You really don’t want to know what orthos do when you are (or are supposed to be at sleep) Lets just say I still have a supply of black and decker electric drills… (they could only use them once because they can’t be cleaned well enough to be sterilized but are fine for their intened purpose)
Here is the difficulty with “criteria” and imaging. For every person that has these same things show up in a study and has symptoms, there are as many as 8 who will have the same things show up in an imaging study and have NO symtoms. The New York Criteria is tough. when you consider the other criteria that has to be met.
Keep in mind It is important to highlight that diagnosis in the radiological section showed a 66.2 sensibility and 9733% specificity. What this means isbased on these variables:
- true positive (TP): an imaging test is positive and the patient has the disease/condition
- false positive (FP): an imaging test is positive and the patient does not have the disease/condition
- true negative (TN): an imaging test is negative and the patient does not have the disease/condition
- false negative (FN): an imaging test is negative and the patient has the disease/condition
On a first pass, we don’t assume some relationship between the test and the disease/condition, but we hope there will be some relationship between the test and the disease/condition, because otherwise the test would be worthless.
Once you have the variables they play this way
For a given test and disease/condition, its sensitivity is how well it can be positive among all those with the condition. Therefore:
sensitivity = TP / (TP + FN)
true positives / (all those with the disease)
For a given test and disease/condition, its specificity is how well it can distinguish those with disease from those without. The test must not just fail to pick up a segment of the population (that might be poor sensitivity), it must distinguish those without the disease… the true negatives (TNs). Therefore:
specificity = TN / (TN + FP)
true negatives / (all those without the disease)
Or in short the chance of your study being significant enough for diagnoses is one in 12 (whats left after the 50:50 chance) The specificity of an xray for a compound fracture for example is 100%
Radiological sacroiliitis grade >2 bilateral or grade 3–4 unilateral is a difficult diagnoses to come by: http://www.scielo.br/pdf/rb/v40n1/en_10.pdf. The images are not enough.
Our other Mod Support person Meli who is pretty busy right now in her first few weeks of med school happens to be a bio-medical engineer first. She explains it as imaging being only one piece of a much larger puzzle. It isn’t even a corner or border piece.
One of the MOST unethical medical practices IMO is the large ortho paractices (especially the spinal practices) who have their own imaging equipment. This was actually illegal at one time. Never before has their been so much unnecessary surgery done. Over 60% of the population is walking around with “herniated discs” and has no idea. But show up at the ortho with back ache which could have been caused by too much golf, and they could be headed to the OR and in many practices were. (insurance companies put the screws on it, because the folks who should have didn’t) Even today its estimated as much as 70% of spinal surgery is unecessary. 80%get better 20% don’t. Among the Unoperated 80%get better 20% don’t.
There frankly isn’t a LOT of answers in imaging. When it comes to the spine unless you have peripheral issues such as you are incontinent, or limbs don’t work, abnormalities are not all that abnormal. The related symptoms need be very specific or the image means nothing.
You guys are going to drive yourself nuts trying to read your own studies. Its hard when you have the 6 years of fellowship training after med school.
Good point, on one hand I can understand the reluctance, but on the other, I have been trying to get a Dx for a few years. I’ve been having SIJ pain since my 30’s, used to notice it when sitting on my surfboard. I have a ruptured disc in my L4/L5, caused by Bertillotti’s syndrome the extra vertebrea L6 is attached with a to my illiac bone on one side, this is what blew out my disc. All my other discs are degenerated, I have radiculopathy in my C5/C6, L5/L6, and now having nerve ssues with my S1, pain down leg and with 3rd, 4th toe, but nothing that diserves surgery. On my 4th radio frequency ablation of my SIJ. So I was just hoping for some answers, which I am very doubtful the medical industry can give me… At least the Remicade is starting to work, but now that the MRI has come back “normal” they will probably deny me medication, while the radiologists sit around with number two pencils stuck in there ear…
Thanks for taking the time and explain how useless the imaging is. It is fascinating to me, I would have thought moderate erosion would make a difference with a diagnosis.
I think that the damage is done with my SIJ, it is starting to fuse together, I told my Pain Management doctor that I heard the pain went away when it fuses, he said "who told you that?"
I am just another frustrated patient, wanting to get a handle on the disease, (if I have it).
One good thing, the biologics are starting to help, I was surprised how much I could bend today, I was practically putting my palms on the floor, always have been to stiff to bend. So maybe I do have something?
