1. Can we order AFOs from Dr. Jordan?
No.  We do not have a central fabrication facility or laboratory.  All AFOs are custom fabricated and not customized from pre-designed or pre-made orthotic shells. 

2.  I hear that Dr. Jordan will be at my child’s surgery to take the plaster impression casts for post operative AFOs.  Is this true?
On occasion, if scheduled well in advance, Dr. Jordan does attend some surgeries.  Dr. Jordan’s office is not part of or linked with any other doctor’s  office.  Our schedules are independent. 

3.  My child has not been evaluated by Dr. Jordan.  Can the Surgeon just send post-operative casts to have Dr. Jordan fabricate and fit the AFOs a few days later?
It is not possible to design AFOs, or any custom fabricated orthoses, without having first examined the child.  There must be a functional benefit to the AFO design.  Often the left and right AFO, if there is need for bilateral, are different in contour, foot to leg angles and leg to ground angles, trimlines, and plantar posting.  This must all come together based on a detailed physical hands-on evaluation and often, discussion with the primary surgeon regarding surgical outcome goals.   The specific design is then translated and discussed with the orthotist who then handcrafts each AFO from plaster impression model to its finished state ready for fitting and fine tuning.
 Can my child can be fit with custom-made AFOs in a day or two?  
   a)  Plaster impression casts are first required to make any custom orthosis.  It makes little sense to mold and shape the impression casts over Pre-Operative legs and feet if the the Achilles mechanism or gastrocnemius (calf muscle) are a limiting factor.   Soft tissue surgery must First be done.
   (b)  At the time of surgical correction of the Achilles, plaster impression casts can then be taken to capture a model of the now corrected foot-leg.  Someone in the operating room must take the casts and mold it while held in the desired position.    In a day or two the cast(s) will be dry enough to send to our office to begin the typical 4-day fabrication process.     This timeframe also presumes that your child has already been evaluated in my office for specific functional design of the orthoses; if it is not about function, why use any orthosis.
   (c)  Now that the impression casts have found their way  into my office, the positive plaster model is built and the specific thermoplastic is heated in order to  mold the hot plastic to the corrective model of the leg and foot.  The physical properties are such that the extremely hot plastic must then be permitted to cool down so that it retains the shape of the cast.   This can take 12-16 hours or so depending on the size of the cast.
   (d)  Once cold, the plastic can be cut by hand in rough design, from the solid plaster model.  The next 4-5 hours will be finer cutting, smoothing and finally adding the straps and SBR plantar posting in three directions to match the child’s current functional needs.   At that time [5-10 days depending on your child’s specific needs], the orthoses can be fit, adjusted and modified.   
So the quick answer for those children flying in for surgery and orthoses is that it is not reasonable or most often not possible to have surgery on a Thursday and be fit with orthoses on a Tuesday.   We are good at what we do but we are not Magical.
5.  When orthoses are mailed back to our office for adjustments and strap changes, please place the Suite number (#98) on the package.  If sent by U.S. mail they will not deliver it without the suite number. 

Also, BEFORE mailing and casts or orthoses:   call the office or send and email to make sure that we are not out of the office for the week. 

QUESTIONS REGARDING PERCS/SPL/SPML and OTHER SIMILAR SURGICAL ACRONYMS:

Talk about confusion, misunderstanding and perceptions that run wild in the professional as well as consumer literature:

1.  Spasticity:     a term thrown around with the meaning being considerably different from one person to the next.    It is difficult, if not impossible to discuss the merits of Botox for spasticity reduction or SDR [selective dorsal rhiztomy] for spasticity relief, and ethanol neurolyses with or without selective myofascial soft tissue surgery IF we don’t speak the language.  In fact, it is downright dangerous to select a kid who exhibits joint constraints that vary throughout the day, call it spasticity and think he/she will do well with SDR.  We see this every week.

Is “spasticity” really that evil?   Talk to the 6 y/o who has mild spasticity so that in walking he has a vaulting or bouncy quality to his walk.  But, he is an independent walker looking a bit like a high school kid who grew real fast and vaults down the hallway at school.  Someone then  thinks ‘we can fix his spastcity!’   So we sign him up for SDR.  Looking back at my office records he seems to have lost the ability to independently ambulate and it has been 2 years post SDR.    Hmmmm.  Spasticity was not really the problem interfering with his independent movements, was it.  So careful in the assessment to determine if spasticity or ‘something else’ is getting in a child’s way.

In the 1940s, 50s, and 60s most central motor disorders of childhood were called ‘spastic’ whether it was clinically factual or not.

