The Verbal Equivalent of "Crunch" (in poetic form)

The Verbal Equivalent of "Crunch"

I have been abusing
"screaming ninnies," misusing
it to describe my spastic, spasming,
painful periods of dystonia.

I say that I have the "screaming ninnies,"
which makes no sense at all.

Still, it's a habit,
and I'll likely continue to misuse it for lack
of words that feel right,
that encompass the realities of screaming
bloody murder on a cellular level,
my cells' uvulae all a-quiver,
feeling bat-shit nuts,
personifying inanity,
all at the same time:
ka-boom!

You stupid git!
I'm so sick.
Don't roll your goddamn eyes.

You want the pretense:
There is a problem list in play,
and as I work the problem,
solutions will come, the list will end, and voilà,
the problems have been put to rest, put to bed, are gone.

You stupid git!
I'm so sick.
Don't roll your goddamn eyes.

Oh, I am thankful, don't worry.
This poem, or that,
as you know, convert into top-notch
inspirational gratitude
with an at-the-ready daily devotional
doily, or - bate-the-breath -
an honest to goodness antimacassar..

Just pick a poem, any poem, read it, and be glad.
Rejoice, rejoice,
rejoice, I say, in the poem.

While screaming obscenities last evening,
I got tickled,in that Southern way,
in the vernacular of greens and hot sauce.
Giggling, weeping, and yelling,
simultaneously.  (The simultaneity of things
is the rip tide in this, my ocean.)

Curse words are satisfying
but somehow all the seats were pews,
all the books psalters, every top
ten hit a hymn..

So, of course, I called out "shitake mushrooms"
over and over, laughing at such
a honed wit
(because laughter demands
an indirect object).

You stupid git!
I'm so sick.
Don't roll your goddamn eyes.

I can't stop talking when I am this sick.
Or I cannot cease the saying of
the same phrases over and over,
and rarely can I sustain conversation
that doesn't reek of, well, onions.

Oh, all right, desperation. That doesn't reek of desperation.
I'm hungry. I'm so sick,
You stupid git.

Replace "screaming ninnies" and "shitake mushrooms,"
all to lose your goddamn rolling eyes.

When "altered" in intensive care,
I wore the world out with "O, God"
exclamations and "O, Dear God" moans.
The result was one crazy Me
screaming to another crazy Me:
"Shut up! Shut up!
God ain't here right now!"

You stupid, goddamn eye-rolled git,
I am so sick.

Further rumination on ninny would yield little.
then as now.
We should honor, though,
the prominence of the gerund
because this term is, frankly, very
verbal, hyperactive, and
stuck that way, like a gerund.

Yes, exactly.
Like Flaubert's Bovary dancing at the ball,
all in the imperfect.

A waltz, hayseeds in high collar.

The ear must be pleased and satisfied.
There needs to be texture,
the aural and verbal equivalent of *crunch*,
You stupid, stupid git.

PHOTO CREDIT:  SCREAM

This is another conversion of a previous prose piece to poetry (if you deign to accept the label!).  I had hoped that the poetry bug would depart once I left the writing site that kept me sane at the beginning of this year -- but I feel the need returning.  It's sad, as I don't want to abandon this venue, the blog -- but my secret writing desires are, believe it or not, very shy.  And it turns out, ha!  Turns out that I need the camaraderie of my brothers and sisters suffering the same delusion:  We're writers.
© 2013 L. Ryan

CRPS Pain

It's been a good while since I've written just to write, writing as if to save my life, writing just to release toxins.  Smiling, offering to make coffee, smiling, asking which coffee he'd like to have this late morning. Saying "excuse me" to the cat whose tail is in my way.  Checking the phone to see if I missed any calls. Setting the mp3 player to recharge, for the third time in 24 hours.  I put up dishes, washed what was in the sink, all interspersed with continued exhortations to Buddy the Maine Coon to please take his prehensile tail elsewhere.

Even in the night I was thinking of the cyclone hitting India.  Between my screams, I'd have a vision of a young man standing on the edge of the spiral, the whorl, knowing that the edge of a spiral, a whorl is a cutting thing.  I kept half-dreaming him saying a cold and swift "good-bye" to what must have been a mother, nodding to an old man, who had nodded first to him, which my mind-state knew was his calling to sacrifice.
He dove into the cyclone, and as I looked down the line of the cliff, the billowing chaotic universal twist not yet touching holy land, I saw young people, serene-faced, push off powerfully, smoothly, launching bodies into the eddy.

I will hate my mind when the pictures roll in, the bodies floating, the water-borne disease predictions, and, surely, the misshapen face of of what must have been a mother, the stoic cold face of an old man in charge of pointless sacrifice.

I was angry at Fred yesterday, which meant I needed to eat.  Fred had done nothing but make sure, at intervals whose meaning meant something only to him (As long as he could stand?  Whenever he remembered?  If i made a moan?  I know that once he came in when he heard me laughing.), that I was still alive, and had taken my meds.  I went to sleep Tuesday evening with a high fever, the chief odd symptom of which was exhaustion, total exhaustion.  I slept and listened to music from Tuesday evening to mid-day Friday.  No food, enough water to take those accursed meds, the spotlight of Fred's face in mine, and that stupid question:  "Are you all right?"

So I tried to be normal yesterday, my normal and a little of what might be your normal.  I cleaned a bit, chatted cheerfully, answered emails, tried, and tried, and tried.

The exhaustion returned, but not the high fever.  I settled in for a normal night of sleep-some, read-some, listen-to-music-some.

And the dystonia, the spasms, the wrenching screaming twists and deformations hit within the hour.  I promptly informed God that "no, I can't do this," and loaded up on antispasmodics, told myself the usual lullaby:  "You will stop jerking in fifteen to twenty minutes, tops.  Whatcha wanna do until then?"

I walked using my forearm crutches, in a back and forth pattern, not wanting to fall but wanting to force my legs into normal shapes.  If I don't, it's grotesque, even for me, to watch, and hell, only for me, to feel.  When my legs decided they weren't going to move any more, and this after about 3 minutes, I grabbed a cat.  I groomed the hell out of that cat, and since it happened to be Dobby, well, that was swell by him.  Why I did not suddenly leap from the bed every night to groom him with ferocity was the mystery between his ears.
The pain increased as I kept denying muscles, tendons, various sheaths and demon parts the right to transmogrify into whatever rhomboid they felt like.  It was blitzkrieg time.

Fifteen to twenty minutes, tops.

Not quite.

Try all night long.  I gave in to the screaming.  I forgave myself the weakness.

I have residual pain in my legs, a new thing to add to their usual pain.  I can only describe it as a leftover electrical burn.  And that is why I try not to put too many words -- ha -- to the work of describing CRPS pain.

It makes you sound like a maniac.

electrocution wallpapers

© 2013 L. Ryan

The Fevered Pitch and Marmy Fluffy Butt

I will be returning to the blogging world soon.  I know you've been holding your breath in bated suspense.

Guess what?  Times are hard!  Physically, financially, emotionally.  I'd get in line except that, at the moment, I eschew the queue.

Monday, my first eye operation has been scheduled -- it's finally definite.  There were some weird shenanigans around getting information to the right people at the right time, but, as usual, it all worked out.
It will likely be a two-fer:  replacement of the lens in the right eye and poking a little hole in the back to help with drainage, thereby treating both cataract and glaucoma.