(edited for right attitude) …
This is why I’m so glad I’m overly cautious about back surgery…I was a “candidate for it” when my back went out. My husband, who’s had two back surgeries, thought I was nuts not having it done. He and some people who’ve had back surgeries seem to think their pain was incredibly worse because nobody could stand the kind of pain they had and not go to the hospital for surgery. I know several people who had discs that were “slipped, bulging, protruding and impinging the nerve” but didn’t have surgery and recovered quite well. It just takes a lot of pain meds, bed rest, mild exercise, TLC and continued caution not to re-injure the back, and then back strengthening exercises ongoing.
I’m not saying back surgery should never be considered, but it should probably be the last resort, in my opinion.
That’s the story of my life!
With all this going on you must sometimes feel desperate to untangle what exactly is causing what and to nail what if anything can be done to help over and above the treatment for PsA. But is your PsA diagnosis in question Jon? On the part of your rheumy, that is?
It’s great that Remicade is starting to help though, palms near the floor is a good thing, right? Not necessarily according to my last rheumy who saw it as due to hypermobility. But just being able to move, bend, get stuff done that’s (nearly) enough for me … Quite a few questions always seem to remain with this disease and its treatment but ultimately feeling better or not is the acid test.
That is good news Jon, isn’t it?
Yes, it sounds like my new Rheumy is questioning the Dx, and trying to reverse it. It has taken 4 years to get to a place where I can get biologic treatment, and like I said it is helping, I don’t want to be religated back to a Dx of OA and given NISAIDS, because of obscure out of date imaging interpretations, and lack of consensus among peers. I need a Rheumy that will not start making judgement calls, like she did with the Raynauds, putting it down to the use of vibrating power tools without any solid evidence, but ignoring all the imaging and ultrasound reports, to bend the diagnosis to her desired outcome.
Yes, I would think it should be, I don’t see my Rheumy until next month. If it is determaned that I do not have SPA, then she might right this off, because how can it improve if it is not there?
Right. It took me 3 years to get on biologics, 3 really lousy years, I can see the problem and then some. My main problem was one rheumy who didn’t question the dx of inflammatory arthritis but was downplaying it in stages, it was pretty obvious where he was going. OA loomed large.
What about other signs of PsA though, apart from imaging? There has to be a way forward, I really hope things turn out well for you. You’d hope that a good response to remade might influence your rheumy’s thinking.
My old Rheumy didn’t keep notes, so then she forged tyem when I left the practice, been on biologics for 1 1/2 years, nails have cleared, Ps has also cleared; enter new Rheumy- suspisious of Dx because of fraudulant notes, no sign of Ps or nail involvement, Biologics are keeping inflamation down especially during the appointment time, around 1pm. I do not want to go back to square one, and be in systemic pain from inflammation just to satisfy some Rheumy’s suspisions.
Also, if I go off Remicade, it will probably not work after I restart, because the body makes antibodies… It is a real pickle, if I dump this doctor, she will write up that there is no sign of PsA and she does not recommend further treatment.
Sorry for another missive but the following is about two years of post medical school fellowship experience (for a rheumy not me)
The type of studies being described are for ‘information’ and have zero to do with diagnoses. diagnoses comes from the following table:
FWIW these criteria have a sensitivity of 0.914 and a specificity of 0.987 How they interptet spinal films means nothing when qualifying for Biologic medications, escept in the case of Anklylosing spondylitis, but that diagnoses is going away so i wouldn’t worry about it.
Inflammatory articular disease (Required for all to have PsA) is NOT determined by imaging but is a differential diagnoses (physical exam) obtained by pressing on "PsA tenderpoints until the white shows upr in the fingernail of the examiner. Occasionally a flat screen X-ray helps, but is usually just a reference item to prove treatment isn’t working (not evidence if it is) More particularly the exam follows this list:
Differential diagnoses for regional musculoskeletal pain
Referred pain may derive from cervical disorders, Pancoast tumor of the lung, subphrenic pathology, or entrapment neuropathies and brachial neuritis (see Brachial Neuritis).
Rotator cuff tendinitis (see Rotator Cuff Injuries)  is inflammation of the rotator cuff tendons, arising acutely as a result of a recognizable injury (throwing) or insidiously as a result of repeated impingement on the overlying acromion, coracoacromial ligament, acromioclavicular joint, or coracoid.
