Balls!

[Northernspy]

I've had -- whatever this is -- since February 2004. It started as epididymitis, and later prostate pain, and later pain in lots of places (rectal, upon sitting, sitbones). The urinary symptoms are rare (no frequency, no voiding issues).

Levaquin helped the prostate aspect a lot --- but it was not prescribed until June, and the epididymitis is as bad as ever. No, worse -- I increasingly have lumps that come and go. A testicular sonogram reported cysts.

I stopped Levaquin because of side-effects (joint pains).

Blood and swab tests post-Levaquin found nothing. Never had a TRUS, never had an EPS never had a semen culture (no one suggested them).

Any suggestions? The pain is bad -- I sit around with ice on my left nut. If only they made refrigerated underwear...

I live in NYC and have seen many urologists who all have made wacky statements -- I don't trust any of them, and I'm open to suggestions.

I have trouble believing muscle spasms or pundendal nerve damage have anything to do with this --- my prostate was swollen and now is less so, and the left epididymis has swellings some and go (no muscles there!).

- Carlos

PS My PSA is low -- 0.6 while on antibiotics.

[webslave]

First things first: have you had a possible strain in the area from lifting/exertion? See https://ucpps.men/lifting-and-testicular-pain-epididymitis

[Northernspy]

First things first: have you had a possible strain in the area from lifting/exertion? See https://ucpps.men/lifting-and-testicular-pain-epididymitis

Not likely. I know you are a skeptic of the infection school (and for good reason, in light of the number of people not cured by antibiotics), but:

- my prostate was abnormal ("boggy", "hard") before antibiotics

- it's less abnormal now (a little hard on one side)

- the epididymis pain has been getting worse -- in pain, and in the frequence of pain -- steadily during the past year

- the testicular cysts and swellings seem to move around (but almost always left-sided)

I'm another desparate character, open to more things than I was a year ago, but urologists have been so disppointing (not just in results) I have no idea what sort of doctor might be able to identify a strain from lifting.

- Carlos

[webslave]

Why not give the Stanford/Wise-Anderson Protocol a try?

[Northernspy]

Why not give the Stanford/Wise-Anderson Protocol a try?

For a couples of reasons:

1. One of my quintet of urologists checked me on 2 occassions and proclaimed I have no muscle disorder (he pushed on various internal points and I felt no internal pain at all).

2. I undertand that pelvic muscles can spasm, and I'm reasonably certain that mine have. And the Stanford thing might even be a good pain management thing, if nothing else, and help prevent future spasm-induced injury. But:

- I have epididymal lumps that change in size and position. I don't see how muscle spasms can cause that

- didn't I don't see how they could make my prostate boggy

- and why would Levaquin make me better (60% or more), and improvement that continued after Levaquin.

3. IT IS EXPENSIVE -- 2x a week initially at $150 per session for something I have no great confidence in

4. I've been to different massage therapists, who claim to find different things wrong. Factor in that the doctor finds nothing, and it makes the whole thing seem pretty unscientific.

I'll eventually do it if my other options run out, but I've never had an EPS culture or rectal sonogram... so I'm reluctant to go to the non-traditional stuff until after the traditional stuff is more check out. Not that it's easy for me to have faith in ANYTHING at this point, or even to get the full traditional stuff.

- Charles

[webslave]

One of my quintet of urologists checked me on 2 occassions and proclaimed I have no muscle disorder (he pushed on various internal points and I felt no internal pain at all).

Urologists are notoriously unable to diagnose trigger points.

I have epididymal lumps that change in size and position. I don't see how muscle spasms can cause that

Many men have that, and they can be normal.

didn't I don't see how they could make my prostate boggy

Well, you have not read enough then. Read this page carefully:
https://ucpps.men/chronic-prostatitis-is-a-psychoneuromuscular-condition

and why would Levaquin make me better (60% or more), and improvement that continued after Levaquin.

Read https://ucpps.men/antibiotics-are-anti-inflammatory-agents

I've been to different massage therapists, who claim to find different things wrong. Factor in that the doctor finds nothing, and it makes the whole thing seem pretty unscientific.

You are quite wrong. There is a lot of science behind it (neurology, immunology, psychiatry etc), and I don't think Stanford would waste time with fringe nonsense,

..so I'm reluctant to go to the non-traditional stuff until after the traditional stuff is more check out. Not that it's easy for me to have faith in ANYTHING at this point, or even to get the full traditional stuff.