Should it be a matter of concern that out of 250 publications reviewed in 2010 that 31% used the Lance definition, 35% used spasticity and increased muscle tone synonymously. While 31% offered no definition at all?   It bothers me if no one else.

We haven’t yet come to terms or agreed on the same definition of Cerebral Palsy, much less “spastic CP”.

‘Spasticity’ referred to the whole motor disorder as a syndrome comprising perceived [muscle] weakness, lack of distal selective motor control, poor motor planning and deformity. The treatment of spasticity then implied the complete management of the motor syndrome.

Spasticity should be a “precise sign” rather than the syndrome of old. Traditional habits die hard in medical arenas that often prevent new ways of understanding nervous system endpoint – motor disorders (or neuromotor) in children; something that I find strange in a disorder of the nervous system and not the muscle; yet we continue to discuss the “motor” the “muscle” as though we are dealing with a muscular disease or disorder.

Maybe, it is just easier to visualize it this way and easier to ‘see’ the musculoskeletal compensations rather than find the primary problems that need to be addressed. Addressed, not a cure for the damage to the brain just yet. Other neural pathways? Sure. Plasticity? Absolutely but not a ‘fix’ or ‘repair’ of the already damaged brain tissue.

Maybe I’m just too picky and don’t think that kids with CP should be random guinea pigs for all of the existing tools that we have in medicine and surgery.

2.  BOTOX:
Its been around so we should be quite good at patient selection and very good at objective selective neuromuscular testing during the procedure.  Yet, all too often the injection is performed by volume injecting with hopes of eventually affecting a targeted nerve ending.   Meanwhile, Botox was wasted and other nerve endings that we did not want to ‘touch’ were also affected.  Hard to measure outcomes that way.

Intramuscular botulinum toxin-A (BoNT-A) injections are used to reduce spasticity in children with cerebral palsy. Clinical studies have documented this, but also indicate variability in outcomes.   There it is again, “spasticity”; a term we still have yet to define in a clinical setting so that we are all talking the same language.

Multiple factors, including injection technique, are responsible for this inconsistency and even more problematic, injecting children thought to be spastic simply due to restricted joint ranges that were often the result of facial limitations of anatomical origin. In the cases of such contracture, any muscle relaxant injected or given by mouth is doomed to fail. Non-contracting, reactive, or contractile muscle tissue, if injected with a neurolytic agent will not have impact on acquiring useful, active range at those joints.

BoNT-A blocks neurotransmission at the neuromuscular junction by inhibiting the release of acetylcholine at the motor endplate (MEP); therefore, the toxin should be administered not only into the correct muscle, but also close to the MEP zone using a ‘nerve finder’ during the procedure.    The MEPs, as an aside, are located within the FASCIA; just in case anyone might wonder if SMPL has any impact or indirect affect on spasticity.

3.  SPML/SPL/Pecutaneous Myofascial Release performed Selectively:   (a “tool”  ; a surgical technique rather than a following or cult)
1. Can SPML be performed on 2 or 3 year old:     Sure.  It can be performed on an infant.  One has to revisit the WHY are you doing this?  WHAT are your goals?  And then, if it appears that the myofascial constraints/contractures/limitations are interfering with that specific child’s active skills then yes, he/she is a candidate.    Going for PROM [passive range of motion] as the goal or end point?  Stop, don’t do it.  You will be disappointment.

2.  Can  SPML help reduce the spasticity or is it the alcohol blocks that do that?

Well yes and yes are the answers.  Some surgeons will combine use of Botox for smaller neuromuscular groups (example upper limb), ethanol (50% EtOH) for lower limbs and Selective surgical release of palpably constraining fascia for both upper and lower limbs where the neurolytic injections alone could not possibly offer benefit.

Don’t confuse SPML as a named technique for the old, common technique of superficial ‘tendon’ release [such as with Ponsetti clubfoot technique].  Not the same and clearly for different reasons.  Interesting enough, there has never been a study showing that the tendons of a CP child become short.  Presumed short by reduced muscle length of limited sarcomeres or by fascial constraint but not within the tendon.  So what does ‘tendon elongation’ offer?  A long tendon with a still shortened muscle excursion or limited sacromere length [i.e. a much weaker muscle that has not been ‘weak’ in the first place?]

EtOH neurolysis does selectively RELIEVE the hyper-reactivity/ spaticity.  The alcohol (ethanol) does not act at the MEP (motor end plate) but does slow the velocity of axonal nerve conduction by denaturing focal points along the peripheral nerve   This procedure must be performed with a “nerve stimulator “ to be of maximum benefit.

Note:  EtOH is not phenol   And phenol is not an alcohol; a common mistake frequently  seen in neurolytic writings.