The principal symptom of rotator cuff tendinitis is pain in the deltoid region of the shoulder, aggravated by an overhead motion of the arm. The patient may also describe shoulder pain when sleeping on the affected side. Examination findings include the following  :
Tenderness in the subacromial region, between the greater tubercle of the humerus and acromial process
Pain in the middle of the arc of active abduction, usually between 60° and 120°
Reproduction of pain when midarc abduction and external rotation are resisted isometrically
Range of passive shoulder abduction exceeding that of active abduction
Treatment includes avoidance of overhead reaching, administration of nonsteroidal anti-inflammatory drugs (NSAIDs) for 2-3 weeks, and physical therapy with stretching and strengthening exercises. Subacromial corticosteroid injections may be used if symptoms do not improve.
Rotator cuff tears (see Rotator Cuff Injuries) are transverse or longitudinal tears of the supraspinatus or infraspinatus tendons. They occur at the musculotendinous juncture, approximately 1 cm from their insertion on the humerus. They may arise as a result of an acute injury (eg, a fall on an outstretched arm, hyperabduction, or a fall onto the side of the shoulder) or gradual attrition in the setting of chronic rotator cuff tendonitis.
With acute injury, symptoms include sharp shoulder pain followed by weakness of abduction. In the setting of chronic rotator cuff tendinitis, a tear is signaled by weakness of abduction or loss of smooth motion during abduction. Examination findings include the following:
Weakness and pain in the midarc of abduction and external rotation
Loss of smooth overhead reaching (partial tears) or inability to reach overhead (complete tears)
Initial management is conservative. Young patients with acute tears should be evaluated by an orthopedic surgeon.
Bicipital tendinitis is inflammation of the long head of the biceps as it passes through the bicipital groove of the anterior humerus. It usually arises as a result of overuse with activities that require repetitive lifting. The primary symptom is pain in the anterior aspect of the shoulder (over the humeral head), which is aggravated by lifting or overhead pushing or pulling. Examination findings include the following:
Tenderness of the bicipital groove
Pain aggravated by isometric resistance to elbow flexion or supination of the arm flexed to 90°
Treatment includes elimination of lifting, avoidance of over-the-shoulder reaching, and 3-4 weeks of NSAID therapy. Corticosteroids may be injected into the bicipital groove if symptoms persist.
Subacromial bursitis is the accumulation of fluid within the subacromial bursa, arising as a result of rotator cuff tendonitis. Significant fluid may be detected during a physical examination. Treatment is similar to that of rotator cuff tendinitis. For a significant effusion, drainage is indicated, followed by corticosteroid instillation.
Frozen shoulder (adhesive capsulitis) is a term for conditions in which the range of motion of the glenohumeral joint is significantly reduced as a result of pathology within the joint capsule. Associated medical conditions include diabetes mellitus, recent myocardial infarction, stroke, a recent neurosurgical procedure, Parkinson disease, and hypothyroidism.
The primary symptoms of frozen shoulder are pain and gradual loss of shoulder motion without any known injury. Examination findings include a reduced range of motion during both active and passive motion. Pain is present particularly at the extreme ranges of motion. Radiographic images do not show evidence of glenohumeral arthritis.
The initial treatment regimen includes NSAIDs, nonnarcotic analgesics, and physical therapy. Occasionally, a 2- to 4-week course of oral corticosteroids combined with aggressive physical therapy may result in decreased pain and increased shoulder motion.
In acromioclavicular syndrome (see Acromioclavicular Joint Injury), pain arises from the acromioclavicular joint as a result of arthritis or injury to the acromioclavicular ligaments. Osteoarthritis of the acromioclavicular joint with inferior osteophytes can lead to rotator cuff impingement and associated tendinitis. This injury may be acute or chronic, and patients may report a history of trauma (eg, fall during a contact sport).
Examination findings include the following:
Swelling of the acromioclavicular joint
Deformity of the joint may result from subluxation. Pain in the joint is aggravated by downward traction of the ipsilateral arm or forced passive adduction. An acute acromioclavicular injury is treated with a shoulder immobilizer.
Elbow, wrist, and hand
Lateral epicondylitis (tennis elbow) is the most common cause of elbow pain. Pain is felt along the lateral aspect of the elbow. Tenderness is present over the lateral epicondyle at the attachment of the extensor tendons of the forearm. Resisting wrist dorsiflexion with the elbow in extension produces increased pain. Elbow extension is normal. Treatment includes rest, NSAIDs, and local steroid injections.