Because of my spasticity, it will be under general anesthesia, which does not make me happy.

Oddly, this bit of news cheered my new pain managaement doctor immensely.  He said,"O!  Maybe they will use propofol.  I think you will enjoy that."

I do a lot of just looking at this man, and wondering.

My previous "health care professional" at the PainDude's office will not be returning following maternity leave.  I wish I could say it was because of her simple (profound!) love of being a mom, but it's more driven by the fact that the baby has Down's Syndrome and needs lots of care.  She's a lucky baby to have been born to such a mom.

But it's my loss!  We had just hit our stride, after a rough start last year -- I met her just after freeing myself from the confinement of the Long Term Acute Care Facility, otherwise known as a place to hide the sick and disabled until they can be permanently stashed out of sight.  So when Natalie and I first met, I was a snarling beast, ready to run, trusting no one, and very, very debilitated.

We worked our way through it.  She was smart and reasonable.

This extremely trained and brand new physician who was supposed to just sub for her... is smart, very compassionate, and close to being idiotic.  He knows a bunch of stuff and knows hardly anything about what to do with it.  He's cost me beaucoup bucks already in the pursuit of dream treatments, and has given me advice that proved faulty -- prompting a phone message that bordered on hysteria.  "Disregard what I told you..."

Not to worry!

He is very sweet and extremely over-involved.  He has never seen anyone suffer as much as I suffer.  Do you think I need to hear that?  Would anyone garner anything positive from hearing that?

Anyway, he thinks I will get a kick out of general anesthesia, being unconscious and all, thereby not feeling my usual pain.  I'd love to point out that scoring me a dozen or so joints and letting me smoke them at my leisure would be something more likely to be remembered as relief.

"Hey, man, I really loved being unconscious.  That was great."

I'm sorry.  He'll grow.  I'll grow.  It'll be touching and rewarding.

The second surgery will be on the 26th.  After each surgery, we have to drive every day to the eye doc's office to have my pressures checked, because any eye surgery causes a spike in intraocular pressures.  For most folks, no biggie -- but since I have a pretty nasty case of glaucoma, it could wreck my optic nerve and so on and so forth.  The surgeon asked me if I could handle extra "emergency" surgeries.  That, again, is a weird thing to say/ask to someone.  Were I to say "no," what would that change?  As it was, I told her it was a familiar scenario, albeit never before with my eyesight at stake. Usually just limbs.

She's very cool -- about as tall as my knees, hair down to her ass, lovely, lovely high-heels, beautifully tailored clothes, tough as nails, focused, super technical and precise.  If I had only followed my intuition a few years earlier and ditched the old fart who was following the glaucoma earlier... I'd be in better shape.

He also had a love for reuben sandwiches and garlicky things that did not endear me to him overly much as we communed face-to-face during eye exams.

Anyway.

That's that.

But the purpose of this ramble -- the first decent photo of Ms. Marmy Fluffy Butt in close to five years.  She appears before you recently groomed by moi, willing to be seen (ears to the front, the "i tolerate you" stare), and knowing that the "boys" have been getting all the photographic glory.

Without further ado, here's my girl:

Marmy, August 2013

She remains feral, usually during the daylight hours.  When darkness descends upon our segment of the planet, she becomes a fur ball of flaming love, head-butting for pets, offering up her tiny, warm, round belly.
She's remarkably small, never crossing the 8 pound mark, except for the one vet visit soon after we first took her hissing and ack-ack-ing self in, when her stomach almost hit the floor due to the five kittens she unwillingly harbored.  Only eight months old at the time, you could tell she was hoping to meet the Law and Order: SVU team.


Today, I need to capture her, as she got into it with Buddy the Outrageously Large Maine Coon, and he slashed her face, managing to leave a large puncture wound near her mouth.  She's going to love me -- for capturing her, as well as for cleaning what looks to be a painful wound.  But we are not having any abscesses around these parts.  Not right now.

My other plans to get me through the weekend without going bonkers?  Well, first, I am not naive.  Well, not too much.  The Spaz Attacks have been BRUTAL.  Fred says I've turned part pretzel.  When the Spaz Attacks hit, and they no longer have predilections for the night alone, I darken the room, take meds, put on my earbuds and try to get lost in music.  Still, I end up screaming in 15 to 40 second intervals, with a string of curses to follow.  I have taken to getting very mobile in bed.  Sideways, with legs hanging off.  Head at the bottom of the mattress, allowing me to press the spasming leg into the black metal headboard festooned, festooned, I say, with pillows of various densities and shapes.  This goes on for hours at a time.

Dobby and Buddy are my little saviors.  Marmy would be, as well, but Buddy is so freaking territorial, he chases her -- and not at all playfully or gently -- away.  I will be moaning, attempting to sing along with some 1950s classic on my sweet Sansa Clip player, or belting it out with Nina Simone -- my God, I'd have gone crazy months ago without Nina Simone -- without Mary Black, without Bob Dylan and Neil Young, without, even, Deadman.  Definitely without my darling dead Townes Van Zandt.  I know Nina's dead, too, and that kills me, but Townes... man, did he fuck up.  Bonnie Raitt, JT, the Stones, Michelle Shocked, Sweet Honey, Paul Simon.  Even the soundtracks to The Sopranos, God bless "Tony"'s soul.

Anyway... I'm laying around being a moaning unsalted pretzel and I will feel a rough tongue tentatively flick my forearm, or forehead.  And it's one of the boys, registering their solidarity.  It's a real crap shoot for them as when I move from side to bottom to top to catty-cornered, they get no notice, so there is no deep cat snoozing possible, not without risking a major bonk attack from a spinning dystonic.

Marmy is different.  She would nestle in, and ride me like a broncin' buck.

I should not forget John Prine or Art Garfunkel, solo.  Jackson Browne.  The Raveonettes. The Roches. Phil Ochs.

When was the last time you listened to Phil Ochs?

Anyway, again:  It still takes a boatload of drugs to stop the jerky jerks, and why I don't just take the boatload of drugs first thiing, I cannot explain.  It can't be good for me.  But neither can all that suffering.

The risk of respiratory depression, euphemism for death, versus the risk of insane pain, forever?  What a battle, fought in a truly fevered pitch.










© 2013 L. Ryan

An Unusual Case Study of CRPS Movement Disorder: Drexel Cheerleaders!

Drexel Cheerleaders

As my struggle with CRPS evolves -- we are in our eleventh year together -- more and more, the pain that I cannot tolerate is born from dystonia / spasticity / Jerk-O-Rama sessions.  Much time and mental energy is wasted as CRPS endeavors to turn my feet and legs into some sort of fancy artisinal pretzel.  The solution is an intrathecal delivery device for a sufficient amount of baclofen to render my muscles, nerves, and connective tissues all loosey-goosey and amenable to the instructions delivered by the central nervous system.  Because of my body's decision to harbor bacteria in my bones (osteomyelitis) in the form of evil biofilm communities, I cannot have any further "implants," as they'll only become another petri dish for bacterial growth.  

Alas!

I joke, but it is hell.  

RSDSA has an excellent little library subsection on CRPS movement disorders/dystonia.  Check it out!