You've had absolutely no luck with the "traditional" (read old and outmoded) stuff, but you won't give a second look at something from the best colleges in the USA that actually helps sufferers. OK.

[Northernspy]

> You've had absolutely no luck with the "traditional"

That's not true. The ONLY thing that's helped were antibiotics. In May I was an invalid, disabled -- in constant pain sitting or standing. After a month of Levaquin my symptoms were 70% less. That benefit remained even after I stopped.

And I'm no Levauqin salesman. It's disgusting stuff. I took it (stupidly switching at one point to Cipro) for 2 more months chasing that other 30%) and all I got were quinolone side effects. And no doctor ever told me that quinolone side effects are NOT rare if you eat that stuff more than 2 weeks. At 3 months they're nearly inevitable.

But my 70% improvement was measureable -- a dramatically different prostate, not just the perception of improvement.

> won't give a second look at something from the best colleges in the
> USA that actually helps sufferers

I've had 5 trigger point sessions (3 with one practitioner, 2 with another). I can see the possibility it is a snappy method of pain management. But the trigger point girls had different ideas about what exactly was wrong. I just didn't trust the stuff enough to spill $150 x 2 a week.

And anyone with this condition is not going to be awed by the likes of Stanford. One of my quintet of urologists is at a top hospital in NYC and is an assistant professor. He was the biggest idiot of a terrifiyingly stupid bunch -- among other things having seemingly no knowledge of the Stanford prototocol. An ivy pedigree does not give a theory any weight.

> Urologists are notoriously unable to diagnose trigger points.

Oh, ho! Which puts this condition in the land of the mystics! One of the trigger point girls identified some muscles as a the problem, and another identified another muscle as the problem and the doctor said none of the muscles were in spasm. Any "treatment" which is that subjective has problems.

>> I have epididymal lumps that change in size and position. I don't see
>> how muscle spasms can cause that

> Many men have that, and they can be normal.

Many men have cysts. Lumps that come and go suggest to me an active pathological process.

- Charles

[Northernspy]

>> and why would Levaquin make me better (60% or more), and
>> improvement that continued after Levaquin.

> Read https://ucpps.men/antibiotics-are-anti-inflammatory-agents

I've read it many times, thanks.

In my case, the benefit of antiobitics persisted after I stopped taking them -- weeks after and so far continuously.

This makes me believe that they had some material benefit -- not just the temporary benefit of antibiotic anti-inflammation.

I actually believe the following, which is not so far from your point of view:

- the Standford protocol benefits some people, and it may be useful for pain management for most

- antibotics are over prescribed and doctors do not sufficient warn about the dangers of quinolones

But to suggest that all persistent epididymitis is the result of muscle spasms seems closed minded. Do you deny that ANYONE can get bacterially infected? Do you deny that quinolones don't kill some bugs that other antibiotics kill handily? And how about the possiblity of physical damage -- from bicycle riding, from the infection itself, or from why ever it is people develop strictures and blockages?

But advocating Stanford no matter what the symptoms & history are you perhaps go too far.

- Charles

[webslave]

In May I was an invalid, disabled -- in constant pain sitting or standing. After a month of Levaquin my symptoms were 70% less. That benefit remained even after I stopped.

Two possibilities: either you had an infection superimposed on your underlying condition, and the Levaquin eradicated it, or 2) you are very genetically susceptible to the anti-inflammatory effects of Levaquin and the initial anti-inflammatory effects allowed some of the guarding spasm to subside, leading to a permanent decrease in symptoms.

I've had 5 trigger point sessions (3 with one practitioner, 2 with another). I can see the possibility it is a snappy method of pain management. But the trigger point girls had different ideas about what exactly was wrong. I just didn't trust the stuff enough to spill $150 x 2 a week.

At this stage, and according to DW and others, there are very few people in the USA reliably diagnosing male internal pelvic point triggers. Read this forum a bit and you'll see what I mean. The fact that you've had a bad experience with some generic PTs doesn't really signify anything.

And anyone with this condition is not going to be awed by the likes of Stanford.

You should read up more on DW's history, stories related by people treated with his protocol, and his book.