Medial epicondylitis (golfer elbow) is less common than lateral epicondylitis. Resisted wrist flexion with the elbow in extension produces pain. Tenderness may occur at the insertion of the common flexor tendon at the medial epicondyle.
In olecranon bursitis, the anatomically superficial position of the bursa predisposes it to injury and inflammation. The patient reports pain when leaning on the elbow and during flexion. Examination findings include tenderness at the tip of the olecranon process and an occasional friction rub. Visible swelling of the bursa may be evident. In acute cases, warmth and erythema are present. Patients with acute bursitis must undergo aspiration for culture and crystal examination.
De Quervain tenosynovitis is a stenosing tenosynovitis of the abductor pollicis longus and extensor pollicis brevis tendons, resulting from repetitive motion or overuse. Pain is noted along the radial aspect of the wrist and thumb during pinching, grasping, and similar movements. Ulnar deviation of the wrist, with the thumb held in abduction by the flexed fingers of the same hand (Finkelstein test), reproduces the pain. Crepitus of the tendons may be evident.
Treatment of de Quervain tenosynovitis includes use of a thumb spica splint, avoidance of repetitive thumb flexion or abduction, and NSAIDs.
Trigger finger and trigger thumb (see Trigger Finger) are also known as stenosing digital tenosynovitis, snapping finger, and snapping thumb. Injury is the result of overuse. Examination findings include the following:
Pain and tenderness
Snapping, triggering, or catching during movement of the finger or thumb
A nodule is felt in the palm on the flexor tendon just proximal to the digital-palmar crease.
Pain in the posterior aspect of the hip is often referred from the lumbar spine. Sacroiliac disorders can also cause buttock pain. Pain from arthritis of the thoracolumbar junction may be referred pain to the area of the greater trochanters and may mimic trochanteric bursitis. Radiculopathies of the L2-L4 nerve roots may produce pain in the inguinal area and the anterior thigh; this may mimic hip disease. Iliopsoas abscesses, retroperitoneal appendicitis, tuberculous abscesses, or pelvic inflammatory disease can cause pain in the hip region.
Thrombosis or aneurysm formation in the branches of the aorta or iliac vessels may produce buttock, thigh, or leg pain that may be confused with hip pain. True intra-articular hip pain is most often felt in the groin and anterior thigh. Occasionally, hip disease can manifest with isolated knee pain.
Trochanteric bursitis is the most common cause of pain in the hip region (felt over the lateral aspect of the hip). Pain increases with activities such as walking, squatting, and climbing stairs; pain typically decreases at rest. Patients note increased pain when lying on their ipsilateral side. The pain may be associated with a limp. The area over the greater trochanter may be tender and boggy. Resisted abduction of the hip reproduces the pain. Local corticosteroids with anesthetics may help.
Iliopsoas bursitis can occur in patients with osteoarthritis, RA, pigmented villonodular synovitis, osteonecrosis, and septic arthritis. Most patients are asymptomatic or present with a painful inguinal mass. Computed tomography (CT) is the best diagnostic test. Instillation of corticosteroids is effective therapy.
Ischiogluteal bursitis occurs most commonly in patients with occupations that favor repeated friction of the ischial bursa. Patients note pain over the ischial tuberosities; the pain is aggravated by sitting and lying down. Local tenderness of the ischial tuberosities is found upon palpation. Symptoms may be alleviated through avoidance of pressure or friction on the ischial tuberosities (ie, by using doughnut-shaped cushions) and local instillation of corticosteroids.
Adductor tendinitis occurs in patients engaged in sports activities that involve straddling (eg, horseback riding, gymnastics, or dancing). Pain is typically felt in the groin and the inner aspect of the thigh. Tenderness can be elicited by local palpation of the adductor muscles, especially near their insertion on the front of the pelvis. Pain is increased by passive abduction of the thighs and active adduction against resistance.
Treatment of adductor tendinitis consists of rest and ice packs during the acute phase. NSAIDs, ultrasonography, and progressive stretching exercises are used in the subacute phase. Local corticosteroid injections are reserved for patients resistant to these conservative modalities.
Knee and ankle
Prepatellar bursitis (housemaid knee) is related to recurrent trauma and usually occurs in persons who spend significant time kneeling. Etiologies include trauma, gout, and infection. In chronic cases, a well-circumscribed area of fluctuance is present over the prepatellar area. In acute cases, warmth, edema, and erythema are noted over the anterior knee. Fluctuance may be subtler. Tenderness is maximal over the prepatellar bursa. Knee flexion increases the pain, whereas knee extension does not. A joint effusion, if present, is small.
