are addressed, may address localized inflammation/tendonistis that I suspect is also present.
A sports medicine physican should be consulted regarding the causative nerve root damage. I have no idea if this condition has been reported among other long-term power lifters. Restorative training may be needed following nerve depolarization resolution (if possible). As I said, this appears to be a unique condition.
The nephrologist should be consulted regarding kidney function for ion balance. Taurine depletion is typically observed in chronically stressed patients; I suspect that it is also a common condition in patients with gastrointestinal disorders. Given the prevalence of GERD in particular within the adult population (>50% by age 45), I suggest that you *might* have a magnesium, calcium absorption, and taurine deficiency associated with damaged (leaky) intestinal mucosa. Note that ion uptake and mucosal cell transport has reported to be a primary secondary deficiency, along with vitamin absorption shortage.
Simply taking a magnesium and calcium supplement may not be enough (as indicated in the last website). Note that diuretics and high blood pressure medication are known to cause hypokalemia as well.
This technical reply and its content is not meant to replace professional evaluation and treatment afford via a medical specialist. Is is provided for informational purposes only.
Good luck. We empathize with your present treatment dilemma (lack of medical coverage at present). I would visit the American Consulate and ask for assistance with this severe debiliating medical condition. It will worsen over time if left untreated.
The problem could be many things.
I could go to ao doctor.
As you are describing it, it sounds like "bowstringing" of the finers. Where the flexor pullys ruputre and create an extended moment arm (the fingers curl).
I could go to ao doctor.
As you are describing it, it sounds like "bowstringing" of the finers. Where the flexor pullys ruputre and create an extended moment arm (the fingers curl).
Thank you for your prompt and most insightful reply -- it's appreciated. I do suffer from GERD and have been on several medications for about a year, currently Nexium. As an additional FYI which may be germain, I have been in full remission from polymyositis for close to a year. During the active treatment phase I was on prednisone, azathioprine, calcium carbonate and Fosamax. I'm assuming that this is not a p-m-s flair as I'm as strong as I've ever been.
Again, thanks for your response to my post.
Again, thanks for your response to my post.
Thanks for both of your replies. I retired at the end of last year, so I don't spend much time on the computer except for a few daily emails and the like. As this condition started about a month ago - some eight months after my computer time became insignificant, I doubt if its that. (Are you thinking maybe carpal tunnel?)
I'll do some research on bowstring and see if it sounds like it fits. Would it afflict both hands starting at the precise same time?
Thanks again for your interest and prompt response.
I'll do some research on bowstring and see if it sounds like it fits. Would it afflict both hands starting at the precise same time?
Thanks again for your interest and prompt response.
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Yes sir, that would be confirmatory, with respect to my previous post.
You will note co-presentation of polymyositis with gastrointestinal complications:
http://www.emedicine.com/med/topic3441.htm
Also note the suggested correlation in both conditions (polymyositis with focal neuromyotonia) with autoimmune disease.
Sir, on a intuitive hunch, please have a GI or internal medicine specialist evaluate you for asymptomatic biliary cirrhosis. An important connection between bile acids and various P450 steroid hydroxylases (including CYP27A1) have been implicated in the autoimmune repsonse to mitochondrial DNA gene products. These same bile acids and various combinations of cholesterol hydroxylating genes are also implicated in lack of pregnenalone production (via alteration in adrenodoxin binding). The result: lack of important natural corticosteroid control (and excess inflammation). This inflammation in your hands, sir, would perhaps be the cause for site directed expression of localized antibodies (autoimmune attack on muscle tissue).
While this is an intuitive (and therefore hypothetical) connection, sir, my particular research, for many years, has included the liver and adrenal P450 proteins and their various actions within the body.
http://www.wjgnet.com/1007-9327/10/894.pdf.
I believe there is a connection between imbalances within bile acids produced under GERD and their activation of immune controlling liver microsomal nuclear receptors. This has been implicated in the etiology of related autoimmune disorders. You will also need to be seen by a rheumatologist.
An interesting case; your FYI was most enlightening. Thank-you for the feedback.
I suspect you will be unable to secure adequate evaluation, diagnosis and treatment in Aruba, sir. Your medical history and present complications from previous corticosteroid treatment require expert, if not top notch, medical attention.
You will note co-presentation of polymyositis with gastrointestinal complications:
http://www.emedicine.com/med/topic3441.htm
Also note the suggested correlation in both conditions (polymyositis with focal neuromyotonia) with autoimmune disease.
Sir, on a intuitive hunch, please have a GI or internal medicine specialist evaluate you for asymptomatic biliary cirrhosis. An important connection between bile acids and various P450 steroid hydroxylases (including CYP27A1) have been implicated in the autoimmune repsonse to mitochondrial DNA gene products. These same bile acids and various combinations of cholesterol hydroxylating genes are also implicated in lack of pregnenalone production (via alteration in adrenodoxin binding). The result: lack of important natural corticosteroid control (and excess inflammation). This inflammation in your hands, sir, would perhaps be the cause for site directed expression of localized antibodies (autoimmune attack on muscle tissue).
While this is an intuitive (and therefore hypothetical) connection, sir, my particular research, for many years, has included the liver and adrenal P450 proteins and their various actions within the body.
http://www.wjgnet.com/1007-9327/10/894.pdf.
I believe there is a connection between imbalances within bile acids produced under GERD and their activation of immune controlling liver microsomal nuclear receptors. This has been implicated in the etiology of related autoimmune disorders. You will also need to be seen by a rheumatologist.
An interesting case; your FYI was most enlightening. Thank-you for the feedback.
I suspect you will be unable to secure adequate evaluation, diagnosis and treatment in Aruba, sir. Your medical history and present complications from previous corticosteroid treatment require expert, if not top notch, medical attention.
Last edited:
Re:
At first I thought it might be Dupuytren's contracture. But I highly doubt it, but it seems that you have a problem with your tendons being entrapped somehow (can't really remember the name of the condition as I don't have my orthopaedics book around), I would recommend that you see an orthopaedic surgeon as this is an Orthopaedic problem and general practitioner/doctor would eventually refer you for an orthopaedic surgeon anyways. The question is, how long have you had this problem and what caused it exactly (like what did you do the day/night before). Cramps can't curl fingers to that extend so better check it out.
At first I thought it might be Dupuytren's contracture. But I highly doubt it, but it seems that you have a problem with your tendons being entrapped somehow (can't really remember the name of the condition as I don't have my orthopaedics book around), I would recommend that you see an orthopaedic surgeon as this is an Orthopaedic problem and general practitioner/doctor would eventually refer you for an orthopaedic surgeon anyways. The question is, how long have you had this problem and what caused it exactly (like what did you do the day/night before). Cramps can't curl fingers to that extend so better check it out.