Oh, ho! Which puts this condition in the land of the mystics!

No, which puts this condition in the land of the very knowledgeable and experienced.

Any "treatment" which is that subjective has problems.

There is no blood test for trigger points, nothing one can auscultate, no visual signs. But trigger points are becoming an accepted part of medicine today, requiring a degree of skill to find and diagnose properly. Myofascial pain syndromes are painful musculoskeletal conditions, and a quite common cause of chronic pain. That's known, although not yet well accepted. These syndromes are characterized by the development of trigger points that are locally tender when active, and refer pain through specific patterns to other areas of the body. Etiological factors are various; trauma, vertebral column diseases, systemic disorders, psychological distress, lack of motion, and chilling of the body parts, and more.

I regard it as neuropathic pain (my suspicion: it is mediated by the brain, because I have aborted flares with opioids).

This shows that it is serious science:

Pain Med. 2000 Dec;1(4):332-9.

Clonazepam open clinical treatment trial for myofascial syndrome associated chronic pain.

Fishbain DA, Cutler RB, Rosomoff HL, Rosomoff RS.
Department of Psychiatry, University of Miami School of Medicine, FL, USA.

OBJECTIVE: A number of case reports and nonplacebo controlled studies have documented the efficacy of clonazepam (Klonopin) in the treatment of a number of chronic pain syndromes including lancinating and neuropathic/deafferentation pain. There are, however, no data on the efficacy of clonazepam for chronic pain (CP) associated with myofascial pain syndrome (MFPS). Therefore, we wish to report the results of an open clinical treatment trial of clonazepam for CP associated with MFPS. DESIGN: Forty-six patients with chronic pain (PWCP) and a diagnosis of MFPS were recruited into a clonazepam pain treatment open clinical trial. At entrance and completion of the study the patients completed a 10-cm visual analog scale (VAS) requesting them to rate their pain over the last 24 hours. Clonazepam was titrated upwards from 0.5 mg per day, at 0.5 mg increments, every 2 days. These patients rated their perceived pain relief daily on a 3-point rating scale: none, partial, total. Once a patient claimed partial pain relief clonazepam increases were stopped. Patients who complained of intolerable side effects before partial pain relief were withdrawn from the study. For a subgroup of patients claiming partial pain relief, clonazepam serum levels were determined. Because of the reported efficacy of clonazepam for neuropathic/deafferentation type of pain, patients with this diagnosis were withdrawn from the partial response group. Statistical analyses were performed on this remaining patient group with myofascial pain syndrome without a secondary diagnosis of neuropathic/deafferentation pain and partially responsive to clonazepam. Descriptive statistics were calculated for this group. Drop in pain level from entrance to partial response was tested for statistical significance via t test. In addition, 17 independent variables such as presence of trigger points, presence of burning pain etc, were utilized in a regression analysis, with drop in pain level as the dependent variable. A Pearson correlation analysis was first performed in order to determine which of the independent variables significantly correlated with decrease in pain level. Independent variables having a Pearson r of.3687 or greater were selected for the regression procedure. SETTING: Multidisciplinary pain facility. PATIENTS: Patients with chronic pain with a diagnosis of MFPS and without neuropathic/deafferentation pain. RESULTS: Of the 46 patients entered into the study, 9 were not titrated to partial pain relief because of intolerable sedation and 9 had a diagnosis of neuropathic/deafferentation pain. For the remaining group (n = 28), mean drop in VAS pain level from beginning of the study to partial response was 2.78 (SD = 1.94). This was statistically significant (t = 5.49, P <.001). Mean clonazepam dosage to reach partial response was 2.41 (SD = 1.62) mg/day and the mean dosage per kilogram body weight per day was 0.04 (SD = 0.03) mg. Mean clonazepam serum level was 30.58 (SD = 24.53) microg/L. Decrease in pain level was associated with the presence of the following independent variables: trigger points (r =.451); range of motion restriction (r =.653); non anatomical sensory abnormalities (r =.370); chronic low back pain (r =.451); and burning pain (r =.482). In the regression analysis, restricted range of motion and presence of burning pain accounted for 42% and 16% of the variance respectfully. CONCLUSION: Clonazepam may have an antinociceptive effect for pain associated with myofascial pain syndrome.