Aspiration of acute bursitis is necessary to assess for the presence of an infection or crystals. Traumatic bursitis improves with rest and avoidance of kneeling.
In anserine bursitis (see Pes Anserinus Bursitis), pain is noted over the medial aspect of the knee, is made worse by climbing stairs, and is often present at night. It is most common in overweight women with osteoarthritis of the knees. Examination reveals exquisite tenderness over the anserine bursa, located over the medial aspect of the knee approximately 2 inches below the joint line. Treatment includes a corticosteroid injection into the bursa and an exercise regimen to stretch the adductor and quadriceps muscles.
Patellar tendinitis (jumper’s knee) most commonly affects young athletes who are engaged in sports that require repetitive running, kicking, and jumping. Pain is noted at the inferior pole of the patella during activities such as climbing stairs, running, and jumping. Treatment consists of rest, NSAIDs, knee bracing, and an exercise regimen to stretch and strengthen the quadriceps and hamstring muscles.
Achilles tendinitis (see Achilles Tendon Injuries and Tendinitis) is characterized by pain, swelling, tenderness, and crepitus over the tendon near its insertion. This form of tendinitis is usually caused by repetitive trauma and microscopic tears from excessive use of the calf muscles in ballet dancing, distance running, basketball, jumping, and other athletic activities. Faulty footwear with a rigid shoe counter also may produce Achilles tendonitis.
Examination findings include thickening and irregularity of the tissues surrounding the tendon and palpable nodule or nodules within the tendon (occasionally representing xanthomata, tophi, or rheumatoid nodules). Passive dorsiflexion of the ankle intensifies the pain. Abnormalities of the tendon and peritendinous tissues can be demonstrated on images from ultrasonography and magnetic resonance imaging (MRI).
Treatment of Achilles tendinitis consists of rest, avoidance of the provocative occupational or athletic activity, shoe modification, a heel lift to reduce tendon stretching during walking, and NSAID therapy. Physical therapy includes local heat application, gentle stretching exercises, and a temporary splint with slight plantar flexion.
Retrocalcaneal bursitis (see Achilles Tendon Injuries and Tendinitis) is inflammation of the retrocalcaneal bursa, resulting in pain and tenderness at the back of the heel. The area anterior to the Achilles tendon and posterior to the calcaneus is tender; passive dorsiflexion of the ankle produces pain. Bursal distention is palpable and produces bulging on both sides of the tendon.
Retrocalcaneal bursitis may occur as a result of repetitive trauma or as a manifestation of gout or a systemic inflammatory arthritis. The diagnosis can be confirmed by means of radiography (showing obliteration of the retrocalcaneal recess), ultrasonography, or MRI.
For most patients with retrocalcaneal bursitis, rest, activity modification, moist heat application, slight heel elevation using a felt heel pad, and NSAIDs constitute sufficient therapy. A walking cast or cautious corticosteroid injection into the bursa is sometimes required.
Generally speaking you have to have 5 “tenderpoints” for it to be systemic. I listed the initial treatment for the basic areas as that is how they eliminate injury form "inflammation in a number of instances. Anyway though you might be interested in what all the pressing, poking, wiggling etc is all about in an exam. He isn’t determining if it “hurts” its far more complicated. We stop thinking about it if it "hurts and figure “we’ve got it.” Nothing could be further from the truth. Its WHY it hurts
One last thing about the physical exam (until I think of several more things:)
Synovial hypertrophy is the most reliable sign of an inflammatory arthritis. The synovial membrane is normally too thin to palpate. In a person with chronic inflammatory arthritis, the synovial membrane has a doughy or boggy consistency, a feature best appreciated at the joint line or margin. You can’t see it (even on imaging studies) BUT you can feel it. In this day and age if your doc isn’t typing and talking poking and typing, your gettin short changed in the records department.
Thanks, still digesting this…
Just been to see my rhuematologist and had a top to toe physical examination. She found bits I didn’t know hurt and was able to tell me which bits were more troublesome than others. All through her hands. Just her hands. So impressive.
