Members do not see these Ads. Sign Up.

I viewed this video on the redefinition of plantar fasciitis to plantar fasciosis with interest and then alarm. I had no idea that plantar fasciitis/fasciosis was 'caused' by a "piece of dead tissue' in the heel, and that it was all down to the blood supply being shut down by the abductor hallucis. In a related video I was told that fasciosis was the same as gangrene.. how horrid.. I had no idea!
thoughts everyone?
http://www.youtube.com/watch?v=tNPf...il&utm_term=0_88b0f78996-e06ded846f-300038858

 

Seems a popular model nowadays:

Step 1 - Invent a product
Step 2 - Describe why product needed (dubious science not mandatory but encouraged)
Step 3 - Scaremonger public into believing you've described them in step 2, thus having to purchase product described in step 1
Step 4 - Sit back and wait for the big bucks to roll in...

 

What shall we invent Griff?

 

Given that Abductor Hallucis only really tightens at a certain point in the contact phase of gait, and then momentarily (in relation to rest of gait cycle), I guess I am meant to believe that throughout swing phase and initial heel contact it still compresses the circulation (if this is fact) sufficient to starve the tissues of oxygen etc in each case of Plantar Fasciosis.

Maybe a toe springless trainer Simon?

 

Not in a normal foot but in a habituated foot where the adductor and extensor remain activated when at rest it seems quite plausible to me.

Actually I did invent one. I had an orthotist cast a half depth tennis ball and a half depth golf ball and a half depth shooter marble each with a 2 inch space between on each side of a square in a box with a 1/4 inch lip around the edge.
He then filled it with silicone and embedded a stiffener in the surface.
When cured and removed from the mold it makes a convenient training platform. The first metatarsal is placed beside one of the larger bulges and the hallucis is abducted and hooked behind the smaller one ahead of it. With persistence the hallucis is trained to planterflex and use the ground force for the adductor to close the angle.

 

I,m sure that we could all devise some sort of "theory" regarding fasciitis or whatever you wish to call it (does it actually matter?) but there are some statements in this presentataion that are misleading, surely the artery will be the medial plantar by this stage? what is this plantar fascial ligament? If the blood supply was so limited to cause tissue death in the fascia surely this would be more widespread and effect the function of the "villain of the piece" namely the over active abductor hallucis, if this was inadequately perfused then surely its ability to contract and thereby constrict the local perfusion would be reduced? How can the mechanics of the forward windlass be ignored when discussing fasciitis? The proposed elevation of the 1MTPJ is in my mind ill advised, although the mobilisation of the joint and the stretches for the extensors are good (and something that I routinely advise in this condition) Lots of confliction and inaccuracies in anatomy, ignoring the basic mechanaics but a good sales pitch.
If you really want to learn something about fasciopathy (another descriptor!)please see Dr Landorff's recent research as presented at the Liverpool conference.

 

This guy does not know the meaning of 'osis'
basically it means diseased tissue. I could not find any mention of dead tissue

just sounds good and scares his clients.

ischaemic pain hurts= just think about the blood pressure cuff blown up high and left on. it hurts and ceases when the pressure is released.

also when one looks anatomically I cannot see how it would compress these vessels. Evolution would not have let that one continue,

No rain but trying, drought and all the grass is dead, only 25 should be 37+
regards from the south coast.
Paul Conneely
www.musmed.com.au