The latest paper I've come across comes from some of the best -- the CRPS Brethren of Drexel's Department of Neurology:


Complex regional pain syndrome with associated chest wall dystonia: a case report.

David J. Irwin and Robert J. Schwartzman
Drexel University College of Medicine, Department of Neurology, Philadelphia, PA, USA

David J Irwin MD
Robert J Schwartzman MD
Department of Neurology
Drexel University College of Medicine
New College Building
245 N 15tl1 St
Philadelphia P A USA 19102
TEL: (215) 762-7090; FAX: (215) 762-3161;
e-mail: dirwin@drexelmed.edu (corresponding author),
robert.schwartzman@drexelmed.edu


Abstract
Patients with complex regional pain syndrome (CRPS) often suffer from an array of associated movement disorders, including dystonia of an affected limb. We present a case of a patient with long standing CRPS after a brachial plexus injury, who after displaying several features of the movement disorder previously, developed painful dystonia of chest wall musculature. Detailed neurologic examination found palpable sustained contractions of the pectoral and intercostal muscles in addition to surface allodynia. Needle electromyography of the intercostal and paraspinal muscles supported the diagnosis of dystonia. In addition, pulmonary function testing showed both restrictive and obstructive features in the absence of a clear cardiopulmonary etiology. Treatment was initiated with intrathecal baclofen and the patient had symptomatic relief and improvement of dystonia. This case illustrates a novel form of the movement disorder associated with CRPS with response to intrathecal baclofen treatment.

Keywords: complex regional pain syndrome, dystonia, movement disorder, dyspnea













© 2013 L. Ryan

Movement Disorder in CRPS: Not Typical Dystonia... But What Is It?

It's on my mind again, what I've become accustomed to name "CRPS Dystonia."  It's rearing its incredibly ugly head again -- in my case, we theorize, in conjunction to a worsening of the infection in my bones.  It's just a theory, and like many theories, was devised to give us a gracious way out to a difficult conversation.

It's the standard reaction of an entrenched medical establishment to accord psychogenic causalities to that which lacks sufficiently convincing research to support another explanation.

I believe that it says a lot that I could give a royal crap whether anyone thinks my sustained, severe, hours-long sessions spent twitching and spasming, all to the tune of some very fine moaning and intermittent screams, is a psychological problem or the result of some CNS misfiring.  If a psychiatrist can find a way to stop them, all praise psychiatry!  If my neurologist manages to do something beyond shake his pretty, pretty head, and give me a painful hug, all hail that sweet guy, too!  Mostly, though, it is me, my MDVIP go-to-guy medico, and the poor slob assigned my case over at the Pain Management Dood's Place -- It's the three of us against the world of CRPS dystonia, or, as the kids say, "what-ev-er."

The fact that baclofen tends to work, if one is able to take the dose needed, is one huge argument for CNS involvement, but, hey!  Don't let decades of clinical practice hammered and honed into an unofficial "Best Practices" sway you.

Seriously, don't.

While those of us dealing with it must also deal with managing symptoms based on the blank areas of a road map, we also want the pure research to continue.  The problem seems to be the necessity of basing the scientific inquiries on what is known to those who study movement disorder.  And these disorders are weird enough to witness that one of the first things medicos want to weed out are those infamous "fakers." 

It's the Turdish Ochoa effect!

Finally, researchers are getting down to the infamous brass tacks.  Some basic understanding about weird and obsessive guarding, weird and excessive non-use has helped.  That leaves the rest of us with eyes rolling up into our skulls and one leg lost in space, while the other is making pretzels.

Here is the most recent study I've found, from the May 2013 issue of Clinical Neurophysiology.

Clinical Neurophysiology is the official journal of the International Federation of Clinical Neurophysiology, the Brazilian Society of Clinical Neurophysiology, the Czech Society of Clinical Neurophysiology, the Italian Clinical Neurophysiology Society and the International Society of Intraoperative Neurophysiology.The journal is dedicated to fostering research and disseminating information on all aspects of both normal and abnormal functioning of the nervous system. The key aim of the publication is to disseminate scholarly reports on the pathophysiology underlying diseases of the central and peripheral nervous system of human patients. Clinical trials that use neurophysiological measures to document change are encouraged, as are manuscripts reporting data on integrated neuroimaging of central nervous function including, but not limited to, functional MRI, MEG, EEG, PET and other neuroimaging modalities.

The Journal has special emphases on epilepsy and on studies of cognitive function and cognitive disorders. Motor neurone and neuromuscular diseases, vestibular disorders, motor control and somatosensory physiopathology are also covered by the Journal. Studies on animals and technical notes must have clear relevance and applicability to human disease, and studies reporting normative data for specific tests must have clear novelty. Case Reports are not generally accepted as full length submissions but may be considered as peer-reviewed Letters.

Note, please, that the article concentrates on hand postures.  I recall rolling down the hall at the orthopedic clinic where I was having a follow-up visit after reconstruction of my right elbow.  I was holding my arm in the way that caused the least amount of pain (the skin felt on fire, yadda yadda), which amounted to a sharp bend at that very elbow, with the entire arm, though, held tucked and away from potential accidental touch or jostling.  My surgeon was walking down the hall toward me and called out, "Why are you holding your arm like that?" The simple question made me aware that I was doing something that looked strange, and also made clear (to me) why I was doing it -- to avoid pain.  

I made a conscious effort to NOT hold my arm in that manner while in that doctor's presence, and then noted, on the drive home, that I'd reverted to the less painful pose.  Nutty, huh?

This is a photo of one of Dr. Anthony Kirkpatrick's patients, Ana English.  First, I so understand her

apparent mood.  Second, the signs of CRPS just leap off the page.  Third, I believe she is doing wonderfully well now following his ketamine protocol.  But yes, that is exactly the posture I had also adopted, and to which my surgeon responded so negatively.  But when it is you and your painful limb against the world?  You find the "posture" that protects you best. 

From Kirkpatrick's Clinical Practice Guidelines

I happen to be just that simple a thinker -- that "posturing" is something related purely to the attraction of positions that cause the least pain.  A nonscientific statement, which I'd make even more embarrassing by requesting a greater emphasis put on first quantifying the variables that are assessable during spasm/tics/dystonia movement disorder manifestations.  I can be such a bitch.

Electromyography can be pretty painful for CRPS patients but I hope they keep recruiting willing subjects, because that gives impressive information about what muscles/nerves are up to, and how.

Interestingly enough, I've had two divergent doctor-types make the same very self-assured statement:  "It's a sign of insufficient pain control." I couldn't get them to ruminate further, as they'd only reassert the belief and did not spout supporting research.  Again, they were going with their decades of "best clinical practice." 

Clin Neurophysiol. 2013 May 18. pii: S1388-2457(13)00310-6. doi: 10.1016/j.clinph.2013.03.029. [Epub ahead of print]

Deficient muscle activation in patients with Complex Regional Pain Syndrome and abnormal hand postures: An electromyographic evaluation.

Bank PJ, Peper CL, Marinus J, Beek PJ, van Hilten JJ.

Source

Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands; Research Institute MOVE, Faculty of Human Movement Sciences, VU University Amsterdam, The Netherlands.