There you go. That’s how it’s done…
BTW one should refer to: Entheses and Fibromyalgia Tender Points This is where they are “poking”
Still kind of subjective, I would think if you could get imaging of the Enthetis and synovitis, it would narrow the Dx down, seems like the lazy Rheumy’s might be quick to go with a Fibro Dx, as a lot of these spots are also tender point locations for fibro…
The Fibro spots:
There is not as much overlap (granted its inches) as one would think, especially after a year or so living with a cadaver… Attempts to manage the practice medicine by “formula/science” as has been somewhat of a trend recently is a formula for failure.
For the most part “skill” replaces “science” which is left behind and becomes the stuff of quacks and internet forums.
The best example is a medication called “Anacin” (my grandfathers invention) He discovered by combining acetylsalicylic acid and Caffeine he could treat a number of conditions headaches being primary. IF he were on the internet, a quack (alternative medicine practitioner) or a scientist he could use science to prove headaches are the result of a shortage of acetylsalicylic acid and Caffeine in the body. He could make a quick pile of money hawking his headache cure (actually he did make a lot of money with his headache cure but thats a different story) in health food stores and the internet and do so with scientific evidence. If he was practicing in 2010 instead of 1910 he could really double down and get literally piles of money from the government, pharmaceutical companies, universities foundations etc. researching why the body had a shortage of acetylsalicylic acid and Caffeine.
Why heck they might even develop a test for acetylsalicylic acid and Caffeine levels. An industry would spring up around him with all kinds of ways to add acetylsalicylic acid and Caffeine to the body along would come someone else who said "wait its NOT a shortage of acetylsalicylic acid and Caffeine, its a shortage of Acetaminophen and caffeine, and suddenly excedrin would be the “thing” (and it was, hardly anyone uses aspirin anymore let alone Anacin.)
A doctor would look at it differently when a headache patient presents himself. Instead of running a blood test for acetylsalisylic acid and caffeine levels despite the fact those two compounds cure a headache. If the test was negative he wouldn’t send the guy packing, saying you are IMAGINING that headache, your blood work proves it. My totally OBJECTIVE test for acetylsalisylic acid and caffeine levels was normal.
Instead a doctor would look at the guys head. He might find a bloody spot. Which would lead him to wonder why there was a bloody spot. Eventually he might even have an x-ray taken only to discover there was another reason for the headache. (this guy was days not knowing the nail was there and only showed up to the doc when Tylenol wouldn’t fix it.
Of course it could have been this guy:
He didn’t need the xray to find out what was causing the headach, but rather how many nails he needed to get out… (BTW the guy lived and did just fine speaking of suicide failure)
Ouch, that is a lot of nails! He could use your grandfathers invention!
Thanks for the info, I appreciate it. I understand where you are coming from with your comments, for me I am just frustrated by lack of professional doctors.
To recap; 1st Rheumy was ready to retire, didn’t want to do any tests, just labeled me with OA relying on a left hand x-ray, she retired after telling me that they really didn’t have a clue, they just throw medications and see what helps, she referred me to the 2nd Rheumy went to her for for over two years, she never kept notes, the ones she did keep, she typed wrong, miss typing IgM for IgA, then thinking I had bone cancer… (BTW this resulted in being Dx’d with WM cancer, possibly caused by inflammation.) After leaving the practice she forged notes, saying I was on two biologics simultaneously, when in fact she didn’t give me any. The 3rd Rheumy read the bogus notes and made changes with my treatment without going over them with me, so she got fired. the 4th just wanted to write scripts, and told me to come back in 3 months, without any treatment for the disease. My current one has been the most promising… So, you might see why I am suspicious of doctors, and would rather verify with imaging…
As far as tender points, I thought I would check to see if my mother had FMS, she has had all the symptoms, but being a military dependent, VA never really diagnosed her, so I casually touched one of the tender points on her leg, she jumped about a foot off her seat! She said “what did you do?” (She is 90, but very spry, good reflexes)… I have been Dx’d with FMS 3 times, by two doctors, mainly because of the brain fog, insomnia, and muscle pain, but I can endure deep tissue massage, so highly unlikely. Both of these “Rheumy’s” didn’t bother to do the exam of tender points.
The biologics are helping, so maybe that will be proof enough to continue treatment, this is the first time after trying several.
I didn’t like my first rheumy even though his diagnosis was right. He just wasn’t interested enough in the disease. This second one came highly recommended as being one of the very best for PsA in the whole of the UK. And she is impressive most especially given her head to toe physical examination, the first one never did that. She’s 200 miles away but worth the effort. Are the rheumys you’re seeing specialists in PsA, do they do research and get all the grants for such research? Are they acclaimed by their peers?