PMID: 15101879 [PubMed]

But there are sceptics:

Eur Neurol. 2004;52(2):67-72. Epub 2004 Jul 13.

Myofascial pain, fibromyalgia or fibrositis?

Pearce JM.
Emeritus Consultant Neurologist, Department of Neurology, Hull Royal Infirmary, Hull, UK.

The terms myofascial pain, fibromyalgia and fibrositis are critically examined. They constitute diagnostic labels for non-specific musculoskeletal aches and pains. Analysis of the evidence shows that none of these labels is substantiated by hard physical signs or by laboratory evidence of consistent pathological or biochemical abnormality. What is the objective evidence for disorder(s) of muscle, fascia or fibrous tissues, so clearly indicated by these diagnostic names? Alternative terms such as 'regional pain syndrome' or 'chronic pain syndrome' merely redefine the clinical problem without providing a mechanism or basis for diagnosis. Despite different diagnostic criteria, these conditions, along with chronic fatigue syndrome, have many demographic and clinical similarities, most notably tender trigger points. Indeed, the terms are often used interchangeably. There are few differences in the symptoms, physical findings, laboratory tests, functional status, psychosocial features and psychiatric disorders. This paper seeks not to deny the existence of aches and pains, but to critically examine the utility of these terms. The only claimed physical sign is the presence of tender trigger points over muscles or muscle attachments. Research suggests that tender points are a measure of general distress related to pain complaints but separately associated with fatigue and depression. They are present in some normal subjects and are variable in occurrence in time in the same individual. They reflect no demonstrable pathology. It is therefore argued that none of these commonly used diagnoses represent distinct disease entities. A possible but unproven alternative hypothesis is that such symptoms relate to neural pain with both peripheral and central components, and in some instances psychological or wilful embellishment. Copyright 2004 S. Karger AG, Basel
Publication Types: * Editorial

Typical British reserve and traditionalism at work here ("wilful embellishment"), but even he admits this may be a neurogenic condition.

Many men have cysts. Lumps that come and go suggest to me an active pathological process.

All I can tell you is that I have had them for years, and my uro said they were insignificant. If you obsess about these "lumps" and palpate them frequently, they can become tender and painful quite quickly. Leave them be.

[webslave]

Another interesting recent study underlining the newness of these concepts and their slow acceptance:

J Electromyogr Kinesiol. 2004 Feb;14(1):95-107.

Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction.

Simons DG.
Department of Rehabilitation Medicine, Emory University, 3176 Monticello Street, Atlanta, GA 20014-3535, USA. [email protected]

This article explores how myofascial trigger points (MTrPs) may relate to musculoskeletal dysfunction (MSD) in the workplace and what might be done about it. The cause of much MSD and pain is often enigmatic to modern medicine and very costly, just as the cause of MTrPs has been elusive for the past century, despite an extensive literature that is confusing because of restricted regional approaches and a seemingly endless variety of names. MTrPs are activated by acute or persistent muscle overload, which is characteristic of MSD in the workplace. MTrPs can involve any, and sometimes many, of the skeletal muscles in the body and are a major, complex cause of musculoskeletal pain. The clinical and etiological characteristics of MTrPs have been underexplored by investigators, leading to undertraining of health care professionals, underappreciation of their clinical importance. MTrPs have no gold standard diagnostic criterion, and no routinely available laboratory or imaging test. MTrPs require a specific non-routine examination and muscle-specific treatment for prompt relief when acute, and also resolution of perpetuating factors when chronic. After identifying a critical false assumption, electrodiagnostic studies are now making encouraging progress toward clarifying the etiology of MTrPs based on the 5- or 6-step positive-feedback model of the integrated hypothesis. Specific research needs are noted. MTrPs are treatable and they deserve increased attention and consideration by research investigators and clinicians.

Publication Types:

* Review
* Review Literature


PMID: 14759755 [PubMed - indexed for MEDLINE]

[Northernspy]

> Two possibilities: either you had an infection superimposed on your underlying condition

Jeeze, don't you accept that SOME people have an infection? :)

If you need a talented trigger point girl and none are available I wonder how useful this will be. I also question why if klonopin helps stop seizures, the seizures restart unless there is a continuing pain stimulus.

Btw, I have self treated klonopin and it helps a little.

But thanks for your gathered research. I'll check it.

- Charles