Abstract

OBJECTIVE:

Motor abnormalities in Complex Regional Pain Syndrome (CRPS) are common and often characterized by a restricted active range of motion (AROM) and an increased resistance to passive movements, whereby the affected body part preferably adopts an abnormal posture. The objective of the present study was to obtain a better understanding of the factors that are associated with these abnormal postures and limitations of the AROM, and to investigate whether these motor impairments reflect dystonia.

METHODS:

We evaluated characteristics of surface EMG of the flexor carpi radialis and extensor carpi radialis muscles during active maintenance of various flexion-extension postures of the wrist of the affected and unaffected side in 15 chronic CRPS patients, and in 15 healthy controls.

RESULTS:

Deviant joint postures in chronic CRPS - at least in those patients with some range of active movement - were not characterized by sustained muscle contractions, and limitations of the AROM were not attributable to excessive co-contraction. Rather, the agonistic muscle and its antagonist were activated in normal proportions, albeit over a limited range.

CONCLUSIONS:

The AROM limitations and abnormal postures that are often observed in chronic CRPS patients are not associated with excessive muscle activity and hence do not exhibit the characteristics typical of dystonia.

SIGNIFICANCE:

We hypothesize that structural alterations in skeletal muscle tissue and pain-induced adaptations of motor function may contribute to the observed motor impairments. Our findings may have important clinical implications, since commonly prescribed treatments are aimed at reducing excessive muscle contraction.

Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

PMID:

 

23692976

 

[PubMed - as supplied by publisher]

Other articles that may elucidate the matter further:

Stretch reflex responses in Complex Regional Pain Syndrome-related dystonia are not characterized 
by hyperreflexia.

Antagonist motor responses correlate with kinesthetic illusions induced by tendon vibration.

Thalamic single neuron activity in patients with dystonia: dystonia-related activity and somatic 
sensory reorganization.

[A case of post-hemiplegic painful dystonia following thalamic infarction with good response to botulinus toxin].

Functional anatomy of thalamus and basal ganglia.

Intrathecal Baclofen in CRPS

Anesthesia & Analgesia 2013 Jan; 116(1):211-5.

Efficacy of intrathecal baclofen on different pain qualities in complex regional pain syndrome.

van der Plas AA, van Rijn MA, Marinus J, Putter H, van Hilten JJ.

Department of Neurology, Leiden University Medical Center, PO Box 9600, 2300 RC
Leiden, the Netherlands.  A.A.van_der_Plas@lumc.n.

BACKGROUND: Complex regional pain syndrome (CRPS) is characterized by severe
debilitating chronic pain. Patients with CRPS may experience various pain
sensations, which likely embody different pathophysiologic mechanisms. In this
study, we evaluated the differential effects of central γ-aminobutyric acid (B)
receptor stimulation on the different pain qualities in CRPS patients with
dystonia.

METHODS: The 10 pain qualities of the neuropathic pain scale, dystonia severity,
and changes in use of antinociceptive drugs were evaluated every 3 months for a
period of 1 year in 42 CRPS patients with dystonia receiving titrated doses of
intrathecal baclofen (ITB) treatment in an open design.

RESULTS: Using a linear mixed model analysis and controlling for global dystonia
severity and the use of supplemental analgesics, we found a significant
improvement in global intense pain, sharp pain, dull pain, and deep pain during
the first 6 months. After this period, the scores leveled off despite further
improvement of dystonia and continued ITB dose escalation.

CONCLUSIONS: γ-Aminobutyric acid (B) receptor stimulation by ITB exerts
differential antinociceptive effects on specific pain qualities in CRPS patients
with dystonia.

PMID: 23223108  [PubMed - in process]


RELATED CITATIONS (101 results)

Cat Videos and Pity Parties

The plan, which I never hide from my Dear Readers, is to salvage this post with a few lame videos of the cats of Marlinspike Hall.  I've been trying to put together some footage of Dobby the Runt and his affinity for all things "butt," however, the little guy has an uncanny awareness of the camera and refuses to be cute or even very butt oriented in its presence.

He senses that I'm drifting into Trouble Territory, however, and may just think that wasting my troubled time recording his predilection for tail pulls and rear whacks is a little too ridiculous, even for me.  Dobby has never before been a lap cat but now gently climbs all over me -- still causing a few episodes of spontaneous screaming when he missteps -- and stares.  I've noted before that he never got the "staring is aggression" memo.  

Dobby will stare at you, pupils huge, all placid-faced and irresistibly pink-nosed -- absolutely luminous -- for as long as 15 or 20 minutes.  He doesn't mind in the least should you stare back, though he does pick up on *your* aggression, should you harbor any.  Should you be thinking, for example, "Why the hell is this cat staring at me?  What, do I have mustard greens stuck to my teeth?  Does he know about that vet appointment?"

The iconic photograph of Dobby, iconic for those of us who know his unique character and weirdnesses, is called "Dobbox."  The love of boxes is not unique, of course, but he seemed to consider this small one a sort of home base, from whence he could survey the world, and particularly, Fred, with immunity from accusations  of Stare Aggression.  He'd trot over to it, hop  in, do the "perfect cat" pose, and immerse himself in the pleasure of staring at Fred, who kept the box next to his office chair.

We used to enjoy yelling out "olly olly oxen free," and then watching Dobby careen around the corner, head high, ears flattened, tail whipping in his own wake, flying to his box.

One night, Fred was working (assiduously, always assiduously -- there's no time wasting going on, no, not ever) and felt The Runt's eyes boring through the back of his lovely curly head.  Dobby sat in his box, adoring Fred, with hardly a blink of a break, for over 20 minutes.  At the 20 minute mark, in fact, Fred snapped this picture.  You know, the iconic one.

Dobbox

I created one of those "Magic Movies"  that Flip video offers for videographers afflicted with shaking hands and not much imagination, using what little The Dobster allowed to be recorded -- a couple of lame butt whacks, tail pulls, and the obligatory scene with a brush.  Excuse me, *The* Brush.  We've purchased five different brushes in an attempt to get him to give up chirping and grabbing for the worn out one seen here, to no avail.  He sniffs them, then bats them on the floor, and begins the most god-awful wailing you've ever heard.

It's lame but hey, it's a cat video, and that buys me a few paragraphs for a Pity Party and enough space for a CRPS / RSD update of my feet and hands -- the going rate for the blogger who navel-gazes.

I see the orthopedic surgeon, Dr. ShoulderMan, this afternoon, for the second post-op visit.  It's not going to be pleasant, I fear.  Although the decision about whether my immune system can support another prosthesis has already been made, by my body, I still don't look forward to hearing it from him.  

The fistula has reappeared right next to the newly closed wound from the February 13 surgery, which is just below the healed incision from the January 23 operation.  It ain't pretty.  I've been febrile for the last 8 days, with sweats and increased pain, and an almost constant headache.  The Infectious Disease folks didn't bat a proverbial eye before changing the antibiotic, accepting without question my suggestion that the bleeping infection is back, or more likely, has never left, lurking as it does behind the teflon shield of its biofilm.

I have completely dropped the ball regarding the port that is implanted in my chest.  I called the cancer clinic that usually takes care of flushing it every 6 weeks, to keep it patent, and they required a new physician order.  Well, I made that call, but haven't followed up with the appointment, because in the course of conversing with MDVIP Go-To-Guy, he got a little too animated at the idea that the biofilm infectious phenomena might well be happening to/on that port.  My mind shut down.  According to legend, the first culpable biofilm identified came from someone's pacemaker:

[Two years after Costerton coined the word/concept biofilm] Tom Marrie, a young doctor working in Halifax, Nova Scotia, examined a feverish homeless man who had wandered off the street and into his emergency room. The man had a raging staph infection and, on his chest, a lump the size and shape of a cigarette pack. It was an infected pacemaker, Marrie reasoned. For three weeks the man was given huge doses of antibiotics but did not get better, so Marrie and his team decided to operate. They invited Costerton to sit in. “If there were ever going to be a biofilm infection in a human being, it was going to be on the end of that pacemaker,” Costerton says. “We took out the pacemaker and there was our first medical biofilm. It was a great big thick layer of bacteria and slime, just caked on.”


Biofilms on implants are now recognized as a serious and growing health problem. Bacterial infections hit 2 percent to 4 percent of all implants. Of the 2 million hip and knee replacements performed worldwide each year, 40,000 become infected. More than a third of these infections lead to amputation, and not with very successful results: Most of those people die. “Implant operations have a 98 percent success rate, so people don’t want to talk about the infections,” Costerton says. “They’re a bit of a disgrace, really.”


Biofilm infections are not limited to implants. They can be found in the bodies of the young and the healthy. Many children suffer from undiagnosed biofilm infections in their ears, which require months of oral antibiotic therapy while the underlying infection smolders untouched. Millions of others live with chronic biofilms: urinary tract infections in women that last for years; prostatitis that no antibiotics permanently cure; bone infections (osteomyelitis) that cripple and immobilize people for the rest of their lives. Each year roughly 500,000 people in the United States die of biofilm-associated infections, nearly as many as those who die of cancer.


As Marrie’s experience shows, biofilms repel antibiotics, although scientists do not fully understand how. Some drugs cannot fully penetrate the biofilm’s protective matrix. In other cases, even though most of the germs die, enough remain alive to regroup and develop another biofilm. The matrix also keeps its resident germs under cover, hiding the chemical receptors on the bacteria so that drugs cannot latch onto them and kill the germs.


The study of this newly discovered behavior is rooted in the basic and ancient biology of bacteria. Geneticist Bonnie Bassler of Princeton University thinks group-living bacteria may give us a window onto the origins of multicellular life. “Bacteria grow best when each one does its own thing…together,” she says. “Bacteriologists had it wrong for the past 300 years—bacteria don’t live alone.”

Today, then, I must do two things, beyond hearing that my best bet is to be left shoulderless, with a flail arm -- I must arrange for this thing to be flushed, if, indeed, it still can be, and I must call the surgeon who put it in, and arrange for it to be removed.  I got it at the insistance of the doctor who oversaw my subanesthetic ketamine infusions, my last ditch effort to quell the advances of CRPS.  Every doctor and nurse that I have asked, except for MDVIP Go-To-Guy, has insisted that I should keep it -- saying vague things like "you never know,"  voices trailing off with much drama.  Do they USE it?  No!  "It's too close to the infection site, to the incision site..."  "I am not trained to use it..."  "We could use it, but we'd have to get the IV Team..."

Go-To-Guy, I trust him.  He thinks things through, has no interests in play other than my welfare and avoiding as many bumps in the road of this journey as possible.

I was hoping to have the blood work results from Monday before visiting ShoulderMan, as they might give a hint of a clue as to what is going on, but the results aren't in.  Of particular interest, beyond white counts, are the C-Reactive Protein and the sedimentation rate.  Both are indicators of inflammation/infection, but one is elevated in a more acute situation and the other indicates a more chronic course.  Historically, when I've been under the gun from these bacterial miscreants, BOTH tests have been greatly elevated.

I know you are tired of hearing about it.  Well, I am tired of living it.  How I wish that this osteomyelitis and this insane CRPS were deadly instead of causing unlimited pain and disability!

I did a video update of what my feet and hands look like, since the last one was from May 2011, if you don't count the ones I did in January 2012 -- and I don't, because the circumstances then were... what?  Extraordinary?!

My right foot/leg looks about the same, to me.  The left foot is awful, is worse, though it doesn't seem to show the change, visually, not the way I feel it.  Both legs are peeling and have larger areas of "ash."  This despite being cleaned daily, and -- for the past three nights, at least -- coated in lotion.  The skin seems to no longer absorb lotion or oils.

The left leg and foot are the banes of my existence, right now.  Spasming, severely spasming, burning, aching.

My hands are much worse in terms of pain but -- apart from both sets of middle finger and thumb nails (ah, the perverse symmetry of this disorder!) -- look about the same.  Both hands were peeling, much like my feet, so I suppose I have the benefit of "new" skin!  I have significant tremor now, and not the greatest grip in the world, on either side.  It used to be that the pain sort of followed the areas of discoloration, but now the burning and aching extend beyond those former borders.  In the left arm -- all the way to the shoulder.  I very much hope that is going to change.

Dobby is now asleep.  I think I will sit here and stare at him for a while, and try to see the way that he sees.

Or I could get on the phone and start the process of getting this port flushed and yanked.  Wish us luck chez ShoulderMan -- and wish him patience, and insight, as he must surely be as sick of all this as I am.

Recent CRPS Research

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I'm not feeling much like blogging these days, being about as busy as a body can be hosting Tête de Hergé's most anticipated Pity Party of the 2011 season.  Nonetheless, having run across some interesting newly published research, I did some wicked-fast copying and pasting, cogitating and perusing, and hope that you will find some of this CRPS work helpful and interesting.  I confess to having focused on aspects of this Sucky Disorder that are posing a challenge and raising questions in my life at present:  sensory dysfunction, disorder of body schema, hemilateral sensory disturbances, dystonia, and -- what the heck! -- ketamine induced liver injury!

There is some comfort in noting the many articles and topics being published and discussed -- just not enough comfort to warrant ending the Pity Party.  Maybe come August.  (Actually, ManorFest is about a week away, at which time my rabid navel-gazing will no longer be tolerated around here.  Already, people are strumming their fingers and rolling their eyes at my wailing and cultivated introspection.  I saw a preliminary ManorFest schedule in which I am relegated to working night shifts, exclusively, far from the public eye.  Harrumph.)

************************************************************************

Title
Comparable disorder of the body schema in patients with complex regional pain syndrome (CRPS) and phantom pain.

Author(s)
Reinersmann A, Haarmeyer GS, Blankenburg M, Frettlöh J, Krumova EK, Ocklenburg S, Maier C

Institution
Abteilung für Schmerztherapie, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbH Bochum, Ruhr-Universität Bochum, Bochum, Deutschland, annika.reinersmann@rub.de.

Source
Schmerz 2011 Jul 9.

Abstract
In patients with complex regional pain syndrome (CRPS) a disruption of the body schema has been shown in an altered cortical representation of the hand and in delayed reaction times (RT) in the hand laterality recognition task. However, the role of attentional processes or the effect of isolated limb laterality training has not yet been clarified.The performance of healthy subjects (n=38), CRPS patients (n=12) and phantom limb pain (PLP) patients (n=12) in a test battery of attentional performance (TAP) and in a limb laterality recognition task was compared and the effect of limb laterality training in CRPS patients and healthy subjects evaluated.The RTs of both CRPS and PLP patients were significantly slower than those of healthy subjects despite normal TAP values. The CRPS and PLP patients showed bilaterally delayed RTs. Through training RTs improved significantly but the RTs of CRPS patients remained slower than those of healthy subjects. In this study an equal disruption of the body schema was found in both CRPS and PLP patients which cannot be accounted for by attentional processes. For CRPS patients this disorder cannot be fully reversed by isolated limb laterality recognition training.

Language
GER

PubMed ID
21739258

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Title
Impaired Hand Size Estimation in CRPS.

Author(s)
Peltz E, Seifert F, Lanz S, Müller R, Maihöfner C

Institution
Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany.

Source
J Pain 2011 Jul 7.

Abstract
A triad of clinical symptoms, ie, autonomic, motor and sensory dysfunctions, characterizes complex regional pain syndromes (CRPS). Sensory dysfunction comprises sensory loss or spontaneous and stimulus-evoked pain. Furthermore, a disturbance in the body schema may occur. In the present study, patients with CRPS of the upper extremity and healthy controls estimated their hand sizes on the basis of expanded or compressed schematic drawings of hands. In patients with CRPS we found an impairment in accurate hand size estimation; patients estimated their own CRPS-affected hand to be larger than it actually was when measured objectively. Moreover, overestimation correlated significantly with disease duration, neglect score, and increase of two-point-discrimination-thresholds (TPDT) compared to the unaffected hand and to control subjects' estimations. In line with previous functional imaging studies in CRPS patients demonstrating changes in central somatotopic maps, we suggest an involvement of the central nervous system in this disruption of the body schema. Potential cortical areas may be the primary somatosensory and posterior parietal cortices, which have been proposed to play a critical role in integrating visuospatial information. PERSPECTIVE: CRPS patients perceive their affected hand to be bigger than it is. The magnitude of this overestimation correlates with disease duration, decreased tactile thresholds, and neglect-score. Suggesting a disrupted body schema as the source of this impairment, our findings corroborate the current assumption of a CNS involvement in CRPS.

PubMed ID
21741321

************************************************************************

Title
The Specificity and Mechanisms of Hemilateral Sensory Disturbances in Complex Regional Pain Syndrome.

Author(s)
Knudsen L, Finch PM, Drummond PD

Institution
School of Psychology, Murdoch University, Perth, Western Australia.

Source
J Pain 2011 Jun 22.

Abstract
Hyperalgesia often extends from the affected limb to the ipsilateral forehead in patients with complex regional pain syndrome (CRPS). To investigate whether this is more common in CRPS than other chronic pain conditions, pressure-pain thresholds and sharpness to a firm bristle were assessed on each side of the forehead, at the pain site, and at an equivalent site on the contralateral side in 32 patients with chronic pain other than CRPS (neuropathic or nociceptive limb pain, radicular pain with referral to a lower limb or postherpetic neuralgia), and in 34 patients with CRPS. Ipsilateral forehead hyperalgesia to pressure pain was detected in 59% of CRPS patients compared with only 13% of patients with other forms of chronic pain. Immersion of the CRPS-affected limb in painfully cold water increased forehead sensitivity to pressure, especially ipsilaterally, whereas painful stimulation of the healthy limb reduced forehead sensitivity to pressure pain (albeit less efficiently than in healthy controls). In addition, auditory discomfort and increases in pain in the CRPS-affected limb were greater after acoustic startle to the ear on the affected than unaffected side. These findings indicate that generalized and hemilateral pain control mechanisms are disrupted in CRPS, and that multisensory integrative processes may be compromised. PERSPECTIVE: The findings suggest that hemilateral hyperalgesia is specific to CRPS, which could be diagnostically important. Disruptions in pain-control mechanisms were associated with the development of hyperalgesia at sites remote from the CRPS limb. Addressing these mechanisms could potentially deter widespread hyperalgesia in CRPS.

PubMed ID
21703937

************************************************************************

Title
Fixed Dystonia in Complex Regional Pain Syndrome: a Descriptive and Computational Modeling Approach.

Author(s)
Munts AG, Mugge W, Meurs TS, Schouten AC, Marinus J, Moseley GL, van der Helm FC, van Hilten JJ

Source
BMC Neurol 2011 May 24; 11(1):53.

ABSTRACT:
BACKGROUND: Complex regional pain syndrome (CRPS) may occur after trauma, usually to one limb, and is characterized by pain and disturbed blood flow, temperature regulation and motor control. Approximately 25% of cases develop fixed dystonia. Involvement of dysfunctional GABAergic interneurons has been suggested, however the mechanisms that underpin fixed dystonia are still unknown. We hypothesized that dystonia could be the result of aberrant proprioceptive reflex strengths of position, velocity or force feedback.
METHODS: We systematically characterized the pattern of dystonia in 85 CRPS-patients with dystonia according to the posture held at each joint of the affected limb. We compared the patterns with a neuromuscular computer model simulating aberrations of proprioceptive reflexes. The computer model consists of an antagonistic muscle pair with explicit contributions of the musculotendinous system and reflex pathways originating from muscle spindles and Golgi tendon organs, with time delays reflective of neural latencies. Three scenarios were simulated with the model: (i) increased reflex sensitivity (increased sensitivity of the agonistic and antagonistic reflex loops); (ii) imbalanced reflex sensitivity (increased sensitivity of the agonistic reflex loop); (iii) imbalanced reflex offset (an offset to the reflex output of the agonistic proprioceptors).
RESULTS: For the arm, fixed postures were present in 123 arms of 77 patients. The dominant pattern involved flexion of the fingers (116/123), the wrists (41/123) and elbows (38/123). For the leg, fixed postures were present in 114 legs of 77 patients. The dominant pattern was plantar flexion of the toes (55/114 legs), plantar flexion and inversion of the ankle (73/114) and flexion of the knee (55/114). Only the computer simulations of imbalanced reflex sensitivity to muscle force from Golgi tendon organs caused patterns that closely resembled the observed patient characteristics. In parallel experiments using robot manipulators we have shown that patients with dystonia were less able to adapt their force feedback strength.
CONCLUSIONS: Findings derived from a neuromuscular model suggest that aberrant force feedback regulation from Golgi tendon organs involving an inhibitory interneuron may underpin the typical fixed flexion postures in CRPS patients with dystonia.

PubMed ID
21609429

************************************************************************

Title
Drug-induced liver injury following a repeated course of ketamine treatment for chronic pain in CRPS type 1 patients: A report of 3 cases.

Author(s)
Noppers IM, Niesters M, Aarts LP, Bauer MC, Drewes AM, Dahan A, Sarton EY

Institution
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands.

Source
Pain 2011 May 3.

Abstract
Studies on the efficacy of ketamine in the treatment of chronic pain indicate that prolonged or repetitive infusions are required to ensure prolonged pain relief. Few studies address ketamine-induced toxicity. Here we present data on the occurrence of ketamine-induced liver injury during repeated administrations of S(+)-ketamine for treatment of chronic pain in patients with complex regional pain syndrome type 1 as part of a larger study exploring possible time frames for ketamine re-administration. Six patients were scheduled to receive 2 continuous intravenous 100-hour S(+)-ketamine infusions (infusion rate 10-20mg/h) separated by 16days. Three of these patients developed hepatotoxicity. Patient A, a 65-year-old woman, developed an itching rash and fever during her second exposure. Blood tests revealed elevated liver enzymes (alanine transaminase, alkaline phosphatase, aspartate transaminase, and γ-glutamyl transferase, all⩾3 times the upper limit of normal) and modestly increased eosinophilic leukocytes. Patient E, a 48-year-old woman, developed elevated liver enzymes of similar pattern as Patient A during her second ketamine administration and a weakly positive response to antinuclear antibodies. In a third patient, Patient F, a 46-year-old man, elevated liver enzymes (alanine transaminase and γ-glutamyl transferase) were detected on the first day of his second exposure. In all patients, the ketamine infusion was promptly terminated and the liver enzymes slowly returned to reference values within 2months. Our data suggest an increased risk for development of ketamine-induced liver injury when the infusion is prolonged and/or repeated within a short time frame. Regular measurements of liver function are therefore required during such treatments. During repeated ketamine infusion for treatment of CRPS1, three patients developed liver injury probably allergic in nature.

PubMed ID
21546160

Changing the Channel: Court TV and Two Abstracts

I've never been a Court TV junky -- mostly because, you know, I've been busy being some other kind of junky -- Mwa ha ha ha!  Sorry, Beloved Readers, that's Street Drug Humor, something at which I am fantastically adept but have kept hidden as an attribute.  Now, though, I've decided not to hide my light under a basket. A bushel.  A bushel basket. Or whatever.

No, I am not suffering from Hinky Methadone Withdrawal.  What I am suffering from is this twit of a woman, this Casey Anthony person upon whom we are wasting such incredible resources of money, time, and emotion.  Yes, my television is tuned to her first-degree murder trial in Florida, where she is accused of having killed her two year old daughter back in 2008.   

Change the channel, you say?

Oh.  Right!

If I can redirect the miscued energy of a kitten, surely I can train myself to change the television channel -- even {gasp} turn the machine off.  Let's do that, then, and see what happens.

Why, look!  Here are some CRPS updates that I've failed to pass on.  Oh, and there is a Pink Elephant hanging from the ceiling fan!  (Just let me know when you've had enough Hinky Methadone Withdrawal humor.  Why are the lights blinking?)

This first research paper has a very specific target audience -- so, attention all orthopods!

The use of beta-tricalcium phosphate bone graft substitute in dorsally plated, comminuted distal radius fractures.Journal of Orthopaedic Surgery and Research

Michael G Jakubietz , Joerg G Gruenert and Rafael G Jakubietz
2011, 6:24
doi:10.1186/1749-799X-6-24


Published:  22 May 2011


Abstract (provisional)

Background:  Intraarticular distal radius fractures can be treated with many methods. While internal fixation with angle stable implants has become increasingly popular, the use of bone graft substitutes has also been recommended to address comminution zones and thus increase stability. Whether a combination of both methods will improve clinical outcomes was the purpose of the study


Methods:  The study was thus conducted as a prospective randomized clinical trial. 39 patients with unilateral, intraarticular fractures of the distal radius were included and randomized to 2 groups, one being treated with internal fixation only, while the second group received an additional bone graft substitute.


Results:  There was no statistical significance between both groups in functional and radiological results. The occurrence of complications did also not show statistical significance.


Conclusions:  No advantage of additional granular bone graft substitutes could be seen in this study. Granular bone graft substitutes do not seem to provide extra stability if dorsal angle stable implants are used. Dorsal plates have considerable complication rates such as extensor tendon ruptures and development of CRPS.

I know, I know -- where did that last line of the conclusion come from?  Is it really there or am I imagining things again?  Like I said, this has a definite target -- orthopedic surgeons -- and, well, I hope it doesn't keep any of them up at night!

Mwa ha ha ha!

Ahem.

Okay, on to something more "relatable," though not less specialized -- fixed dystonia in CRPS.  Just a few observations:  Classical dystonia is mobile;  Fixed dystonia is usually classified as part of functional movement disorders and is often labelled a contracture -- (though I think a better descriptor is fixed flexion postures);  All of that is code for "psychogenic."  Most studies will make quick mention that fixed dystonia happens mostly in females, many of whom suffer from dissociative and affective disorders. 

Sigh.

(Please note that I am sighing as I look down at my twisted and distorted foot... as I recall the initial days of CRPS, when my left hand looked like the infamous psychogenic claw!  I'm also flashing on some really cool concerts from back in the day, but that could be the DTs.  Mwa ha ha!)

So... once again, if you're a CRPS patient experiencing dystonia, be sure to see someone who is not going to automatically categorize you as a nut.  The authors of the study below are searching for an explanation beyond the easy and lazy classification of "functional," and posit that the neurotransmitters used by interneurons are misfiring or dysfunctional (he he).  If you are like me, you might want to start with this quick intro to interneurons!

Fixed Dystonia in Complex Regional Pain Syndrome: a Descriptive and Computational Modeling Approach

Alexander G. Munts, Winfred Mugge, Thomas S. Meurs, Alfred C. Schouten, Johan Marinus, G. LORIMER Moseley, Frans C.T. van der Helm and Jacobus J. van Hilten

BMC Neurology 2011, 11:53
doi:10.1186/1471-2377-11-53

Published: 24 May 2011

Abstract (provisional)

Background: Complex regional pain syndrome (CRPS) may occur after trauma, usually to one limb, and is characterized by pain and disturbed blood flow, temperature regulation and motor control. Approximately 25% of cases develop fixed dystonia. Involvement of dysfunctional GABAergic interneurons has been suggested, however the mechanisms that underpin fixed dystonia are still unknown. We hypothesized that dystonia could be the result of aberrant proprioceptive reflex strengths of position, velocity or force feedback.

Methods: We systematically characterized the pattern of dystonia in 85 CRPS-patients with dystonia according to the posture held at each joint of the affected limb. We compared the patterns with a neuromuscular computer model simulating aberrations of proprioceptive reflexes. The computer model consists of an antagonistic muscle pair with explicit contributions of the musculotendinous system and reflex pathways originating from muscle spindles and Golgi tendon organs, with time delays reflective of neural latencies. Three scenarios were simulated with the model: (i) increased reflex sensitivity (increased sensitivity of the agonistic and antagonistic reflex loops); (ii) imbalanced reflex sensitivity (increased sensitivity of the agonistic reflex loop); (iii) imbalanced reflex offset (an offset to the reflex output of the agonistic proprioceptors).

Results: For the arm, fixed postures were present in 123 arms of 77 patients. The dominant pattern involved flexion of the fingers (116/123), the wrists (41/123) and elbows (38/123). For the leg, fixed postures were present in 114 legs of 77 patients. The dominant pattern was plantar flexion of the toes (55/114 legs), plantar flexion and inversion of the ankle (73/114) and flexion of the knee (55/114). Only the computer simulations of imbalanced reflex sensitivity to muscle force from Golgi tendon organs caused patterns that closely resembled the observed patient characteristics. In parallel experiments using robot manipulators we have shown that patients with dystonia were less able to adapt their force feedback strength.

Conclusions: Findings derived from a neuromuscular model suggest that aberrant force feedback regulation from Golgi tendon organs involving an inhibitory interneuron may underpin the typical fixed flexion postures in CRPS patients with dystonia.

In other breaking news, "Ketamine induced selective impairments in timing..."

Put that in the No Kidding File. 

Well, folks, I'd better get back to my soon-to-be "Done"-less life.  I do hope you know I'm just joshing around about the difficulties of tapering off of methadone.  I am NOT having a hard time (yet) or experiencing anything I cannot deal with.  Just don't take away my ibuprofen.

Rotator Cuffs and Intrathecal Baclofen

After posting such a spaz attack as today's earlier contribution, I thought I'd offer up something cut, dry, and relatively boring.  Er... a few infinitely fascinating new studies referencing CRPS/RSD.

The first involves rotator cuff tears and CRPS, and that just makes me chortle. Er... chuckle. Smile. A little.

After my left shoulder "collapsed" from AVN secondary to lupus in 2002, I had it replaced. That hospitalization -- giggle::giggle -- did not go well and the prosthesis never did quite meet my Stringent Standards for Shoulder Membership. Fast forward to 2008 and the Search for the Guilty Pathogen Infecting My Shoulder Hardware... Over the next two years, that left prosthesis was removed, a spacer put in. That spacer was removed... but there was still infection, so a second spacer was put in that had a specially made antibiotic-laced cement ball. All surgeries were followed by at least 6 weeks of intravenous antibiotic via PICC line. Unfortunately, the handcrafted spacer proved highly irritating to the joint, was removed, and I was gifted with a new prosthesis... because no one knew what else to do. I was to live with the pain until I couldn't, then we'd see what limited options remained. I reached that point last Fall, underwent my fifth unsuccessful aspiration under fluoroscopy, and then cried "uncle" in October and went in to see the orthopedic wizard. He snapped some x-rays. His verdict? My rotator cuff was gone!

Have you ever had a day like that? You lose your rotator cuff, can't remember where you last put it?

Anyway... the pain picture is complicated because those muscles and tendons got the hell out of Dodge. Dr. ShoulderMan has since opined that a reverse replacement will be my fate... but has asked me to resume living with it until I can't. It's crazy-making.

I have my suspicions, based on some recent sneaky behavior by the right prosthesis (that underwent more surgeries than it's lefterly brother, even), that the rotator cuff on that side has fled to Mexico.

Now, we do not EVER badmouth, or allow anyone else to badmouth, Dr. ShoulderMan, Wizard Surgeon and Kindly Person. Why? Well, complicate my shoulder picture, if you will, with the addition of CRPS/RSD. See? See?!? The fact that my arms are still usable and not completely at the mercy of this neurological disorder is a testament to his abilities.

The disease has spread from one arm to another, just as it has from leg to leg. As it spread, he was busy performing major shoulder operations on both sides approximately every 9 to 12 weeks. Can you imagine what terrible shape I would be in if I hadn't lucked out by finding the best ShoulderMan in all of Tête de Herge?

So I kinda shiver and laugh when I see this in today's MedWord offering:

Shoulder surface temperature and bone scintigraphy findings in patients with rotator cuff tears.Koike Y, Sano H, Kinjyo T, Imamura I, Masahiro O, Goto M, Ooyama M, Kita A, Itoi E.
Upsala Journal of Medical Sciences, 2011 Feb 16
Department of Orthopaedic Surgery, Japanese Red Cross Sendai Hospital, 2-43-3, Yagiyama Honcyo, Taihaku-Ku, Sendai, Miyagi, Japan, 982-8501.


ABSTRACT
Abstract Background. Complex regional pain syndrome (CRPS) is one of the serious complications after surgical treatment of a rotator cuff tear. Both a measurement of body surface temperature and bone scintigraphy have been used as diagnostic tools for the early phase of CRPS.Unfortunately, few studies have been carried out that applied these methods to the patients after rotator cuff repair.
Purposes. To clarify both shoulder surface temperature and bone scintigraphy findings in patients with rotator cuff tears. Subjects and methods. Subjects comprised patients with unilateral rotator cuff tears (five men and five women, mean age 61 years). For measurements of shoulder surface temperature, a Thermochron was attached to both shoulders. As for bone scintigraphy, intravenous injection of technetium-labelled hydroxymethylenebisphosphonic acid (99mTc-HMDP)was performed, and then images were taken with a gamma camera.
Results. During the measurements, the changes in body surface temperature for the affected and healthy shoulders remained within the standard deviation of the reference group. The intensity of radioisotope (RI) uptake for the affected shoulder joint was significantly increased compared to that for the healthy shoulder joint (P < 0.05).
Conclusion. RI uptake is increased in shoulders with rotator cuff tears, whereas shoulder surface temperature shows no differences on the affected and unaffected sides.

When you've sufficiently recovered from that bit of hilarity, check out the second item caught by my little CRPS bot, as published in the 18 February issue of Pain Medicine.  Watch out, though, because it's exciting.  You might be up all night.  I'm just sayin':

The Lack of Efficacy of Different Infusion Rates of Intrathecal Baclofen in Complex Regional Pain Syndrome: A Randomized, Double-Blind, Crossover Study

Anton Adriaan van der Plas MD,  Johan Marinus PhD,  Sam Eldabe MD,  Eric Buchser MD,  Jacobus Johannes van Hilten MD, PhD

ABSTRACT
Objective.  Intrathecal baclofen (ITB) is effective in the treatment of dystonia related to complex regional pain syndrome (CRPS). In a previous study, we noted that the responsiveness to ITB declined in 30% of patients once drug delivery was switched from an external to an implanted device associated with a reduction of the infusion rate (IR).


Design.  In a double-blind study, we investigated the effect of varying the IR at a fixed daily dose on the efficacy and safety of ITB in patients with CRPS-related dystonia. Patients were randomized to either slower infusion rate delivery (SIRD) or four-times faster infusion rate delivery (FIRD) for 2 weeks and were crossed over after a 1-week washout period.


Patients.  Patients were eligible if they experienced no beneficial response to ITB on dystonia despite a minimum dose of 600 µg/day, or because side effects limited dose escalation.


Outcome Measures.  Primary outcome measures were changes in global dystonia and pain severity.


Results.  There were no significant differences between the FIRD and the SIRD groups for the median change of numeric rating scale dystonia (–0.3 [interquartile range {IQR} −1.1–0.5]), pain (0.1 [IQR –0.8–1.3]), and secondary outcomes, except for the frequency of adverse events, which was significantly higher during FIRD (12 vs 2). FIRD was preferred only by patients who were included because side effects to ITB prevented dose escalation.


Conclusions.  Increasing the IR at a fixed daily dose is not associated with improvement of dystonia or pain but warrants further investigation in patients in whom side effects prevent further dose escalation.

  I tried to share the preceding fascination with Bianca and Fred, but I developed a terrible lisp talking about the FIRD and SIRD groups... 

Back when I was shooting for implantation of a SCS, I also had interest in pursuing intrathecal baclofen.  Some prognosticator mentioned something, blahblahblah, about the potential for infection, and ruled me ineligible for both.  And the band played on...

I'm outta here.